Angioscopic findings 1 year after percutaneous coronary intervention for chronic total occlusion.

BACKGROUND: Chronic total occlusion (CTO) is a high-risk factor for stent thrombosis, but little is known about the difference in neointimal healing between CTO and non-CTO lesions regarding implanted stents. We investigated factors affecting neointimal healing after stent implantation for CTO and non-CTO lesions using angioscopy. METHODS: We retrospectively evaluated 106 stents in 85 consecutive patients between March 2016 and July 2020. Their average age was 68 ±â€¯11 years, and participants (73 male and 12 female) underwent follow-up angiography and angioscopy 1 year after percutaneous coronary intervention (PCI). The stents (n = 106) were divided into three groups according to the lesion status at the previous PCI: CTO (n = 17), acute coronary syndrome (ACS) (n = 35), and stable coronary artery disease without CTO or non-CTO (n = 54). RESULTS: The neointimal stent coverage grade was significantly lower in the CTO and ACS groups than in the non-CTO group (0.4 ±â€¯0.5, 0.9 ±â€¯0.8, and 1.4 ±â€¯0.8, respectively, p < 0.001). Thrombi were significantly more frequent in CTO and ACS than in non-CTO (71 %, 51 %, and 15 %, respectively, p < 0.001). The yellow grade in CTO was comparable to that in ACS but significantly higher in CTO than in non-CTO (CTO vs. ACS vs. non-CTO 1.5 ±â€¯0.7, 1.4 ±â€¯0.6, and 0.9 ±â€¯0.7, respectively, p = 0.007). CONCLUSIONS: Delayed healing occurs in stents implanted for CTO lesions. Longer dual-antithrombotic therapy may be beneficial.

External Validation of the Kumamoto Criteria in Transthyretin Amyloid Cardiomyopathy Screening　- A Retrospective Cohort Study.

Background: The Kumamoto criteria have been proposed as a non-invasive screen for transthyretin amyloid cardiomyopathy. This study assessed the validity of the Kumamoto criteria externally. Methods and Results: The study included 138 patients (median age 73 years; 65% male) who underwent 99 mTc-pyrophosphate (PYP) scintigraphy. Patients were divided into 4 groups according to total scores on the Kumamoto criteria (i.e., 0-3) for the following 3 factors: high-sensitivity cardiac troponin T ≥0.0308 ng/mL, wide (≥120 ms) QRS, and left ventricular posterior wall thickness ≥13.6 mm. The diagnostic performance and positive predictive value (PPV) of the Kumamoto criteria for positive 99 mTc-PYP scintigraphy were validated. Eighteen (13%) patients were positive on 99 mTc-PYP scintigraphy. The Kumamoto criteria had a favorable diagnostic performance (area under the curve 0.808). The PPV for groups with scores of 0, 1, 2, and 3 was 0% (n=0/42), 11% (n=6/57), 21% (n=7/33), and 83% (n=5/6), respectively, which is lower, particularly for those with a score of 2, than in the original Kumamoto cohort. However, the PPV increased after combining the Kumamoto criteria with a history of orthopedic diseases (spinal canal stenosis and/or carpal tunnel syndrome). Conclusions: This study suggests that the Kumamoto criteria have a favorable diagnostic performance; however, the PPV may decrease depending on the study population. Combining the Kumamoto criteria with the presence of orthopedic disease may improve the PPV.

Vascular Endothelial Dysfunction in Myeloproliferative Neoplasms and Gene Mutations.

Essential thrombocythemia (ET) and polycythemia vera (PV), are common Philadelphia-negative myeloproliferative neoplasms (MPN). Patients with MPN have a high rate of cardiovascular complications and often have acquired JAK2V617F and CALR genetic mutations. In this study, we aimed to analyze vascular endothelial function in patients with MPN.We evaluated 27 outpatients, including 10 patients diagnosed with MPN, flow-mediated dilatation (FMD), and nitroglycerin-mediated dilation (NMD), between September 2014 and August 2016. We measured serum adiponectin, which protects vascular endothelial function, and serum asymmetric dimethyl arginine (ADMA), which inhibits the production of adiponectin. The presence or absence of JAK2V617F and CALR mutations was evaluated in patients with MPN.Venous thrombosis was observed more frequently in patients with MPN than in those without. Seven MPN patients were diagnosed with PV, and 3 MPN patients were diagnosed with ET. JAK2V617F and CALR mutations were found in 5 and 3 MPN patients, respectively. FMD was significantly lower in JAK2V617F-positive MPN patients than in JAK2V617F-negative MPN patients, although NMD, adiponectin, and ADMA were similar in both groups. Adiponectin levels were higher and ADMA levels were lower in CALR-positive MPN patients than in CALR-negative MPN patients. There was no difference in FMD and NMD prevalence between the 2 groups. Furthermore, we had 3 representative MPN patients who were complicated with coronary spasm, possibly caused by MPN-related endothelial dysfunction.We found that patients with MPN presented with endothelial dysfunction, which was related to the presence of genetic mutations and was sometimes associated with cardiovascular disease.

