Recurrence of left ventricular systolic dysfunction and its risk factors in heart failure with improved ejection fraction patients receiving guideline-directed medical therapy: A trajectory analysis based on echocardiography.

BACKGROUND: Despite the better prognosis of heart failure (HF) with improved ejection fraction (HFimpEF), remnant cardiovascular risks, including cardiovascular death, rehospitalization, and future deterioration of left ventricular (LV) systolic function, remain in HFimpEF. However, for HFimpEF patients, especially for those receiving guideline-directed medical therapy (GDMT), the recurrent LV systolic dysfunction and its risk factors is still unclear. METHODS: A total of 1098 HF patients under HF follow-up management system were initially screened. Echocardiography was re-evaluated at 3-, 6-, and 12-month follow-up. After exclusion, a total of 203 HFimpEF patients on GDMT were enrolled in our final analysis. Cox regression analysis was conducted to select risk factors. RESULTS: During the 1-year follow-up, a total of 28 (13.8%) patients had recurrent LV systolic dysfunction. The trajectory analysis of echocardiographic parameters illustrated that persistent decline of left ventricular ejection fraction (LVEF) and worsening LV remodeling was observed in patients with recurrent LV systolic dysfunction. Multivariable Cox regression analysis identified that ischemic cardiomyopathy, atrial fibrillation, higher left ventricular end-diastolic diameter index (LVEDDI), elevated serum potassium, and a lack of sodium-glucose co-transporter-2 inhibitors (SGLT2i) treatment were confirmed as independent risk factors for recurrent LV systolic dysfunction. Recurrent LV systolic dysfunction was associated with higher rehospitalization rate. CONCLUSION: In our longitudinal cohort study, almost 14% HFimpEF receiving GDMT suffered recurrent LV systolic dysfunction. Ischemic cardiomyopathy, atrial fibrillation, higher LVEDDI, higher serum potassium, and a lack of SGLT2i therapy were tightly associated with recurrence of LV systolic dysfunction. Relapse of LV systolic dysfunction correlated with poor prognosis.

Association Between Epicardial Adipose Tissue and Left Atrial and Ventricular Function in Patients With Heart Failure: A Systematic Review and Meta-Analysis.

Existing evidence suggested that the role of epicardial adipose tissue (EAT) in heart failure with reduced and preserved ejection fraction (HFrEF/HFpEF) might be divergent. Here, we conducted a systematic review and meta-analysis to evaluate the association between EAT and HF. Several databases were searched from their inception to January 20, 2023. We calculated the standard mean difference (SMD) in EAT between the HF and control groups, as well as the correlation coefficient between EAT and left atrial (LA) and left ventricular (LV) function. This meta-analysis included 23 studies, involving 1563 HFrEF and 1351 HFpEF patients. Our findings indicated that EAT was significantly higher in HFpEF patients (SMD: 0.61, 95% CI: 0.27-0.94), but not in total HF or HFrEF patients compared to controls. In HFrEF, EAT was positively correlated with LVEF, LV end-diastolic volume index (LVEDVI), LA global longitudinal strain (LAGLS), and negatively correlated with N-terminal pro-B-type natriuretic peptide (NT-ProBNP). However, no significant relationship existed between EAT and LV mass index (LVMI) or LVGLS. For HFpEF, EAT correlated positively with LVMI, LVEDVI, LV end-systolic volume index (LVESVI), LA volume index (LAVI), cardiac troponin T, and extracellular volume (ECV), but negatively with LVGLS and LAGLS. EAT was shown to be higher in HFpEF, but not in HFrEF. Less EAT was linked with worse LA function but not worse LV function in HFrEF, while more EAT was associated with worse LA/LV function in HFpEF.

Efficacy and safety of sacubitril/valsartan after six months in patients with heart failure with reduced ejection fraction and asymptomatic hypotension.

BACKGROUND: It is not clear whether sacubitril/valsartan is beneficial for patients with heart failure (HF) with reduced ejection fraction (HFrEF) and low systolic blood pressure (SBP). This study aimed to investigate the efficacy and tolerability of sacubitril/valsartan in HFrEF patients with SBP < 100 mmHg. METHODS & RESULTS: An observational study was conducted on 117 patients, 40.2% of whom had SBP < 100 mmHg without symptomatic hypotension, and 59.8% of whom had SBP ≥ 100 mmHg in an optimized HF follow-up management system. At the 6-month follow-up, 52.4% of patients with SBP < 100 mmHg and 70.0% of those with SBP ≥ 100 mmHg successfully reached the target dosages of sacubitril/valsartan. A reduction in the concentration of N-terminal pro-B-type natriuretic peptide was similar between patients with SBP < 100 mmHg and SBP ≥ 100 mmHg (1627.5 pg/mL and 1340.1 pg/mL, respectively; P = 0.75). The effect of sacubitril/valsartan on left ventricular ejection fraction was observed in both SBP categories, with a 10.8% increase in patients with SBP < 100 mmHg (P < 0.001) and a 14.0% increase in patients with SBP ≥ 100 mmHg (P < 0.001). The effects of sacubitril/valsartan on SBP were statistically significant and inverse across both SBP categories (P = 0.001), with an increase of 7.5 mmHg in patients with SBP < 100 mmHg and a decrease of 11.5 mmHg in patients with SBP ≥ 100 mmHg. No statistically significant differences were observed between the two groups in terms of the occurrence of symptomatic hypotension, deteriorating renal function, hyperkalemia, angioedema, or stroke. CONCLUSIONS: Within an optimized HF follow-up management system, sacubitril/valsartan exhibited excellent tolerability and prompted left ventricular reverse remodeling in patients with HFrEF who presented asymptomatic hypotension.

Nascent SecM chain outside the ribosome reinforces translation arrest.

SecM, a bacterial secretion monitor protein, contains a specific amino acid sequence at its C-terminus, called arrest sequence, which interacts with the ribosomal tunnel and arrests its own translation. The arrest sequence is sufficient and necessary for stable translation arrest. However, some previous studies have suggested that the nascent chain outside the ribosome affects the stability of translation arrest. To clarify this issue, we performed in vitro translation assays with HaloTag proteins fused to the C-terminal fragment of E. coli SecM containing the arrest sequence or the full-length SecM. We showed that the translation of HaloTag proteins, which are fused to the fragment, is not effectively arrested, whereas the translation of HaloTag protein fused to full-length SecM is arrested efficiently. In addition, we observed that the nascent SecM chain outside the ribosome markedly stabilizes the translation arrest. These results indicate that changes in the nascent polypeptide chain outside the ribosome can affect the stability of translation arrest; the nascent SecM chain outside the ribosome stabilizes the translation arrest.