Risk Stratification and Prognosis of Human Immunodeficiency Virus Infected Patients with Known or Suspected Coronary Artery Disease Referred for Stress Echocardiography
Background—Patients with Human Immunodeficiency Virus (HIV) infection are at increased risk of accelerated coronary artery disease (CAD) and cardiovascular events. Stress echocardiography (SE) is routinely used for risk stratification and prognosis of patients with known or suspected CAD. The prognostic value of SE in this high-risk group is unknown. The purpose of this study was to evaluate the prognostic value of SE in HIV infected patients with known or suspected CAD.
Methods and Results—We evaluated 311 patients (52 ± 9 years; 74% males, left ventricular ejection fraction (LVEF) 54 ± 12%) with history of HIV undergoing SE (56% dobutamine). LV wall motion was evaluated on a 16-segment model 5-point scale. An abnormal SE was defined by a fixed (infarction), biphasic or new (ischemia) wall motion abnormality on stress. Follow-up for cardiac death and myocardial infarction (MI) was obtained. Seventy-nine (26%) patients had an abnormal SE. After 2.9 ± 1.9 years, 17 confirmed MI and 14 cardiac deaths occurred. SE risk stratified patients into normal versus abnormal subgroups (event rate 0.6%/year vs. 11.8%/year; p <0.0001). Both abnormal SE (HR 28.2, 95% CI 6.2-128.0, p<0.0001) and the presence of any ischemia on SE (HR 3.4, 95% CI 1.3-8.6, p=0.009) were independent predictors of cardiac events. On a forward conditional Cox proportional hazards regression model, SE provided incremental prognostic value over clinical, stress electrocardiographic and resting echocardiographic variables (global Chi-square increased from 17.8 to 24.5 to 65 to 109, p<0.05 across all groups).
Conclusions—SE can effectively risk stratify and prognosticate patients with HIV. The presence of ischemia and scar during SE provides independent and incremental prognostic value over traditional variables. A normal SE response portends a benign prognosis even in this high-risk subset.
- Received September 27, 2010.
- Accepted May 10, 2011.
- Copyright © 2011, American Heart Association, Inc. All rights reserved. Unauthorized use prohibited