Empagliflozin confers reno-protection in acute myocardial infarction and type 2 diabetes mellitus.

AIMS: Although the reno-protective effects of sodium-glucose cotransporter 2 inhibitors are known in patients with heart failure or type 2 diabetes mellitus (T2DM), this effect has not been confirmed in patients with acute myocardial infarction (AMI). METHODS AND RESULTS: The prospective, multicentre, randomized, double-blind, placebo-controlled EMBODY trial investigated patients with AMI and T2DM in Japan. The eligible patients included adults aged 20 years or older, diagnosed with AMI and T2DM, and who could be discharged within 2-12 weeks after the onset of AMI. One hundred and five patients were randomized (1:1) to receive once daily 10 mg empagliflozin or placebo within 2 weeks of AMI onset. In this sub-analysis, we investigated the time course of renal functional parameters such as serum creatinine levels and estimated glomerular filtration rate (eGFR) from baseline to Weeks 4, 12, and 24. Ninety-six patients (64 ± 11 years, 78 male) were included in the full analysis (n = 46 and 50 in the empagliflozin and placebo groups, respectively). We used serum creatinine and eGFR as indicators of renal function. In the placebo group, eGFR decreased from 66.14 mL/min/1.73 m2 at baseline to 62.77 mL/min/1.73 m2 by Week 24 (P = 0.023) but remained unchanged in the empagliflozin group (from 64.60 to 64.36 mL/min/1.73 m2 , P = 0.843). In the latter group, uric acid improved from 5.8 mg/dL at baseline to 4.9 mg/dL at Week 24 (P < 0.001). In the earlier analysis of 56 patients with eGFR ≥ 60 mL/min/1.73 m2 , the eGFR decreased and the serum creatinine increased from baseline to 24 weeks in the placebo group, significantly different to the empagliflozin group (-6.61 vs. +0.22 mL/min/1.73 m2 , P = 0.008 and +0.063 vs. -0.001 mg/dL, P = 0.030, respectively). The changes in serum creatinine and eGFR from baseline to Week 24 were significantly correlated with those in uric acid in the placebo group (r = 0.664, P < 0.001 and r = -0.675, P < 0.001, respectively) but not in the empagliflozin group. CONCLUSIONS: Empagliflozin prevented the kidney functional decline in patients with AMI and T2DM, especially those with baseline eGFR ≥ 60 mL/min/1.73 m2 . Early administration of sodium-glucose cotransporter 2 inhibitors in these patients is considered desirable for renal protection.

Bisoprolol transdermal patch for perioperative care of non-cardiac surgery in patients with hypertrophic obstructive cardiomyopathy.

BACKGROUND: Non-cardiac surgery for hypertrophic obstructive cardiomyopathy (HOCM) is considered to require meticulous perioperative care. ß-blockers are considered the first-line drugs for patients with HOCM, and they play a key role in preventing cardiovascular complications in perioperative care. The bisoprolol transdermal patch has recently become available in Japan, and it is useful for patients who are unable to take oral medication during perioperative care. The aim of this case series was to assess the hemodynamic features of patients with HOCM who used the bisoprolol transdermal patch during perioperative care for non-cardiac surgery. METHODS: Between August 2016 and August 2018, we retrospectively analyzed 10 consecutive cases of HOCM with the patients using the bisoprolol transdermal patch during perioperative care. Hemodynamic and echocardiographic features were evaluated before and after patients were switched from oral bisoprolol to transdermal patch therapy or started transdermal patch therapy as a new ß-blocker medication. In addition, cardiovascular complications (all-cause death, cardiac death, heart failure, ventricular tachycardia, and ventricular fibrillation) during the perioperative period were evaluated. RESULTS: There was no significant change in the patients' heart rate, blood pressure, ejection fraction, and pressure gradient in the left ventricle after switching from oral bisoprolol to the transdermal patch therapy. On the other hand, patients who started using the bisoprolol transdermal patch as a new ß-blocker medication tended to have a decreased heart rate and pressure gradient thereafter, but there was no significant difference in blood pressure or ejection fraction. No cardiovascular complications occurred during the perioperative period. CONCLUSIONS: We described the utilization of the bisoprolol transdermal patch during perioperative care for non-cardiac surgery in patients with HOCM. We determined that the hemodynamic features of these patients did not change significantly after switching to patch therapy. Further, initiation of the bisoprolol transdermal patch as a new ß-blocker medication sufficiently tended to decrease the pressure gradient. This unique approach can be an alternate treatment option for HOCM. TRIAL REGISTRATION: The registry was registered in the University Hospital Medical Information Network Clinical Trials Registry (UMIN000036703). The date of registration was 10/5/2019 and it was "Retrospectively registered".

