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Background & Aims: The aim of this study was to determine whether liver fibrosis is associated with heart failure in a general population cohort, and if genetic polymorphisms (PNPLA3 rs738409; TM6SF2 rs58542926), linked to increased risk of liver fibrosis and decreased risk of coronary artery disease, modify this association.
Methods: Using UK Biobank data, we prospectively examined the relationship between noninvasive fibrosis markers (nonalcoholic fatty liver disease [NAFLD] fibrosis score [NFS], Fibrosis-4 [FIB-4] and aspartate transaminase [AST] to platelet ratio index [APRI]) and incident hospitalization/death from heart failure (n = 413,860). Cox-regression estimated hazard ratios (HRs) for incident heart failure. Effects of PNPLA3 and TM6SF2 on the association between liver fibrosis and heart failure were estimated by stratifying for genotype and testing for an interaction between genotype and liver fibrosis using a likelihood ratio test.
Results: A total of 12,527 incident cases of heart failure occurred over a median of 10.7 years. Liver fibrosis was associated with an increased risk of hospitalization or death from heart failure (multivariable adjusted high-risk NFS score HR, 1.59; 95% confidence interval [CI],1.47-1.76; P < .0001; FIB-4 HR, 1.69; 95% CI, 1.55-1.84; P < .0001; APRI HR, 1.85; 95% CI, 1.56-2.19; P < .0001; combined fibrosis scores HR, 1.90; 95% CI, 1.44-2.49; P < .0001). These associations persisted for people with metabolic dysfunction-associated steatotic liver disease (MASLD), MASLD with alcohol consumption (Met-ALD), and harmful alcohol consumption. PNPLA3 rs738409 GG and TM6SF2 rs58542926 TT did not attenuate the positive association between fibrosis markers and heart failure. For PNPLA3, a statistically significant interaction was found between PNPLA3 rs738409, FIB-4, APRI score, and heart failure.
Conclusion: In the general population, serum markers of liver fibrosis are associated with increased hospitalization/death from heart failure. Genetic polymorphisms associated with liver fibrosis were not positively associated with elevated heart failure risk.
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http://dx.doi.org/10.1016/j.cgh.2024.03.045 | DOI Listing |
JACC Heart Fail
September 2025
Université de Lorraine, Inserm, Centre d'Investigations Cliniques Plurithématique 1433, Centre Hospitalier Régional Universitaire de Nancy, Nancy, France.
Cardiol Rev
September 2025
Departments of Cardiology and Medicine, Westchester Medical Center and New York Medical College, Valhalla, NY.
Heart failure (HF) remains one of the leading causes of 30-day hospital readmissions, presenting a major challenge to healthcare systems worldwide. This comprehensive review synthesizes recent evidence on effective strategies to reduce readmission rates through patient education, self-care interventions, and systemic reforms. Structured education-particularly when reinforced postdischarge through methods like teach-back, tele-coaching, and home visits-has consistently demonstrated improved self-management, symptom recognition, and quality of life.
View Article and Find Full Text PDFAnn Am Thorac Soc
September 2025
Brigham and Women's Hospital, Division of Sleep and Circadian Disorders, Boston, Massachusetts, United States.
Rationale: There are insufficient data to inform the management of central sleep apnea (CSA) in patients with heart failure (HF) with reduced ejection fraction (HFrEF). Nocturnal oxygen therapy (NOT) has been postulated to benefit CSA patients with HFrEF, but has not been rigorously studied. This article is open access and distributed under the terms of the Creative Commons Attribution Non-Commercial No Derivatives License 4.
View Article and Find Full Text PDFAnnu Rev Pathol
September 2025
3Department of Pathology, Stanford University, Stanford, California, USA;
Clonal hematopoiesis, originally identified as a precursor to hematologic malignancies, has emerged as a significant factor in various nonmalignant diseases. Recent research highlights how somatic mutations in hematopoietic stem cells lead to the expansion of circulating mutated immune cells that exert profound effects on organ function and disease progression. These mutated clones display altered inflammatory profiles and tissue-specific functional consequences, contributing to various diseases including atherosclerotic cardiovascular disease, osteoporosis, heart failure, and neurodegenerative conditions.
View Article and Find Full Text PDFEur Heart J Cardiovasc Pharmacother
September 2025
Department of Internal Medicine, University of Genova, Genova, Italy.
Aims: Several diuretic strategies, including furosemide iv boluses (FB) or continuous infusion (FC), are used in acute heart failure (AHF).
Methods And Results: We systematically searched phase 3 randomized clinical trials (RCTs) evaluating diuretic regimens in admitted AHF patients within 48 hours and irrespective of clinical stabilization. We calculated the odds ratio (OR) of FC or FB plus another diuretic (sequential nephron blockade, SNB) compared to FB alone on 24-hour weight loss (WL) and worsening renal function (WRF), with a random-effects model with inverse variance weighting.