Early changes in the time course of myocardial contraction after correcting aortic regurgitation.

BACKGROUND: Correcting aortic regurgitation causes significant changes in left ventricular loading conditions, but few observations have been made intraoperatively of early effects on myocardial function. METHODS: We studied 18 patients (mean age, 59+/-12 years; 14 men) in whom aortic regurgitation was corrected with a stentless biologic valve. Overall left ventricular function was studied by thermodilution cardiac output, ventricular filling pressure, and systemic arterial pressure. Regional myocardial function was assessed from intraoperative transesophageal M-mode echocardiography and high fidelity ventricular pressure recordings before cardiopulmonary bypass, and 0.5, 1, 3, 6, 12, and 20 hours after operation. Time course of contraction, and magnitude of left ventricular systolic wall stress, dimensional shortening, myocardial power, and stroke work were measured. RESULTS: Global hemodynamics: there was an immediate decrease in left ventricular stroke volume (58+/-31 mL versus 80+/-30 mL, p = 0.004) and stroke work index (250+/-86 mJ/m versus 401+/-198 mJ/m, p = 0.005), but systemic arterial pressure (79+/-11 mm Hg versus 65+/-10 mm Hg, p = 0.002), increased at constant heart rate and end-diastolic pressure. Regional myocardial function and timing: peak systolic wall stress, dimensional shortening rate, and myocardial power production were all unchanged with operation. However, myocardial stroke work decreased (3.0+/-1.3 mJ/cm versus 4.8+/-2.4 mJ/cm, p = 0.009), attributable to shortening of the duration of systole (475+/-91 ms versus 543+/-67 ms, p<0.001). Diastolic time increased from 34%+/-18% to 71%+/-33% of systolic pulse duration (p<0.001). CONCLUSIONS: Correcting aortic regurgitation causes an early decrease in regional and global stroke work and increases diastolic time, although systolic wall stress does not decrease immediately. These beneficial effects are achieved by reducing the duration rather than altering the peak intensity (power) of myocardial contraction.