A novel application of the culotte stent technique to bail out a jailed common iliac artery.

Implanting a self-expandable stent at the ostium of the common iliac artery (CIA) may lead to coverage of the orifice of the contralateral CIA. Here, we describe a novel application of the culotte stent technique using a balloon-expandable stent to bail out an ostial stenotic legion of a jailed CIA due to prior self-expandable stent placement. The bilateral CIAs were revascularized by culotte stenting, and patency of the stents was confirmed 3 years after the procedure. The culotte stent technique was successfully applied to an ostial stenotic lesion of a jailed CIA.

Superiority of the extracellular volume fraction over the myocardial T1 value for the assessment of myocardial fibrosis in patients with non-ischemic cardiomyopathy.

PURPOSE: This study aimed to assess the efficacies of the myocardial T1 value and the extracellular volume fraction (ECV) for determining the severity of myocardial fibrosis in patients with non-ischemic cardiomyopathy. MATERIALS AND METHODS: Myocardial fibrosis is considered the most important indicator of cardiac damage associated with non-ischemic cardiomyopathy. Recently, modified Look-Locker inversion recovery imaging (MOLLI) has been used for T1 mapping and measurement of the ECV for the assessment of myocardial fibrosis. The present study included 22 patients (mean age, 61.5±12.7; 21 male) with non-ischemic heart failure. Motion corrected myocardial T1 mapping was automatically performed using a MOLLI sequence, and the ECV was estimated from the pre- and post-contrast blood and myocardial T1 values corrected for the hematocrit level. All endomyocardial biopsy specimens were obtained from the inferoposterior left ventricular wall. The percentage of myocardial fibrosis (%F) was determined after Elastica Masson-Goldner staining as follows: (fibrosis area/[fibrosis area+myocardial area])×100. RESULTS: No correlation was noted between the %F and the pre- (r=0.290, p=0.191) or post-contrast T1 values (r=-0.190, p=0.398); however, a significant correlation was noted between the %F and ECV (r=0.750, p<0.001). CONCLUSIONS: In this study, the ECV reflected the extent of myocardial fibrosis, but the pre- and post-contrast T1 values did not. The ECV may be used to estimate the severity of myocardial fibrosis in patients with non-ischemic cardiomyopathy.

Autophagic vacuoles in cardiomyocytes of dilated cardiomyopathy with initially decompensated heart failure predict improved prognosis.

Autophagy is a process of bulk protein degradation and organelle turnover, and is a current therapeutic target in several diseases. The present study aimed to clarify the significance of myocardial autophagy of patients with dilated cardiomyopathy (DCM). Left ventricular endomyocardial biopsy was performed in 250 consecutive patients with DCM (54.9±13.9 years; male, 79%), initially presenting with decompensated heart failure (HF). The association of these findings with HF mortality or recurrence was examined. Myofilament changes, which are apparent in the degenerated cardiomyocytes of DCM, were recognized in 164 patients (66%), and autophagic vacuoles in cardiomyocytes were identified in or near the area of myofilament changes in 86 patients (34%). Morphometrically, fibrosis (odds ratio [OR], 0.96; 95% confidence interval [CI], 0.93 to 0.99) and mitochondrial abnormality (OR, 2.24; 95% CI, 1.23 to 4.08) were independently related with autophagic vacuoles. During the follow-up period of 4.9±3.9 y, 24 patients (10%) died, including 10 (4%) who died of HF, and 67 (27%) were readmitted for HF recurrence. Multivariate analysis identified a family history of DCM (hazard ratio [HR], 2.117; 95% CI, 1.199 to 3.738), hemoglobin level (HR, 0.845; 95% CI, 0.749 to 0.953), myofilament changes (HR, 13.525; 95% CI, 5.340 to 34.255), and autophagic vacuoles (HR, 0.214; 95% CI, 0.114 to 0.400) as independent predictors of death or readmission due to HF recurrence. In conclusion, autophagic vacuoles in cardiomyocytes are associated with a better HF prognosis in patients with DCM, suggesting autophagy may play a role in the prevention of myocardial degeneration.

