Citations

Abstract Aims Left ventricular assist devices (LVADs) are a critical intervention for advanced heart failure (HF), serving as destination therapy or bridge to transplantation. Obesity and diabetes impact outcomes in patients with LVADs. Glucagon-like peptide-1 receptor agonists (GLP1-RAs) demonstrate cardiovascular benefits; however, their role in patients with LVADs remains underexplored. We evaluated the association of GLP1-RA therapy with cardiovascular outcomes in patients with LVADs. Methods This retrospective cohort study used the TriNetX database, a research network database from 98 healthcare organizations. We queried for all adult LVAD recipients (≥18 years) and were stratified into GLP1-RA users and non-users. Propensity score matching (PSM) (1:1) balanced demographics, comorbidities, medication use and laboratory data. Outcomes included heart transplantation rates, heart failure hospitalizations, all-cause mortality, all-cause hospitalizations and cardiovascular events. Logistic regression models were used to estimate adjusted odds ratios (aOR). Results After PSM, we included a total of 1036 adult LVAD recipients (518 GLP1-RA users, 518 matched non-users) with a mean follow-up time of 311.6 ± 98.4 days for the GLP1-RA cohort and 304.0 ± 111.5 days for the non-GLP1-RAs cohort. Mean age was 56.7 ± 12.2 years in the GLP1-RA cohort and 58.0 ± 12.5 years in the non-GLP1-RA cohort. Females comprised 28.0% of both cohorts while White patients represented 52.1% of the GLP1-RA group and 53.1% of the non-GLP1-RA group. GLP1-RA users had higher heart transplantation rates [n = 98 (18.9%) vs. n = 44 (8.5%); aOR 2.514 (95% CI: 1.720–3.673)]. Acute HF events and all-cause hospitalizations were lower among GLP1-RA users compared with non-users [n = 288 (55.6%) vs. n = 357 (68.9%); aOR 0.565 (95% CI: 0.438–728) and n = 324 (62.5%) vs. n = 390 (75.3%); aOR 0.548 (95% CI: 0.420–0.716)]. No differences were observed when comparing the GLP1-RA cohort with the non-GLP1-RA cohort in regard to all-cause mortality [n = 32 (6.2%) vs. n = 44 (8.5%); aOR 0.709 (95% CI: 0.442–1.138)], stroke [n = 42 (8.1%) vs. n = 58 (11.2%); aOR 0.700 (95% CI: 0.461–1.062)] or cardiac arrest [n = 18 (3.5%) vs. n = 17 (3.3%); aOR 1.061 (95% CI: 0.541–2.082)]. Conclusions GLP1-RA therapy in patients with advanced HF and LVADs is potentially associated with improved heart transplantation rates while decreasing hospitalization and acute HF event rates.

Atrial fibrillation (AF) is the most common cardiac arrhythmia and is associated with increased morbidity, mortality, and healthcare expenses. Meanwhile, effective management of AF requires a comprehensive, patient-centered approach that includes risk factor modification, rate and rhythm control strategies, and prevention of thromboembolic events. Multidisciplinary AF clinics have emerged as a model for comprehensive management to improve patient outcomes and reduce healthcare burden. This review discusses the rationale, structure, benefits, challenges, and future directions of multidisciplinary AF clinics, emphasizing their role in optimizing AF management.

Introduction: Sex-based differences in outcomes among patients with heart failure with reduced ejection fraction (HFrEF) treated with sodium-glucose cotransporter 2 inhibitors (SGLT2is) remain underexplored. This study aimed to evaluate sex-specific differences in cardiovascular outcomes in patients with HFrEF receiving SGLT2 inhibitors alongside guidelinedirected medical therapy (GDMT). Methods: We conducted a retrospective cohort study using the TriNetX global research network. Adults with HFrEF treated with SGLT2is and GDMT were stratified by sex. Propensity score matching (PSM) was used to balance baseline demographics, comorbidities, medications, and laboratory data. Primary outcomes were all-cause mortality and acute heart failure (HF) events; secondary outcomes included hospitalizations, arrhythmias, renal outcomes, and advanced therapies. Results: After PSM, 17,408 male and 17,408 female patients were analyzed. Male patients had lower odds of acute HF events (aOR: 0.949; 95% CI: 0.909–0.991), all-cause hospitalizations (aOR: 0.933; 95% CI: 0.895–0.973), and renal failure (aOR: 0.915; 95% CI: 0.870–0.962). No significant differences were observed in all-cause mortality (aOR: 1.003; 95% CI: 0.926–1.087) or heart transplantation, although LVAD use was more frequent in males (aOR: 1.416; 95% CI: 1.053–1.905). Discussion: The findings highlighted potential sex-based disparities in outcomes for patients with HFrEF on SGLT2is. Differential prescribing patterns, comorbidity burden, or timing of therapy initiation may contribute to observed differences. Conclusion: Among HFrEF patients treated with SGLT2is, males experienced lower risks of HF events, hospitalizations, and renal failure compared to females, despite similar mortality. Further research is needed to understand and address sex-specific disparities in HFrEF management.

