Cardiac Failure Review最新文献

Background: Right ventricular (RV) failure remains a major cause of morbidity and mortality after continuous flow left ventricular assist device (CF-LVAD) implantation. Previous risk assessment tools using pre-operative data to predict RV failure have performed only modestly well. We retrospectively evaluated the potential of a non-invasive measure of right ventricular contractility - RV dP/dt, derived from the echocardiographic Doppler signal of tricuspid regurgitation (TR) both without and with inotropes - to predict RV failure post-CF-LVAD.

Methods: We studied 65 consecutive CF-LVAD recipients at Vanderbilt University Medical Center from 2013-2019 who had a baseline off inotrope echocardiogram with an evaluable TR signal within 3 months prior to LVAD implantation. Of the 65 patients, 40 were started on inotropes before LVAD implantation, 32 of whom had an evaluable TR signal on a repeat echocardiogram prior to LVAD. RV dP/dt was evaluated using spectral Doppler recordings from the TR and calculated by obtaining the time required from the TR velocity to increase from 0.5 m/s to 2 m/s. Off inotrope RV dP/dt of the 65 patients and on inotrope RV dP/dt of the 32 patients were collected. Post-CF-LVAD RV failure was defined by Interagency Registry for Mechanically Assisted Circulatory Support criteria. Overall survival was estimated by Kaplan-Meier curves and compared by log-rank test among different subgroups. Receiver operative characteristic curves were constructed to determine the optimal thresholds for prediction of severe RV failure post-LVAD.

Results: Of the 65 patients, 30 had no/mild RV failure; RV failure was moderate in 17 and severe in 18 patients after LVAD. Subjects with severe RV failure had worse survival than patients with no/mild and moderate RV failure. Either a baseline off inotrope, or on inotrope RV dP/dt of greater than or equal to 300 mmHg/s predicted a low risk of severe RV failure with high sensitivity (89% and 80%, respectively) and negative predictive value (91% and 88% respectively). Persistently low RV dP/dt <300 mmHg/s despite being on inotrope was associated with a high likelihood of post-LVAD RV failure (OR 10.5; 95% CI [1.8-59.4]) compared with the rest of the cohort on inotropic therapy.

Conclusion: Echocardiographic RV dP/dt may be a valuable adjunct tool for predicting post-operative RV failure in patients undergoing evaluation for CF-LVAD implantation.

Background: In recent heart failure (HF) trials, the win ratio statistical approach, developed to address the limitations of conventional methods, has been increasingly applied to better capture clinical benefits. The TOPCAT study was a randomised controlled trial designed to evaluate the efficacy of spironolactone in patients with HF and a left ventricular ejection fraction (LVEF) ≥45%. This study evaluated the cardiovascular benefits of spironolactone according to their clinical importance using the win ratio method.

Methods: A post hoc analysis was conducted using data from the TOPCAT Americas cohort. The primary outcome was a hierarchical composite comprising the time to cardiovascular death, time to first aborted cardiac arrest, time to first hospitalisation for HF, time to first hospitalisation for arrhythmia and change in the Kansas City Cardiomyopathy Questionnaire Overall summary score at 36 months. Outcomes were analysed using the win ratio statistical model.

Results: In all, 1,767 patients were included; 886 were assigned to receive spironolactone and 881 to receive placebo. Hierarchical analysis of the primary composite outcome revealed a significant higher probability of win (28.3%) compared to loss (23.1%) in the spironolactone group, yielding a win ratio of 1.22 (95% CI [1.05-1.42]; p=0.008) and a net clinical benefit (win difference) of 5.2% (95% CI [1.36-9.04]). Detailed assessment of the win differences revealed a concordant positive benefit (win difference >0) across all components of the outcome hierarchy. Subgroup analyses indicated no significant effect of age (<75 years versus ≥75 years), sex (male versus female) or LVEF (<50% versus ≥50%) on the efficacy of spironolactone (p for interaction>0.05).

Conclusion: This post hoc analysis, using a novel statistical approach, demonstrates the consistent benefits of spironolactone across adverse cardiovascular events, patient symptoms, functional status and quality of life in individuals with HF and mildly reduced or preserved LVEF.

