Congestive heart failure following chronic tachycardia

The mechanics of left ventricular contraction were analyzed in quantitative terms from isovolumic contractions in six dogs in which congestive heart failure developed following 13 to 29 days of chronic pacemaker-induced ventricular tachycardia. Twenty-four hours following cessation of stimulation, heart failure was evidenced in the intact sedated dogs by elevated left ventricular end-diastolic pressures (average, 28 mm. Hg), ascites, and the presence of a protodiastolic gallop sound. Aortic pressure, heart rate, and the ratio of stroke volume to end-diastolic volume were decreased while the ratio of left ventricular mass to body weight was unchanged, and cardiac output was increased, presumably secondary to hypervolemia. Left ventricular function was substantially reduced, contractile element velocity-tension relations were altered, and V max was significantly reduced (failure 2.37 ± 0.40 circumferences per second vs. control 3.0 ± 0.03). The maximum isovolumic tension development for any given end-diastolic volume also was decreased in five of six animals. Left ventricular myocardial stores of creatine, creatine phosphate, and adenosine triphosphate were significantly depressed. These findings indicate that the syndrome of heart failure following chronic tachycardia, characterized by elevated left ventricular end-diastolic pressure and ascites, is associated with significant depression of the left ventricular contractile state and total energy stores.