Contribution of ventricular remodeling to pathogenesis of heart failure in rats

• Published in: American journal of physiology. Heart and circulatory physiology Vol. 280; no. 2; pp. H674 - H683
• Main Authors: Brower, Gregory L, Janicki, Joseph S
• Format: Journal Article
• Language: English
• Published: United States 01.02.2001
• Subjects: Animals; Arteriovenous Fistula - mortality; Arteriovenous Fistula - physiopathology; Cardiac Volume - physiology; Disease Models, Animal; Heart Failure - etiology; Heart Failure - mortality; Heart Failure - physiopathology; Hypertrophy, Left Ventricular - etiology; Hypertrophy, Left Ventricular - mortality; Hypertrophy, Left Ventricular - physiopathology; Hypertrophy, Right Ventricular - etiology; Hypertrophy, Right Ventricular - mortality; Hypertrophy, Right Ventricular - physiopathology; Male; Matrix Metalloproteinases - metabolism; Myocardium - enzymology; Rats; Rats, Sprague-Dawley; Systole - physiology; Ventricular Dysfunction, Left - etiology; Ventricular Dysfunction, Left - mortality; Ventricular Dysfunction, Left - physiopathology; Ventricular Remodeling - physiology
• ISSN: 0363-6135; 1522-1539
• DOI: 10.1152/ajpheart.2001.280.2.h674

Department of Anatomy, Physiology, and Pharmacology, Auburn University, Auburn, Alabama 36849-5517 We previously reported an approximately 50% incidence of rats with symptoms of congestive heart failure (CHF) at 8 wk postinfrarenal aorto-caval fistula. However, it was not clear whether compensatory ventricular remodeling could continue beyond 8 wk or whether the remaining animals would have developed CHF or died. Therefore, the intent of this study was to complete the characterization of this model of sustained volume overload by determining the morbidity and mortality and the temporal response of left ventricular (LV) remodeling and function beyond 8 wk. The findings demonstrate an upper limit to LV hypertrophy and substantial increases in LV volume and compliance, matrix metalloproteinase activity, and collagen volume fraction associated with the development of CHF. There was an 80% incidence of morbidity and mortality following 21 wk of chronic volume overload. These findings indicate that the development of CHF is triggered by marked ventricular dilatation and increased compliance occurring once the myocardial hypertrophic response is exhausted. aorto-caval fistula; matrix metalloproteinase activity; ventricular hypertrophy; ventricular dilatation; ventricular function