Successful early diagnosis and treatment in a case of Toxocara canis-induced eosinophilic myocarditis with eosinophil-rich pericardial effusion.

Fulminant myocarditis can become fatal if left untreated. Treatments for most types of myocarditis, including mechanical support, are limited. However, immediate systemic corticosteroids are known to be effective against eosinophilic myocarditis; therefore, prompt diagnosis of this disease is crucial. Unfortunately, the standard diagnostic tool for myocarditis, endomyocardial biopsy, does not provide immediate histopathological findings. Thus, a rapid diagnostic tool for identifying types of myocarditis is urgently required. We report here the first case of Toxocara canis-induced eosinophilic fulminant myocarditis which was diagnosed based on eosinophil-rich pericardial effusion where the patient recovered with early corticosteroid therapy.

Patients with reduced heart rate response to adenosine infusion have low myocardial flow reserve in (13)N-ammonia PET studies.

To assess the effect of adenosine infusion by evaluating the relationship between heart rate (HR) response to adenosine and myocardial flow reserve (MFR) of remote regions supplied by normal coronary arteries in (13)N-ammonia PET. Thirty-one consecutive subjects (20 known coronary artery disease patients, 4 chronic heart failure patients, and 7 normal volunteers) except cases having 3-vessel disease underwent rest and adenosine stress (13)N-ammonia myocardial perfusion PET. Semi-quantitative, quantitative, and gated analyses were performed. Subjects were divided into two groups with regard to HR response to adenosine. Twenty-two subjects had normal HR response (peak/rest HR > 1.20), while reduced HR response (≤ 1.20) was observed in nine subjects. There were no differences in rest myocardial blood flow (MBF) of remote regions between the groups. Subjects with reduced HR response had significantly lower stress MBF and MFR of remote regions than those with normal HR response (stress MBF: 1.559 ± 0.517 vs. 2.279 ± 0.530, p = 0.004, MFR: 1.59 ± 0.36 vs. 2.35 ± 0.53, p = 0.001). There were no significant differences between the groups by means of semi-quantitative scoring. Rest and stress ejection fraction (EF) in the reduced HR response group was lower than that in the normal HR response group. In a multiple stepwise regression analysis, HR ratio, dyslipidemia, and Brinkman index were identified as predictors of the change in MFR of remote regions. Subjects with reduced HR response to adenosine had lower stress MBF and MFR of remote regions and lower EF. Moreover, HR response was one of the predictors of the change in MFR of remote regions.

Impact of time-of-flight on qualitative and quantitative analyses of myocardial perfusion PET studies using (13)N-ammonia.

BACKGROUND: The impact of time-of-flight (TOF) in myocardial perfusion (13)N-ammonia positron emission tomography (PET) is unclear. METHODS AND RESULTS: Twenty consecutive subjects underwent rest and adenosine stress (13)N-ammonia myocardial perfusion PET. Two sets of images were reconstructed using TOF-ordered subset expectation maximization (TOF-OSEM) and 3-dimensional row-action maximum likelihood algorithm (3D-RAMLA). Qualitative and quantitative analyses from the TOF-OSEM and 3D-RAMLA reconstructions were compared. Count profile curves revealed that TOF relatively increased the uptake of (13)N-ammonia at the lateral walls, and apical thinning was emphasized on the TOF images. Both segmental rest and stress myocardial blood flow (MBF) values were higher with TOF-OSEM use than with 3D-RAMLA use (rest MBF: 0.955 ± 0.201 vs 0.836 ± 0.185, P < .001; stress MBF: 2.149 ± 0.697 vs 2.058 ± 0.721, P < .001). The differentiation of MBF between reconstructions was more enhanced under rest conditions. Thus, segmental myocardial flow reserve (MFR) observed using TOF-OSEM reconstruction was lower than that observed using 3D-RAMLA (2.25 ± 0.57 vs 2.46 ± 0.75, P < .001). No remarkable differences were observed between segmental and territorial results. CONCLUSIONS: TOF increased lateral wall counts and emphasized apical thinning. Quantitatively, TOF reconstruction showed increased MBF, especially under relatively low perfusion conditions.

