Introduction: High sensitive Troponin (hsTn) assays enable detection of minimal marker elevation in heart failure patients previously deemed Troponin negative. Biovariability, reference change values (RCV), and index of individuality (II) have not been previously described for hsTnT although serial testing is important in interpreting low concentrations. For these values, a difference between ischemic heart disease (IHD) and dilated cardiomyopathy (dCMP) appears conceivable.
Methods: Change in hsTnT was determined alongside with clinical variables in 41 patients with stable chronic systolic dysfunction at 2-week-, 1-month-, 2-month-, and 3-month-intervals (IHD n = 17; dCMP n = 24).
Results: HsTnT was detectable in all patients. Individual hsTnT-variations at 2-week, 1-month, 2-month, and 3-month follow-up were 7.2, 22.6, 28.9, and 15.7%, respectively, corresponding to RCVs of 20.1, 62.5, 80.0, and 43.3%, respectively, for crude values. For log-normalised values, individual variations were 3.2, 2.8, 2.7, and 3.5%, respectively, corresponding to RCVs of 8.8, 7.9, 7.6, and 9.7%, respectively. The II was 0.03 to 0.33 according to interval. Aetiology of heart failure was not a consistent determinant of variation (p = 0.28; p = 0.07; p = 0.98; p = 0.03 for 2-week, 1-month, 2-month, and 3-month follow-up, respectively).
Conclusion: While short-term biological variation of hsTnT is low, it becomes relatively more important for intermediate follow-up. It is not related to aetiology of heart failure. The corresponding indices of individuality indicate high individuality of values.
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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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