Mitochondrial DNA (mtDNA) copy number variation (CNV), which reflects the oxidant-induced cell damage, has been observed in a wide range of human diseases. However, whether it correlates with heart failure, which is closely related to oxidative stress, has never been elucidated before. We aimed to systematically investigate the associations between leukocyte mtDNA CNV and heart failure risk and prognosis. A total of 1700 hospitalized patients with heart failure and 1700 age- and sex-matched community population were consecutively enrolled in this observational study, as well as 1638 (96.4%) patients were followed prospectively for a median of 17 months (12-24 months). The relative mtDNA copy number of leukocyte of peripheral blood or cardiac tissue was measured in triplicate by quantitative real-time PCR method. Patients with heart failure possessed much lower relative mtDNA copy number compared with control subjects (median 0.83, interquartile range [IQR] 0.60-1.16 vs median 1.00, IQR 0.47-2.20; P < 0.001), especially for the patients with ischemic etiology (median, 0.77 for ischemic and 0.91 for non-ischemic, P < 0.001). Patients with lower mtDNA copy number exhibited 1.7 times higher risk of heart failure (odds ratio 1.71, 95% confidence interval [CI] 1.48-1.97, P < 0.001). Long-term follow-up (median of 17 months) showed that decreased mtDNA copy number was significant associated with both increased cardiovascular deaths (hazard ratio [HR] 1.58, 95% CI 1.16-2.16, P = 0.004) and cardiovascular rehospitalization (HR 1.48, 95% CI 1.21-1.82, P < 0.001). After adjusting for the conventional risk factors and medications, lower mtDNA copy numbers were still significantly associated with 50% higher cardiovascular mortality (P = 0.035). In conclusion, mtDNA copy number depletion is an independent risk factor for heart failure and predicts higher cardiovascular mortality in patients with heart failure.

MiR-124 aggravates failing hearts by suppressing CD151-facilitated angiogenesis in heart MiR-124 aggravates failing hearts by suppressing CD151-facilitated angiogenesis in heart

Background: To determine the effects of inspiratory muscle training (IMT) alone on inspiratory muscle strength and endurance, pulmonary function, pulmonary complications, and length of hospital stay in patients undergoing coronary artery bypass graft surgery (CABG). Methods: We conducted a literature search across databases (Ovid MEDLINE(R) and Epub Ahead of Print, In-Process & Other Non-Indexed Citations and Daily; Ovid Embase; Ovid Cochrane Central Register of Controlled Trials; Ovid Cochrane Database of Systematic Reviews; and Scopus) from inception to December 2021. The eligibility criteria were randomized controlled trials that investigated the effects of IMT versus usual care or sham IMT in patients undergoing CABG. Results: A total of 12 randomized clinical trials with 918 patients were included in the meta-analysis. Postoperative IMT was associated with improved maximal inspiratory pressure (MIP), maximum inspiratory pressure (PImax), and six-minute walking test (6MWT) and with a decrease in length of hospital stay (LOS). For preoperative IMT, there was statistical significance between intervention and MIP, PImax, forced expiratory volume in one second (FEV1), forced vital capacity (FVC), postoperative pulmonary complications (PPCs), and LOS. Pre- and postoperative IMT resulted in improvements in MIP. Conclusions: Isolated IMT in patients who underwent CABG improved their inspiratory muscle strength and endurance, pulmonary function, and 6MWT and helped decrease postoperative pulmonary complications and the length of hospital stay.

Objective: Global longitudinal strain (GLS) is a sensitive and reproducible predictive factor in patients with ischemic heart disease (IHD), although its correlation with exercise tolerance is unknown. We aimed to identify the correlation between global longitudinal strain (GLS) and cardiopulmonary exercise testing (CPX) parameters and assess the prognostic implications and accuracy of GLS in predicting exercise intolerance in populations with ischemic heart disease (IHD) using CPET criteria. Methods: Prospectively, 108 patients with IHD underwent CPX and 2D speckle-tracking echocardiography. Correlation between GLS and multiple CPX variables was assessed using Spearman’s correlation analysis and univariate regression analysis. A receiver operating characteristic (ROC) curve analysis was performed on GLS to detect exercise intolerance. Results: GLS was correlated with peak oxygen uptake (peak VO₂; r = −0.438, p = 0.000), %PPeak VO₂ (−0.369, p = 0.000), peak metabolic equivalents (METs@peak; r = −0.438, p < 0.01), and the minute ventilation–carbon dioxide production (VE/VCO₂) slope (r = 0.257, p < 0.01). Weak-to-moderate correlations were also identified for the respiratory exchange rate at the anaerobic threshold (RER@AT), end-tidal carbon dioxide at the anaerobic threshold (PETCO₂@AT), oxygen consumption at the anaerobic threshold (VO₂@AT), carbon dioxide production at the anaerobic threshold (VCO₂@AT), and metabolic equivalents at the anaerobic threshold (METs@AT; p < 0.01). On multivariate analysis, the results showed that age, the BMI, and GLS are independent predictors for reduced exercise capacity in patients with IHD (p < 0.01). The area under the ROC curve value of GLS for identifying patients with a peak VO₂ of <14 mL/kg/min was 0.73 (p = 0.000). Conclusion: As a sensitive echocardiographic assessment of patients with ischemic heart disease, global longitudinal strain is an independent predictor of reduced exercise capacity and has a sensitivity of 74.2% and a specificity of 66.7% to detect exercise intolerance.