Does hypotension during dobutamine stress echocardiography correlate with anatomic or functional cardiac impairment?

Journal Article (Journal Article)

The development of hypotension during various exercise stress tests has been correlated with the presence of multivessel coronary artery disease and impaired left ventricular contractility. Hypotension may also occur during dobutamine stress echocardiography; however, its anatomic and functional significance remains unknown. As part of an ongoing study of restenosis, dobutamine stress echocardiography and diagnostic cardiac catheterization were performed on the same day in 105 outpatients approximately 6 months after percutaneous coronary revascularization (balloon angioplasty or directional coronary atherectomy) to determine the anatomic and functional significance of dobutamine-induced hypotension. Dobutamine was infused in stepwise increments to a maximum rate of 30 micrograms/kg/min. Hypotension was defined as a reduction in systolic blood pressure of > or = 15 mm Hg. Anatomic abnormalities were defined by quantitative coronary angiography and functional abnormalities by digitized two-dimensional stress echocardiography. Clinical, angiographic, hemodynamic, and electrocardiographic data underwent multivariable regression analysis to determine their ability to predict independently the development of dobutamine-induced hypotension. Dobutamine-induced hypotension was not associated with the presence of severity of coronary artery disease or with echocardiographic wall motion abnormalities. Univariable predictors of stress-induced hypotension included high baseline systolic blood pressure, advanced age, and high left ventricular ejection fraction. Only a high baseline systolic blood pressure contributed independent predictive information in multivariable stepwise logistic regression analysis. Therefore, the development of hypotension during dobutamine stress echocardiography, unlike that during traditional exercise stress tests, is not associated with the presence of significant coronary artery disease or left ventricular dysfunction.

Full Text

Duke Authors

Cited Authors

  • Lieberman, EB; Heinle, SK; Wildermann, N; Waugh, RA; Kisslo, JA; Bashore, TM

Published Date

  • June 1995

Published In

Volume / Issue

  • 129 / 6

Start / End Page

  • 1121 - 1126

PubMed ID

  • 7754942

International Standard Serial Number (ISSN)

  • 0002-8703

Digital Object Identifier (DOI)

  • 10.1016/0002-8703(95)90392-5


  • eng

Conference Location

  • United States