Peak exercise oxygen consumption (Vo(2)) and the Heart Failure (HF) Survival Score (HFSS) were developed in middle-aged patient cohorts referred for heart transplantation with HF. The prognostic value of Vo(2) in patients >65 years has not been well studied. Accordingly, the prognostic value of peak Vo(2) was evaluated in these patients with HF. A retrospective analysis of 396 patients with HF >65 years with cardiopulmonary exercise testing was performed. Peak Vo(2) and components of the HFSS (presence of coronary artery disease, left ventricular ejection fraction, heart rate, mean arterial blood pressure, presence of intraventricular conduction defects, and serum sodium) were collected. Follow-up averaged 1,038 +/- 983 days. Outcome events were defined as death, implantation of a left ventricular assist device, or urgent transplantation. Patients were divided into risk strata for peak Vo(2) and HFSS based on previous cut-off points. Survival curves were derived using Kaplan-Meier analysis and compared using log-rank analysis. Survival differed markedly by Vo(2) stratum (p <0.0001), with significantly better survival rates for the low- (>14 ml/kg/min) versus medium- (10 to 14 ml/kg/min), low- versus high- (<10 ml/kg/min), and medium- versus high-risk strata (all p <0.05). Survival also differed markedly by HFSS stratum (p <0.0001), with significantly better survival rates for the low- (> or =8.10) versus medium- (7.20 to 8.09), low- versus high- (< or =7.19), and medium- versus high-risk strata (all p <0.0001). In conclusion, peak Vo(2) and the HFSS were both excellent parameters to predict survival in patients >65 years with HF.
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http://dx.doi.org/10.1016/j.amjcard.2008.12.010 | DOI Listing |
Curr Cancer Drug Targets
January 2025
Department of Cardiology, Affiliated Zhongshan Hospital of Dalian University, Dalian 116001, Liaoning, China.
Introduction: The cardiotoxicity and subsequent Heart Failure (HF) induced by Doxorubicin (DOX) limit the clinical application of DOX. Valsartan (Val) is an angiotensin II receptor blocker that could attenuate the HF induced by DOX. However, the underlying mechanism of Val in this process is not fully understood.
View Article and Find Full Text PDFHypertension
January 2025
Department of Cardiovascular Research, Shinshu University School of Medicine, Matsumoto, Nagano, Japan. (Y. Zhao, T. Sakurai, A.K., M.T., Y.I.-S., H.K., Y.M., Y. Zhang, Q.G., P.L., K.H., M.H., J.L., T. Shindo).
Background: Adrenomedullin 2 (AM2) plays critical roles in regulating blood pressure and fluid balance. However, the specific involvement of AM2 in cardiac hypertrophy has not been comprehensively elucidated, warranting further investigation into its molecular mechanisms and therapeutic implications.
Methods: Cardiac hypertrophy was induced in adult mice lacking AM2 (AM2-/-) using transverse aortic constriction surgery.
Circ Cardiovasc Qual Outcomes
January 2025
Department of Medicine, New York Presbyterian-Weill Cornell Medical Center (N.S., L.C.P., J.D.L., M.R.S., M.M.S., P.G.).
Background: Increased burden of socially determined vulnerabilities (SDV), which include nonmedical conditions that contribute to patient health, is associated with incident heart failure (HF). Mediators of this association have not been examined. We aimed to determine if a healthy lifestyle mediates the association between SDV and HF.
View Article and Find Full Text PDFAn atrial septal defect (ASD) is a common congenital heart anomaly that results in irregular blood flow between the systemic and pulmonary circulations due to an opening in the atrial septum. Ostium secondum ASD accounts for a large proportion of these defects and often goes unnoticed during childhood and adolescence. Pulmonary hypertension (PH), affecting a significant number of patients with ostium secondum ASD, is associated with functional limitations, heart failure, and tachyarrhythmias.
View Article and Find Full Text PDFWorld J Diabetes
January 2025
National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20810, United States.
Diabetes mellitus (DM) is a debilitating disorder that impacts all systems of the body and has been increasing in prevalence throughout the globe. DM represents a significant clinical challenge to care for individuals and prevent the onset of chronic disability and ultimately death. Underlying cellular mechanisms for the onset and development of DM are multi-factorial in origin and involve pathways associated with the production of reactive oxygen species and the generation of oxidative stress as well as the dysfunction of mitochondrial cellular organelles, programmed cell death, and circadian rhythm impairments.
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