Background: Recent studies have shown the efficacy for using spironolactone to treat heart failure with reduced ejection fraction (HFrEF), but the efficacy of spironolactone for heart failure with mid-range ejection fraction (HFmrEF) and heart failure with preserved ejection fraction (HFpEF) is unclear. This meta-analysis investigated the efficacy and safety of spironolactone in patients with HFmrEF and HFpEF. Methods and results: We searched several databases including PubMed and the Cochrane Collaboration, for randomized controlled trials (RCTs) that assessed spironolactone treatment in HFmrEF and HFpEF. Eleven RCTs including 4539 patients were included. Spironolactone reduced hospitalizations (odds ratio [OR], 0.84; 95% confidence interval [CI], 0.73–0.95; P = .006), improved New York Heart Association functional classifications (NYHA-FC) (OR, 0.35; 95% CI, 0.19–0.66; P = .001), decreased the levels of brain natriuretic peptide (BNP) (mean difference [MD], − 44.80 pg/mL; 95% CI, −73.44–−16.17; P = .002), procollagen type I C-terminal propeptide (PICP) (MD, −27.04 ng/mL; 95% CI, −40.77–−13.32, P < .001) in HFmrEF and HFpEF. Besides, it improved 6-minute walking distances (6-MWD) (standard weighted mean difference [SMD], 0.45 m; 95% CI, 0.27–0.64; P < .001), decreased amino-terminal peptide of procollagen type-III (PIIINP) (SMD, −0.37 μg/L; 95% CI, −0.59–−0.15; P = .001) in HFpEF only. The risks of hyperkalemia ( P <.001) and gynecomastia ( P <.001) were increased. Conclusion: Patients with HFmrEF and HFpEF could benefit from spironolactone treatment, with reduced hospitalizations, BNP levels, improved NYHA-FC, alleviated myocardial fibrosis by decreasing serum PICP in HFmrEF and HFpEF, decreased PIIINP levels and increased 6-MWD only in HFpEF. The risks of hyperkalemia and gynecomastia were significantly increased with the spironolactone treatment.
No previous meta-analysis has evaluated the efficacy and safety of pulmonary vasodilators in Fontan physiology. Recent relative trials have obtained conflicting results regarding improvements in peak oxygen consumption; the relatively small number of patients in each study may be a limiting factor. We aimed to evaluate the efficacy and safety of pulmonary vasodilators in Fontan patients. Relevant studies were identified by searching the PubMed, Embase, and Cochrane Library databases. Pooled outcomes were determined to assess the efficacy and safety of pulmonary vasodilators in Fontan patients. Nine randomized controlled studies involving 381 patients with Fontan circulation were included. Pulmonary vasodilator therapy led to significant improvement (mean difference = −0.39, 95% CI: [−0.72, −0.05]) in the New York Heart Association (NYHA) functional class. The 6-minute walking distance (6MWD) was significantly increased by 134 m (95% CI: [86.07, 181.94]), and the peak VO2 was also significantly improved (mean difference = 1.42 ml·(kg·min)-1, 95% CI: [0.21, 2.63]). Additionally, the mean pulmonary artery pressure (mPAP) was significantly reduced (mean difference = −2.25 mmHg, 95% CI: [−3.00, −1.50]). No significant change was found in mortality or in brain natriuretic peptide (BNP) or N-terminal pronatriuretic peptide (NT-proBNP). Four studies reported no side effects and good drug tolerance, and two studies reported mild adverse effects. The present meta-analysis indicated that pulmonary vasodilators (primarily the PDE-5 inhibitor and endothelin-1 receptor antagonist) significantly improved the hemodynamics of Fontan patients, reduced the NYHA functional class and increased the 6MWD. The peak oxygen consumption was also improved. No significant change was observed in mortality or in the BNP or NT-proBNP level. Overall, the pulmonary vasodilators were well tolerated. This finding needs to be confirmed in future studies.
Pulmonary arterial hypertension (PAH) is an incurable disease with high mortality. Chemerin has been found to be associated with pulmonary hypertension (PH). However, the specific role of chemerin in mediating PH development remains unclear. This study aimed to elucidate the regulatory effects and the underlying mechanism of chemerin on PH and to investigate the expression levels of chemerin protein in plasma in PAH patients. In vivo, two animal models of PH were established in rats by monocrotaline (MCT) injection and hypoxia. We found that the expression levels of chemerin and its receptor, chemokine-like receptor 1 (CMKLR1), were significantly upregulated in the lungs of PH rats. Primary cultured pulmonary arterial smooth muscle cells [(PASMCs) (isolated from pulmonary arteries of normal healthy rats)] were exposed to hypoxia or treated with recombinant human chemerin, we found that CMKLR1 expression was upregulated in PASMCs in response to hypoxia or chemerin stimulation, whereas the exogenous chemerin significantly promoted the migration and proliferation of PASMCs. Notably, the regulatory effects of chemerin on PASMCs were blunted by PD98059 (a selective ERK1/2 inhibitor). Using enzyme linked immunosorbent assay (ELISA), we found that the protein level of chemerin was also markedly increased in plasma from idiopathic pulmonary arterial hypertension (IPAH) patients compared to that from healthy controls. Moreover, the diagnostic value of chemerin expression in IPAH patients was determined through receiver operating characteristic (ROC) curve analysis and the result revealed that area under ROC curve (AUC) for plasma chemerin was 0.949. Taken together, these results suggest that chemerin exacerbates PH progression by promoting the proliferation and migration of PASMCs via the ERK1/2 signaling pathway, and chemerin is associated with pulmonary hypertension.
Objective: To investigate the relationship between ST-segment resolution (STR) and myocardial scar thickness after percutaneous coronary intervention (PCI) in patients with ST-segment elevation myocardial infarction (STEMI).Methods: Forty-two STEMI patients with single-branch coronary artery stenosis or occlusion were enrolled. ST-segment elevations were measured at emergency admission and at 24 h after PCI. Late gadolinium-enhanced cardiac magnetic resonance imaging (CMR-LGE) was performed 7 days after PCI to evaluate myocardial scars. Statistical analyses were performed to assess the utility of STR to predict the development of transmural (>75%) or non-transmural (<75%) myocardial scars.Results: The sensitivity and specificity of STR for predicting transmural scars were 96% and 88%, respectively, at an STR cut-off value of 40.15%. The area under the curve was 0.92. Multivariate logistic proportional hazards regression analysis disclosed that patients with STR<40.15% had a 112.95-fold higher probability of developing transmural scars compared with patients with STR≥40.15%. STR percentage was negatively correlated with myocardial scar thickness (β=-0.838, P<0.001) and size (β=-0.714, P<0.001).Conclusion: STR<40.15% at 24 h after PCI may provide meaningful diagnostic nformation regarding the extent of myocardial scarification in STEMI patients.
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