Language：English   Publishing type：Research paper (scientific journal)  

BACKGROUND: Angiopoietin-like protein 3 (ANGPTL3) regulates lipoprotein metabolism, and its genetic deficiency reduces the risk of atherosclerotic cardiovascular disease. However, the association between ANGPTL3 expression and atherosclerotic plaque formation remains unclear. METHODS: We analyzed 58 patients with coronary artery disease (89 non-culprit lesions) who underwent optical coherence tomography (OCT)-guided percutaneous coronary intervention. ANGPTL3 levels were measured by an enzymatic method (Immuno-Biological Laboratories, Gunma, Japan). Clinical demographics and OCT-derived plaque features were compared among patients stratified according to tertiles of ANGPTL3 levels. RESULTS: The ANGPTL3 level was 356.2 ± 158.9 ng/mL (statin = 98.2%; low-density lipoprotein cholesterol = 74.5 ± 21.7 mg/dL). Patients in tertile 3 of ANGPTL3 level were older (P = 0.025) and had a lower estimated glomerular filtration rate (eGFR; P = 0.010). On OCT imaging, the lipid arc (P = 0.139), fibrous cap thickness (P = 0.826), and other plaque microstructures did not significantly differ among the 3 groups, whereas increased ANGPTL3 levels were associated with a larger calcification arc (P < 0.001) and a longer calcification length (P < 0.001). Multivariate analysis demonstrated that ANGPTL3 (β-coefficient = 0.143, 95% confidence interval [CI] = 0.07-0.21, P < 0.001) and eGFR (β-coefficient = -1.380, 95% CI = -2.53-0.22, P = 0.019) are independent factors affecting the maximum calcification arc. ANGPTL3 (β-coefficient = 0.013, 95% CI = 0.010-0.016, P < 0.001) levels remained independently associated with calcification length. Receiver operating characteristic curve analyses revealed that ANGPTL3 ≥ 410.9 ng/mL (area under the curve = 0.815, 95% CI = 0.718-0.913, P < 0.001) and eGFR ≤ 65.2 mL/min per 1.73 m2 (area under the curve = 0.759, 95% CI = 0.645-0.873, P < 0.001) are the best cutoff values for predicting OCT-derived greater calcification (calcification arc > 87.7° + calcification length > 5.6 mm). The proportion of patients with greater calcification increased with the number of these features (P < 0.001). CONCLUSIONS: ANGPTL3 expression was associated with plaque calcification in patients with coronary artery disease. Further studies are required to confirm ANGPTL3 as a therapeutic target for modulating calcification.

DOI： 10.1016/j.cjco.2025.06.006

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

BACKGROUND: Idiopathic pericarditis generally has a favorable prognosis, but contemporary data on treatment patterns and outcomes remain limited. METHODS AND RESULTS: Using a nationwide Japanese database, we analyzed 8,020 pericarditis patients hospitalized between April 2016 and March 2021, and identified 3,963 (49%) patients with idiopathic pericarditis after excluding those with infectious, autoimmune or other causes. During the study period, the median age increased from 62 to 68 years (Ptrend<0.001), and prescription rates of non-steroidal anti-inflammatory drugs (NSAIDs) and colchicine, and the simultaneous administration of NSAIDs and colchicine increased over time (from 65.9 to 72.6% [P=0.049], from 17.4 to 44.3% [P<0.001], and from 8.0 to 22.7% [P<0.001], respectively). The mean incidence of in-hospital death and rehospitalization for recurrence was 1.4% and 5.7%, respectively; neither changed over time. The mean length of hospitalization increased from 8 to 10 days and the cost of hospitalization increased from JPY 417,000 to JPY 525,000. Multivariable analysis showed that age and steroid use were significant predictors of in-hospital death, whereas cardiac tamponade was not (adjusted odds ratio 1.32; 95% confidence interval 0.56-3.14). CONCLUSIONS: Among hospitalized patients with idiopathic pericarditis, prescription rates of medications recommended by European Society of Cardiology guidelines have increased, although the concurrent use of NSAIDs and colchicine remains uncommon; there have been no changes in the incidence of in-hospital death. Prospective studies, including outpatients, are needed to clarify the prognosis and recurrence rate of idiopathic pericarditis.

DOI： 10.1253/circj.CJ-24-0697

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1093/ejcts/ezaf084

Web of Science

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

With the increasing number of transcatheter aortic valve replacements (TAVR) performed annually, coronary cannulation in post-TAVR patients has gained importance. The aim of this study was to investigate the effectiveness of the en face view for post-TAVR coronary cannulation. Between March 2015 and March 2024, we evaluated coronary cannulation based on the period when the en face view was initiated post-TAVR in December 2021. To assess the impact of the transcatheter heart valve on cannulation success, we excluded patients whose cannulation was conducted outside the stent frame. During the study period, 82 consecutive coronary cannulations were evaluated (en face era/pre-en face era = 47/35). Balloon-expandable valves were used in 48.8% of cases, and cannulation was performed in 31.7% of cases involving acute coronary syndromes. The overall cannulation success rate was 64.6%. Notably, the success rate was significantly higher during the en face era compared to the pre-en face era (78.7% vs. 45.7%, p = 0.003). Cannulation success was more frequently achieved during the en face era in both types of prostheses (self-expandable valve: 83.3% vs. 50.0%, p = 0.049; balloon-expandable valve: 75.9% vs. 36.4%, p = 0.03). Moreover, multivariate analysis identified the en face era as an independent predictor of cannulation success (adjusted odds ratio = 4.57, 95% confidence interval = 1.37-15.30, p = 0.01). The success rate of cannulation was significantly higher during the en face era. This study suggests that the en face view enhances the success rate of coronary cannulation, regardless of the prosthesis type.

DOI： 10.1007/s12928-025-01112-x

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

BACKGROUND AND AIMS: Calcified nodule (CN) is a plaque phenotype characterized by protruding calcification, associated with repeat revascularization after percutaneous coronary intervention (PCI). The severity of calcification increases the risk of future target lesion revascularization (TLR). This study was conducted to determine whether calcification severity in the adjacent zone is associated with TLR. METHODS: We analyzed 204 patients who received PCI for de-novo CN using intravascular ultrasound (IVUS). The calcium volume index (CVI) was calculated for each 1-mm cross-sectional frame in both the CN and adjacent zones. RESULTS: TLR occurred in 63 patients (30.9 %) during a median follow-up period of 2.8 years (interquartile range, 2.4-3.2). CVIs in both the CN and adjacent zones, along with minimum lumen area (MLA) after PCI, were significant predictors of TLR. The ROC curve-derived values for the CVIs in the CN and adjacent zones (10.52 and 5.33, respectively) and the MLA after PCI (6.65 mm2) were associated with higher TLR incidence. Among those requiring TLR, 27.0 % experienced multiple TLRs, with higher CVIs associated with recurrence. In a multi-state model, CVIs in both the CN and adjacent zones were significantly associated with the first TLR (no TLR as reference) and the second TLR (first TLR as reference). The CVI in the adjacent zone showed a higher hazard ratio for the second TLR (1.31; 95 % confidence interval [CI]: 1.16-1.48) compared to the first TLR (1.12; 95 % CI: 1.07-1.17). CONCLUSIONS: Our findings highlight the importance of not only the calcification severity in the CN zone, but also in the adjacent zones, for TLR.

DOI： 10.1016/j.atherosclerosis.2025.119116

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

BACKGROUND: The role of cyclic guanosine 3',5'-monophosphate (cGMP) after acute myocardial infarction (AMI) is not well understood despite its significance as a second messenger of natriuretic peptides (NPs) in cardiovascular disease. We investigated the association between the NP-cGMP cascade and left ventricular reverse remodelling (LVRR) in anterior AMI. METHODS: 67 patients with their first anterior AMI (median age, 64 years; male, 76%) underwent prospective evaluation of plasma concentrations of the molecular forms of A-type and B-type natriuretic peptide (BNP) and cGMP from immediately after primary percutaneous coronary intervention (PPCI) to 10 months post-AMI. The estimated mature BNP (emBNP) concentration was calculated as the difference between total BNP and prohormone of BNP (proBNP) concentrations. Patients were divided into LVRR and non-LVRR groups on the basis of residuals between observed change in left ventricular end-systolic volume index on MR during the first 11 months after AMI and change adjusted for proBNP concentration immediately post-PPCI, which was calculated with regression. The LVRR group (n=33) had residuals below the median; the non-LVRR group (n=34) had residuals at or above the median. RESULTS: The LVRR group had higher freedom from major adverse cardiac and cerebrovascular events (MACCEs) than the non-LVRR group during a median follow-up of 9.9 years (p=0.008). The presence of LVRR (HR 0.256; 95% CI 0.081 to 0.809; p=0.028) and peak creatine phosphokinase-myocardial band level (per 100 IU/L) (HR 1.22; 95% CI 1.02 to 1.46; p=0.027) were independent predictors of MACCE after adjusting for age, male sex, infarct size and hypertension. Multivariable analyses identified logarithmic proBNP and emBNP concentrations from 12 hours to 5 days post-AMI and logarithmic cGMP concentration from immediately post-PPCI to 3 days post-AMI as independent predictors of LVRR (p<0.05). CONCLUSIONS: Early-phase BNP-cGMP cascade activation might play a crucial role in LVRR in anterior AMI.

DOI： 10.1136/openhrt-2024-002927

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

BACKGROUND: The ongoing residual cardiovascular risks despite lowering low-density lipoprotein cholesterol (LDL-C) levels suggest the need to identify additional drivers associated with atherosclerosis. Circulating lipoprotein(a) [Lp(a)]promotes formation of foam cells via its proatherogenic properties. However, whether a lower Lp(a) level in combination with favorable LDL-C control could induce a more stable form of disease remains unknown. Near-infrared spectroscopy (NIRS) generates maximum lipid-core burden index in 4 mm (MaxLCBI4 mm) which is a histologically validated measure of lipidic plaque material in vivo. Therefore, the current study employed NIRS imaging to characterize lipidic plaque in association with LDL-C < 70 mg/dL and Lp(a) <50 mg/dL. METHODS: We analyzed 439 patients with coronary artery disease (CAD) (554 de-novo target lesions receiving percutaneous coronary intervention) in the REASSURE-NIRS registry (NCT04864171). Clinical characteristics and NIRS-derived MaxLCBI4mm were compared among 4 groups according to LDL-C of 70 mg/dL and Lp(a) of 50 mg/dL. RESULTS: Almost one-third of study subjects (33.4%) exhibited both LDL-C < 70 mg/dL and Lp(a) <50 mg/dL. They were more likely male with a lower frequency of acute coronary syndrome and lipid lowering therapies were more frequently used in those with LDL-C < 70 mg/dL and Lp(a) <50 mg/dL. On NIRS imaging analysis, a smaller MaxLCBI4mm (P < .001) and a lower frequency of MaxLCBI4mm ≥400 (P = .001) were observed in those with both LDL-C < 70 mg/dL and Lp(a) <50 mg/dL. On multivariable logistic regression analysis, the coexistence of these 2 lipid controls showed an approximately 70% lower risk (adjusted odds ratio: 0.30; 95% confidence interval: 0.13-0.68) of MaxLCBI4mm ≥400 compared with the reference group (LDL-C ≥ 70 mg/dL and Lp(a) ≥50 mg/dL). CONCLUSION: Our findings suggest circulating Lp(a) as a potential therapeutic target to stabilize coronary atherosclerosis in CAD patients who achieved LDL-C < 70 mg/dL.

DOI： 10.1016/j.jacl.2024.12.019

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

BACKGROUND: Type 2 diabetic patients exhibited an increased secretion of triglyceride-rich lipoproteins and low high-density lipoprotein cholesterol levels with a greater amount of small dense low-density lipoprotein (LDL). Given that apolipoprotein B (apoB), a proatherogenic lipoprotein, exists at both triglyceride-rich lipoproteins and LDL particles, circulating apoB may associate with diabetic coronary atherosclerosis. METHODS: The OPTIMAL study was a prospective randomized-controlled study which employed serial near-infrared spectroscopy (NIRS)/intravascular ultrasound (IVUS) imaging to evaluate the efficacy of glycemic control on coronary atherosclerosis in 94 statin-treated type 2 diabetic patients with coronary artery disease (CAD) (UMIN000036721). Of these, 78 patients with both serial apoB levels and NIRS/IVUS images at baseline and week 48 were analyzed. NIRS/IVUS-derived plaque measures were compared in those with and without any reduction of apoB levels. RESULTS: All of the study subjects received a statin, and 60.6% of the study subjects exhibited any reduction of apoB levels. There was no significant difference in the atheroma progression rate between the 2 groups (-0.27 ± 0.15% vs -0.33 ± 0.51%, P = .44). However, patients with any reduction of apoB levels exhibited a greater frequency of change in maximal lipid-core burden index at 4-mm segment (maxLCBI4mm) (-13.4 ± 22.2% vs 70.3 ± 28.7%, P = .03) and maxLCBI4mm regression (61.1 ± 0.08% vs 31.0 ± 0.09%, p = .02). Multivariate analysis demonstrated change in apoB as an independent factor associated with maxLCBI4mm regression (odds ratio = 0.92, 95% CI = 0.87-0.98, P = .01). CONCLUSIONS: In statin-treated type 2 diabetic patients with CAD, a greater delipidation of coronary atherosclerosis was observed in association with a reduction of apoB levels. The current findings indicate a potential anti-atherosclerotic effect of lowering apoB levels, which may ultimately mitigate future coronary events risk in statin-treated type 2 diabetic patients with CAD.

DOI： 10.1016/j.jacl.2025.04.204

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

BACKGROUND: The Society of Cardiovascular Angiography and Intervention (SCAI) has defined 5 stages of cardiogenic shock (CS). In patients with acute myocardial infarction (AMI) who initially present in stable hemodynamic condition (SCAI CS stage: A or B), CS stages could deteriorate despite therapeutic management. However, deterioration of SCAI CS stages after AMI remains to be fully characterized. Therefore, the current study sought to investigate the frequency and clinical characteristics about deterioration of SCAI CS stages after AMI. METHODS: We retrospectively analyzed 347 patients in a derivation cohort and 163 patients in a validation cohort who had AMI (SCAI shock stage upon arrival: A/B) and underwent percutaneous coronary intervention (PCI) at National Cerebral and Cardiovascular Center, Suita, Japan (enrolment period of study subjects: 2019.07.01-2022.09.30). Deterioration of CS (D-CS) was defined as SCAI shock stage C-E after PCI. Clinical characteristics and in-hospital mortality were compared according to D-CS status. Adjusted hazard ratios (HRs) for in-hospital mortality were calculated with multivariate Cox proportional hazards models that included variables with P<0.10 in univariate models. Uni- and multivariate logistic regression analyses were used to identify predictors of D-CS. RESULTS: D-CS occurred in 17.3% (60/347) of the derivation cohort. Patients with D-CS had lower systolic blood pressure (BP) (P<0.001) and left ventricular ejection fraction (LVEF) (P<0.001) upon arrival with a higher proportion of initial Thrombolysis in Myocardial Infarction (TIMI) grade flow 0 or 1 (P=0.002). During hospitalization (13.9±9.4 days), D-CS was associated with higher in-hospital mortality [adjusted HR, 12.95; 95% confidence interval (CI): 1.46-114.97; P=0.02]. Initial systolic BP, LVEF, and TIMI grade flow 0 or 1 independently predicted D-CS. The D-CS risk score including these variables satisfactorily predicted D-CS [area under the curve (AUC), 0.749; 95% CI: 0.651-0.848] and in-hospital mortality (AUC, 0.961; 95% CI: 0.914-1.000) in the validation cohort. CONCLUSIONS: D-CS occurred in 17.3% of patients with AMI initially presenting in stable condition and increased the risk of in-hospital mortality. Our D-CS risk score (initial systolic BP, LVEF, and TIMI grade flow) could be helpful to predict D-CS.