Ultrastructural features of cardiomyocytes in dilated cardiomyopathy with initially decompensated heart failure as a predictor of prognosis.

AIMS: The aim of the present study was to clarify the significance of myocardial ultrastructural changes in patients with dilated cardiomyopathy (DCM). METHODS AND RESULTS: Endomyocardial biopsy of the left ventricle was performed in 250 consecutive DCM patients (54.9 ± 13.9 years, 79% men), presenting initially as decompensated heart failure (HF). Myofilament changes of cardiomyocytes were evaluated by electron microscopy and compared with clinical and morphometric data. Mortality and HF recurrence were evaluated during the follow-up period. During the follow-up period (4.9 ± 3.9 years), 24 patients (10%) died and 67 (27%) were readmitted because of HF recurrence, including those who had died because of HF. Myofilament changes, classified as either focal derangement of myofilaments (sarcomere damage) or diffuse myofilament lysis (disappearance of most sarcomeres in cardiomyocytes), were identified in 164 patients (66%). Multivariate analysis identified a family history of DCM [hazard ratio (HR) 4.763; 95% confidence interval (CI) 1.012-12.518], atrial fibrillation (HR 6.132; 95% CI 2.188-17.180), haemoglobin level (HR 0.685; 95% CI 0.528-0.889), and diffuse myofilament lysis (HR 4.048; 95% CI 1.427-11.481) as independent predictors of mortality. A family history of DCM (HR 2.268; 95% CI 1.276-4.030), haemoglobin level (HR 0.876; 95% CI 0.785-0.979), focal derangement of myofilaments (HR 7.431; 95% CI 2.916-18.934), and diffuse myofilament lysis (HR 6.480; 95% CI 2.403-17.473) were predictors of readmission due to HF recurrence. CONCLUSIONS: In DCM patients with first-decompensated HF, myofilament changes are strongly associated with mortality and HF recurrence.

Impact of sleep-disordered breathing and efficacy of positive airway pressure on mortality in patients with chronic heart failure and sleep-disordered breathing: a meta-analysis.

BACKGROUNDS: To conduct a meta-analysis to investigate whether sleep-disordered breathing (SDB) is an independent risk factor for mortality and whether positive airway pressure (PAP) decreases mortality in patients with chronic heart failure (HF). The impact of SDB and the effects of PAP on mortality in patients with chronic HF remain unclear. METHODS: We searched the MEDLINE, EMBASE, and Cochrane databases. Clinical trials that addressed mortality and the effect of PAP on mortality in chronic HF patients with SDB were included in this meta-analysis. RESULTS: Eleven studies (1,944 participants in total) that addressed mortality in chronic HF patients with SDB were included in this study. Patients with SDB showed a significantly increased mortality risk compared to those without SDB [risk ratio (RR) 1.66 (1.19-2.31)]. In sub-analyses, a significant increase in risk of mortality was observed for central sleep apnea versus no-SDB [RR 1.48 (1.15-1.91)], whereas no significant increase in risk was observed for obstructive sleep apnea versus no-SDB. Five randomized controlled studies (395 participants) that assessed the effect of PAP in chronic HF patients with SDB were analyzed. Adaptive servo-ventilation (ASV) significantly reduced all-cause mortality in chronic HF patients with SDB [RR 0.13 (0.02-0.95)], whereas continuous PAP did not significantly reduce all-cause mortality [RR 0.71 (0.32-1.57)]. CONCLUSIONS: The prevalence of SDB in patients with chronic HF is associated with worse survival, and ASV reduces all-cause mortality in patients with chronic HF concomitant with SDB.

Myocardial alterations and clinical implications associated with recovery of cardiac function in dilated cardiomyopathy with obesity.

