Plasma renin activity (PRA) increases during heart failure; however, PRA is altered by drug therapy, and it is difficult to study the natural progression of elevated PRA in humans and the possible factors that contribute to its rise. This study evaluated PRA in a drug-naive hypertensive rat model (SHHF/Mcc-facp) that has a genetic program resulting in heart failure (HF). Mean arterial blood pressure and PRA were determined and correlated to heart weight index in conscious normotensive, spontaneously hypertensive rats and HF rats of various ages. PRA, atrial natriuretic peptide, and aldosterone levels progressively increase with age in male HF rats. PRA and blood pressure are independently correlated to cardiac hypertrophy in male HF rats. Atrial natriuretic peptide was elevated in spontaneously hypertensive compared with normotensive rats. Female HF rats have elevated PRA, but the increase is temporally delayed compared with that in male HF rats. Hypertension, PRA, and male gender are independent factors contributing to cardiac hypertrophy and heart failure in the HF model. The HF rat model may prove useful in determining the contribution of these factors in the progression from cardiac hypertrophy to heart failure.
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http://dx.doi.org/10.1152/ajpheart.1997.273.1.H228 | DOI Listing |
Cardiooncology
January 2025
Division of Cardiovascular Medicine, Gill Heart Institute, University of Kentucky, Lexington, KY, USA.
Background: Heart failure (HF) is associated with systemic inflammation and hypercatabolic syndrome, impacting body metabolism. The advanced lung cancer inflammation index (ALI) is a novel inflammatory and nutritional biomarker. We aimed to investigate the prognostic role of ALI in patients with HF.
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January 2025
Department of Intensive Care Medicine, Army Medical Center of PLA, No. 10 Changjiang Road, Yuzhong District, Chongqing, 400010, People's Republic of China.
Background: Pregnancy-associated atypical hemolytic uremic syndrome (aHUS) is a form of thrombotic microangiopathy (TMA) caused by uncontrolled activation of the complement system during pregnancy or the postpartum period. In the intensive care unit, aHUS must be differentiated from sepsis-related multiple organ dysfunction, thrombotic thrombocytopenic purpura (TTP), hemolysis, elevated liver enzymes, and low platelet (HELLP) syndrome. Early recognition of aHUS is critical for effective treatment and improved prognosis.
View Article and Find Full Text PDFBMC Pregnancy Childbirth
January 2025
Royal Hospital for Women and UNSW, School of Clinical Medicine, Level 0, Royal Hospital for Women, Barker Street (Locked Bag 2000), Sydney, NSW, 2031, Australia.
Background: Congenital heart disease (CHD) is the most common fetal malformation, and it can result first in cardiac remodeling and dysfunction and later in cardiac failure and hydrops. A limited number of studies have evaluated cardiac function in fetuses affected by CHD. Functional parameters could potentially identify fetuses at risk of cardiac failure before its development.
View Article and Find Full Text PDFNPJ Digit Med
January 2025
School of Electrical and Computer Engineering, Georgia Institute of Technology, Atlanta, GA, USA.
Monitoring fluid intake and output for congestive heart failure (CHF) patients is an essential tool to prevent fluid overload, a principal cause of hospital admissions. Addressing this, bladder volume measurement systems utilizing bioimpedance and electrical impedance tomography have been proposed, with limited exploration of continuous monitoring within a wearable design. Advancing this format, we developed a conductivity digital twin from radiological data, where we performed exhaustive simulations to optimize electrode sensitivity on an individual basis.
View Article and Find Full Text PDFNat Commun
January 2025
Smidt Heart Institute, Cedars-Sinai Medical Center, Los Angeles, California, CA, USA.
Myocardial fibrosis leads to cardiac dysfunction and arrhythmias in heart failure with preserved ejection fraction (HFpEF), but the underlying mechanisms remain poorly understood. Here, RNA sequencing identifies Forkhead Box1 (FoxO1) signaling as abnormal in male HFpEF hearts. Genetic suppression of FoxO1 alters the intercellular communication between cardiomyocytes and fibroblasts, alleviates abnormal diastolic relaxation, and reduces arrhythmias.
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