Dennis R. Trumble

Component analysis of bilateral anterior cardiomyoplasty

This experiment was designed to analyze the mechanism of ventricular augmentation generated with bilateral anterior cardiomyoplasty by comparing it in an acute setting with its components, the left anterior cardiomyoplasty and the right anterior cardiomyoplasty. Hemodynamic variables were measured in 8 dogs before and after each flap was positioned around the heart. Stimulation was achieved by R-wave synchronous latissimus burst pacing at a ratio of 1:4, an amplitude of 5 V, a frequency of 33 Hz, and a duration of 30% of the R-R interval. Hemodynamic changes were again recorded during latissimus stimulation. Construction of the bilateral anterior wrap (static cardiomyoplasty) caused some depression of baseline hemodynamic function, which was greater than that caused by either the static right or left anterior cardiomyoplasty. With stimulation of the muscles (dynamic cardiomyoplasty), the bilateral wrap caused significant biventricular augmentation. Evaluation of the components of the bilateral wrap demonstrated that dynamic right anterior cardiomyoplasty also provided significant biventricular augmentation, but the dynamic left anterior cardiomyoplasty augmented only right-sided variables. The mechanism of biventricular compression by the bilateral procedure is due mostly to the right wrap. The right anterior cardiomyoplasty may provide significant biventricular compression for treatment of heart failure, without the complexity associated with bilateral anterior cardiomyoplasty.

Catecholamines restore myocardial contractility in dilated cardiomyopathy at the expense of increased coronary blood flow and myocardial oxygen consumption (MvO2 cost of catecholamines in heart failure)

To investigate the metabolic cost of catecholamine use in heart failure, we administered intravenous dobutamine or norepinephrine to dogs with moderate and severe LV dysfunction until LV contractile function was restored to normal levels. Both drugs were associated with significant increases in myocardial O2 consumption, increased coronary blood flow requirements and decreased myocardial mechanical efficiency. These mechanisms may contribute to the deleterious effects of catecholamines in heart failure.

Right latissimus dorsi cardiomyoplasty augments left ventricular systolic performance

We hypothesized that the right latissimus dorsi cardiomyoplasty augments left ventricular performance. Five dogs underwent staged right latissimus dorsi cardiomyoplasty. Ventricular function was studied 1 to 3 weeks later. Left ventricular pressure was measured with a micromanometer and left ventricular dimensions with piezoelectric crystals. Inferior vena caval occlusion was used to vary preload. Pressure-volume data were collected with the muscle unstimulated and stimulated at 1:2 and 1:1 muscle/heart ratios. The end-systolic pressure-volume relation (mm Hg/mL), stroke work, preload recruitable stroke work, left ventricular end-diastolic volume, and the diastolic relaxation constant were calculated and expressed as mean +/- standard deviation. Stimulated beats at a 1:2 ratio showed an increase in stroke work of 42.1% (978 +/- 381 to 1,390 +/- 449 g.cm; p < 0.01) and preload recruitable stroke work of 28.8% (59.4 +/- 20.7 to 76.6 +/- 11.0 g.cm/cm3; p = 0.05) compared with the unstimulated beats. With the stimulator on at 1:1, smaller changes occurred: stroke work increased 9% (1,167 +/- 390 to 1,273 +/- 363 g.cm; not significant) and preload recruitable stroke work increased 27% (63.9 +/- 22.7 to 80.9 +/- 23.1 g.cm/cm3; p = 0.05). There were no significant changes in the end-systolic pressure-volume relation. The diastolic relaxation constant did not change at 1:1 (36 +/- 9.7 to 37 +/- 6.4 ms; not significant) or 1:2 (36 +/- 9.3 to 39 +/- 8.2 ms; not significant). Left ventricular end-diastolic volume was unchanged at 1:1 (34 +/- 10.7 to 32 +/- 10.3 mL) and at 1:2 (31 +/- 9.0 to 32 +/- 8.7 mL).(ABSTRACT TRUNCATED AT 250 WORDS)