Heart Failure Reviews最新文献

Introduction: Acute heart failure (AHF) is a leading cause of hospitalization among older adults and is associated with high rates of rehospitalization and mortality. Intravenous diuretics are the cornerstone of treatment, but diuretic response is highly variable. Spot urine sodium measurement has emerged as a novel tool to guide diuretic titration. We aim to evaluate the efficacy and safety of urine sodium-guided diuresis (USGD) compared to standard of care (SOC) in AHF.

Methods: Online databases were searched. Outcomes included 48-hour natriuresis, 48-hour diuresis, 48-hour weight loss, length of stay (LOS), all-cause mortality, heart failure (HF) rehospitalization, acute kidney injury (AKI), hypotension and hypokalemia. These were reported as risk ratio (RR) for categorical outcomes and mean difference (MD) for continuous outcomes with a random effects model using 95% confidence intervals (CI).

Results: Five studies with 920 patients were selected. USGD was associated with an increased 48-hour natriuresis (MD = 139.13 mmol [95% CI: 4.84, 273.43], p = 0.047) and diuresis (MD = 1.12 L [95% CI: 0.09, 2.15], p = 0.043) and a lower risk of AKI (RR = 0.51 [95% CI: 0.27, 0.97], p = 0.039). There were no significant differences in 48-hour weight loss (MD = 0.45 kg), LOS (MD=-0.38 days), all-cause mortality (RR = 0.93), HF rehospitalization (RR = 0.91), hypotension (RR = 1.06), or hypokalemia (RR = 0.97).

Conclusion: USGD was associated with an increased 48-hour natriuresis and diuresis and a lower risk of AKI compared to SOC in AHF. However, there was no difference in 48-hour weight loss, LOS, all-cause mortality, HF rehospitalization, hypotension, or hypokalemia. While USGD improved short-term natriuresis and renal safety endpoints, further randomized trials are needed to determine optimal urine sodium thresholds and long-term outcomes.

Chronic heart failure with reduced ejection fraction (HFrEF) is a progressive syndrome associated with substantial residual morbidity and mortality despite contemporary guideline-directed medical therapy (GDMT) - angiotensin-converting enzyme inhibitors (ACEIs)/angiotensin receptor blockers (ARBs)/angiotensin receptor-neprilysin inhibitors (ARNIs), beta-blockers, mineralocorticoid receptor antagonists (MRAs) and sodium-glucose cotransporter-2 inhibitors (SGLT2is) [1]. Consequently, the need for novel therapeutic strategies has led to the exploration of new drug classes and pathways. In HF, impaired nitric-oxide (NO) signaling, reduced soluble guanylate cyclase (sGC) responsiveness/abundance, and downstream attenuation of cyclic guanosine monophosphate (cGMP) contribute to disease progression [2]. Vericiguat-an oral sGC stimulator-sensitizes sGC to endogenous NO and directly stimulates the enzyme, thereby restoring cGMP signaling in vascular smooth muscle and cardiomyocytes.

Subcutaneous glucagon-like peptide-1 receptor agonists (GLP-1 RAs) have been shown to reduce risk of major adverse cardiac events (MACE) for patients with type 2 diabetes (T2DM) who have or are at high risk of cardiovascular disease, but the evaluation of cardiovascular efficacy of oral GLP-1 RAs has yet to be performed. This article reviews results from the SOUL (Semaglutide Cardiovascular Outcomes) trial, whose aim was to assess the cardiovascular benefit in oral semaglutide in high-risk individuals. SOUL was a randomized, double blind, parallel-group, placebo-controlled superiority trial that enrolled 9,650 adults with T2DM who had established atherosclerotic cardiovascular disease (ASCVD), chronic kidney disease (CKD), or both, to receive a maximum daily dose of 14 mg oral semaglutide or placebo. The primary outcome in this study was a composite of time to first CV death, non-fatal MI, or non-fatal stroke. In prespecified secondary analyses, treatment groups were analyzed for an expanded list of CV, CKD, PAD, and HF outcomes. Over a median follow-up of 49.5 months, the risk for MACE was significantly lower in the oral semaglutide compared with the placebo group (HR 0.86; 95% CI, 0.77; 0.96; p = 0.006), and these results were consistent across subgroup analysis, including by sodium glucose co-transporter 2 inhibitor (SGLT2i) drug use. Oral semaglutide reduces the risk of MACE in high-risk patients with T2DM.