DOI： 10.21037/cdt-24-226

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

BACKGROUND: Acute autoimmune pericarditis (AAP) is an uncommon disease with diverse etiology. Data regarding AAP diagnosis and outcomes are scant. OBJECTIVES: This study sought to describe the diagnosis and the rates of in-hospital mortality, cardiac tamponade, and readmission of AAP. METHODS: This study used a nationwide Japanese claim-based database to identify patients with AAP from April 2016 to March 2020 compared with patients with acute idiopathic pericarditis (AIP). RESULTS: Of 20,469 hospitalized patients with acute pericarditis, 170 had AAP and 5,027 had AIP of new onset. The diagnosis for AAP was systemic lupus erythematosus in 23.5% (40 of 170), rheumatoid arthritis in 19.4% (33 of 170), systemic sclerosis in 8.2% (14 of 170), other in 17.7% (30 of 170), and undifferentiated in 31.2% (53 of 170). During hospitalization, 1.8% (3 of 170) of patients with AAP and 1.5% (73 of 5,027) of patients with AIP died, and cardiac tamponade occurred in 8.8% (15 of 170) of AAP patients and 4.7% (237 of 5,027) of AIP patients. The incidence of cardiac tamponade was highest in patients with systemic lupus erythematosus (15.0%; 6 of 40). AAP was more associated with cardiac tamponade than AIP (adjusted OR: 1.82; 95% CI: 1.02-3.23). There was no difference between the AAP and AIP groups with regard to rehospitalization, although this was more common in patients with undifferentiated forms of autoimmune disease (P = 0.001). CONCLUSIONS: This Japanese national registry study of acute pericarditis revealed no differences in rehospitalization for recurrence between patients with AAP and AIP. It also underscored the diversity in AAP diagnosis, with more than 30% of patients lacking a differentiated diagnosis.

DOI： 10.1016/j.jacasi.2024.06.008

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

BACKGROUND: Left ventricular (LV) thrombus is not common but poses significant risks of embolic stroke or systemic embolism. However, the distinction in embolic risk between nonischemic cardiomyopathy (NICM) and ischemic cardiomyopathy (ICM) remains unclear. METHODS AND RESULTS: In total, 2738 LV thrombus patients from the JROAD-DPC (Japanese Registry of All Cardiac and Vascular Diseases Diagnosis Procedure Combination) database were included. Among these patients, 1037 patients were analyzed, with 826 (79.7%) having ICM and 211 with NICM (20.3%). Within the NICM group, the distribution was as follows: dilated cardiomyopathy (DCM; 41.2%), takotsubo cardiomyopathy (27.0%), hypertrophic cardiomyopathy (18.0%), and other causes (13.8%). The primary outcome was a composite of embolic stroke or systemic embolism (SSE) during hospitalization. The ICM and NICM groups showed no significant difference in the primary outcome (5.8% vs. 7.6%, p = 0.34). Among NICM, SSE occurred in 12.6% of patients with DCM, 7.0% with takotsubo cardiomyopathy, and 2.6% with hypertrophic cardiomyopathy. Multivariate logistic regression analysis for SSE revealed an odds ratio of 1.4 (95% confidence interval [CI], 0.7-2.7, p = 0.37) for NICM compared to ICM. However, DCM exhibited a higher adjusted odds ratio for SSE compared to ICM (2.6, 95% CI 1.2-6.0, p = 0.022). CONCLUSIONS: This nationwide shows comparable rates of embolic events between ICM and NICM in LV thrombus patients, with DCM posing a greater risk of SSE than ICM. The findings emphasize the importance of assessing the specific cause of heart disease in NICM, within LV thrombus management strategies.

DOI： 10.1016/j.ijcard.2024.132329

PubMed

researchmap

Language：Japanese   Publisher：(一社)日本集中治療医学会  

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

Background: Cardiovascular events still occur at intermediate stenosis with fractional flow reserve (FFR) ≥0.81, underscoring the additional measure to evaluate this residual risk. A reduction in distal coronary artery pressure/aortic pressure from baseline to hyperemia (i.e., change in Pd/Pa) reflects lipidic burden within vessel walls. We hypothesized that this physiological measure might stratify the risk of future cardiac events at deferrable lesions. Methods: Lesion- (899 intermediate lesions) and patient-based (899 deferred patients) analyses in those with FFR ≥0.81 were conducted to investigate the association between change in Pd/Pa and target lesion failure (TLF) and major adverse cardiac events (MACE) at 7 years, respectively. Results: The occurrence of TLF and MACE was 6.7% and 13.4%, respectively. The incidence of target lesion-related non-fatal myocardial infarction was 0.6%. Lesions with TLF had greater change in Pd/Pa (0.11±0.03 vs. 0.09±0.04; P=0.002), larger diameter stenosis (51.0±9.2% vs. 46.4±12.4%; P=0.048), and smaller FFR (0.84 (0.82-0.87) vs. 0.86 (0.83-0.90); P=0.02). Change in Pd/Pa (per 0.01 increase) predicted TLF (odds ratio, 1.16; 95% confidence interval (CI), 1.05-1.28; P=0.002) and MACE (odds ratio, 1.08; 95% CI, 1.01-1.16; P=0.03). Lesions with change in Pd/Pa ≥0.10 had 2.94- and 1.85-fold greater likelihood of TLF (95% CI, 1.30-6.69; P=0.01) and MACE (95% CI, 1.08-3.17; P=0.03), respectively. Lesions with FFR ≤0.85 had substantially higher likelihood of TLF when change in Pd/Pa ≥0.10 (12.4% vs. 2.9%; hazard ratio, 3.60, 95% CI, 1.01-12.80; P=0.04). However, change in Pd/Pa did not affect TLF risk in lesions with FFR ≥0.86 (3.8% vs. 3.7%; hazard ratio, 0.56; 95% CI, 0.06-5.62; P=0.62). Conclusions: Despite deferrable FFR values, lesions and patients with change in Pd/Pa ≥0.10 had higher cardiovascular risk. Change in Pd/Pa might help stratify lesion- and patient-level risk of future cardiac events in those with FFR ≥0.81.

DOI： 10.1161/CIRCINTERVENTIONS.124.013830

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

BACKGROUND AND AIMS: Randomized clinical trials have demonstrated the ability of glucagon-like peptide-1 analogues (GLP-1RAs) to reduce atherosclerotic cardiovascular disease events in patients with type 2 diabetes (T2D). How GLP-1RAs modulate diabetic atherosclerosis remains to be determined yet. METHODS: The OPTIMAL study was a prospective randomized controlled study to compare the efficacy of 48-week continuous glucose monitoring- and HbA1c-guided glycemic control on near infrared spectroscopty (NIRS)/intravascular ultrasound (IVUS)-derived plaque measures in 94 statin-treated patients with T2D (jRCT1052180152, UMIN000036721). Of these, 78 patients with evaluable serial NIRS/IVUS images were analyzed to compare plaque measures between those treated with (n = 16) and without GLP-1RAs (n = 72). RESULTS: All patients received a statin, and on-treatment LDL-C levels were similar between the groups (66.9 ± 11.6 vs. 68.1 ± 23.2 mg/dL, p = 0.84). Patients receiving GLP-1RAs demonstrated a greater reduction of HbA1c [-1.0 (-1.4 to -0.5) vs. -0.4 (-0.6 to -0.2)%, p = 0.02] and were less likely to demonstrate a glucose level >180 mg/dL [-7.5 (-14.9 to -0.1) vs. 1.1 (-2.0 - 4.2)%, p = 0.04], accompanied by a significant decrease in remnant cholesterol levels [-3.8 (-6.3 to -1.3) vs. -0.1 (-0.8 - 1.1)mg/dL, p = 0.008]. On NIRS/IVUS imaging analysis, the change in percent atheroma volume did not differ between the groups (-0.9 ± 0.25 vs. -0.2 ± 0.2%, p = 0.23). However, GLP-1RA treated patients demonstrated a greater frequency of maxLCBI4mm regression (85.6 ± 0.1 vs. 42.0 ± 0.6%, p = 0.01). Multivariate analysis demonstrated that the GLP-1RA use was independently associated with maxLCBI4mm regression (odds ratio = 4.41, 95%CI = 1.19-16.30, p = 0.02). CONCLUSIONS: In statin-treated patients with T2D and CAD, GLP-1RAs produced favourable changes in lipidic plaque materials, consistent with its stabilization.

DOI： 10.1016/j.athplu.2024.03.001

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

INTRODUCTION: Cerebral microbleeds (CMBs) on brain magnetic resonance imaging (MRI) are predictive of intracerebral hemorrhage (ICH). However, the risk of ICH in patients with CMBs who undergo percutaneous coronary intervention (PCI) while receiving dual antiplatelet therapy (DAPT) is unclear. MATERIALS AND METHODS: We conducted a study on 329 consecutive patients with coronary artery disease who underwent PCI and were evaluated using a 3T MRI scanner. Based on T2*-weighted imaging, patients were classified into three groups: no CMBs, < 5 CMBs, or ≥ 5 CMBs. We determined the occurrence of ICH during follow-up. RESULTS: At least 1 CMB was found in 109 (33%) patients. The mean number of CMBs per patient was 2.9 ± 3.6. Among the 109 patients with CMBs, 16 (15%) had ≥ 5 CMBs. Coronary stent implantation was performed in 321 patients (98%). DAPT was prescribed for 325 patients (99%). During a mean follow-up period of 2.3 years (interquartile range, 1.9-2.5 years), ICH occurred in one patient (1.1%) with four CMBs. There were no significant differences in the incidence of ICH (0% vs. 1.1% vs. 0%; p = 0.28). However, the rate of DAPT at 6 months of follow-up was significantly lower in patients with ≥ 5 CMBs than in patients with no CMBs or < 5 CMBs (89% vs. 91% vs. 66%, p = 0.026). Furthermore, there were no significant differences in systemic blood pressure during follow-up (123 ± 16 vs. 125 ± 16 vs. 118 ± 11 mmHg; p = 0.40). CONCLUSION: Although a substantial number of patients who underwent PCI had cerebral microbleeds, at approximately two years of follow-up, intracerebral hemorrhage was very rare in our study population.

DOI： 10.1007/s00380-024-02404-7

PubMed

researchmap

Language：English   Publisher：(一社)日本循環器学会  

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

Objective Earlobe crease (ELC) is an easily detectable physical sign of cardiovascular risk and coronary artery disease (CAD). However, the relationship between ELC and CAD severity in patients with ST-segment elevation myocardial infarction (STEMI) requiring urgent clinical judgment is unknown. Using the residual synergy between percutaneous coronary intervention with taxus and cardiac surgery (SYNTAX) score, we investigated the relationship between ELC and anatomical severity of CAD. Methods, patients or materials We studied 219 consecutive patients with STEMI (median age, 71 years old) and divided them into 2 groups according to the presence of ELC (ELC group, n=161; non-ELC group, n=58). Results The ELC group had a significantly higher number of diseased vessels than the non-ELC group (≥2 diseased vessels, 79% vs. 46%; ≥3 diseased vessels, 35% vs. 12%; P<0.001). In addition, a higher median residual SYNTAX score was observed after primary percutaneous coronary intervention than the non-ELC group [8 (4-12) vs. 3 (0-8), P<0.001]. Furthermore, a multivariable regression analysis showed that ELC was an independent predictor of the residual SYNTAX score (β=3.620, P<0.001). Conclusions The presence of ELC was significantly associated with the anatomical severity of diseased coronary vessels in patients with STEMI who required emergency clinical judgment and treatment.

DOI： 10.2169/internalmedicine.2997-23

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

AIM: Omega-3 fatty acids have emerged as a new option for controlling the residual risk for coronary artery disease (CAD) in the statin era. Eicosapentaenoic acid (EPA) is associated with reduced CAD risk in the Reduction of Cardiovascular Events with Icosapent Ethyl-Intervention trial, whereas the Statin Residual Risk with Epanova in High Cardiovascular Risk Patients with Hypertriglyceridemia trial that used the combination EPA/docosahexaenoic acid (DHA) has failed to derive any clinical benefit. These contradictory results raise important questions about whether investigating the antiatherosclerotic effect of omega-3 fatty acids could help to understand their significance for CAD-risk reduction. METHODS: The Attempts at Plaque Vulnerability Quantification with Magnetic Resonance Imaging Using Noncontrast T1-weighted Technic EPA/DHA study is a single-center, triple-arm, randomized, controlled, open-label trial used to investigate the effect of EPA/DHA on high-risk coronary plaques after 12 months of treatment, detected using cardiac magnetic resonance (CMR) in patients with CAD receiving statin therapy. Eligible patients were randomly assigned to no-treatment, 2-g/day, and 4-g/day EPA/DHA groups. The primary endpoint was the change in the plaque-to-myocardium signal intensity ratio (PMR) of coronary high-intensity plaques detected by CMR. Coronary plaque assessment using computed tomography angiography (CTA) was also investigated. RESULTS: Overall, 84 patients (mean age: 68.2 years, male: 85%) who achieved low-density lipoprotein cholesterol levels of ＜100 mg/dL were enrolled. The PMR was reduced in each group over 12 months. There were no significant differences in PMR changes among the three groups in the primary analysis or analysis including total lesions. The changes in CTA parameters, including indexes for detecting high-risk features, also did not differ. CONCLUSION: The EPA/DHA therapy of 2 or 4 g/day did not significantly improve the high-risk features of coronary atherosclerotic plaques evaluated using CMR under statin therapy.

DOI： 10.5551/jat.64063

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

BACKGROUND: While internal mammary artery (IMA) has become a major conduit of coronary artery bypass graft (CABG) surgery, subclavian artery stenosis (SAS) could cause subsequent coronary events due to ischemia of myocardial territory supplied by IMA. Clinical characteristics and cardiovascular outcomes of SAS-related IMA failure (SAS-IMAF) remain to be fully determined yet. Therefore, the current study was designed to characterize SAS-IMAF in patients receiving CABG with IMA. METHODS: This is a retrospective observational study which analyzed 380 patients who presented acute coronary syndrome/stable ischemic heart disease (ACS/SIHD) after CABG using IMA (2005.01.01-2020.10.31). SAS-IMAF was defined as the presence of myocardial ischemia/necrosis caused by SAS. Clinical characteristics and cardiovascular outcomes [major adverse cardiovascular events (MACE) = cardiac death + non-fatal myocardial infarction + non-fatal ischemic stroke], were compared in subjects with and without SAS-IMAF. Multivariate Cox proportional hazards model and propensity score-matched analyses were used to compare cardiovascular outcomes between those with and without SAS-IMAF. RESULTS: SAS-IMAF was identified in 5.5% (21/380) of study subjects. Patients with SAS-IMAF are more likely had a history of hemodialysis (P<0.001), stroke (P<0.001) and lower extremity artery disease (P<0.001). Furthermore, SAS-IMAF patients more frequently presented ACS (P=0.002) and required mechanical support (P=0.02). Despite SAS as a culprit lesion causing ACS/SIHD, percutaneous coronary intervention was firstly selected in 47.6% (10/21) of them. Consequently, 33.3% (7/21) of SAS-IMAF patients required additional revascularization procedure (vs. 0.3%, P<0.001). During 4.9-year observational period, SAS-IMAF exhibited a 5.82-fold [95% confidence interval (CI): 2.31-14.65, P<0.001] increased risk of MACE. Multivariate Cox proportional hazards model [hazard ratio (HR) 4.04, 95% CI: 1.44-11.38, P=0.008] and propensity score-matched analyses (HR 2.67, 95% CI: 1.06-6.73, P=0.038) consistently demonstrated the association of SAS-IMAF with MACE. CONCLUSIONS: SAS-IMAF reflects a high-risk phenotype of polyvascular disease, underscoring meticulous evaluation of subclavian artery after CABG using IMA.

