Mechanisms of Hypotension During Dobutamine Stress Echocardiography in Patients With Coronary Artery Disease

Fifty-nine consecutive patients with angiographically documented coronary artery disease were prospectively studied during dobutamine stress echocardiography. Twelve patients (20%) developed hypotension, defined as a decrease in systolic blood pressure of ≥ 20 mm Hg compared with baseline. The transmitral flow velocities, isovolumic relaxation time (IVRT), and flow in the left ventricular (LV) outflow tract were measured at baseline, at maximal dobutamine dose, or during a hypertensive episode; stroke volume, cardiac output, and systemic vascular resistance (SVR) were computed. Correlates of hypotensive response to dobutamine stress echocardiography included therapy with angiotensin-converting enzyme inhibitors (p = 0.032), a longer IVRT at baseline (121 ± 25 vs 103 ± 28 ms, p = 0.047), a greater decrease in LV end-diastolic (−6.0 ± 3.1 vs −2.2 ± 2.1 mm, p < 0.0001) and end-systolic (−8.3 ± 7.0 vs −5.1 ± 3.7 mm, p = 0.037) dimensions, and a greater decrease in stroke volume (−10 ± 10 vs −2 ± 11 ml, p = 0.023) compared with those with a normal response. The groups did not differ significantly with regard to baseline stroke volume, cardiac output, SVR, and LV ejection fraction or LV mass. The predominant mechanism for hypotension among individual patients included: (1) inadequate increase in cardiac output due to impaired systolic reserve (n = 5), (2) marked prolongation of IVRT due to induced myocardial ischemia with abbreviated LV filling period (n = 2), (3) marked isolated reduction in SVR (n = 1), (4) decrease in cardiac output associated with cavity obliteration and reflex bradycardia (n = 2), and (5) a combination of all these mechanisms (n = 2).