Functional and Morphological Characteristics of Compensated and Decompensated Cardiac Hypertrophy in Dogs With Chronic Infrarenal Aorto-caval Fistulas

• Published in: Circulation research 1990-03, Vol.66 (3), p.846-859
• Main Authors: Legault, Francine, Rouleau, Jean L, Juneau, Carl, Rose, Colin, Rakusan, Karel
• Format: Article
• Language: English
• Subjects: Adaptation, Physiological; Animals; Aorta - surgery; Arteriovenous Shunt, Surgical; Biological and medical sciences; Biomechanical Phenomena; Blood and lymphatic vessels; Capillaries - pathology; Cardiac Output, Low - etiology; Cardiology. Vascular system; Cardiomegaly - etiology; Cardiomegaly - pathology; Cardiomegaly - physiopathology; Diseases of the aorta; Dogs; Drug Resistance; Isoproterenol - pharmacology; Male; Medical sciences; Papillary Muscles - physiopathology; Physical Exertion; Space life sciences; Venae Cavae - surgery; Water - pharmacology
• ISSN: 0009-7330; 1524-4571
• DOI: 10.1161/01.RES.66.3.846

The relation between cardiac hypertrophy, shunt size, myocardial contractility, capillary density, adrenergic responsiveness, and neurohumoral stimulation was evaluated in dogs with compensated and decompensated cardiac hypertrophy caused by an infrarenal aorto-caval shunt. Shunt size varied from 5 to 35 mm due to an inability to create a uniform size. Dogs that developed heart failure within 4 months had 25 ± 2 mm shunts, whereas those that developed it after 4 months had 19 ± 3 mm shunts; those that did not develop heart failure had 10 ± 1 mm shunts. Hypertrophy developed at the same rate in all the dogs that developed heart failure, which occurred at a critical heart weight (hypertrophy) for a given load (shunt size). In the dogs with heart failure there was a decrease in myocardial contractility (tension = 5.7 ± 0.6 vs. 7.3 ± 0.3 g/mm, p < 0.05), a decrease in adrenergic responsiveness (maximal heart rate with isoproterenol=203 ± 7 vs. 249 ± 5 beats/min, p < 0.01), an increase in circulating neurohor-mones, and a decrease in urinary sodium excretion (0.4 ± 0.1 vs. 5.0 ± 1.3 meq/3 hr, p < 0.01). None of these abnormalities occurred in dogs with compensated hypertrophy. There were no differences in cardiac capillary density between the control dogs and the dogs with compensated cardiac hypertrophy or heart failure. Thus, it would appear that if heart failure is to develop after an initial toleration of a sudden volume overload, it will develop at a given combination of cardiac hypertrophy and volume overload, with cardiac hypertrophy developing at the same rate in all cases. In this model, once heart failure develops, myocardial contractility and cardiac adrenergic responsiveness are decreased and there is pronounced neurohumoral activation. All these changes are absent in hearts with compensated hypertrophy.