Hemodynamic effects of nitroglycerin in an experimental model of acute aortic regurgitation

AbstractAfterload reduction is an accepted therapeutic modality for the treatment of congestive heart failure caused by chronic aortic regurgitation. However, the role of vasodilator therapy in acute aortic incompetence has not been established. To investigate this, left ventricular volume overload was produced in 18 dogs by constructing a valved conduit from the descending thoracic aorta to the left ventricular apex. The time course of aortic, pulmonary and conduit flows was analyzed in eight control studies and established stability of the experimental model.In the remaining 10 dogs, intravenous nitroglycerin, titrated to reduce mean aortic blood pressure by 40%, and placebo (ethanol) were each infused for 20 min periods. Compared with placebo, nitroglycerin significantly reduced aortic flow (3,945 ± 324 to 3,397 ± 362 ml/min, p < 0.01), regurgitant flow (1,304 ± 131 to 764 ± 90 ml/min, p < 0.001), septal-lateral end-diastolic diameter (47.5 ± 1.8 to 46.5 ± 1.8 mm, p < 0.001), left ventricular end-diastolic pressure (6.9 ± 0.8 to 6.0 ± 0.6 mm Hg, p < 0.05), left ventricular stroke work (19.0 ± 2.6 to 10.8 ± 1.7 g-m/beat, p < 0.001) and systemic vascular resistance (2,253 ± 173 to 1,433 ± 117 dyne-s/cm5, p < 0.001). In contrast, pulmonary flow, left anterior descending coronary flow and subendocardial pH did not change during infusion of either nitroglycerin or placebo.These data indicate that by decreasing preload and afterload, and by preserving coronary flow and tissue pH, nitroglycerin effectively reduced ventricular and regurgitant volumes in the setting of acute volume overload. This study supports the clinical use of nitroglycerin in severe acute aortic incompetence