Cardiac Strangulation Due to Partial Pericardial Defect Presenting as Acute Myocardial Infarction.

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. (Level of Difficulty: Advanced.).

Association Between Liver Function and Peak Oxygen Uptake in Heart Failure Patients: A Retrospective Observational Study.

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 (VO2). 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 VO2, 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 VO2. RESULTS: The mean peak VO2 was 10.7±2.9 ml/kg/min. Peak VO2 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 VO2 were treatment with statin (ß=-3.19, P=0.015) and T-bil levels (ß=-4.27, P=0.002). CONCLUSION: Our findings demonstrated that liver function may contribute to the functional capacity in heart failure patients.

Association between adiponectin production in coronary circulation and future cardiovascular events in patients with coronary artery disease.

Adiponectin has antiatherosclerotic properties and is also produced in the local coronary circulation. We previously reported that significantly 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 defined as the plasma adiponectin level at the great cardiac vein minus that at the orifice 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 significantly 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 significantly 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.

A better effect of cilostazol for reducing in-stent restenosis after femoropopliteal artery stent placement in comparison with ticlopidine.

PURPOSE: The purpose of this study was to assess the preventive effect of cilostazol on in-stent restenosis in patients after superficial femoral artery (SFA) stent placement. MATERIALS AND METHODS: Of 28 patients with peripheral arterial disease, who had successfully undergone stent implantation, 15 received cilostazol and 13 received ticlopidine. Primary patency rates were retrospectively analyzed by means of Kaplan-Meier survival curves, with differences between the two medication groups compared by log-rank test. A multivariate Cox proportional hazards model was applied to assess the effect of cilostazol versus ticlopidine on primary patency. RESULTS: The cilostazol group had significantly better primary patency rates than the ticlopidine group. Cumulative primary patency rates at 12 and 24 months after stent placement were, respectively, 100% and 75% in the cilostazol group versus 39% and 30% in the ticlopidine group (P = 0.0073, log-rank test). In a multivariate Cox proportional hazards model with adjustment for potentially confounding factors, including history of diabetes, cumulative stent length, and poor runoff, patients receiving cilostazol had significantly reduced risk of restenosis (hazard ratio 5.4; P = 0.042). CONCLUSION: This retrospective study showed that cilostazol significantly reduces in-stent stenosis after SFA stent placement compared with ticlopidine.