Cardio-double myoplasty was performed in eight mongrel dogs. Both latissimus dorsi muscles were dissected from the chest wall and wrapped around the heart. They were then stimulated using an R wave synchronous stimulator. Hemodynamic measurements were obtained, first with the stimulator off and then with stimulator activated. After measuring hemodynamic effects in a normal heart, acute heart failure was induced by the infusion of propranolol (5 mg/kg). Hemodynamic data were then obtained in the same fashion. In a normal heart state, cardio-double myoplasty increased the cardiac output 9.9% +/- 2.24 (p less than 0.005), the left ventricular pressure 18.7% +/- 3.53 (p less than 0.001), the pulmonary artery pressure 72.2% +/- 25.4 (p less than 0.01), and the stroke volume 13.4% +/- 5.73 (p less than 0.05). In a failing heart, the cardiac output increased 21.6% +/- 3.34 (p less than 0.005), the left ventricular pressure increased 20.8% +/- 3.34 (p less than 0.005), the pulmonary artery pressure increased 87.2% +/- 39.9 (p less than 0.05), and the stroke volume increased 46.9% +/- 22.9 (p less than 0.05). The left ventricular end-diastolic pressure decreased slightly and the central venous pressure did not change in either the normal state or during cardiac failure. Cardio-double myoplasty resulted in a significant circulatory augmentation particularly in the setting of cardiac failure.
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http://dx.doi.org/10.1111/jocs.1991.6.1s.124 | DOI Listing |
J Card Surg
March 1991
Division of Cardiothoracic Surgery, Wayne State University, School of Medicine, Detroit, Michigan 48201.
Cardio-double myoplasty was performed in eight mongrel dogs. Both latissimus dorsi muscles were dissected from the chest wall and wrapped around the heart. They were then stimulated using an R wave synchronous stimulator.
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