DOI： 10.21037/cdt-23-211

PubMed

researchmap

Language：English  

BACKGROUND: Non-contrast T1-weighted imaging (T1WI) with cardiac magnetic resonance enables to evaluate the intensity of coronary plaque. Plaque-to-myocardial signal intensity ratio (PMR) has been shown to associate with an elevated risk of future coronary events. Of note, PMR >1.4 is a best cut-off value to identify high-risk plaque causing future coronary events. One recent study has reported intraluminal thrombus as a contributor to PMR. However, whether plaque material itself is associated with PMR has not been fully characterized yet. We present three cases with coronary artery stenosis evaluated by non-contrast T1WI-magnetic resonance imaging, optical coherence tomography (OCT) and near-infrared spectroscopy (NIRS)-intravascular ultrasound (IVUS) imaging. CASE DESCRIPTION: Case 1 exhibited one lesion with high PMR (2.79) at the proximal segment of left anterior descending (LAD) artery. OCT imaging did not identify any obvious intra-luminal thrombus but the presence of lipid-rich plaque harboring cholesterol crystal at the corresponding lesion. In addition, an elevated maximum 4-mm lipid-core burden index (maxLCBI4mm) (=873) was observed at this lesion by NIRS/IVUS imaging. In case 2, PMR of coronary stenosis at the middle segment of LAD artery was 1.88. This lesion harboured lipidic materials without any thrombus on OCT imaging. NIRS-derived maxLCBI4mm was 725. Case 3 had a severe stenosis at the middle segment of LAD artery. This lesion exhibited a low PMR (0.90). On OCT and NIRS/IVUS imaging, this lesion was characterized as the presence of small lipid arc with a low maxLCBI4mm (=386). CONCLUSIONS: These cases showed the possible relationship of T1WI-derived PMR with the degree of lipidic plaque components.

DOI： 10.21037/cdt-23-125

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

BACKGROUND: Continuous glucose monitoring (CGM) improves glycemic fluctuation and reduces hypoglycemic risk. Whether CGM-guided glycemic control favorably modulates coronary atherosclerosis in patients with type 2 diabetes (T2DM) remains unknown. METHODS: The OPTIMAL trial was a prospective, randomized, single-center trial in which 94 T2DM patients with CAD were randomized to CGM- or HbA1c-guided glycemic control for 48 weeks (jRCT1052180152). The primary endpoint was the nominal change in total atheroma volume (TAV) measured by serial IVUS. The secondary efficacy measure was the nominal change in maxLCBI4mm on near-infrared spectroscopy imaging. RESULTS: Among the 94 randomized patients, 82 had evaluable images at 48 weeks. Compared to HbA1c-guided glycemic control, CGM-guided control achieved a greater reduction in %coefficient of variation [-0.1 % (-1.8 to 1.6) vs. -3.3 % (-5.1 to -1.5), p = 0.01] and a greater increase in the duration with glucose between 70 and 180 mg/dL [-1.5 % (-6.0 to 2.9) vs. 6.7 % (1.9 to 11.5), p = 0.02]. TAV increased by 0.11 ± 1.9 mm3 in the HbA1c-guided group and decreased by -3.29 ± 2.00 mm3 in the CGM-guided group [difference = -3.4 mm3 (95%CI: -8.9 to 2.0 mm3), p = 0.22]. MaxLCBI4mm, increased by 90.1 ± 25.6 in the HbA1c-guided group and by 50.6 ± 25.6 in the CGM-guided group (difference = -45.6 (95%CI: -118.1 to 26.7) p = 0.21]. A post-hoc exploratory analysis showed a greater regression of maxLCBI4mm in the CGM-guided group [difference = 20.4 % (95%CI:1.3 to 39.5 %), p = 0.03]. CONCLUSIONS: CGM-guided control for 48 weeks did not slow disease progression in T2DM patients with CAD. A greater regression of lipidic plaque under CGM-guided glycemic control in the post-hoc analysis requires further investigation.

DOI： 10.1016/j.jdiacomp.2023.108592

PubMed

researchmap

Language：English   Publisher：(一社)日本心血管インターベンション治療学会  

researchmap

Language：English   Publisher：(一社)日本心血管インターベンション治療学会  

researchmap

Language：English   Publisher：(一社)日本心血管インターベンション治療学会  

researchmap

Language：English   Publisher：(一社)日本心血管インターベンション治療学会  

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

Nitroglycerin dilates the radial artery and prevents spasm, which increases the success rate of sheath cannulation through the conventional transradial approach. However, the effects of nitroglycerin on distal radial approach (DRA) procedures are not known. The aim of this study is to elucidate whether a transdermal nitroglycerin patch improves the rate of successful DRA cannulation. A total of 92 patients scheduled for coronary angiography by means of DRA randomly received (1:1) a transdermal nitroglycerin patch preintegrated with the covering material or only the covering material on their upper arm on the side of the puncture. The diameter of the distal radial artery was evaluated with ultrasound at baseline and after application. DRA procedures were performed in a double-blind fashion. The primary outcome was the rate of successful palpation-guided distal radial artery cannulation with the first puncture. The nitroglycerin group had larger distal radial artery diameter after patch application than that of the no-treatment group (mean, 3.21 mm vs 2.71 mm, p <0.001), but not at baseline (mean, 2.64 mm vs 2.64 mm, p = 0.965).The nitroglycerin group had a significantly higher success rate of DRA cannulation with the first puncture than that of the no-treatment group (59% vs 24%, p = 0.001; odds ratio 4.5, 95% confidence interval 1.9 to 11.0). The nitroglycerin group required fewer punctures than did the no-treatment group (median, 1 vs 3, p = 0.019). There were no significant differences in the occurrence of hypotension between the 2 groups. No patients experienced radial artery occlusion. In conclusion, transdermal nitroglycerin patch application safely facilitates DRA cannulation. Trial Registration: Japan Registry of Clinical Trials, https://jrct.niph.go.jp/ (identifier: jRCTs051210128).

DOI： 10.1016/j.amjcard.2023.07.068

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

Inflammation has been considered to promote atheroma instability. Coronary computed tomography angiography (CCTA) visualizes pericoronary adipose tissue (PCAT) attenuation, which reflects coronary artery inflammation. While PCAT attenuation has been reported to predict future coronary events, plaque phenotypes exhibiting high PCAT attenuation remains to be fully elucidated. The current study aims to characterize coronary atheroma with a greater vascular inflammation. We retrospectively analyzed culprit lesions in 69 CAD patients receiving PCI from the REASSURE-NIRS registry (NCT04864171). Culprit lesions were evaluated by both CCTA and near-infrared spectroscopy/intravascular ultrasound (NIRS/IVUS) imaging prior to PCI. PCAT attenuation at proximal RCA (PCATRCA) and NIRS/IVUS-derived plaque measures were compared in patients with PCATRCA attenuation ≥ and < -78.3 HU (median). Lesions with PCATRCA attenuation ≥ -78.3 HU exhibited a greater frequency of maxLCBI4mm ≥ 400 (66% vs. 26%, p < 0.01), plaque burden ≥ 70% (94% vs. 74%, p = 0.02) and spotty calcification (49% vs. 6%, p < 0.01). Whereas positive remodeling (63% vs. 41%, p = 0.07) did not differ between two groups. On multivariable analysis, maxLCBI4mm ≥ 400 (OR = 4.07; 95%CI 1.12-14.74, p = 0.03), plaque burden ≥ 70% (OR = 7.87; 95%CI 1.01-61.26, p = 0.04), and spotty calcification (OR = 14.33; 95%CI 2.37-86.73, p < 0.01) independently predicted high PCATRCA attenuation. Of note, while the presence of only one plaque feature did not necessarily elevate PCATRCA attenuation (p = 0.22), lesions harboring two or more features were significantly associated with higher PCATRCA attenuation. More vulnerable plaque phenotypes were observed in patients with high PCATRCA attenuation. Our findings suggest PCATRCA attenuation as the presence of profound disease substrate, which potentially benefits from anti-inflammatory agents.

DOI： 10.1007/s10554-023-02907-w

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

Calcified atheroma has been viewed conventionally as stable lesion which less likely increases no-reflow phenomenon. Given that lipidic materials triggers the formation of calcification, lipidic materials could exist within calcified lesion, which may cause no-reflow phenomenon after PCI. The REASSURE-NIRS registry (NCT04864171) employed near-infrared spectroscopy and intravascular ultrasound imaging to evaluate maximum 4-mm lipid-core burden index (maxLCBI4mm) at target lesions containing small (maximum calcification arc < 180°: n = 272) and large calcification (maximum calcification arc ≥ 180°: n = 189) in stable CAD patients. The associations of maxLCBI4mm with corrected TIMI frame count (CTFC) and no-reflow phenomenon after PCI were analyzed in patients with target lesions containing small and large calcification, respectively. No-reflow phenomenon occurred in 8.0% of study population. Receiver-operating characteristics curve analyses revealed that optimal cut-off values of maxLCBI4mm for predicting no-reflow phenomenon were 585 at small calcification (AUC = 0.72, p < 0.001) and 679 at large calcification (AUC = 0.76, p = 0.001). Target lesions containing small calcification with maxLCBI4mm ≥ 585 more likely exhibited a greater CTFC (p < 0.001). In those with large calcification, 55.6% of them had maxLCBI4mm ≥ 400 [vs. 56.2% (small calcification), p = 0.82]. Furthermore, a higher CTFC (p < 0.001) was observed in association with maxLCBI4mm ≥ 679 at large calcification. On multivariable analysis, maxLCBI4mm at large calcification still independently predicted no-reflow phenomenon (OR = 1.60, 95%CI = 1.32-1.94, p < 0.001). MaxLCBI4mm at target lesions exhibiting large calcification elevated a risk of no-reflow phenomenon after PCI. Calcified plaque containing lipidic materials is not necessarily stable lesion, but could be active and high-risk one causing no-reflow phenomenon.

DOI： 10.1007/s10554-023-02905-y

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

The feasibility of rotational atherectomy (RA) during percutaneous coronary intervention (PCI) in patients who present with acute coronary syndrome (ACS) remains fully unsettled. We retrospectively evaluated 198 consecutive patients who underwent RA during PCI from 2009 to 2020. All patients underwent intracoronary imaging (intravascular ultrasound 96.5%, optical coherence tomography 9.1%, both 5.6%) during PCI. Patients who underwent RA during PCI were divided into two groups: ACS (n = 49; unstable angina pectoris, n = 27; non-ST-elevation myocardial infarction, n = 18, and ST-elevation myocardial infarction, n = 4) and chronic coronary syndrome (CCS) (n = 149). The RA procedural success rate was comparable between in the ACS and CCS groups (93.9 vs. 89.9%, P = 0.41). No significant differences were observed in procedural complications and in-hospital death between the groups. The incidence of major adverse cardiovascular event (MACE) after 2 years was significantly higher in ACS group compared with CCS group (38.7 vs. 17.4%, log-rank P = 0.002). Multivariable Cox regression analysis identified SYNTAX score or CABG SYNTAX score > 22 (hazard ratio (HR) 2.66, 95% confidence interval (CI) 1.40-5.06, P = 0.002) and mechanical circulatory support during the procedure (HR 2.61, 95% CI 1.21-5.59, P = 0.013) as predictors of MACE at 2 years, but not ACS on index admission (HR 1.58, 95% CI 0.84-2.99, P = 0.151). RA procedure is feasible as a bail-out strategy for ACS lesions. However, more complexed coronary atherosclerosis and mechanical circulatory support during RA procedure, but no ACS lesions were associated with worse mid-term clinical outcomes.

DOI： 10.1007/s00380-023-02272-7

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

BACKGROUND: Current guidelines recommend prophylactic defibrillator implantation in patients with acute myocardial infarction (AMI) and left ventricular ejection fraction (LVEF) ≤40% or LVEF ≤35% plus heart failure symptoms or inducible ventricular tachyarrhythmias during an electrophysiology study at 40 days after AMI or 90 days after revascularization. In-hospital predictors of sudden cardiac death (SCD) after AMI during the index hospitalization remain unsettled. We sought to examine in-hospital predictors of SCD in patients with AMI and LVEF ≤40% evaluated during the index hospitalization. METHODS: We retrospectively evaluated 441 consecutive patients with AMI and LVEF ≤40% admitted to our hospital between 2001 and 2014 (77% male gender; median age: 70 years; median hospitalization length: 23 days). The primary endpoint was a composite of SCD or aborted SCD at ≥30 days after AMI onset (composite arrhythmic event). LVEF and QRS duration (QRSd) on electrocardiography were measured at a median of 12 days and 18 days, respectively. RESULTS: During a median follow-up of 7.6 years, the incidence of composite arrhythmic events was 7.3% (32 of 441 patients). In multivariable analysis, QRSd ≥100 msec (beta-coefficient=1.54, p=0.003), LVEF ≤23% (beta-coefficient=1.14, p=0.007), and onset-reperfusion time >5.5 hours (beta-coefficient=1.16, p=0.035) were independent predictors of composite arrhythmic events. The combination of these 3 factors was associated with the highest rate of composite arrhythmic events compared with 0-2 factors (p<0.001). CONCLUSIONS: The combination of QRSd ≥100 msec, LVEF ≤23%, and onset-reperfusion time >5.5 hours during the index hospitalization provides precise risk stratification for SCD in patients early after AMI.

DOI： 10.1016/j.jjcc.2023.05.003

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

BACKGROUND: Intravascular imaging has shown better response of coronary atheroma to statin-mediated lowering of low-density lipoprotein cholesterol in women. However, its detailed mechanism remains to be determined yet. Modifiability of coronary atheroma under lipid-lowering therapies is partly driven by lipidic plaque component. Given a smaller plaque volume in women, lipidic plaque features including their density may differ between sex. Therefore, the current study sought to characterize sex-related differences in the density of lipidic plaque. METHODS: We analyzed 1429 coronary lesions (culprit/nonculprit lesions=825/604) in 758 coronary artery disease patients (men/women=608/150) from the REASSURE-NIRS multicenter registry (Revelation of Pathophysiological Phenotypes of Vulnerable Lipid-Rich Plaque on Near-Infrared Spectroscopy). Total atheroma volume at 4-mm segment, maximum 4-mm-lipid-core burden index, and lipid plaque density index (=maximum 4-mm-lipid-core burden index/total atheroma volume at 4-mm segment) on near-infrared spectroscopy/intravascular ultrasound imaging at culprit and nonculprit lesions were compared in men and women. RESULTS: Statin and high-intensity statin were used in 72.4 (P=0.81) and 22.9% (P=0.32) of study subjects, respectively. Women exhibited a smaller adjusted total atheroma volume at 4-mm segment (culprit lesions: 50.3±0.4 versus 54.2±0.3mm3, P<0.001, nonculprit lesions: 31.5±3.0 versus 44.4±2.1mm3, P<0.001), whereas their adjusted maximum 4-mm-lipid-core burden index did not differ between sex (culprit lesions: 544.7±29.9 versus 501.7±19.1, P=0.11, nonculprit lesions: 288.8±26.7 versus 272.7±18.9, P=0.51). Furthermore, a greater adjusted lipid plaque density index was observed in women (culprit lesions: 18.2±0.9 versus 9.8±0.6, P<0.001, nonculprit lesions: 23.0±2.0 versus 7.8±1.4, P<0.001). These adjustments of total atheroma volume at 4-mm segment, maximum 4-mm-lipid-core burden index, and lipid plaque density index included age, body mass index, hypertension, dyslipidemia, diabetes, smoking, a history of myocardial infarction and chronic kidney disease, low-density lipoprotein cholesterol level, statin and ezetimibe use, vessel volume, and hospital unit. The aforementioned plaque features consistently existed in both acute coronary syndrome and stable coronary artery disease subjects. CONCLUSIONS: Women harbored greater condensed lipidic plaque features, accompanied by smaller atheroma volume. These observations indicate potentially better modifiable disease in women, which underscores the need to intensify their lipid-lowering therapies for further improving their outcomes. REGISTRATION: URL: https://www. CLINICALTRIALS: gov/; Unique identifier: NCT04864171.

