Gap in the prognostic impact of short physical performance battery among phenotypes of heart failure.

BACKGROUND: The Short Physical Performance Battery (SPPB) has been reported to predict clinical outcomes in patients with heart failure (HF). However, whether the discriminative capacity of SPPB score for adverse outcomes varies according to the phenotypes of HF, such as HF with reduced, mid-range, and preserved left-ventricular ejection fraction (HFrEF, HFmrEF, and HFpEF) remains unclear. The aim of this study was to investigate the difference in discriminative capacity of SPPB score for predicting 2-year mortality among phenotypes of HF. METHODS: We consecutively enrolled 542 adult patients admitted for HF (HFrEF, n = 187; HFmrEF, n = 94; HFpEF, n = 261). The patients underwent SPPB score when discharged from hospital. The primary endpoint was all-cause mortality during the 2 years after hospital discharge. We assessed the discriminative capacity of SPPB score for predicting mortality by using receiver operating characteristic (ROC) curve analysis. RESULTS: A total of 95 events (17.5%) occurred during the follow-up period. The area under the curve of ROC (95% confidence interval) was 0.80 (0.71-0.88) in HFrEF, 0.61 (0.46-0.76) in HFmrEF, and 0.70 (0.61-0.79) in HFpEF group. After adjustment for potential confounders, the hazard ratios (95% confidence interval) of the lower SPPB score were 5.38 (2.34-14.6) in HFrEF group, 1.12 (0.36-3.29) in HFmrEF group, and 3.19 (1.68-6.22) in HFpEF group. CONCLUSIONS: Prognostic value of SPPB score varies according to the HF phenotype. SPPB score predicts mortality in patients with HFrEF and HFpEF, but not in patients with HFmrEF. These findings lead to more precise risk prediction by SPPB score in patients with HF.

The ReACT Trial: Randomized Evaluation of Routine Follow-up Coronary Angiography After Percutaneous Coronary Intervention Trial.

OBJECTIVES: The purpose of this study was to evaluate long-term clinical impact of routine follow-up coronary angiography (FUCAG) after percutaneous coronary intervention (PCI) in daily clinical practice in Japan. BACKGROUND: The long-term clinical impact of routine FUCAG after PCI in real-world clinical practice has not been evaluated adequately. METHODS: In this prospective, multicenter, open-label, randomized trial, patients who underwent successful PCI were randomly assigned to routine angiographic follow-up (AF) group, in which patients were to receive FUCAG at 8 to 12 months after PCI, or clinical follow-up alone (CF) group. The primary endpoint was defined as a composite of death, myocardial infarction, stroke, emergency hospitalization for acute coronary syndrome, or hospitalization for heart failure over a minimum of 1.5 years follow-up. RESULTS: Between May 2010 and July 2014, 700 patients were enrolled in the trial among 22 participating centers and were randomly assigned to the AF group (n = 349) or the CF group (n = 351). During a median of 4.6 years of follow-up (interquartile range [IQR]: 3.1 to 5.2 years), the cumulative 5-year incidence of the primary endpoint was 22.4% in the AF group and 24.7% in the CF group (hazard ratio: 0.94; 95% confidence interval: 0.67 to 1.31; p = 0.70). Any coronary revascularization within the first year was more frequently performed in AF group than in CF group (12.8% vs. 3.8%; log-rank p < 0.001), although the difference between the 2 groups attenuated over time with a similar cumulative 5-year incidence (19.6% vs. 18.1%; log-rank p = 0.92). CONCLUSIONS: No clinical benefits were observed for routine FUCAG after PCI and early coronary revascularization rates were increased within routine FUCAG strategy in the current trial. (Randomized Evaluation of Routine Follow-up Coronary Angiography After Percutaneous Coronary Intervention Trial [ReACT]; NCT01123291).

Upregulation of redox-regulating protein, thioredoxin, in endomyocardial biopsy samples of patients with myocarditis and cardiomyopathies.

An important role of redox regulation in myocardial diseases and heart failure has been postulated. Thioredoxin (TRX) is a redox-regulating protein. Recent studies indicated a possible association between plasma TRX concentrations and the severity of heart failure. Accordingly, we investigated the myocardial expression of TRX in patients with myocarditis and cardiomyopathies. Four cases of hypertrophic cardiomyopathy (HCM), 10 of dilated cardiomyopathy (DCM), 6 of myocarditis, and 5 of controls were studied. Right and left ventricular endomyocardial biopsy samples were obtained at the diagnostic cardiac catheterization. The samples were processed for immunohistological staining for TRX, which was done by the indirect immunoperoxidase technique. 8-hydoxy-2'-deoxyguanosine (8-OHdG), one of the major DNA base-modified products, was also detected for an established marker for oxidative stress. TRX immunoreactivity was none or trivial in control specimens. Positive TRX staining was found in 6 cases; 3 in active myocarditis and 3 in DCM. The positive staining was found in infiltrating cells and damaged myocytes in the perinecrotic lesions. Damaged myocytes were also positive for 8-OHdG All the 3 cases of DCM positive for TRX stain showed severe left ventricular hypertrophy on electrocardiogram and highly elevated left ventricular end-diastolic pressure (> 24 mmHg), suggesting the overload of oxidative stress by hemodynamic impairment. Myocardial TRX was upregulated in myocarditis and cardiomyopathies with active necrotic stage associated with DNA damage, which may reflect the oxidative stress overload in hemodynamically uncontrolled status.