Background: Blood troponin I (TnI) concentrations, the reasons for increases in TnI after coronary artery bypass grafting (CABG) and the effects of TnI on short- and long-term outcomes are not well understood.

Methods: Patients undergoing off-pump CABG at Anzhen Hospital between 2011 and 2022 were reviewed. Data on peak postoperative TnI and high-sensitivity (hs) TnI were collected, and patients were divided into a high TnI group (TnI ≥10 ≥g/l or hsTnI ≥10,000 pg/ml) and low TnI group. Baseline characteristics, graft flow, perioperative outcomes and long-term mortality were compared between the two groups.

Results: In all, 19,196 patients were included in the study (median age 63 years; interquartile range [IQR] 57-68 years; 14,423 (75.1%) male). Compared with the low TnI group, patients in the high TnI group were more likely to have an intra-aortic balloon pump inserted (17.8% vs. 2.9%; p<0.001), receive extracorporeal membrane oxygenation support (3.6% vs. 0.1%; p<0.001), and undergo early revascularisation (2.81% vs. 0.12%; p<0.001); the high TnI group also had more in-hospital deaths (2.7% vs. 0.2%; p<0.001). After propensity score matching, patients in the high TnI group had fewer grafts to the left circumflex artery (LCX; 0.71 ± 0.58 versus 0.81 ± 0.57; p<0.001) and right coronary artery (RCA; 0.89±0.53 versus 0.95±0.53; p=0.011), as well as less graft flow to the LCX (median 33 [IQR 21-55] versus 41 [IQR 25-67] ml/min; p<0.001) and RCA (30 [IQR 18-50] versus 35 [IQR 22-55] ml/min; p<0.001) than patients in the low TnI group. Patients with high postoperative TnI also had reduced long-term survival (HR 2.59; 95% CI [1.76-3.82]; p<0.001).

Conclusion: Elevated TnI following off-pump CABG may be associated with incomplete revascularisation in the LCX and RCA. It is also associated with increased early and late mortality.

Central sleep apnoea (CSA) is a common comorbidity in patients with heart failure. Due to its insidious and chronic nature, CSA often remains unrecognised. Patients with CSA typically present with symptoms, such as daytime fatigue, recurrent heart failure decompensations and cardiac arrhythmias. Although the pathophysiology of CSA is not yet fully understood, the most widely accepted theory suggests that fluctuations in PaCO₂ levels, particularly crossing the apnoeic threshold, play a central role in its development. CSA is associated with various changes, including activation of the sympathetic nervous system, neurohormonal disturbances and haemodynamic perturbations, all of which contribute to increased morbidity and mortality. Transvenous phrenic nerve stimulation (TPNS) has been demonstrated to be a safe and effective therapy for reducing the apnoea-hypopnoea index and improving both left ventricular ejection fraction and quality of life in patients with CSA. These benefits have been validated in randomised clinical trials (RCTs). New methods of analysing RCTs were recently introduced. Applying the win ratio method in a post hoc analysis of the primary RCTs evaluating TPNS suggested that TPNS may also contribute to reduced mortality and fewer heart failure hospitalisations. In this article we explore the pathophysiology of CSA and evaluate the existing evidence on therapeutic options, with a particular focus on TPNS.

The renin-angiotensin-aldosterone system is integral to cardiorenal health, with aldosterone controlling fluid balance, blood pressure and cardiac remodelling. Despite the widespread use of angiotensin-converting enzyme inhibitors, angiotensin receptor blockers and mineralocorticoid receptor antagonists, 'aldosterone escape' persists, contributing to treatment failure and adverse outcomes. Steroidal mineralocorticoid receptor antagonists also cause hyperkalaemia and anti-androgenic effects, limiting their use. Aldosterone synthase inhibitors (ASIs) selectively block cytochrome P450 11B2, reducing pathological aldosterone levels while preserving basal mineralocorticoid receptor activity, thus potentially lowering hyperkalaemia risk. This narrative review identified 41 relevant publications from a PubMed/MEDLINE search of "aldosterone synthase inhibitor" through 11 January 2025. Early clinical trials of ASIs (baxdrostat, lorundrostat, vicadrostat, dexfadrostat phosphate, JX09) report significant reductions in aldosterone, blood pressure and albuminuria, with promising safety. Challenges include ensuring high selectivity, mitigating hyperkalaemia and establishing long-term benefits. Ongoing Phase III trials will clarify their efficacy, safety and synergy with additional therapies - including sodium-glucose cotransporter 2 inhibitors - and clinical outcomes, positioning ASIs as an important advance in renin-angiotensin-aldosterone system modulation.

