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J Am Coll Cardiol, 1999; 33:1469-1475 © 1999 by the American College of Cardiology Foundation |
* Division of Cardiology, Department of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, USA
Division of Cardiology, Department of Medicine, Rhode Island Hospital, Providence, Rhode Island, USA
Division of Cardiology, Department of Medicine, Allegheny University of the Health Sciences, Pittsburgh, Pennsylvania, USA
Division of Cardiology, Department of Medicine, University of Alabama, Birmingham, Alabama, USA
|| Division of Cardiology, Department of Medicine, University of Florida, Gainesville, Florida, USA
¶ Department of Epidemiology, University of Pittsburgh Graduate School of Public Health, Pittsburgh, Pennsylvania, USA
# Division of Heart and Vascular Diseases, National Heart, Lung, and Blood Institute, Bethesda, Maryland, USA
Manuscript received June 26, 1998; revised manuscript received December 11, 1998, accepted January 21, 1999.
Reprint requests and correspondence: Dr. Steven E. Reis, c/o WISE Coordinating Center, 127 Parran Hall, 130 DeSoto St., Pittsburgh, Pennsylvania 15261
reisse{at}msx.upmc.edu
OBJECTIVES
We sought to develop and validate a definition of coronary microvascular dysfunction in women with chest pain and no significant epicardial obstruction based on adenosine-induced changes in coronary flow velocity (i.e., coronary velocity reserve).
BACKGROUND
Chest pain is frequently not caused by fixed obstructive coronary artery disease (CAD) of large vessels in women. Coronary microvascular dysfunction is an alternative mechanism of chest pain that is more prevalent in women and is associated with attenuated coronary volumetric flow augmentation in response to hyperemic stimuli (i.e., abnormal coronary flow reserve). However, traditional assessment of coronary volumetric flow reserve is time-consuming and not uniformly available.
METHODS
As part of the Women’s Ischemia Syndrome Evaluation (WISE) study, 48 women with chest pain and normal coronary arteries or minimal coronary luminal irregularities (mean stenosis = 7%) underwent assessment of coronary blood flow reserve and coronary flow velocity reserve. Blood flow responses to intracoronary adenosine were measured using intracoronary Doppler ultrasonography and quantitative angiography.
RESULTS
Coronary volumetric flow reserve correlated with coronary velocity reserve (Pearson correlation = 0.87, p < 0.001). In 29 (60%) women with abnormal coronary microcirculation (mean coronary flow reserve = 1.84), adenosine increased coronary velocity by 89% (p < 0.001) but did not change coronary cross-sectional area. In 19 (40%) women with normal microcirculation (mean flow reserve = 3.24), adenosine increased coronary velocity and area by 179% (p < 0.001) and 17% (p < 0.001), respectively. A coronary velocity reserve threshold of 2.24 provided the best balance between sensitivity and specificity (90% and 89%, respectively) for the diagnosis of microvascular dysfunction. In addition, failure of the epicardial coronary to dilate at least 9% was found to be a sensitive (79%) and specific (79%) surrogate marker of microvascular dysfunction.
CONCLUSIONS
Coronary flow velocity response to intracoronary adenosine characterizes coronary microvascular function in women with chest pain in the absence of obstructive CAD. Attenuated epicardial coronary dilation response to adenosine may be a surrogate marker of microvascular dysfunction in women with chest pain and no obstructive CAD.
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