DOI： 10.1161/CIRCIMAGING.122.015107

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

BACKGROUND: Acute pericarditis occasionally requires invasive treatment, and may recur after discharge. However, there are no studies on acute pericarditis in Japan, and its clinical characteristics and prognosis are unknown. METHODS: This was a single-center, retrospective cohort study of clinical characteristics, invasive procedures, mortality, and recurrence in patients with acute pericarditis hospitalized from 2010 to 2022. The primary in-hospital outcome was adverse events (AEs), a composite of all-cause mortality and cardiac tamponade. The primary outcome in the long-term analysis was hospitalization for recurrent pericarditis. RESULTS: The median age of all 65 patients was 65.0 years [interquartile range (IQR), 48.0-76.0 years], and 49 (75.3 %) were male. The etiology of acute pericarditis was idiopathic in 55 patients (84.6 %), collagenous in 5 (7.6 %), bacterial in 1 (1.5 %), malignant in 3 (4.6 %), and related to previous open-heart surgery in 1 (1.5 %). Of the 8 patients (12.3 %) with in-hospital AE, 1 (1.5 %) died during hospitalization and 7 (10.8 %) developed cardiac tamponade. Patients with AE were less likely to have chest pain (p = 0.011) but were more likely to have symptoms lasting 72 h after treatment (p = 0.006), heart failure (p < 0.001), and higher levels of C-reactive protein (p = 0.040) and B-type natriuretic peptide (p = 0.032). All patients complicated with cardiac tamponade were treated with pericardial drainage or pericardiotomy. We analyzed 57 patients for recurrent pericarditis after excluding 8 patients: 1 with in-hospital death, 3 with malignant pericarditis, 1 with bacterial pericarditis, and 3 lost to follow-up. During a median follow-up of 2.5 years (IQR 1.3-3.0 years), 6 patients (10.5 %) had recurrences requiring hospitalization. The recurrence rate of pericarditis was not associated with colchicine treatment or aspirin dose or titration. CONCLUSIONS: In acute pericarditis requiring hospitalization, in-hospital AE and recurrence were each observed in >10 % of patients. Further large studies on treatment are warranted.

DOI： 10.1016/j.jjcc.2023.03.002

PubMed

researchmap

Language：English   Publisher：(一社)日本循環器学会  

researchmap

Language：English   Publisher：(一社)日本循環器学会  

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

Background Acute myocardial infarction (AMI) infrequently occurs after acute stroke. The Heart-brain team approach has a potential to appropriately manage this poststroke cardiovascular complication. However, clinical outcomes of AMI complicating acute stroke (AMI-CAS) with the heart-brain team approach have not been characterized. The current study investigated cardiovascular outcomes in patients with AMI-CAS managed by a heart-brain team. Methods and Results We retrospectively analyzed 2390 patients with AMI at our institute (January 1, 2007-September 30, 2020). AMI-CAS was defined as the occurrence of AMI within 14 days after acute stroke. Major adverse cerebral/cardiovascular events (cardiac-cause death, nonfatal myocardial infarction, and nonfatal stroke) and major bleeding events were compared in subjects with  AMI-CAS and those without acute stroke. AMI-CAS was identified in 1.6% of the subjects. Most AMI-CASs (37/39=94.9%) presented ischemic stroke. Median duration of AMI from the onset of acute stroke was 2 days. Patients with AMI-CAS less frequently received primary percutaneous coronary intervention (43.6% versus 84.7%; P<0.001) and dual-antiplatelet therapy (38.5% versus 85.7%; P<0.001), and 33.3% of them did not receive any antithrombotic agents (versus 1.3%; P<0.001). During the observational period (median, 2.4 years [interquartile range, 1.1-4.4 years]), patients with AMI-CAS exhibited a greater likelihood of experiencing major adverse cerebral/cardiovascular events (hazard ratio [HR], 3.47 [95% CI, 1.99-6.05]; P<0.001) and major bleeding events (HR, 3.30 [95% CI, 1.34-8.10]; P=0.009). These relationships still existed even after adjusting for clinical characteristics and medication use (major adverse cerebral/cardiovascular event: HR, 1.87 [95% CI, 1.02-3.42]; P=0.04; major bleeding: HR, 2.67 [95% CI, 1.03-6.93]; P=0.04). Conclusions Under the heart-brain team approach, AMI-CAS was still a challenging disease, reflected by less adoption of primary percutaneous coronary intervention and antithrombotic therapies, with substantially elevated cardiovascular and major bleeding risks. Our findings underscore the need for a further refined approach to mitigate their ischemic/bleeding risks.

DOI： 10.1161/JAHA.122.027156

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

BACKGROUND: Indwelling urethral catheters (IUCs) are used to measure urine volume, keep patients on bed rest, or keep the groin area clean in patients with acute myocardial infarction (AMI). However, the association between IUC use and in-hospital urinary-related complications is unknown. METHODS: This was a single-center retrospective analysis of 303 patients admitted to our hospital in 2018-2020 who had AMI without cardiogenic shock. An IUC was inserted in the emergency room upon initiation of invasive catheter treatment and removed as soon as possible. The primary outcome was in-hospital adverse urinary event (IHAUE), which consisted of in-hospital urinary tract infection and in-hospital gross hematuria. RESULTS: Of 303 patients, 243 patients (80.2 %) underwent IUC insertion. A lower proportion of patients with IUCs were male (72 % vs. 85 %, p = 0.044). A higher proportion had Killip classification 2 or 3 (13 % vs. 0 %, p = 0.003) or ST-elevation myocardial infarction (65 % vs. 32 %, p < 0.001). IHAUEs occurred significantly more commonly in patients with IUCs than without IUCs (11 % vs. 2 %, p = 0.023). Kaplan-Meier analysis showed that IHAUEs occurred more frequently in patients with IUCs than patients without IUCs (log-rank test p = 0.033). Furthermore, IUC use longer than the median of 2 days was associated with a higher odds ratio (OR) for IHAUE when compared with those without IUC use (OR, 3.65; 95 % confidence interval, 1.28-10.4; p = 0.015). There were no significant differences in in-hospital mortality by IUC status. CONCLUSIONS: IUC use is associated with a higher risk of IHAUEs in patients with uncomplicated AMI. Routine IUC use might not be recommended.

DOI： 10.1016/j.jjcc.2022.12.007

PubMed

researchmap

Language：Japanese   Publisher：医学図書出版(株)  

researchmap

Language：Japanese   Publisher：医学図書出版(株)  

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

BACKGROUND: Recent clinical studies are testing strategies for short (1-3 months) dual antiplatelet therapy following newer-generation drug-eluting stent (DES) placement. However, detailed biological responses to newer-generation DES remain unknown in humans. AIMS: We sought to evaluate early pathologic responses to abluminal biodegradable polymer-coated (BP-) DES compared with circumferential durable polymer-coated (DP-) DES in human autopsy cases. METHODS: The study included 38 coronary lesions with newer-generation DES implanted for <90 days (DP-DES=24, BP-DES=14) in 26 autopsy cases. The degree of strut coverage was defined as follows: grade 0 (bare), grade 1 (with fibrin or tissues/cells without endothelium), grade 2 (with single-layered endothelium), and grade 3 (with endothelium and underlying smooth muscle cell layers). RESULTS:  The duration following implantation was similar in DP- and BP-DES (median=20 vs 17 days). A total of 2,022 struts (DP-DES=1,297, BP-DES=725) were pathologically analysed. Focal grade 2 coverage was observed as early as 5 days after the implantation in both stents. The multilevel mixed-effects ordered logistic regression model demonstrated that BP-DES exhibited greater strut coverage compared with DP-DES (odds ratio [OR]: 3.64, 95% confidence interval [CI]: 1.37-9.67; p=0.009), which remained significant after adjustment for the duration following implantation and underlying tissue characteristics (OR: 2.74, 95% CI: 1.10-6.80; p=0.030). The predictive probability of grade 2 and 3 coverage was comparably limited at 30 days (DP-DES=17.1%, BP-DES=28.7%) and increased at 90 days (DP-DES=76.5%, BP-DES=86.6%). Both stents showed low inflammation and a similar degree of fibrin deposition. CONCLUSIONS: Single-layered endothelial coverage begins in the days after newer-generation DES placement, and BP-DES potentially exhibit faster strut coverage with smooth muscle cell infiltration than DP-DES in humans. Nevertheless, vessel healing remains suboptimal in both stents at 30 days.

DOI： 10.4244/EIJ-D-22-00650

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

BACKGROUND: Although screening for coronary artery disease (CAD) using computed tomography coronary angiography in patients with stable chest pain has been reported to be beneficial, patients with chronic kidney disease (CKD) might have limited benefit due to complications of contrast agent nephropathy and decreased diagnostic accuracy as a result of coronary artery calcifications. Cardiac magnetic resonance (CMR) has emerged as a novel imaging modality for detecting coronary stenosis and high-risk coronary plaques without contrast media that is not affected by coronary artery calcification. However, the clinical use of this technology has not been robustly evaluated. METHODS: AQUAMARINE-CKD is an open parallel-group prospective multicenter randomized controlled trial of 524 patients with CKD at high risk for CAD estimated based on risk factor categories for a Japanese urban population (Suita score) recruited from 6 institutions. Participants will be randomized 1:1 to receive a CMR examination that includes non-contrast T1-weighted imaging and coronary magnetic angiography (CMR group) or standard examinations that include stress myocardial scintigraphy (control group). Randomization will be conducted using a web-based system. The primary outcome is a composite of cardiovascular events at 1 year after study examinations: all-cause death, death from CAD, nonfatal myocardial infarction, nonfatal ischemic stroke, and ischemia-driven unplanned coronary intervention (percutaneous coronary intervention or coronary bypass surgery). DISCUSSION: If the combination of T1-weighted imaging and coronary magnetic angiography contributes to the risk assessment of CAD in patients with CKD, this study will have major clinical implications for the management of patients with CKD at high risk for CAD. TRIAL REGISTRATION: Japan Registry of Clinical Trials (jRCT) 1,052,210,075. Registered on September 10, 2021.

DOI： 10.1186/s13063-022-06820-w

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

BACKGROUND: Mechanism of femoropopliteal in-stent restenosis has been underappreciated. AIM: The aim of this animal study was to elucidate vascular response after femoropopliteal bare nitinol self-expanding stents (SESs) implantation. METHODS: Misago, Smart Flex, or Innova stent was randomly implanted in 36 swine femoropopliteal arteries. At week 4, quantitative vessel analysis (QVA) was performed on 36 legs, of which 18 underwent histological evaluation after angiography. The remaining 18 legs underwent QVA and histological evaluation at week 13. RESULTS: Fibrin deposition was excessive at week 4. Internal elastic lamina (IEL) progressively enlarged over time, and vessel injury developed from mild level at week 4 to moderate level at week 13. Vessel inflammatory reaction was mild to moderate at week 4, and was moderate to severe at week 13. Increased fibrin deposition was an early-acting, IEL enlargement and increased vessel inflammation were long-acting, and increased vessel injury and giant cells infiltration were late-acting contributors to neointimal hyperplasia (NIH). Stent type altered time-dependent process of vessel injury, vessel inflammation, eosinophils and giant cells infiltration. Misago had less fibrin deposition and vessel enlargement, and less progressive vessel injury, vessel inflammation, and eosinophils and giant cells infiltration. Net lumen as assessed by percent diameter stenosis or minimum lumen diameter was preserved with Misago, but was not preserved with the other stents. CONCLUSIONS: In the context of bare nitinol SES platform with less progressive mechanical stress and inflammatory reaction, the advantage of less NIH outweighed the disadvantage of less vessel enlargement, leading to net lumen preservation.

DOI： 10.1007/s12928-022-00889-5

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.21037/cdt-22-306

Web of Science

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

BACKGROUND: Lipid-rich plaque is an important substrate that causes future coronary events. However, the clinical implications of underlying plaque characteristics in coronary lesions after newer-generation drug-eluting stent (DES) implantation remain unknown. METHODS: The current study analyzed 445 target lesions after newer-generation DES implantation in 416 patients with coronary artery disease (CAD) (chronic coronary syndrome/acute coronary syndrome = 264/181) from the REASSURE-NIRS multicentre registry. Near-infrared spectroscopy (NIRS) imaging was used to evaluate maximum lipid core burden index after stent implantation in target lesions (residual maxLCBI4mm). The primary and secondary outcomes were 3-year lesion-oriented clinical outcomes (LOCO): cardiac death, nonfatal target-lesion-related myocardial infarction (MI), or ischemia-driven target-lesion revascularization (ID-TLR) and patient-oriented clinical outcomes (POCO): all-cause death, nonfatal MI, or ID unplanned revascularization. Outcomes were compared by residual maxLCBI4mm tertile. RESULTS: Median residual maxLCBI4mm was 183; 16% of lesions had residual maxLCBI4mm > 400. Higher residual maxLCBI4mm was not associated with a greater likelihood of LOCO or POCO during the observational period (LOCO, log-rank P = 0.76; POCO, log-rank P = 0.84). Mixed-effects logistic regression demonstrated that residual maxLCBI4mm does not predict LOCO (odds ratio [OR], 1.000; 95% confidence interval [CI], 0.997-1.003; P = 0.95). There was no significant relationship between residual maxLCBI4mm and POCO (OR, 1.001; 95% CI, 0.999-1.002; P = 0.30). CONCLUSIONS: Residual maxLCBI4mm is not associated with LOCO or POCO in patients with CAD after newer-generation DES implantation. Our findings suggest that NIRS-derived underlying lipid-rich plaque is not associated with the risk of stent-related events and patient-based outcomes in patients with CAD who have received newer-generation DESs.

DOI： 10.1016/j.cjca.2022.07.004

PubMed

researchmap

Publisher：株式会社 医学書院  

DOI： 10.11477/mf.1438200603

CiNii Research

researchmap

Language：English  

DOI： 10.1016/j.jcmg.2022.02.005

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

BACKGROUND: The distal radial approach (DRA) is a novel catheter cannulation technique to access the distal radial artery for coronary angiography (CAG). It is associated with less occurrence of puncture site occlusion than the conventional transradial approach. However, cannulation failure occasionally occurs due to difficulty in puncturing the smaller distal radial artery. Nitroglycerin is expected to improve the rate of successful DRA via its vasodilative and vasospasm-preventive effects. METHODS: The DRA in CAG using transdermal NitroGlycerin patch (DRANG) study is a single-center, double-arm, parallel-assignment, double-blinded, randomized, controlled trial. Eligible patients with angina pectoris who are scheduled to receive CAG via DRA at the National Cerebral and Cardiovascular Center will be enrolled and allocated to the nitroglycerin group (n = 46) or the no-treatment group (n = 46). The nitroglycerin group will receive a transdermal nitroglycerin patch pre-integrated with a covering material that completely conceals the patch on their upper arm on the puncture side. The no-treatment group will receive only the covering material. Applications are performed 2-8 h before puncture while the patient wears an eye mask. Physicians who are blinded to the allocation and have similar experience with DRA puncture will perform DRA using the Seldinger technique with a 22-gauge needle. The primary outcome is the rate of successful palpation-guided distal radial artery cannulation with the first puncture. The secondary outcomes are the rate of successful distal radial artery cannulation, number of punctures, procedure time, use of ultrasound guidance, diameter of the distal radial artery and changes before and after patch application, and occurrence of arterial vasospasm, occlusion, or hypotension. CONCLUSIONS: This study will allow us to determine the impact of a transdermal nitroglycerin patch on the rate of successful DRA and validate its effectiveness as a DRA pretreatment. TRIAL REGISTRATION: jRCTs051210128.

