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Ann Thorac Surg 1990;49:225-230
© 1990 The Society of Thoracic Surgeons
a Department of Cardiovascular Surgery, Hôpital Broussais, Paris, France
b The Bakken Research Center, Maastricht, The Netherlands
* Address reprint requests to Dr Chachques, Department of Cardiovascular Surgery, Hôpital Broussais, 96 rue Didol, 75014 Paris, France.
The efficacy of skeletal muscle contractile force to augment left ventricular function has been demonstrated experimentally and clinically by the cardiomyoplasty procedure. Another approach in biomechanical cardiac assistance is the use of electrostimulated skeletal muscle in an extracardiac position. We describe an autologous counterpulsating device using the native ascending aorta as a ventricular chamber wrapped by an electrostimulated latissimus dorsi muscle flap (LDMF). This model avoids thrombotic complications observed in skeletal muscle neo-ventricles associated with prosthetic chambers. In 8 goats, a right LDMF was transferred to the thoracic cavity by removal of the second rib. In 4 goats, the diameter of the aorta was enlarged by surgical implantation (using lateral clamping) of an autologous pericardial patch. The LDMF was wrapped around the ascending aorta and electrostimulated using an external diastolic pulse generator connected to a sensing myocardial lead and to LDMF pacing electrodes. Hemodynamic studies were performed (left ventricular, aortic, and pulmonary artery pressures and rate of rise of left ventricular pressure). The LDMF diastolic counterpulsation was performed using a burst of 30 Hz, with a delay from the R wave adjusted to provide optimal diastolic augmentation. Percent increase in the subendocardial viability index was calculated during unassisted and assisted cardiac cycles (1:2) at baseline and after acute heart failure induced by the administration of high doses of propranolol hydrochloride (3 mg/kg intravenously). Diastolic aortic counterpulsation by the stimulated LDMF resulted in a significant improvement in the subendocardial viability index both at baseline and after induced cardiac failure in both groups, though the increase was greater in the group with aortic enlargement.
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