Abstract

Dobutamine stress echocardiography (DSE) has been used as a screening tool for coronary artery disease after heart transplantation and in the identification of patients at risk for development of cardiac events. However, the safety profile of high-dose dobutamine in heart transplant patients has not been systematically examined. Accordingly, we studied the safety profile and hemodynamic responses to escalating doses of dobutamine to determine the influence of denervation. We assessed the hemodynamic responses, heart rate (HR), and arterial BP indexes (mean arterial pressure, systolic BP [SBP], diastolic BP [DBP], and pulse pressure) to dobutamine in 87 heart transplant patients ([mean +/- SD] age, 51 +/- 1 years) and compared the results with 97 nontransplant patients (age, 63.0 +/- 1 years) who served as innervated control subjects. The baseline HR (84 +/- 2 vs 69 +/- 1 beats/minute, respectively; p < 0.001) and peak HR response (144 +/- 2 vs 117 +/- 2 beats/minute, respectively; p < 0.001) were significantly higher in heart transplant patients than in the nontransplant patients. SBP was lower in heart transplant patients than in nontransplant patients at baseline (131 +/- 2 vs 138 +/- 2 mm Hg, respectively; p < 0.02) and at peak (150 +/- 3 vs 158 +/- 3 mm Hg, respectively; p < 0.03). However, baseline DBP was higher in transplant patients than in nontransplant patients (86 +/- 1 vs 77 +/- 1 mm Hg, respectively; p < 0.001). The decrease in DBP was similar in both groups (15 mm Hg). The dose-response curve for HR was shifted leftward in heart transplant patients. Heart transplant patients attained a higher absolute HR at each infusion stage and higher rates of increase, but the decrease in DBP was not significantly different in the two groups. These results show that there is augmented chronotropic response and expected decline in DBP in response to dobutamine infusion in heart transplant patients. This increase in myocardial oxygen demand and a decrease in coronary perfusion pressure may be important mechanisms in the development of ischemic abnormalities that are detectable as regional dysynergy on echocardiography.

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