In the last decade, an increasing number of left ventricular assist devices (LVADs) have been implanted to treat patients with end-stage heart failure. Although LVAD therapy improves hemodynamics and survival, it is also associated with potentially life-threatening complications. A common and significant complication following LVAD implantation is chronic kidney disease (CKD), which is associated with high morbidity and mortality. Despite improvements in kidney function early after LVAD implantation, creatinine levels return to pre-implantation levels or higher in the long term. With the increasing number of LVAD implantations in the last decades, it is essential to focus on LVAD-associated CKD in order to improve the outcomes of LVAD therapy. In addition, identifying potential markers for early diagnosis may optimize perioperative management and prevent disease progression, which may now be the only realistic therapeutic option. This review describes the definition, diagnosis, incidence, pathophysiology, and risk factors for CKD after LVAD implantation. Additionally, future perspectives on the prevention and management of CKD in LVAD patients are discussed.

Surgical repair and clinical management have significantly improved Tetralogy of Fallot (TOF) patient survival rates. Despite these advancements, adults with repaired TOF remain at high risk for long-term complications, particularly heart failure, which constitutes the primary cause of mortality in this population. This review synthesizes current evidence on right heart failure in repaired TOF, with emphasis on pathophysiological mechanisms, diagnostic strategies, and management approaches. The chronic hemodynamic burden of residual lesions and surgical sequalae initiates a maladaptive cascade that results in progressive right ventricular dysfunction and, ultimately, clinical manifestations of right heart failure. The discussion includes the role of multimodal imaging, electrocardiographic monitoring, and exercise testing, as well as the limited evidence for conventional pharmacological therapies in patients with repaired TOF and right heart failure. This review aims to serve as a comprehensive resource to guide clinical decision-making and to highlight key knowledge gaps that warrant further research to improve long-term outcomes in this patient group.

Interatrial shunt devices (IASDs) and implant-free strategies have emerged as novel approaches for heart failure (HF) management by mechanically unloading the left atrium (LA) to reduce left atrial pressure (LAP), a key driver of pulmonary congestion and exercise intolerance. However, evidence from pivotal randomized trials remains mixed, and optimal patient selection is evolving. To provide an updated and balanced review of IASDs and implant-free atrial shunting therapies, integrating recent data from major clinical trials and exploring their current role, limitations, and future perspectives in HF. A comprehensive literature search was conducted using PubMed, Embase, and ClinicalTrials.gov up to August 2025. We summarized available evidence on device designs, procedural approaches, pivotal trials, patient selection, contraindications, and safety considerations. Early feasibility studies demonstrated improvements in hemodynamics, functional capacity, and quality of life. However, REDUCE LAP-HF II failed to show an overall clinical benefit, with potential harm signals in patients with elevated pulmonary vascular resistance. RELIEVE-HF similarly reported no significant improvement in the composite endpoint; however, the HFpEF subgroups showed favorable signals. RESPONDER-HF demonstrated modest but significant quality-of-life improvements in carefully selected HFpEF patients without pulmonary vascular disease. Implant-free strategies, such as Alleviant and InterShunt, aim to minimize device-related risks but remain in early investigation. Interatrial shunt therapy holds promise for a subset of HF patients but is not universally beneficial. Precision-based patient selection, integration with guideline-directed therapy, and validation through ongoing sham-controlled trials are critical before broader clinical adoption.

Recent advancements in oncology have markedly enhanced cancer survival rates; however, anticancer therapies, particularly anthracyclines, pose significant cardiovascular (CV) risks, collectively referred to as cancer therapy-related cardiovascular toxicity (CTR-CVT). This review consolidates evidence on strategies to mitigate CTR-CVT especially associated with anthracyclines. Neurohormonal blockers, including ACE inhibitors, ARBs, and β-blockers, constitute the foundation of prevention, although their efficacy varies: combinations such as ACEi/ARB with βB yield mixed outcomes, whereas carvedilol offers antioxidant benefits beyond β-blockade. Sacubitril/valsartan (ARNI) has demonstrated improvements in global longitudinal strain and LVEF preservation in the SARAH trial, albeit with associated hypotension risks. Aldosterone antagonists show potential, with spironolactone preserving LVEF and diastolic function, though eplerenone has not shown significant effects. Statins present conflicting data; the STOP-CA trial supports atorvastatin for LVEF preservation, while the PREVENT and SPARE-HF trials found no benefit. Emerging evidence suggests sodium-glucose cotransporter-2 inhibitors (SGLT2i), such as dapagliflozin and empagliflozin, as promising agents, with preclinical and early clinical data indicating cardioprotection through metabolic modulation, anti-inflammatory effects, and reduced oxidative stress. Gaps remain in understanding CTR-CVT pathophysiology, risk stratification, and the translation of preclinical findings. Future efforts should prioritize personalized approaches, dynamic risk assessment (e.g., HFA-ICOS tool), and a paradigm shift from oxidative stress to cardiometabolic dysfunction. Multidisciplinary collaboration is essential to optimize oncological outcomes while minimizing CV toxicity, with SGLT2i representing a key frontier for validation in ongoing trials.