BACKGROUND: Obesity is associated with an increased risk of heart failure (HF) but the relationship between changes in cardiac function and the specific pathological features of dilated cardiomyopathy (DCM) with obesity, remains unknown. METHODS: Endomyocardial biopsies from the left ventricle (LV) were obtained from 50 patients with DCM, at the first-onset of decompensated HF. Thirty patients were obese (obese-group: body mass index >30 kg/m(2)) and 20 were non-obese (lean-group). Clinical data were acquired at the admission, after one month and one year. RESULTS: The obese-group had higher systolic blood pressure (142.8 ± 33.9 vs 113.6 ± 18.7 mm Hg; p<0.001) and serum troponin-T level (0.049 ± 0.07 vs 0.020 ± 0.03 ng/mL; p=0.022) than the lean-group. LV ejection fraction (LVEF) was not significantly different between groups, but after one year the obese-group had an improved LVEF (57.0 ± 11.4 vs 44.3 ± 17.1; p=0.003). Light microscopy revealed that the obese-group had larger cardiomyocytes (17.2 ± 1.7 vs 16.4 ± 1.4 µm; p=0.033) and less myofilament lysis (37 vs 75%; p=0.008) with a higher density of lipid droplets (1.93 ± 0.8 vs 0.94 ± 0.7 /µm(2); p<0.001). Multivariate regression analysis revealed that independent predictors of LVEF improvement after 12 months were diuretics use, nuclear diameter, and absence of myofilament lysis (p=0.024, 0.012 and 0.028, respectively). CONCLUSIONS: Cardiac function in most patients with DCM with obesity is reversible and myocardial structural changes are trivial even at the ultrastructural level.

Controlled-release basic fibroblast growth factor for peripheral artery disease: comparison with autologous bone marrow-derived stem cell transfer.

OBJECTIVE: We examined the safety and efficacy of controlled-release basic fibroblast growth factor (b-FGF) for peripheral artery disease (PAD), compared with autologous bone marrow mononuclear cell implantation (BMCI). BACKGROUND: We recently developed a b-FGF-incorporated biodegradable hydrogel that enables slow-releasing drug delivery system. METHODS: PAD patients were divided into a b-FGF group (n=10) and BMCI group (n=15). Injection of gelatin hydrogel containing 600 µg b-FGF or BMCI (0.4-5.1×10(10) cell) was performed. Visual analog pain scale (VAS), (99m)technetium-tetrofosmin (Tc-TF) scintigraphy, transcutaneous oxygen tension (TcPO(2)), and ankle-brachial index (ABI) were evaluated before and 4 weeks after each treatment, and 2-year prognosis was determined. RESULTS: VAS (b-FGF 67±15 to 4±5, p<0.01, BMCI 67±42 to 5±9 mm, p<0.01) and TcPO(2) (b-FGF 16±14 to 47±17, p<0.01, BMCI 13±13 to 37±21 mmHg, p<0.01) were significantly improved in both groups. Tc-TF and ABI were not changed. Prognosis was similar between the groups (b-FGF 91%, BMCI 80%, NS). CONCLUSION: Controlled-release b-FGF is as safe as BMCI, and its efficacy appears to be comparable. Thus, this therapy may be an alternative to BMCI.

Angioscopic study of silent plaque disruption in nonischemic related coronary artery in patients with stable ischemic heart disease.

Plaque disruption, which may be associated with some coronary risk factors, plays a key role in the development of acute coronary syndromes and progression of atherosclerosis. However, the clinical profile of asymptomatic plaque disruption in stable ischemic heart disease has not been well evaluated. The aim of the present study was to investigate the frequency and determinants of silent plaque disruption (SPD) in patients with stable ischemic heart disease using coronary angioscopy. Forty-one patients with stable angina or old myocardial infarction (OMI) without any complaints within 3 months were included in the present study. Angioscopy was successfully performed through 49 nonischemic related coronary arteries. The presence of SPD and coronary risk factors were recorded. Silent plaque disruption was found in 12 patients with stable ischemic heart disease (12/41, 29.3%), and the frequency of SPD in nonischemic related coronary arteries was 26.5% (13/49). A significantly higher frequency of SPD was noted in yellow plaques than in white plaques (35.3% versus 6.7%, P = 0.043). Overall, the independent clinical risk factors of SPD in nonischemic related coronary arteries were diabetes mellitus (P = 0.018; OR, 18.8209; 95% CI, 1.6525 to 214.3523) and hypertension (P = 0.0313; OR, 6.6485; 95% CI, 1.1850 to 37.3019). These results suggest silent plaque disruption was commonly observed in nonischemic related coronary arteries in patients with stable ischemic heart disease and its determinants were diabetes mellitus and hypertension.