Impact of acute propranolol administration on dobutamine-induced myocardial ischemia as evaluated by myocardial perfusion imaging and echocardiography

Adel R. Shehata, Linda Gillam, Victor A. Mascitelli, Steven D. Herman, Alan W. Ahlberg, Michael P. White, Chunguang Chen, David D. Waters, Gary V. Heller

Research output: Contribution to journalArticle

42 Citations (Scopus)

Abstract

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 paints 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 o standard clinical end paint 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.

Original languageEnglish (US)
Pages (from-to)268-272
Number of pages5
JournalAmerican Journal of Cardiology
Volume80
Issue number3
DOIs
StatePublished - Aug 1 1997
Externally publishedYes

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Myocardial Perfusion Imaging
Dobutamine
Propranolol
Myocardial Ischemia
Echocardiography
Paint
Perfusion
Single-Photon Emission-Computed Tomography
Exercise Test
Heart Rate
Technetium Tc 99m Sestamibi
Therapeutics
Exercise
Calcium
Pressure

All Science Journal Classification (ASJC) codes

  • Cardiology and Cardiovascular Medicine

Cite this

Shehata, Adel R. ; Gillam, Linda ; Mascitelli, Victor A. ; Herman, Steven D. ; Ahlberg, Alan W. ; White, Michael P. ; Chen, Chunguang ; Waters, David D. ; Heller, Gary V. / Impact of acute propranolol administration on dobutamine-induced myocardial ischemia as evaluated by myocardial perfusion imaging and echocardiography. In: American Journal of Cardiology. 1997 ; Vol. 80, No. 3. pp. 268-272.
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abstract = "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 paints 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 o standard clinical end paint 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.",
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Impact of acute propranolol administration on dobutamine-induced myocardial ischemia as evaluated by myocardial perfusion imaging and echocardiography. / Shehata, Adel R.; Gillam, Linda; Mascitelli, Victor A.; Herman, Steven D.; Ahlberg, Alan W.; White, Michael P.; Chen, Chunguang; Waters, David D.; Heller, Gary V.

In: American Journal of Cardiology, Vol. 80, No. 3, 01.08.1997, p. 268-272.

Research output: Contribution to journalArticle

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T1 - Impact of acute propranolol administration on dobutamine-induced myocardial ischemia as evaluated by myocardial perfusion imaging and echocardiography

AU - Shehata, Adel R.

AU - Gillam, Linda

AU - Mascitelli, Victor A.

AU - Herman, Steven D.

AU - Ahlberg, Alan W.

AU - White, Michael P.

AU - Chen, Chunguang

AU - Waters, David D.

AU - Heller, Gary V.

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N2 - 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 paints 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 o standard clinical end paint 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.

AB - 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 paints 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 o standard clinical end paint 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.

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