Value of rapid beta-blocker injectionat peak dobutamine-atropine stressechocardiography for detection of coronary artery disease
Wilson Mathias, Jr, MD, PhD, FACC*,*,
Jeane M. Tsutsui, MD, PhD*,
José L. Andrade, MD, PhD*,
Ingrid Kowatsch, MD*,
Pedro A. Lemos, MD*,
Samira M. B. Leal, MD, PhD*,
Bijoy K. Khandheria, MD, FACC* and
José F. Ramires, MD, PhD, FACC*
* Echocardiographic Laboratory, Heart Institute (InCor), University of São Paulo Medical School, São Paulo, Brazil
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Figure 1 Dobutamine-atropine stress echocardiography—metoprolol protocol. EKG = electrocardiogram.
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Figure 2 Sensitivity, specificity, accuracy, positive predictive value (PPV), and negative predictive value (NPV) for the detection of CAD for peak (open bars) and peak plus metoprolol images (solid bars).
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Figure 3 Sensitivity values in patients with single-vessel (solid bars) and multivessel coronary artery disease (open bars) at peak and peak plus metoprolol (Met) images.
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Figure 4 Example of a patient with 90% left anterior descending coronary artery stenosis without new wall motion abnormality at peak stress developed only after metoprolol. Apical four-chamber views at end systole with normal thickening at rest (heart rate of 46 beats/min; rate–pressure product of 6,578 mm Hg/min; and left ventricular end-systolic volume index [LVESVI] of 15.7 ml/m2) and low doses. At peak stress, HR was 139 beats/min, rate–pressure product was 20,850 mm Hg/min, and LVESVI was 12.8 ml/m2. After metoprolol, there is a lack of thickening in the apical septum (white arrows; HR of 103 beats/min; rate–pressure product of 15,450 mm Hg/min; and LVESVI of 33.3 ml/m2). For the accompanying video corresponding to Figure 4, please see the following link: http://www.cardiosource.com/library/journals/journal/suppdata?acronym=JAC&pii=s0735109703002420&filename=Stress_eco_met_3.mpg.
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Figure 5 An electrocardiogram from the patient in Figure 4, demonstrating ST-segment changes in leads D2, D3, aVF, V5, and V6 only during metoprolol (Met).
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