DOI： 10.1016/j.carrev.2022.05.010

PubMed

researchmap

Language：English  

DOI： 10.1016/j.carrev.2021.11.025

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

BACKGROUND AND AIMS: The residual risk of atherosclerotic cardiovascular disease (ASCVD) in patients with diabetes on statin therapy warrants identification of other pro-atherogenic drivers. Lipoprotein(a) [Lp(a)] promotes the formation of necrotic cores within vessel walls. Given that patients with diabetes have an Lp(a)-associated ASCVD risk, Lp(a) might lead to plaque vulnerability in patients with diabetes on statin therapy. METHODS: We analyzed target lesions that underwent PCI in 312 patients with coronary artery disease (CAD) on statin treatment from the REASSURE-NIRS registry (NCT04864171). Maximum 4-mm lipid-core-burden index (maxLCBI4mm) in target lesions was measured with near-infrared spectroscopy (NIRS) imaging. The relationship between Lp(a) levels and maxLCBI4mm was investigated in patients with and without diabetes. RESULTS: High-intensity statin use (p = 0.49) and on-treatment low-density lipoprotein cholesterol (LDL-C) (p = 0.32) and Lp(a) levels (p = 0.09) were comparable between patients with and without diabetes. Lp(a) levels were significantly associated with maxLCBI4mm in patients with diabetes (p = 0.01) but not in patients without diabetes (p = 0.96). Multivariate analysis showed that LDL-C levels (p = 0.03) predict maxLCBI4mm in patients without diabetes, but not Lp(a) levels (p = 0.91). Both LDL-C (p = 0.01) and Lp(a) (p = 0.04) levels were independent predictors of maxLCBI4mm in patients with diabetes. Even in patients with diabetes achieving LDL-C <1.8 mmol/L (70 mg/dL), Lp(a) levels remained associated with maxLCBI4mm (p = 0.04). CONCLUSIONS: A significant relationship between Lp(a) and maxLCBI4mm exists in patients with diabetes and CAD on statin treatment, even with LDL-C <1.8 mmol/L (70 mg/dL). Lp(a) might be associated with more vulnerable coronary atheroma in patients with diabetes despite receiving statin therapy.

DOI： 10.1016/j.atherosclerosis.2022.03.033

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1093/ehjci/jeab295

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1253/circj.CJ-20-1282

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

AIMS: Although comprehensive cardiac rehabilitation (CCR) is recommended for patients with heart failure (HF), participants often show low adherence. The aim of this study was to evaluate the association of CCR completion and response with long-term clinical outcomes. METHODS AND RESULTS: We screened 824 HF patients who participated in a 3 month CCR programme and underwent baseline assessment, including cardiopulmonary exercise testing (CPX). After excluding 52 participants who experienced all-cause death or HF hospitalization within 180 days, long-term outcomes were compared between those who attended 3 month follow-up assessment including CPX (completers) and those who did not (non-completers). We also compared the prognostic value of the changes in peak oxygen uptake (VO2 ) vs. quadriceps muscle strength (QMS) during the 3 month CCR programme. Among the 772 study patients, there were no significant differences in baseline characteristics, including left ventricular ejection fraction, B-type natriuretic peptide levels, and peak VO2 , between the completers (n = 561) and non-completers (n = 211), except for a higher age (63.2 ± 14.2 vs. 59.4 ± 16.2 years; P = 0.0015) and proportion of females (27% vs. 17%; P = 0.0030) among the completers. During a median follow-up of 55.4 months, the completers had lower rates of the composite of all-cause death or HF hospitalization (34.4% vs. 44.6%; P = 0.0015) and all-cause death (16.9% vs. 24.6%; P = 0.0037) than the non-completers. After adjustment for prognostic baseline characteristics, including age and sex, CCR completion was associated with 34% and 44% reductions in the composite outcome and all-cause death, respectively. Among the completers, peak VO2 and QMS increased significantly (8.9 ± 15.8% and 10.5 ± 17.9%, respectively) over 3 months. Patients who had an increase in peak VO2  ≥ 6.3% (median value) during the CCR programme had significantly lower rates of the composite outcome (27.0% vs. 33.8%; P = 0.048) and all-cause mortality (10.0% vs. 17.4%; P = 0.0069) than those who did not. No statistically significant difference was observed in the composite outcome (30.5% vs. 30.4%; P = 0.76) or all-cause mortality (13.0% vs. 14.4%; P = 0.39) between those with and without an increase in QMS ≥8.3% (median value). CONCLUSIONS: In HF patients who participated in a 3 month CCR programme, its completion was associated with lower risks of subsequent HF hospitalization and death. Within the group of patients who completed the programme, the improvement in exercise capacity, but not in skeletal muscle strength, over the 3-month period was associated with better outcomes. These findings highlight the importance of the post-CCR follow-up assessment, including CPX, to identify a patient's adherence and response to the CCR programme.

DOI： 10.1002/ehf2.13838

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

OBJECTIVES: To determine the characteristics of thyroid storm patients with acute decompensated heart failure who should be candidates for temporary percutaneous mechanical circulatory support in addition to beta-blocker treatment to prevent cardiogenic shock. DESIGN: A single-center, retrospective review of treatment details and data collected from electronic medical records. SETTING: Thyrotoxicosis complicated with acute decompensated heart failure. PATIENTS: Eight consecutive patients who were admitted to our hospital for acute decompensated heart failure with thyroid storm between December 2011 and August 2020 were retrospectively reviewed. Of the eight patients, four were treated with percutaneous mechanical circulatory support. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Compared with thyroid storm patients who did not require percutaneous mechanical circulatory support, those who did had a significantly higher initial plasma brain natriuretic peptide level (1,231 [911-3,387] vs 447 pg/mL [243-653 pg/mL], respectively; p = 0.015), as well as a significantly larger left ventricular end-diastolic diameter (56 [54-63] vs 48 mm [38-48 mm], respectively; p = 0.029) and end-systolic diameter (50 [49-58] vs 28 mm [28-30 mm], respectively; p = 0.029) on echocardiogram. In terms of thyroid storm severity, the Burch-Wartofsky score was higher in patients with percutaneous mechanical circulatory support than in those without, although the difference was not significant. All patients survived this index admission. CONCLUSIONS: In thyroid storm patients, the presence of a high brain natriuretic peptide level, "left ventricular dilatation," or both may necessitate hemodynamic assessment to determine the indication of percutaneous mechanical circulatory support before beta-blocker administration.

DOI： 10.1097/CCE.0000000000000599

PubMed

researchmap

Language：Japanese   Publisher：(一社)日本動脈硬化学会  

researchmap

Language：English  

DOI： 10.1016/j.hrcr.2021.04.015

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

A 75-year-old man had recurrent in-stent restenosis (ISR) attributable to calcified nodule. Near-infrared spectroscopy (NIRS) showed a gradual decrease in yellow signals during the process of repeated percutaneous coronary intervention for recurrent ISR that eventually halted. The case indicates that NIRS signals may represent lesion instability even in calcified nodule, and may be potentially predictive of recurrent ISR.

DOI： 10.1016/j.cjca.2021.07.012

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

Background Statin-mediated efficacy of lowering low-density lipoprotein (LDL) cholesterol varies in each individual, and its diminished response is associated with worse outcomes. However, there is no established approach to predict hyporesponse to statins. PCSK9 (proprotein convertase subxilisin/kexin type 9) is a serine-protease associated with LDL metabolism, which circulates as mature and furin-cleaved PCSK9. Since mature PCSK9 more potently degrades the LDL receptor, its evaluation may enable the identification of statin hyporesponders. Methods and Results We analyzed 101 statin-naive patients with coronary artery disease who commenced a statin. PCSK9 subtypes at baseline and 1 month after statin use were measured by ELISA. Hyporesponse to statins was defined as a percent reduction in LDL cholesterol <15%. The relationship between each PCSK9 subtype level and hyporesponse to statins was investigated. Statins significantly lowered LDL cholesterol level (percent reduction, 40%±21%), whereas 11% of study participants exhibited a hyporeseponse to statins. Multivariable logistic regression analysis demonstrated that baseline mature PCSK9 level was an independent predictor for hyporesponse to statins even after adjusting clinical characteristics (mature PCSK9 per 10-ng/mL increase: odds ratio [OR], 1.12; 95% CI, 1.01-1.24 [P=0.03]), whereas furin-cleaved level was not (per 10-ng/mL increase: OR, 1.37; 95% CI, 0.73-2.58 [P=0.33]). Receiver operating characteristic curve analysis identified mature PCSK9 level of 228 ng/mL as an optimal cutoff to predict hyporesponse to statins (area under the curve, 0.73 [sensitivity, 0.91; specificity, 0.56]). Conclusions Baseline mature PCSK9 level >228 ng/mL is associated with hyporesponse to statins. This finding suggests that mature PCSK9 might be a potential determinant of hyporesponse to statins.

DOI： 10.1161/JAHA.120.019525

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

BACKGROUND: Calcified nodule (CN) has a unique plaque morphology, in which an area of nodular calcification causes disruption of the fibrous cap with overlying luminal thrombus. CN is reported to be the least frequent cause of acute coronary thrombosis, and the pathogenesis of CN has not been well studied. OBJECTIVES: The purpose of this study is to provide a comprehensive morphologic assessment of the CN in addition to providing an evolutionary perspective as to how CN causes acute coronary thrombosis in patients with acute coronary syndromes. METHODS: A total of 26 consecutive CN lesions from 25 subjects from our autopsy registry were evaluated. Detailed morphometric analysis was performed to understand the plaque characteristics of CN and nodular calcification. RESULTS: The mean age was 70 years, with a high prevalence of diabetes and chronic kidney disease. CNs were equally distributed between men and women, with 61.5% of CNs found in the right coronary artery (n = 16), mainly within its mid-portion (56%). All CNs demonstrated surface nonocclusive luminal thrombus, consisting of multiple nodular fragments of calcification, protruding and disrupting the overlying fibrous cap, with evidence of endothelial cell loss. The degree of circumferential sheet calcification was significantly less in the culprit section (89° [interquartile range: 54° to 177°]) than in the adjacent proximal (206° [interquartile range: 157° to 269°], p = 0.0034) and distal (240° [interquartile range: 178° to 333°], p = 0.0004) sections. Polarized picrosirius red staining showed the presence of necrotic core calcium at culprit sites of CNs, whereas collagen calcium was more prevalent at the proximal and distal regions of CNs. CONCLUSIONS: Our study suggests that fibrous cap disruption in CN with overlying thrombosis is initiated through the fragmentation of necrotic core calcifications, which is flanked-proximally and distally-by hard, collagen-rich calcification in coronary arteries, which are susceptible to mechanical stress.

DOI： 10.1016/j.jacc.2021.02.016

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

Background: Vulnerable plaque features including lipidic plaque have been shown to affect fractional flow reserve (FFR). Given that formation and propagation of lipid plaque is accompanied by endothelial dysfunction which impairs vascular tone, the degree of lipidic burden may affect vasoreactivity during hyperemia, potentially leading to reduced FFR. Our aim is to elucidate the relationship of the extent of lipidic plaque burden with coronary physiological vasoreactivity measure. Methods: We analyzed 89 subjects requeuing PCI due to angiographically intermediate coronary stenosis with FFR ≤0.80. Near-infrared spectroscopy (NIRS) and intravascular ultrasound were used to evaluate lipid-core burden index (LCBI) and atheroma volume at both target lesion (maxLCBI4mm; maximum value of LCBI within any 4 mm segments) and entire target vessel (LCBIvessel: LCBI within entire vessel). In addition to FFR, delta-FFR was measured by difference of distal coronary artery pressure/aortic pressure (Pd/Pa) between baseline and hyperemic state. Results: The averaged FFR and delta-FFR was 0.74 (0.69-0.77), and 0.17±0.05, respectively. On target lesion-based analysis, maxLCBI4mm was negatively correlated to FFR (ρ=-0.213, P=0.040), and it was positively correlated to delta-FFR (ρ=0.313, P=0.002). Furthermore, target vessel-based analysis demonstrated similar relationship of LCBIvessel with FFR (ρ=-0.302, P=0.003) and delta-FFR (ρ=0.369, P<0.001). Even after adjusting clinical characteristics and lesion/vessel features, delta-FFR (by 0.10 increase) was independently associated with maxLCBI4mm (β=57.2, P=0.027) and LCBIvessel (β=24.8, P=0.007) by mixed linear model analyses. Conclusions: A greater amount of lipidic plaque burden at not only "target lesion" alone but "entire target vessel" was associated with a greater delta-FFR. The accumulation of lipidic plaque materials at both local site and entire vessel may impair hyperemia-induced vasoreactivity, which causes a reduced FFR.

DOI： 10.21037/cdt-20-1024

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

BACKGROUND: Coronary computed tomography angiography (CCTA) non-invasively visualizes lipid-rich plaque. However, this ability is not fully validated in vivo. The current study aimed to elucidate the association of CCTA features with near-infrared spectroscopy-derived lipidic plaque measure in patients with coronary artery disease. METHODS: 95 coronary lesions (culprit/non-culprit = 51/44) in 35 CAD subjects were evaluated by CCTA and NIRS imaging. CT density, positive remodeling, spotty calcification, napkin-ring sign and NIRS-derived maximum 4-mm lipid-core burden index (maxLCBI4mm) were analyzed by two independent physicians. The association of CCTA-derived plaque features with maxLCBI4mm ≥ 400 was evaluated. RESULTS: The median CT density and maxLCBI4mm were 57.7 Hounsfield units (HU) and 304, respectively. CT density (r = -0.75, p < 0.001) and remodeling index (RI) (r = 0.58, p < 0.001) were significantly associated with maxLCBI4mm, respectively. Although napkin-ring sign (p < 0.001) showed higher prevalence of maxLCBI4mm ≥ 400 than those without it, spotty calcification did not (p = 0.13). On multivariable analysis, CT density [odds ratio (OR) = 0.95, 95% confidence interval (CI) = 0.93-0.97; p < 0.001] and positive remodeling [OR = 7.71, 95%CI = 1.37-43.41, p = 0.02] independently predicted maxLCBI4mm ≥ 400. Receiver operating characteristic curve analysis demonstrated CT density <32.9 HU (AUC = 0.92, sensitivity = 85.7%, specificity = 91.7%) and RI ≥ 1.08 (AUC = 0.83, sensitivity = 74.3%, specificity = 85.0%) as optimal cut-off values of maxLCBI4mm ≥ 400. Of note, only 52.6% at lesions with one of these plaque features exhibited maxLCBI4mm ≥ 400, whereas the frequency of maxLCBI4mm ≥ 400 was highest at those with both features (88.5%, p < 0.001 for trend). CONCLUSIONS: CT density <32.9 HU and RI ≥ 1.08 were associated with lipid-rich plaque on NIRS imaging. Our findings underscore the synergistic value of CT density and positive remodeling to detect lipid-rich plaque by CCTA.

DOI： 10.1016/j.atherosclerosis.2021.02.019

PubMed

researchmap

Language：English   Publisher：(一社)日本循環器学会  

researchmap

Language：English   Publisher：(一社)日本循環器学会  

researchmap

Language：English   Publisher：(一社)日本循環器学会  

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

OBJECTIVE: Although there are regional reports that the COVID-19 pandemic is associated with a reduction in acute myocardial infarction presentations and primary percutaneous coronary intervention (PCI) procedures, little is known about the impact of the COVID-19 pandemic on mechanical complications resulting from ST-segment elevation myocardial infarction (STEMI) and mortality. METHODS: This single-centre retrospective cohort study analysed presentations, incidence of mechanical complications, and mortality in patients with STEMI before and after a state of emergency was declared due to the COVID-19 pandemic by the Japanese government on 7 April 2020. RESULTS: We analysed 359 patients with STEMI hospitalised before the declaration and 63 patients hospitalised after the declaration. The proportion of patients with late presentation was significantly higher after the declaration than before (25.4% vs 14.2%, p=0.03). The incidence of late presentation was significantly higher during the COVID-19 pandemic than before (incidence rate ratio (IRR), 2.41; 95% CI, 1.37 to 4.05; p=0.001, even after adjusting for month (IRR, 2.61; 95% CI, 1.33 to 5.13; p<0.01). Primary PCI was performed significantly less often after the declaration than before (68.3% vs 82.5%, p=0.009). The mechanical complication resulting from STEMI occurred in 13 of 359 (3.6%) patients before the declaration and 9 of 63 (14.3%) patients after the declaration (p<0.001). However, the incidence of in-hospital death (before, 6.2% vs after, 6.4%, p=0.95) was comparable. CONCLUSIONS: Following the COVID-19 pandemic, an increased incidence of mechanical complications resulting from STEMI was observed. Instructing people to stay at home, without effectively educating them to immediately seek medical attention when suffering symptoms of a heart attack, may worsen outcomes in patients with STEMI.

