cardiovascular-agents and Atrial-Remodeling

The aim of this study was to investigate the effects of a noninvasive positive pressure ventilation therapy on cardiac structure and function in patients with coronary heart disease combined with obstructive sleep apnea/hypopnea syndrome (OSAHS).. Eighty patients with coronary heart disease OSAHS were divided randomly into treatment (n=40) and control (n=40) groups. Both groups received standard medications. The treatment group received additional noninvasive mechanical ventilation support for at least 3 h (3-6 h) every night. On the first day after selection and 3 months afterwards, participants were examined with echocardiograms, 24-h ambulatory blood pressure monitoring, and blood analyses. Primary endpoints were left ventricular end-diastolic diameter, left ventricular end-systolic diameter, left ventricular ejection fraction, left atrial diameter as well as serum concentrations of N-terminal prohormone of brain natriuretic peptide, and high-sensitive C-reactive protein. Secondary endpoints included cardiac death, nonfatal myocardial infarction, and hospitalization.. After the 3-month study period, patients in the treatment group showed significantly improved left ventricular end-diastolic diameter (P=0.02), left ventricular end-systolic diameter (P=0.035), left ventricular ejection fraction (P=0.05), and left atrial diameter (P=0.02) values, and their serum N-terminal prohormone of brain natriuretic peptide (P=0.01) and high-sensitive C-reactive protein (P=0.04) concentrations were significantly improved compared with the control group. During the 3 months, three cardiovascular complications occurred in the treatment group versus nine in the control group (P<0.05).. For patients with coronary heart disease combined with OSAHS, noninvasive mechanical ventilation therapy can significantly improve heart functions and reduce the occurrence of cardiovascular complications.

Topics: Aged; Atrial Remodeling; Biomarkers; C-Reactive Protein; Cardiovascular Agents; China; Combined Modality Therapy; Coronary Artery Disease; Female; Humans; Male; Middle Aged; Natriuretic Peptide, Brain; Noninvasive Ventilation; Peptide Fragments; Positive-Pressure Respiration; Prospective Studies; Recovery of Function; Sleep Apnea, Obstructive; Stroke Volume; Time Factors; Treatment Outcome; Ventricular Function, Left

Aldosterone induces cardiac electrical and structural remodeling, which leads to the development of heart failure and/or atrial fibrillation (AF). However, it remains unknown whether aldosterone-induced remodeling may modulate the efficacy of anti-AF drugs. In this study, we aimed to jeopardize the structural and functional remodeling by aldosterone in rats with aorto-venocaval shunts (AVS rats) and evaluate the effect of acehytisine in this model. An AVS operation was performed on rats (n = 6, male) and it was accompanied by the intraperitoneal infusion of aldosterone (AVS + Ald) at 2.0 µg/h for 28 d. The cardiopathy was characterized by echocardiography, electrophysiologic and hemodynamic testing, and morphometric examination in comparison with sham-operated rats (n = 3), sham + Ald (n = 6), and AVS (n = 5). Aldosterone accelerated the progression from asymptomatic heart failure to overt heart failure and induced sustained AF resistant to electrical fibrillation in one out of six rats. In addition, it prolonged PR, QT interval and Wenckebach cycle length. Acehytisine failed to suppress AF in the AVS + Ald rats. In conclusion, aldosterone jeopardized electrical remodeling and blunted the electrophysiological response to acehytisine on AF.

Topics: Aldosterone; Animals; Aorta; Arteriovenous Shunt, Surgical; Atrial Fibrillation; Atrial Remodeling; Cardiovascular Agents; Electrophysiological Phenomena; Heart Atria; Heterocyclic Compounds, 4 or More Rings; Male; Rats, Wistar; Venae Cavae