SummaryAdiponectin has antiatherosclerotic properties and is also produced in the local coronary circulation. We previously reported that signifi cantly less adiponectin was produced in the coronary circulation of patients with than without coronary artery disease (CAD). The goal of this study was to determine whether adiponectin production in the coronary circulation could predict future cardiovascular events in patients with CAD.Forty-eight CAD patients whose left anterior descending coronary arteries required percutaneous coronary intervention (PCI) were enrolled. The amount of adiponectin production in the coronary circulation was defi ned as the plasma adiponectin level at the great cardiac vein minus that at the orifi ce of the left coronary artery. All patients were divided by adiponectin production level in the coronary circulation into the adiponectin-positive production group (> 0 µg/ mL) and adiponectin-negative production group (≤ 0 µg/mL). Median follow-up period was 66 months (maximum, 108 months). The primary endpoint was the combined occurrence of major adverse cardiovascular events (MACE), including rehospitalization due to unstable angina, heart failure, nonfatal myocardial infarction, revascularization with PCI or coronary artery bypass grafting, ischemic stroke, and cardiovascular death.Sixteen MACE occurred. The incidence of MACE was signifi cantly higher in the adiponectin-negative production group than in the adiponectin-positive production group (P = 0.02). In multivariate analysis, adiponectin-negative production was a predictor of MACE (P = 0.03). Kaplan-Meier analysis revealed that the MACE-free rate was signifi cantly lower in the adiponectin-negative production group than in the adiponectin-positive production group.Adiponectin production in the coronary circulation with CAD may be associated with MACE. (Int Heart J 2014; 55: 239-243)
Objective: With respect to liver function and heart failure, 46% of acute decompensated heart failure patients exhibit abnormal liver function. However, there have been no reports of the association between liver function and functional capacity in these patients. Our aim was to clarify the relationship between liver function and functional capacity using the peak oxygen uptake (VO 2 ). Methods: We retrospectively identified 36 heart failure patients who were referred to our rehabilitation laboratory. These patients underwent cardiopulmonary exercise testing (CPX). Furthermore, we investigated the correlations between peak VO 2 , blood measurements [e.g., total bilirubin (T-bil) and brain natriuretic peptide], and echocardiographic parameters. Finally, multivariate regression analysis was performed to investigate the independent variables related to peak VO 2 . Results: The mean peak VO 2 was 10.7±2.9 ml/kg/min. Peak VO 2 during CPX correlated inversely with T-bil [r=-0.379, 95% confidence intervals (CI): −0.654 to −0.014, P=0.043], aspartate transaminase (r=-0.426, 95% CI: −0.685 to −0.07, P=0.021), and peak heart rate (r=0.391, 95% CI: 0.029 to 0.663, P=0.036). The significant independent factors associated with peak VO 2 were treatment with statin (β=-3.19, P=0.015) and T-bil levels (β=-4.27, P=0.002). Conclusion: Our findings demonstrated that liver function may contribute to the functional capacity in heart failure patients.
A 79-year-old man with chest pain and dyspnea underwent emergency percutaneous coronary intervention for acute myocardial infarction. However, he died 17 days later due to refractory heart failure. An autopsy revealed cardiac strangulation caused by herniation of the apical heart through a pericardial defect due to partial absence of the pericardium. (
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