Heart failure (HF) is closely linked to endothelial dysfunction, which contributes significantly to its progression. Endothelial dysfunction in HF is marked by reduced nitric oxide bioavailability, increased oxidative stress and inflammation, all of which impair vascular function. Endothelial progenitor cells (EPCs) - vital for vascular repair - are particularly affected, with their dysfunction further exacerbating HF outcomes. Emerging therapies targeting these mechanisms, including antioxidants, gene therapies enhancing endothelial nitric oxide synthase activity and EPCbased strategies, hold promise. Recent advances show encouraging results, especially with treatments improving EPC mobilisation and function. Additionally, pharmacological agents such as statins and sodium-glucose cotransporter 2 inhibitors demonstrate pleiotropic benefits, enhancing endothelial health and EPC activity. This review emphasises the therapeutic potential of these approaches, highlighting the critical need for further research to optimise endothelial-targeted treatments and improve outcomes for HF patients.

Glucagon-like peptide-1 receptor agonists (GLP-1 RAs), initially developed for glycaemic control in patients with type 2 diabetes, have demonstrated significant cardiometabolic benefits beyond glucose regulation. These agents have multiple effects, including reducing body weight, improving insulin sensitivity, anti-inflammatory properties and enhancing endothelial function. All these mechanisms are potentially beneficial in patients with heart failure (HF), specifically those with HF with preserved left ventricular ejection fraction. Recent trials, including STEP-HFpEF and SUMMIT, underscore the efficacy of GLP-1 RAs in improving quality of life and exercise capacity, as well as possibly reducing major adverse cardiovascular events. Furthermore, these trials demonstrated improvements in other endpoints, such plasma N-terminal pro B-type natriuretic peptide, troponin and C-reactive protein concentrations, consistent with the beneficial effects of GLP-1 RAs on myocardial function and inflammation. Further data are needed regarding the effects of GLP-1 RAs on cardiovascular outcomes, and possibly in a broader range of patients with HF, such as those with HF reduced ejection fraction and/or patients without obesity.

Recent advances in medical therapy have significantly improved the prognosis of patients with heart failure and reduced ejection fraction (HFrEF). The established four pillars of HFrEF treatment - β-blockers, angiotensin-converting enzyme inhibitors or angiotensin receptor- neprilysin inhibitors, mineralocorticoid receptor antagonists and sodium-glucose cotransporter 2 inhibitors - serve as the foundation for ongoing innovations in this domain. However, these represent only the starting point for the therapy and management of heart failure. New medications, new devices and improvements in the use of diuretic therapy are fundamental and recent advancements. This article aims to highlight the latest findings in HFrEF treatment. While emphasising the optimism these developments bring, the article also addresses the significant unresolved challenges that persist in the management of this syndrome, which remains a leading global cause of mortality, morbidity and poor quality of life with high use of resources and healthcare costs.

The high risk of adverse outcomes in patients with heart failure with reduced ejection fraction (HFrEF) demands urgent efforts in the initiation of guideline-directed medical therapy to reduce morbidity and mortality. Angiotensin receptor-neprilysin inhibitor showed substantial benefits in reducing the risks of heart failure hospitalisation and cardiovascular mortality in HFrEF patients. Therefore, the European Society of Cardiology 2021 guidelines recommend angiotensin receptor-neprilysin inhibitor as a first-line therapy for HFrEF patients. The guidelines emphasise the importance of the early use and rapid titration of the 'four pillars' in HFrEF: angiotensin receptor-neprilysin inhibitor, β-blockers, sodium-glucose cotransporter 2 inhibitors and mineralocorticoid receptor antagonists. However, real-world application of the guidelines remains suboptimal, limiting patient outcomes. This statement paper investigates the barriers to the use of the 'four pillars', and aims to give guidance to improve their implementation in different HFrEF patient types.