No abstract

The effect of descending thoracic aortomyoplasty using conditioned latissimus dorsi muscle on cardiac output in five mongrel dogs with pharmacologically induced congestive heart failure was evaluated. A neurovascular left latissimus dorsi flap was lifted and through a left thoracotomy placed around the proximal descending thoracic aorta. The flap was conditioned for 4–6 weeks with a neurostlmulator using the following parameters: amplitude 0.5 V. pulse width 210 μs and frequency 2 Hz. The neurostlmulator was then removed and a cardiomyostlmulator inserted and programmed to burst-stimulate the muscle during diastole. Baseline measurements of central venous pressure, heart rate, mean arterial blood pressure, pulmonary capillary wedge pressure, and cardiac output were obtained with the cardiomyostlmulator off and on (study 1). Heart failure was induced with a combination of propranolol and verapamil, and measurements again taken with the stimulator off and on. The neurostimulator was reimplanted to continue stimulation of the latissimus dorsi muscle, and another set of measurements taken at 6 weeks with the cardiomyostlmulator off and on (study 2). Counterpulsation in control conditions (before cardiac failure) in both studies demonstrated no significant increase in cardiac output. However, mean(s.d.) cardiac output was significantly (P < 0.1) increased by muscle stimulation in dogs with heart failure (study 1: from 2.39(1.10) to 3.14(1.41)l/min; study 2: from 1.89(0.64) to 2.38(0.57) l/min). There was no significant difference in the increase in cardiac output associated with muscle stimulation between studies 1 and 2. The results indicate that the model can increase cardiac output in heart failure and that this improvement is constant over a 4–6-week period, suggesting that muscle fatigue may not occur.