Role of tricuspid regurgitation and left ventricular damage in the treatment of right ventricular infarction-induced low cardiac output syndrome

Abstract

To evaluate, in right ventricular (RV) myocardial infarction, the role of tricuspid regurgitation (TR) and left ventricular (LV) damage and the response to treatment of low cardiac output, 20 patients were prospectively studied. Volume infusion increased cardiac output only slightly (11%, p < 0.001), despite a dramatic increase in ventricular filling pressures. Dobutamine (4 μg · kg −1 · min −1) markedly increased cardiac output (24%, p < 0.001) with a decrease in ventricular filling pressures. In the 5 patients with TR, dobutamine only modestly increased cardiac output (9 vs 26%, p < 0.001), white stroke index and LV end-diastolic dimensions decreased in comparison (−5 vs 33% and −6 vs 9%, respectively, p < 0.001). In the absence of TR (n = 15), there was no significant difference in response to volume expansion between patients with normal (n = 7) and depressed LV ejection fraction (n = 8). In contrast, dobutamine, in patients with depressed LV function, induced a greater increase in cardiac output (38 vs 17%, p < 0.01) and RV ejection fraction (36 vs 12%, p < 0.05). All patients with RV infarction-induced low cardiac output responded only modestly to volume loading. Dobutamine is particularly efficacious in patients without TR who have depressed LV function by improving RV function and, consequently, LV preload. In the 5 patients with TR, increasing RV contractility failed to improve the forward stroke volume by increasing the regurgitant fraction.