DOI： 10.1136/openhrt-2020-001497

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1093/eurheartj/ehaa632

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

BACKGROUND AND AIMS: Calcified nodule (CN) is an eruptive calcified mass causing acute coronary syndrome (ACS). Since coronary calcification is associated with an elevated cardiac event's risk, ACS attributable to CN may exhibit worse clinical outcome following percutaneous coronary intervention (PCI). METHODS: We retrospectively analyzed 657 ACS patients receiving PCI with newer-generation drug-eluting stent (DES) implantation under intravascular ultrasound (IVUS) guidance. CN was defined as (1) protruding calcification with its irregular surface and (2) the presence of calcification at adjacent proximal and distal segments. The primary endpoint was a composite of major adverse cardiac event [MACE = cardiac death + ACS recurrence + target lesion revascularization (TLR)]. RESULTS: CN was identified in 5.3% (=35/657) of the study subjects. CN patients were more likely to have coronary risk factors including hypertension (p = 0.005), chronic kidney disease (p < 0.001), maintenance hemodialysis (p < 0.001) and a history of PCI (p < 0.001). During the observational period (median = 1304 days), CN was associated with an increased risk of MACE (HR = 7.68, 95%CI = 4.61-12.80, p < 0.001), ACS recurrence (HR = 12.32, 95%CI = 6.05-25.11, p < 0.001) and TLR (HR = 10.48, 95%CI = 5.80-18.94, p < 0.001). These cardiac risks related to CN were consistently observed by Cox proportional hazards model (MACE: p < 0.001, ACS recurrence: p < 0.001, TLR: p < 0.001) and a propensity score-matched cohort analysis (MACE: p = 0.002, ACS recurrence: p = 0.01, TLR: p = 0.005). Of note, over 80% of TLR at the CN lesion was driven by its re-appearance within the implanted DES. CONCLUSIONS: ACS patients attributable to CN have an increased risk of ACS recurrence and TLR, mainly driven by the continuous growth and protrusion of the calcified mass.

DOI： 10.1016/j.atherosclerosis.2020.11.005

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1016/j.jcin.2020.06.026

PubMed

researchmap

Language：English  

A 75-year-old female patient on hemodialysis presented with non-ST-segment elevation myocardial infarction. After successful primary percutaneous coronary intervention, in-stent restenosis (ISR) occurred 3 consecutive times. Intravascular imaging assessment during the repeated percutaneous coronary intervention indicated that the ISR was not associated with neointimal hyperplasia but was mainly attributed to a calcified nodule, which protruded into the lumen. We applied excimer laser catheter ablation to avoid another ISR. (Level of Difficulty: Intermediate.).

DOI： 10.1016/j.jaccas.2020.06.035

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

In vivo imaging of plaque instability has been considered to have a great potential to predict future coronary events and evaluate the stabilization effect of novel anti-atherosclerotic medical therapies. Currently, there are several intravascular imaging modalities which enable to visualize plaque components associated with its vulnerability. These include virtual histology intravascular ultrasound (VH-IVUS), integrated backscatter IVUS (IB-IVUS), optical coherence tomography (OCT), near-infrared spectroscopy and coronary angioscopy. Recent studies have shown that these tools are applicable for risk stratification of cardiovascular events as well as drug efficacy assessment. However, several limitation exists in each modality. The current review paper will outline advantages and limitation of VH-IVUS, IB-IVUS, OCT, NIRS and coronary angioscopy imaging.

DOI： 10.21037/cdt-20-238

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)   Publisher：AME Publishing Company  

DOI： 10.21037/cdt-20-415

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

Background: Lowering low-density lipoprotein cholesterol (LDL-C) levels using a statin is a cornerstone of preventive therapeutic management following acute myocardial infarction (AMI). In addition to its anti-atherosclerotic effects, recent studies reported a lower occurrence of heart failure (HF) under statin therapy. However, there is a wide variability in statin response. The association between the response to statin and the occurrence of HF in AMI subjects remains unclear. The purpose of present study is to examine whether the variability in statin response affects HF risk after AMI. Methods: We analyzed 505 statin-naïve AMI subjects undergoing primary percutaneous coronary intervention (PCI) who commenced atorvastatin, rosuvastatin, or pitavastatin. Statin hyporesponse was defined as a reduction in LDL-C levels <15% from baseline to 1 month after statin therapy. HF outcomes were compared between patients with and without statin hyporesponse. Results: Statin hyporesponse was identified in 15.2% (77/505) of study subjects. During a median 4.4-year observational period, statin hyporesponse was associated with a greater likelihood of HF [hazard ratio (HR) =3.01, 95% confidence interval (CI): 1.27-6.79, P=0.01]. This increased HF risk in statin hyporesponders was consistently observed in a multivariate Cox proportional hazards model (HR =2.74, 95% CI: 1.01-6.75, P=0.04), a propensity score-matched cohort (HR =12.30, 95% CI: 1.50-100.3, P=0.01) and in an inverse probability of treatment weights analysis with average treatment effects (coefficient =7.02, 95% CI: 2.29-21.58, P=0.0006). Conclusions: Hyporesponse to statins increases HF risk after AMI. Our findings highlight statin hyporesponse as a high-risk feature associated with HF events.

DOI： 10.21037/cdt-20-415

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1007/s12928-019-00601-0

PubMed

researchmap

Language：English  

In the original publication of the article, the first author name "Yuji Nishimoto" was repeated in the author group.

DOI： 10.1007/s12928-019-00605-w

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

BACKGROUND: Struts have been considered as covered when tissue overlying the struts is >0 μm by optical coherence tomography (OCT). However, there is no confirmatory study to validate this definition by histology which is the gold standard. The aim of the present study was to assess the appropriate cutoff value of neointimal thickness of stent strut coverage by OCT with histology confirmation. METHODS: We performed ex vivo OCT imaging of human coronary arteries with stents at autopsy. A total of 46 stents in 39 vessels from 25 patients were examined in this study, and a total of 165 cross-sectional images were co-registered with histology to determine the optimal cutoff value for strut coverage by OCT which was defined as luminal endothelial cells with 2 abluminal layers of smooth muscles cells and matrix. Considering the resolution of OCT is 10 to 20 μm, the cutoff values were assessed at ≥20, ≥40, and ≥60 μm. RESULTS: A total of 2235 struts were reviewed by histology, 1216 were considered as well-matched struts which were analyzed in this study. By histology, 160 struts were identified as uncovered, while 1056 struts were covered. The OCT assessment without consideration of neointimal thickness yielded a poor specificity of 37.5% and sensitivity 100%. Of 3 cutoff values, the cutoff value of ≥40 μm yielded the best sensitivity (99.3%), specificity (91.0%), positive predictive value (98.6%), and negative predictive value (95.6%) as compared with ≥20 and ≥60 μm. CONCLUSIONS: Neointimal thickness ≥40 μm by OCT yielded the most accurate cutoff value to identify stent strut coverage validated by histology.

DOI： 10.1161/CIRCINTERVENTIONS.119.008869

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

In the original publication of this article [1] the wording of '3Di-PMR' was different between the text and figures.

DOI： 10.1186/s12968-020-00620-4

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1253/circj.CJ-19-1109

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

BACKGROUND: Periprocedural myocardial injury (pMI) is a common complication of elective percutaneous coronary intervention (PCI) that reduces some of the beneficial effects of coronary revascularization and impacts the risk of cardiovascular events. We developed a 3-dimensional volumetric cardiovascular magnetic resonance (CMR) method to evaluate coronary high intensity plaques and investigated their association with pMI after elective PCI. METHODS: Between October 2012 and October 2016, 141 patients with stable coronary artery disease underwent T1-weighted CMR imaging before PCI. A conventional 2-dimensional CMR plaque-to-myocardial signal intensity ratio (2D-PMR) and the newly developed 3-dimensional integral of PMR (3Di-PMR) were measured. 3Di-PMR was determined as the sum of PMRs above a threshold of > 1.0 for voxels in a target plaque. pMI was defined as high-sensitivity cardiac troponin T > 0.07 ng/mL. RESULTS: pMI following PCI was observed in 46 patients (33%). 3Di-PMR was significantly higher in patients with pMI than those without pMI. The optimal 3Di-PMR cutoff value for predicting pMI was 51 PMR*mm3 and the area under the receiver operating characteristic curve (0.753) was significantly greater than that for 2D-PMR (0.683, P = 0.015). 3Di-PMR was positively correlated with lipid volume (r = 0.449, P < 0.001) based on intravascular ultrasound. Stepwise multivariable analysis showed that 3Di-PMR ≥ 51 PMR*mm3 and the presence of a side branch at the PCI target lesion site were significant predictors of pMI (odds ratio [OR], 11.9; 95% confidence interval [CI], 4.6-30.4, P < 0.001; and OR, 4.14; 95% CI, 1.6-11.1, P = 0.005, respectively). CONCLUSIONS: 3Di-PMR coronary assessment facilitates risk stratification for pMI after elective PCI. TRIAL REGISTRATION: retrospectively registered.

DOI： 10.1186/s12968-019-0588-6

PubMed

researchmap

Language：English  

DOI： 10.1007/s10554-019-01641-6

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

Introduction: In CKD subjects, atherosclerotic cardiovascular disease (ASCVD) is a major cause of their morbidity and mortality (1-3). Current therapeutic guidelines recommend lowering LDL-C level to prevent ASCVD (4, 5). However, it remains uncertain how this therapeutic approach effectively modifies atherosclerosis of CKD. These findings suggest the need to further understand pathophysiology of atherosclerosis. Given that intravascular imaging modalities have contributed to characterize the natural history of coronary atherosclerosis (13-23), the integration of plaque imaging is expected to help to elucidate targets associated with stabilizing atheroma.Areas covered: This review will outline atherogenic stimuli in patients with CKD. In addition, the characteristics of their coronary atheroma will be presented from finding in clinical studies using a variety of intravascular imaging modalities. The efficacy of current guideline recommended anti-atherosclerotic therapies in CKD patients will be also summarized. All related articles were searched through PubMed.Expert opinion: Integration of intravascular imaging has a great potential to establish effective therapies for slowing progression of atherosclerosis in subjects with CKD. More efforts toward searching therapeutic target associated with atherosclerosis of CKD are required. In particular, identifying drivers associated with plaque calcification will lead to the development of new agents which regress calcium accumulation.

DOI： 10.1080/14779072.2019.1676150

PubMed

researchmap

Language：English  

Background: Histopathological studies have reported the presence of cholesterol crystals in the culprit lesion in patients with sudden cardiac death. Given that cholesterol crystals themselves promote pro-inflammatory cascades, they may destabilize atherosclerotic plaques, leading to the occurrence of acute coronary events. Case summary: A 60-year-old man presented with ST-segment elevation myocardial infarction. Emergent coronary angiography revealed a severely stenotic lesion (=culprit lesion) and another non-obstructive lesion in the proximal and middle segments of the left anterior descending artery (LAD), respectively. Optical coherence tomography (OCT) imaging showed that both lesions exhibited lipid-rich plaque with cholesterol crystals, and the non-obstructive lesion in the mid-LAD did not have a thin fibrous cap (its thickness = 230 μm). A drug-eluting stent was successfully implanted at the culprit lesion in the proximal LAD. On non-contrast T1-weighted magnetic resonance imaging performed 10 days after percutaneous coronary intervention (PCI), a high-intensity signal was identified at the non-obstructive mid-LAD lesion. This lesion was medically managed with aspirin, clopidogrel, and rosuvastatin due to the absence of myocardial ischaemia. However, 12 months after PCI, the patient was hospitalized again due to unstable angina pectoris. Coronary angiography revealed substantial progression of the mid-LAD lesion. Optical coherence tomography imaging prior to the second PCI showed a severely narrowed lesion containing cholesterol crystals and covered by organized thrombus. This lesion harbored an extensive amount of lipidic materials on near-infrared spectroscopy (maximum 4-mm lipid core burden index = 809). Discussion: In our case, atherosclerotic plaques containing cholesterol crystals was associated with the occurrence of acute coronary syndrome. Our findings suggest that plaque with cholesterol crystals is a potential precursor to future acute coronary events.

DOI： 10.1093/ehjcr/ytz128

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

The association between low-dose combined oral contraceptives (COCs) and anticoagulation factors in Japanese women has been rarely studied. A total of 394 Japanese women with a new beginning cycle of COC use were enrolled, of whom 335 women visited the clinic within 4 weeks after starting the first cycle of COC. Visits occurred in the active phase (272 women) and the placebo phase (63 women). Free protein S (PS) antigen and activity levels and antithrombin activity levels decreased significantly in both the active and placebo phase groups. Protein C (PC) activity levels increased significantly in both groups. Larger reductions in free PS antigen and activity levels occurred with COC comprising either 30 µg ethinylestradiol/desogestrel or 20 µg ethinylestradiol/drospirenone than that comprising 35 µg ethinylestradiol/norethisterone. In four women with the Japanese-specific PS K196E mutation, mean PS activity was 65% before COC use and 57% during COC use, indicating further decrease with COC use. In conclusion, decreased antigen and activity levels of PS and antithrombin and increased activity levels of PC were observed even during the first cycle of low-dose COC use. The effects on PS and PC activities were also observed in the hormone-free interval.

DOI： 10.1007/s12185-019-02633-x

PubMed

researchmap

Language：English   Publisher：(一社)日本循環器学会  

researchmap

Language：English   Publisher：(一社)日本循環器学会  

researchmap

Language：English   Publisher：(一社)日本循環器学会  

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

Aims: Coronary high-intensity plaques (HIPs) with a high plaque-to-myocardial signal intensity ratio (PMR) on non-contrast T1-weighted imaging in patients with stable coronary artery disease (CAD) are associated with future coronary events. To characterize the morphological substrate of HIP, we performed a correlative optical coherence tomography (OCT) study. Methods and results: We examined 137 lesions in 105 patients with stable angina pectoris or silent myocardial ischaemia scheduled for percutaneous coronary intervention (PCI) using a 3 T magnetic resonance scanner. Pre-interventional OCT was performed for PCI target lesions. HIP was defined as PMR ≥ 1.4. Of the 137 lesions, 34% were HIP and 66% were non-HIP. The prevalence of lipid-rich plaque (96% vs. 70%, P < 0.001), macrophage accumulation (65% vs. 46%, P = 0.046), cholesterol crystals (46% vs. 22%, P = 0.006), and healed plaque rupture (multiple layers of different optical densities overlaying a large lipid accumulation, 72% vs. 18%, P < 0.001) was significantly higher in the HIP group than the non-HIP group; no significant differences were observed for the presence of thin cap fibroatheroma, intracoronary thrombus, and plaque rupture between the two groups. Multivariable stepwise logistic regression analysis showed that HIP was significantly associated with the presence of healed plaque rupture [odds ratio (OR) 9.32; 95% confidence interval (95% CI) 4.05-22.71; P < 0.001] and lipid-rich plaque (OR 4.38; 95% CI 1.08-29.77; P = 0.038). Conclusions: The significant association between HIP- and OCT-derived healed plaque rupture and large lipid core provides new insights into the characteristics of high-risk plaques, even in clinically stable CAD.

