Author + information
- Received January 7, 1991
- Revision received April 29, 1991
- Accepted May 10, 1991
- Published online November 1, 1991.
- William A. Zoghbi, MD, FACC∗,
- Jorge Cheirif, MD, FACC,
- Neal S. Kleiman, MD, FACC,
- Mario S. Verani, MD, FACC and
- Anatole Trakhtenbroit, MD
- ↵∗Address for reprints: William A. Zoghbi, MD, The Methodist Hospital, Section of Cardiology, 6535 Fannin, MS F-905, Houston, Texas 77030.
To assess the feasibility, safety and diagnostic accuracy of adenosine infusion combined with echocardiography, 73 patients with suspected or known coronary artery disease underwent echocardiography at baseline and during a maximal intravenous adenosine infusion of 140 μg/kg per min. Compared with baseline values, adenosine caused an increase in heart rate, a decrease in systolic and diastolic blood pressure and a slight but significant increase in rate-pressure product. The echocardiographic images were digitized and randomly assigned in a quad-screen format for nonbiased interpretation.
An ischemic response, defined as a new or worsening wall motion abnormality, developed in 25 patients; a fixed wall motion abnormality was present in 27 and no abnormality in 21. All patients underwent coronary angiography. The sensitivity of adenosine echocardiography for ≥75% coronary artery diameter stenosis was 85% (46 of 54), with a specificity of 92% in patients with normal coronary arteries.
In the 35 patients with a normal baseline electrocardiogram the sensitivity was 60%; 9 (82%) of 11 patients with multivessel disease were correctly identified. The sensitivity for adenosine electrocardiography (≥1.mm ST depression) was 35% with a specificity of 100%. Side effects were transient and mild; aminophylline was used in two patients.
Thus, ischemic changes can be induced in patients with coronary artery disease with intravenous adenosine that, combined with echocardiography, is sensitive for the assessment of ischemic heart disease, particularly in patients with multivessel disease.
☆ Computational assistance was provided by the CLINFO Project funded by Grant RR00350 from the Division of Research Resources, National Institutes of Health, Bethesda, Maryland. This study was supported in part by a grant from Medco Research, Inc., Los Angeles, California. It was presented in part at the 63rd Annual Meeting of the American Heart Association. November 1990, Dallas, Texas.
- Received January 7, 1991.
- Revision received April 29, 1991.
- Accepted May 10, 1991.