Chronic left bundle branch block (LBBB) has been associated with adverse cardiac remodeling and the development of cardiomyopathy. This retrospective cohort study evaluated the impact of angiotensin II receptor blocker (ARB) therapy on cardiovascular outcomes in adults with isolated LBBB with no known heart failure (HF), cardiomyopathy, or ischemic heart disease. Using the TriNetX global research network, patients were stratified by ARB use and followed for up to 5 years. Propensity score matching was performed to balance characteristics. Three thousand two hundred sixty-six patients were included in each group with comparable baseline characteristics. The ARB therapy was not associated with a reduction in new-onset acute HF events (4.9% vs 4.4%; hazard ratio (HR) 1.05 (95% CI 0.84–1.32)). Similarly, there were no significant differences in rates of all-cause hospitalizations, cardiac arrest, or ventricular tachycardia. However, ARB use was associated with a significantly lower, all-cause mortality rate (8.6% vs 12.1%; HR 0.67 (95% CI 0.57–0.77)). This is the first real-world study examining ARB use in a cohort with isolated LBBB, highlighting a potential mortality benefit, despite no difference in acute HF risk. While ARBs are not effective in preventing LBBB-induced cardiomyopathy based on these findings, the observed survival advantage warrants further investigation. Prospective studies are needed to elucidate mechanisms underlying this mortality benefit and to determine whether ARBs should be considered in the management of patients with isolated LBBB.

Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia, contributing to significant morbidity and mortality worldwide. The relationship between physical exercise and AF is complex, with studies showing both beneficial and potentially adverse effects. Moreover, evidence suggests a U-shaped association between exercise intensity and AF risk. Moderate exercise has been shown to reduce AF burden by improving cardiovascular risk factors, enhancing autonomic regulation, and mitigating atrial fibrosis. In contrast, excessively high-intensity endurance exercise may increase AF risk, particularly in young athletes, due to atrial stretching, dilation, fibrosis, autonomic imbalances, and heightened inflammation. The current guidelines emphasize exercise as a core lifestyle intervention for AF management, recommending moderate-intensity aerobic activity for optimal outcomes. This review examines the current evidence on the effects of exercise on AF, identifies knowledge gaps, and proposes potential future research directions.

Arrhythmogenic cardiomyopathies (ACMs) are a phenotypically and etiologically heterogeneous group of myocardial disorders characterized by fibrotic or fibro-fatty replacement of ventricular myocardium, electrical instability, and an elevated risk of sudden cardiac death. Initially identified as a right ventricular disease, ACMs are now recognized to include biventricular and left-dominant forms. Genetic causes account for a substantial proportion of cases and include desmosomal variants, non-desmosomal variants, and familial gene-elusive forms with no identifiable pathogenic mutation. Nongenetic etiologies, including post-inflammatory, autoimmune, and infiltrative mechanisms, may mimic the phenotype. In many patients, the disease remains idiopathic despite comprehensive evaluation. Cardiac magnetic resonance imaging has emerged as a key tool for identifying non-ischemic scar patterns and for distinguishing arrhythmogenic phenotypes from other cardiomyopathies. Emerging classifications propose the unifying concept of scarring cardiomyopathies based on shared structural substrates, although global consensus is evolving. Risk stratification remains challenging, particularly in patients without overt systolic dysfunction or identifiable genetic markers. Advances in tissue phenotyping, multi-omics, and artificial intelligence hold promise for improved prognostic assessment and individualized therapy.

Advances in plaque imaging have transformed cardiovascular diagnostics through detailed characterization of atherosclerotic plaques beyond traditional stenosis assessment. This review outlines the clinical applications of varying modalities, including dual-layer spectral CT, photon-counting CT, dual-energy CT, and CT-derived fractional flow reserve (CT-FFR). These technologies offer improved spatial resolution, tissue differentiation, and functional assessment of coronary lesions. Additionally, artificial intelligence has emerged as a powerful tool to automate plaque detection, quantify burden, and refine risk prediction. Collectively, these innovations provide a more comprehensive approach to coronary artery disease evaluation and support personalized management strategies.

Introduction: Amyloidosis complicated by heart failure (HF) poses significant mortality. We sought to identify trends in comorbid amyloidosis and HF mortality in the recent 22- year period. Methods: Mortality due to amyloid and HF as contributors of death were queried from death certificates using the CDC database from 1999 to 2020. Mortality rates and their 95% confidence intervals were adjusted for age (AAMR) through the Direct method and compared by demographic subpopulations. The Monte-Carlo permutation test was used to estimate the annual percentage change (APC). Log-linear regression models were utilized to assess temporal variation in mortality. Results: Age-adjusted mortality rates (AAMR) increased from 0.09 [0.08-0.10] in 1999 to 0.27 [0.25-0.29] in 2020. Mortality increased from 1999 to 2013 (APC +1.4, p=0.048) with an accelerating inflection point in 2013 to 2020 (APC +13.3, p<0.001). AAMR was higher among male populations (AAMR 0.20 [0.20-0.21]) compared to female populations (AAMR 0.07 [0.07- 0.07]). A significant inflection point in uprising mortality rates was observed for both male and female populations in 2013 (p<0.001). Mortality was highest among Black populations (AAMR 0.33), followed by White (AAMR 0.10), Asian/Pacific Islander (AAMR 0.06), and American Indian/Alaska Native populations (AAMR 0.04). Among Black populations, mortality remained consistent from 1999 to 2012 (APC +1.1, p=0.184), followed by an increase from 2012 to 2020 (APC +14.0, p<0.001). Among White populations, mortality remained stagnant from 1999 to 2013 (APC +0.7, p=0.302), followed by an increase starting in 2013 to 2020 (APC +13.5, p<0.001). Discussion: Our findings of a marked rise in HF-related mortality in patients with amyloidosis since 2013 highlighted the profound impact of enhanced diagnostic awareness, novel imaging techniques, and emerging therapeutics. Our analysis also showed mortality disparities between sexes, and geographic locations, races, and ethnicity that warrant targeted public health interventions. Conclusions: Amyloid and HF mortality increased in the recent 22-year period, primarily starting in 2013, emphasizing the urgent need for targeted intervention to address these disparities.