DOI： 10.1093/ehjci/jey035

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

BACKGROUND: The histopathological validation of optical coherence tomography (OCT) in visualizing atherosclerotic plaques has been reported only in ex vivo studies. We sought to evaluate the accuracy of OCT in tissue characterization in vivo. METHODS AND RESULTS: A total of 25 patients with stable angina pectoris who underwent directional coronary atherectomy (DCA) were included in the investigation, whereby OCT was performed before and after a single debulking. The debulked region was determined on OCT and classified into fibrous tissue, lipid, calcification, thrombus, and macrophage accumulation, which were compared with histology. Changes in OCT signal intensity in the deeper intimal region after DCA were also visually evaluated. Fibrous tissues were detected in all cases, while thrombus was identified only in 1 case, by both OCT and histology. The sensitivity, specificity, positive and negative predictive values, and predictive accuracy for lipid detection by OCT were 88.9%, 75.0%, 66.7%, 92.3%, and 80.0%; those for calcification were 50.0%, 100%, 100%, 91.3%, and 92.0%; and those for macrophage accumulation were 85.7%, 88.9%, 75.0%, 94.1%, and 88.0%, respectively. The false positive diagnoses for lipid were mostly attributed to the extracellular matrix accumulation containing less collagen. The false negative diagnoses for calcification were explained by the presence of lipid around the calcification. The OCT signal intensity in the deeper intimal region substantially increased after DCA in all cases. CONCLUSIONS: The current study showed excellent predictive accuracy of in vivo OCT in tissue characterization, whereas the limitations of OCT were highlighted by an over-detection of lipid, under-detection of calcification, and underestimation of the deeper intimal matrix.

DOI： 10.1016/j.ijcard.2018.05.022

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

A 53-year-old male presented with acute myocardial infarction and was subsequently implanted with a 4.0 × 28 mm everolimus-eluting platinum chromium stent in his proximal left anterior descending artery. Eight months after the implantation, he developed exertional angina and underwent coronary angiography, which revealed significant in-stent restenosis (ISR). Percutaneous coronary intervention was performed 1 month later, and the pre-procedural optical coherence tomography (OCT) revealed a diffusely bordered and rapidly attenuated signal-poor region with invisible stent struts at ISR site, potentially indicating a "lipid-laden" neointima. The ISR lesion was excised using a novel directional coronary atherectomy catheter. The histological analysis of the retrieved restenotic tissues revealed substantial inflammation characterized by abundant foamy macrophages and T-cell infiltration. This "inflammatory" neointimal tissue with numerous macrophages (without a necrotic core) detected on OCT was not expected owing to the absence of a known feature of macrophages on OCT (i.e., high backscattering with remarkable attenuation). The current histological confirmation of in vivo OCT findings of restenotic neointima indicated that a "lipid-laden" neointima on OCT may not necessarily reflect necrotic core accumulation, and this could be attributed to substantial inflammation with abundant macrophages.

DOI： 10.1536/ihj.17-602

PubMed

researchmap

Language：English   Publisher：(一社)日本心血管インターベンション治療学会  

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

Early identification of high-risk or vulnerable atherosclerotic plaques prone to rupture and performing preemptive therapy prior to catastrophic cardiovascular events are optimal goals of plaque imaging. Despite the advances in imaging modalities to identify vulnerable characteristics, the predictive value of the imaging techniques in the clinical setting is still developing. In this regard, reliable and high-sensitive imaging modalities identifying vulnerable plaque characters that may lead to future cardiovascular events will be useful. In this review article, we describe a current non-invasive plaque imaging technique to identify high-risk coronary plaque features.

DOI： 10.5551/jat.RV17019

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

Intake of hemoglobin by the hemoglobin-haptoglobin receptor CD163 leads to a distinct alternative non-foam cell antiinflammatory macrophage phenotype that was previously considered atheroprotective. Here, we reveal an unexpected but important pathogenic role for these macrophages in atherosclerosis. Using human atherosclerotic samples, cultured cells, and a mouse model of advanced atherosclerosis, we investigated the role of intraplaque hemorrhage on macrophage function with respect to angiogenesis, vascular permeability, inflammation, and plaque progression. In human atherosclerotic lesions, CD163+ macrophages were associated with plaque progression, microvascularity, and a high level of HIF1α and VEGF-A expression. We observed irregular vascular endothelial cadherin in intraplaque microvessels surrounded by CD163+ macrophages. Within these cells, activation of HIF1α via inhibition of prolyl hydroxylases promoted VEGF-mediated increases in intraplaque angiogenesis, vascular permeability, and inflammatory cell recruitment. CD163+ macrophages increased intraplaque endothelial VCAM expression and plaque inflammation. Subjects with homozygous minor alleles of the SNP rs7136716 had elevated microvessel density, increased expression of CD163 in ruptured coronary plaques, and a higher risk of myocardial infarction and coronary heart disease in population cohorts. Thus, our findings highlight a nonlipid-driven mechanism by which alternative macrophages promote plaque angiogenesis, leakiness, inflammation, and progression via the CD163/HIF1α/VEGF-A pathway.

DOI： 10.1172/JCI93025

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1161/CIRCINTERVENTIONS.117.006175

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

BACKGROUND: Despite the success of HMG-CoA reductase inhibitor (statin) therapy in reducing atherosclerotic cardiovascular events, a residual risk for cardiovascular events in patients with coronary artery disease (CAD) remains. Long-chain n-3 polyunsaturated fatty acids (LC n-3 PUFAs), especially eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), are promising anti-atherosclerosis agents that might reduce the residual CAD risk. Non-contrast T1-weighted imaging (T1WI) with cardiac magnetic resonance (CMR) less invasively identifies high-risk coronary plaques as high-intensity signals. These high-intensity plaques (HIPs) are quantitatively assessed using the plaque-to-myocardium signal intensity ratio (PMR). Our goal is to assess the effect of EPA/DHA on coronary HIPs detected with T1WI in patients with CAD on statin treatment. METHODS/DESIGN: This prospective, controlled, randomized, open-label study examines the effect of 12 months of EPA/DHA therapy and statin treatment on PMR of HIPs detected with CMR and computed tomography angiography (CTA) in patients with CAD. The primary endpoint is the change in PMR after EPA/DHA treatment. Secondary endpoints include changes in Hounsfield units, plaque volume, vessel area, and plaque area measured using CTA. Subjects are randomly assigned to either of three groups: the 2 g/day EPA/DHA group, the 4 g/day EPA/DHA group, or the no-treatment group. DISCUSSION: This trial will help assess whether EPA/DHA has an anti-atherosclerotic effect using PMR of HIPs detected by CMR. The trial outcomes will provide novel insights into the effect of EPA/DHA on high-risk coronary plaques and may provide new strategies for lowering the residual risk in patients with CAD on statin therapy. TRIAL REGISTRATION: The University Hospital Medical Information Network (UMIN) Clinical Trials Registry, ID: UMIN000015316 . Registered on 2 October 2014.

DOI： 10.1186/s13063-017-2353-1

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1016/j.atherosclerosis.2017.10.014

Web of Science

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

INTRODUCTION: Polymers are an essential component of drug-eluting stents (DES) used to control drug release but remain the most controversial component of DES technology. There are two types of polymers employed in DES: durable polymer based DES (DP-DES) and biodegradable polymer DES (BP-DES). First-generation DES were exclusively composed of DP and demonstrated increased rates of late stent failure due in part to poor polymer biocompatibility. Newer generations DES use more biocompatible durable polymers or biodegradable polymers. Areas covered: We will cover issues identified with 1st-generation DP-DES, areas of success and failure in 2nd-generation DP-DES and examine the promise and shortcomings of BP-DES. Briefly, fluorinated polymers used in 2nd-generation DP-DES have excellent anti-thrombogenicity and better biocompatibility than 1st-generation DES polymers. However, these devices lead to persistent drug exposure to the endothelium which impairs endothelial function and predisposes towards neoatherosclerosis. Meanwhile, BP-DES has shortened the duration of drug exposure which might be beneficial for endothelial functional recovery leading to less neoatherosclerosis. However, it remains uncertain whether the long-term biocompatibility of bare metal surfaces is better than that of polymer-coated metals. Expert commentary: Each technology has distinct advantages, which can be optimized depending upon the particular characteristics of the patient being treated.

DOI： 10.1080/14779072.2017.1386098

PubMed

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1253/circj.CJ-16-1175

Web of Science

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1093/ehjci/jew153

Web of Science

PubMed

researchmap

Language：English  

DOI： 10.1016/j.jccase.2016.10.016

PubMed

researchmap

Language：Japanese   Publisher：(株)メジカルビュー社  

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

The process of early atherosclerotic plaque progression is characterized by the development of pathologic intimal thickening (PIT) with lipid pool that may transform into the necrotic core to form fibroatheroma, where infiltration of foamy macrophages plays a crucial role. The expansion of the necrotic core is also attributable to intraplaque hemorrhage. Thin-cap fibroatheroma (TCFA) is characterized by a relatively large necrotic core with an overlying thin fibrous cap measuring <65 µm typically containing numerous macrophages, and is considered to be the precursor lesion of plaque rupture which is the most common cause of coronary thrombosis. The second common cause of acute thrombosis is plaque erosion, while calcified nodules is known to be the least frequent cause of coronary thrombosis. Coronary thrombosis can occur without symptoms to form healed lesions, which contributes to an increase in plaque burden and luminal narrowing. The process of plaque progression is generally accompanied by the progression of calcification. An understanding of the histomorphological characteristics of coronary plaques should provide important insights into the pathogenesis, diagnosis, and treatment of atherosclerotic coronary disease for both basic and clinical researchers as well as for clinicians.

DOI： 10.21037/cdt.2016.06.01

PubMed

researchmap

Language：English   Publisher：(一社)日本心血管インターベンション治療学会  

researchmap

Language：Japanese   Publishing type：Research paper (scientific journal)  

PubMed

researchmap

Language：Japanese   Publishing type：Research paper (scientific journal)  

PubMed

researchmap

Language：English  

DOI： 10.1016/j.jcmg.2015.01.012

Web of Science

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1016/j.jcmg.2015.07.011

Web of Science

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1038/nrcardio.2015.164

Web of Science

PubMed

researchmap

Language：English  

DOI： 10.1093/eurheartj/ehv223

Web of Science

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1093/eurheartj/ehv205

Web of Science

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1016/j.jcin.2015.03.029

Web of Science

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1016/j.atherosclerosis.2015.05.011

Web of Science

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1161/CIRCULATIONAHA.114.012658

Web of Science

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1007/s00330-014-3404-6

Web of Science

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1161/CIRCINTERVENTIONS.114.001720

Web of Science

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1253/circj.CJ-14-0897

Web of Science

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1253/circj.CJ-14-1069

Web of Science

PubMed

researchmap

Language：English  

DOI： 10.1016/j.jcmg.2014.08.005

Web of Science

PubMed

researchmap

Language：English  

DOI： 10.1038/nrcardio.2014.62-c2

Web of Science

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.4244/EIJV10I7A143

Web of Science

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.4244/EIJV10I6A124

Web of Science

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1016/j.jacc.2014.03.059

Web of Science

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1093/eurheartj/eht422

Web of Science

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1038/nrcardio.2014.62

Web of Science

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1016/j.jacc.2014.02.607

Web of Science

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1161/CIRCRESAHA.114.302721

Web of Science

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1161/CIRCINTERVENTIONS.113.000990

Web of Science

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.3109/14017431.2014.900185

Web of Science

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

Acute coronary syndrome is the leading cause of death worldwide and plaque rupture is the most common underlying mechanism of coronary thrombosis. During the last 2 decades the understanding of atherosclerotic plaque progression advanced dramatically and pathology studies provided fundamental insights of underlying plaque morphology, which paved the way for invasive imaging modalities, which bring a new area of atherosclerotic plaque characterization in vivo. The development of intravascular ultrasound (IVUS) allowed the field to evaluate the principles of vascular anatomy, which is often underestimated by coronary angiography. Furthermore, IVUS image technologies were developed to obtain improved characterization of plaque composition. However, since spatial resolution of IVUS is insufficient to distinguish details of plaque morphology, a broad adoption of this technology in clinical practice was missing. Optical coherence tomography is a light-based imaging modality with higher spatial resolution compared to IVUS, which enables the assessment of vascular anatomy with great detail.

DOI： 10.1586/14779072.2014.902749

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1161/ATVBAHA.113.302642

Web of Science

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1002/ccd.25010

Web of Science

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1161/CIRCULATIONAHA.113.001790

Web of Science

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1002/ccd.24995

Web of Science

PubMed

researchmap

Language：English  

DOI： 10.1161/CIRCULATIONAHA.113.007267

Web of Science

PubMed

researchmap

Language：English  

DOI： 10.1093/eurheartj/eht259

Web of Science

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

AIMS: Restenosis in drug-eluting stents (DESs) occurs infrequently, however, it remains a pervasive clinical problem. We interrogated our autopsy registry to determine the underlying mechanisms of DES restenosis, and further we investigated the neointimal characteristics of DESs and compared with bare metal stents (BMSs). METHODS AND RESULTS: Coronary lesions from patients with DES implants (n = 82) were categorized into four groups based on cross-sectional area narrowing: patent (<50%), intermediate (50-74%), restenotic (≥ 75% with residual lumen), and total occlusion (organized thrombus within the stent). Restenosis and occlusion were significantly dependent on the total stented length: restenosis (26.7 mm) and occlusion (25.7 mm) compared with patent DESs (17.3 mm). Further, restenotic and occluded lesions were located more distally in the coronary arteries and had greater vessel injury and uneven strut distribution suggesting local drug gradient. Multivariate analysis revealed that normalized maximum inter-strut distance was associated with DES restenosis (OR: 17.4, P = 0.04) while medial tear length was a predictor of DES occlusion (OR: 5.1, P = 0.03). No differences were observed between different DESs (sirolimus-, paclitaxel-, and everolimus-eluting stents) for restenosis and occlusion. Further, neointimal compositions of restenotic DESs demonstrated greater proteoglycan deposition and less smooth muscle cellularity over time, when compared with BMS with greater cell density and collagen deposition. CONCLUSIONS: Our study indicates the impacts of inadequate drug concentration due to wider inter-strut distance and vessel injury as primary mechanisms of DES restenosis and occlusion, respectively. Moreover, the differences in neointimal compositions between DESs and BMSs might serve as a potential target for the suppression of late neointima growth via inhibition of proteoglycans in DESs.

DOI： 10.1093/eurheartj/eht241

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

Mice with homozygous null mutations in the HDL receptor (scavenger receptor class B, type I, or SR-BI) and apolipoprotein E (apoE) genes [SR-BI/apoE double KO (SR-BI(-/-)/apoE(-/-) or dKO) mice] spontaneously develop occlusive, atherosclerotic coronary artery disease (CAD) and die prematurely (50% mortality at 42 d of age). Using microarray mRNA expression profiling, we identified genes whose expression in the hearts of dKO mice changed substantially during disease progression [at 21 d of age (no CAD), 31 d of age (small myocardial infarctions), and 43 d of age (extensive myocardial infarctions) vs. CAD-free SR-BI(+/-)/apoE(-/-) controls]. Expression of most genes that increased >sixfold in dKO hearts at 43 d also increased after coronary artery ligation. We examined the influence and potential mechanism of action of apolipoprotein D (apoD) whose expression in dKO hearts increased 80-fold by 43 d. Analysis of ischemia/reperfusion-induced myocardial infarction in both apoD KO mice and wild-type mice with abnormally high plasma levels of apoD (adenovirus-mediated hepatic overexpression) established that apoD reduces myocardial infarction. There was a correlation of apoD's ability to protect primary cultured rat cardiomyocytes from hypoxia/reoxygenation injury with its potent ability to inhibit oxidation in a standard antioxidation assay in vitro. We conclude that dKO mice represent a useful mouse model of CAD and apoD may be part of an intrinsic cardioprotective system, possibly as a consequence of its antioxidation activity.

