Impact of Acute Propranolol Administration on Dobutamine-Induced Myocardial Ischemia as Evaluated by Myocardial Perfusion Imaging and Echocardiography

Beta-blocker therapy may delay or completely prevent myocardial ischemia during exercise testing, as assessed by ST-segment shifts, myocardial perfusion defects, or echocardiographic wall motion abnormalities. However, the impact of β-blocker therapy on these end points during dobutamine stress testing has not been well established. The purpose of this study was to determine the impact of propranolol on dobutamine stress testing with ST-segment monitoring, technetium-99m (Tc-99m) sestamibi single-photon emission computed tomography (SPECT) imaging, and echocardiography. In 17 patients with known reversible perfusion defects, dobutamine stress tests with and without propranolol were performed in randomized order and on separate days, following discontinuation of oral β blockers and calcium antagonists. Propranolol was administered intravenously to a cumulative dose of 8 mg or to a maximum heart rate reduction of 25% and dobutamine was infused in graded doses in 3 minute stages until a standard clinical end point or the maximum dose of 40 μg/kg/min was achieved. The dobutamine stress test after propranolol was associated with a lower maximum heart rate (83 ± 18 vs 125 ± 17, p <0.001) and rate pressure product (14,169 ± 4,248 vs 19,894 ± 3,985, p <0.001) despite a higher infusion dose. The SPECT myocardial ischemia score was also lower (6.9 ± 5.8 vs 10.1 ± 7.1, p = 0.047) and fewer echocardiographic segments were abnormal (3.4 ± 3.0 vs 4.6 ± 3.4, p = 0.042). In 4 of 17 patients, reversible perfusion defects and echocardiographic wall motion abnormalities were detected during the control but not during the propranolol test. Thus, during dobutamine stress testing, β-blocker therapy attenuates, and in some cases eliminates, evidence of myocardial ischemia.