DOI： 10.1073/pnas.1315986110

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

BACKGROUND: Re-endothelialization is delayed after drug-eluting stent (DES) implantation. In this setting, neointima is more prone to become lipid laden and develop neoatherosclerosis (NA), potentially increasing plaque vulnerability. METHODS AND RESULTS: Optical coherence tomography and near-infrared spectroscopy with intravascular ultrasound were used to characterize NA in 65 (51 DES and 14 bare-metal stents) consecutive symptomatic patients with in-stent restenosis. Median duration poststent implantation was 33 months. Optical coherence tomography-verified NA was observed in 40 stents with in-stent restenosis (62%), was more prevalent in DES than bare-metal stents (68% versus 36%; P=0.02), and demonstrated significantly higher prevalence of thin-cap neoatheroma (47% versus 7%; P=0.01) in DES. Near-infrared spectroscopy assessment demonstrated that the total lipid core burden index (34 [interquartile range, 12-92] versus 9 [interquartile range, 0-32]; P<0.001) and the density of lipid core burden index (lipid core burden index/4 mm, 144 [interquartile range, 60-285] versus 26 [interquartile range, 0-86]; P<0.001) were higher in DES compared with bare-metal stents. Topographically, NA was classified as I (thin-cap NA), II (thick-cap NA), and III (peri-strut NA). Type I thin-cap neoatheroma was more common in DES (20% versus 3%; P=0.01) and in areas of the stented segment without significant in-stent restenosis (71%). Periprocedural myocardial infarction occurred only in DES (11 versus 0; P=0.05), of which 6 (55%) could be attributed to segments with >70% in-stent restenosis. By logistic regression, prior DES was the only independent predictor of both NA (odds ratio, 7.0; 95% confidence interval, 1.7-27; P=0.006) and periprocedural myocardial infarction (odds ratio, 1.8; 95% confidence interval, 1.1-2.4; P=0.05). CONCLUSIONS: In-stent thin-cap neoatheroma is more prevalent, is distributed more diffusely across the stented segment, and is associated with increased periprocedural myocardial infarction in DES compared with bare-metal stents. These findings support NA as a mechanism for late DES failure.

DOI： 10.1161/CIRCINTERVENTIONS.112.000248

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

Web of Science

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1093/cvr/cvt115

Web of Science

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

The internal mammary artery (IMA) grafts have been associated with long-term patency and improved survival as compared to saphenous vein grafts (SVGs). Early failure of IMA is attributed to poor surgical technique and less with thrombosis. Similarly, bypass surgery especially with the use of IMA has also been shown to be superior at 1-year as well as over five years compared to percutaneous procedures, including the use of drug-eluting stents for the treatment of coronary artery disease. The superiority of IMAs over SVGs can be attributed to its striking resistance to the development of atherosclerosis. Structurally its endothelial layer shows fewer fenestrations, lower intercellular junction permeability, greater anti-thrombotic molecules such as heparin sulfate and tissue plasminogen activator, and higher endothelial nitric oxide production, which are some of the unique ways that make the IMA impervious to the transfer of lipoproteins, which are responsible for the development of atherosclerosis. A better comprehension of the molecular resistance to the generation of adhesion molecules that are involved in the transfer of inflammatory cells into the arterial wall that also induce smooth muscle cell proliferation is needed. This basic understanding is crucial to championing the use of IMA as the first line of defense for the treatment of coronary artery disease.

DOI： 10.3978/j.issn.2225-319X.2013.07.06

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1016/j.atherosclerosis.2012.12.032

Web of Science

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1161/CIRCULATIONAHA.112.001091

Web of Science

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1016/j.hlc.2013.03.001

Web of Science

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1016/j.jcmg.2012.09.015

Web of Science

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

Saphenous vein grafts (SVGs) are the most used conduits in coronary artery bypass graft (CABG) surgery; however, they are susceptible to accelerated atherosclerosis. Clinical studies have shown 10-year patency rates of SVG can be as low as 50% to 60%. This article highlights changes that are observed following CABG surgery using SVG, including intimal thickening to the development of atherosclerotic changes, and how these changes in vein graft are different from those observed in native atherosclerosis. It also discusses the role of risk factors that contribute to acceleration of SVG atherosclerosis.

DOI： 10.1016/j.iccl.2012.11.002

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1016/j.jacc.2012.12.018

Web of Science

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1194/jlr.P030890

Web of Science

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1016/j.jcmg.2012.03.019

Web of Science

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1002/msj.21353

Web of Science

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1016/j.atherosclerosis.2012.06.021

Web of Science

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1016/j.atherosclerosis.2012.04.028

Web of Science

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1038/nrcardio.2012.64

Web of Science

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

It has been more than 3 decades since the introduction of percutaneous transluminal coronary angioplasty for the treatment of coronary artery disease, and the introduction of bare metal stents and drug-eluting stents (DES) has significantly improved clinical outcomes by decreasing rates of acute vessel closure and restenosis. This article reviews pathologic findings from male and female patients who had received coronary stents for acute coronary syndrome and died suddenly with or without complications of stent implantation, at early (<30 days) and late (>30 days) time points after DES implantation.

DOI： 10.1016/j.iccl.2012.01.003

PubMed

researchmap

Language：English  

DOI： 10.1161/CIRCINTERVENTIONS.111.967927

Web of Science

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1161/ATVBAHA.111.240101

Web of Science

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1016/j.jacc.2011.10.852

Web of Science

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1016/j.jcmg.2011.09.015

Web of Science

PubMed

researchmap

DOI： 10.1016/j.carrev.2011.08.001

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

Several randomized and observational studies have reported steady increase in cumulative incidence of late and very late ST (LST/VLST) following first-generation drug-eluting stents (DES: sirolimus-(SES) and paclitaxel-(PES)) up to 5 years. Pathologic studies have identified uncovered struts as the primary substrate responsible for LST/VLST following DES, where delayed arterial healing is associated with stent struts penetrating into the necrotic core, long/overlapping stents, and bifurcation stenting especially in flow divider region. Grade V stent fracture also induces LST/VLST and restenosis. Hypersensitivity reaction is exclusive to SES as an etiology of LST/VLST, whereas malapposition secondary to excessive fibrin deposition is associated with PES. Uncovered struts can be identified in SES and PES with duration of implant beyond 12 months, particularly in stents placed for "off-label" indications. Neoatherosclerosis is another important contributing factor for VLST in DES and bare metal stents (BMS); however, DES shows rapid and more frequent development of neoatherosclerosis than BMS. Future pathologic studies should address the long-term safety of newer generation DES including zotarolimus- and everolimus-eluting stents in terms of the improvement in reendothelialization, decreased inflammation and fibrin deposition as well as a lower incidence of stent fracture-related adverse events, and reduced neoatherosclerosis, which likely contribute to the decreased risk of LST/VLST and better patient outcomes.

DOI： 10.1155/2012/608593

PubMed

researchmap

Language：English  

DOI： 10.1161/CIRCULATIONAHA.111.048736

PubMed

researchmap

Language：English  

DOI： 10.1161/CIRCIMAGING.111.969683

Web of Science

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1016/j.jcin.2011.05.020

Web of Science

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1016/j.jcmg.2011.02.004

Web of Science

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1016/j.jacc.2011.01.011

Web of Science

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1161/CIRCINTERVENTIONS.110.957654

Web of Science

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1016/j.atherosclerosis.2010.09.005

Web of Science

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.4244/EIJV6SUPJA5

Web of Science

PubMed

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1016/j.jcin.2010.01.015

Web of Science

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1097/FJC.0b013e3181c0419c

Web of Science

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1253/circj.CJ-09-0389

Web of Science

PubMed

researchmap

Language：Japanese   Publisher：(NPO)日本冠疾患学会  

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1016/j.jjcc.2008.11.004

Web of Science

PubMed

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：Japanese   Publisher：日本循環制御医学会  

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1253/circj.72.409

Web of Science

PubMed

researchmap

Language：English   Publisher：Japanese Circulation Society  

DOI： 10.1253/circj.72.505

CiNii Books

researchmap

Other Link： http://search.jamas.or.jp/link/ui/2008214974

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1253/circj.71.1703

Web of Science

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1016/j.atherosclerosis.2006.08.023

Web of Science

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1016/j.atherosclerosis.2006.07.028

Web of Science

PubMed

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：Japanese   Publisher：Japan Heart Foundation  

DOI： 10.11281/shinzo1969.39.Supplement3_54

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1016/j.jacc.2006.05.054

Web of Science

PubMed

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1253/circj.69.1154

Web of Science

PubMed

researchmap

J-GLOBAL

researchmap

J-GLOBAL

researchmap

J-GLOBAL

researchmap

J-GLOBAL

researchmap

J-GLOBAL

researchmap

J-GLOBAL

researchmap

J-GLOBAL

researchmap

J-GLOBAL

researchmap

Language：English   Publishing type：Research paper, summary (international conference)  

Web of Science

researchmap

J-GLOBAL

researchmap

J-GLOBAL

researchmap

J-GLOBAL

researchmap

J-GLOBAL

researchmap

J-GLOBAL

researchmap

J-GLOBAL

researchmap

J-GLOBAL

researchmap

J-GLOBAL

researchmap

J-GLOBAL

researchmap

J-GLOBAL

researchmap

Language：English   Publishing type：Research paper, summary (international conference)  

Web of Science

researchmap

Language：English   Publisher：(一社)日本循環器学会  

researchmap

Language：English   Publishing type：Research paper, summary (international conference)  

Web of Science

researchmap

Language：English   Publisher：(一社)日本循環器学会  

researchmap

J-GLOBAL

researchmap

Language：English   Publishing type：Research paper, summary (international conference)  

Web of Science

researchmap

Language：English   Publishing type：Research paper, summary (international conference)  

Web of Science

researchmap

Language：English   Publishing type：Research paper, summary (international conference)  

DOI： 10.1016/j.jacc.2017.09.501

Web of Science

researchmap

Language：Japanese   Publisher：医学書院  

CiNii Books

researchmap

Other Link： http://search.jamas.or.jp/link/ui/2017380440

Language：Japanese   Publisher：(一社)日本心臓病学会  

J-GLOBAL

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：English   Publishing type：Research paper, summary (international conference)  

DOI： 10.1016/S0735-1097(17)34388-7

Web of Science

researchmap

Language：Japanese   Publisher：(一社)日本集中治療医学会  

J-GLOBAL

researchmap

Language：Japanese  

J-GLOBAL

researchmap

Language：English   Publisher：(一社)日本心血管インターベンション治療学会  

researchmap

Language：English   Publisher：(一社)日本心血管インターベンション治療学会  

researchmap

Language：English   Publishing type：Research paper, summary (international conference)  

Web of Science

researchmap

Language：Japanese   Publisher：(一社)日本脈管学会  

researchmap

J-GLOBAL

researchmap

J-GLOBAL

researchmap

Language：Japanese  

J-GLOBAL

researchmap

Language：Japanese  

J-GLOBAL

researchmap

J-GLOBAL

researchmap

Language：English   Publishing type：Research paper, summary (international conference)  

Web of Science

researchmap

Language：English   Publishing type：Research paper, summary (international conference)  

Web of Science

researchmap

Language：English   Publishing type：Research paper, summary (international conference)  

Web of Science

researchmap

Language：Japanese  

J-GLOBAL

researchmap

Language：English  

DOI： 10.3109/14017431.2014.954825

Web of Science

researchmap

Language：English   Publishing type：Research paper, summary (international conference)  

Web of Science

researchmap

Language：English   Publishing type：Research paper, summary (international conference)  

Web of Science

researchmap

Language：English   Publishing type：Research paper, summary (international conference)  

Web of Science

researchmap

Language：English   Publishing type：Research paper, summary (international conference)  

Web of Science

researchmap

Language：English   Publishing type：Research paper, summary (international conference)  

Web of Science

researchmap

Language：English   Publishing type：Research paper, summary (international conference)  

Web of Science

researchmap

Language：English  

DOI： 10.1194/jlr.P030890ERR

Web of Science

researchmap

Language：English   Publishing type：Book review, literature introduction, etc.  

Web of Science

researchmap

Language：English  

DOI： 10.1016/j.hlc.2013.03.001

Web of Science

researchmap

Language：English   Publishing type：Research paper, summary (international conference)  

Web of Science

researchmap

Language：English   Publishing type：Research paper, summary (international conference)  

Web of Science

researchmap

Language：English   Publishing type：Research paper, summary (international conference)  

Web of Science

researchmap

Language：English   Publishing type：Research paper, summary (international conference)  

Web of Science

researchmap

Language：English   Publishing type：Research paper, summary (international conference)  

Web of Science

researchmap

Language：English   Publishing type：Research paper, summary (international conference)  

Web of Science

researchmap

Language：English   Publishing type：Research paper, summary (international conference)  

Web of Science

researchmap

Language：English   Publishing type：Research paper, summary (international conference)  

Web of Science

researchmap

Language：English   Publishing type：Research paper, summary (international conference)  

Web of Science

researchmap

Language：English   Publishing type：Research paper, summary (international conference)  

Web of Science

researchmap

Language：English   Publishing type：Research paper, summary (international conference)  

Web of Science

researchmap

Language：English   Publishing type：Research paper, summary (international conference)  

Web of Science

researchmap

Language：English   Publishing type：Research paper, summary (international conference)  

Web of Science

researchmap

Language：English   Publishing type：Research paper, summary (international conference)  

Web of Science

researchmap

Language：English   Publishing type：Research paper, summary (international conference)  

Web of Science

researchmap

Language：English   Publishing type：Rapid communication, short report, research note, etc. (scientific journal)  

DOI： 10.1161/CIRCULATIONAHA.111.048736

Web of Science

researchmap

Language：English   Publishing type：Research paper, summary (international conference)  

Web of Science

researchmap

Language：English   Publishing type：Research paper, summary (international conference)  

Web of Science

researchmap

Language：English   Publishing type：Research paper, summary (international conference)  

Web of Science

researchmap

Language：English   Publishing type：Research paper, summary (international conference)  

Web of Science

researchmap

Language：English   Publishing type：Research paper, summary (international conference)  

Web of Science

researchmap

Language：English   Publishing type：Research paper, summary (international conference)  

Web of Science

researchmap

Language：English   Publishing type：Research paper, summary (international conference)  

Web of Science

researchmap

Language：English   Publishing type：Research paper, summary (international conference)  

Web of Science

researchmap

Language：English   Publishing type：Research paper, summary (international conference)  

Web of Science

researchmap

Language：English   Publishing type：Research paper, summary (international conference)  

Web of Science

researchmap

Language：English   Publishing type：Research paper, summary (international conference)  

Web of Science

researchmap

Language：English   Publishing type：Research paper, summary (international conference)  

Web of Science

researchmap

Language：English   Publishing type：Research paper, summary (international conference)  

Web of Science

researchmap

Language：English   Publishing type：Research paper, summary (international conference)  

Web of Science

researchmap

Language：English   Publishing type：Research paper, summary (international conference)  

Web of Science

researchmap

Language：English   Publishing type：Research paper, summary (international conference)  

Web of Science

researchmap

Language：English   Publishing type：Research paper, summary (international conference)  

Web of Science

researchmap

Language：English   Publishing type：Research paper, summary (international conference)  

DOI： 10.1016/S0735-1097(11)60629-3

Web of Science

researchmap

Language：English   Publishing type：Research paper, summary (international conference)  

Web of Science

researchmap

Language：Japanese  

CiNii Books

researchmap

Language：English   Publishing type：Research paper, summary (international conference)  

Web of Science

researchmap

Language：English   Publishing type：Research paper, summary (international conference)  

Web of Science

researchmap

Language：English   Publishing type：Research paper, summary (international conference)  

Web of Science

researchmap

Language：English   Publishing type：Research paper, summary (international conference)  

Web of Science

researchmap

Language：English   Publishing type：Research paper, summary (international conference)  

Web of Science

researchmap

Language：English   Publishing type：Research paper, summary (international conference)  

Web of Science

researchmap

Language：English   Publishing type：Research paper, summary (international conference)  

Web of Science

researchmap

Language：English   Publisher：Japanese Circulation Society  

CiNii Books

researchmap

Language：English   Publisher：Japanese Circulation Society  

CiNii Books

researchmap

Language：English   Publishing type：Rapid communication, short report, research note, etc. (scientific journal)  

Web of Science

researchmap