Author + information
- Received November 9, 1982
- Revision received December 7, 1982
- Accepted December 13, 1982
- Published online March 1, 1983.
- Richard Gorlin, MD, FACC*
- ↵*Address for reprints: Richard Gorlin, MD, Department of Medicine, The Mount Sinai Medical Center, 1 Gustave L. Levy Place, New York, New York 10029.
While fixed atherosclerotic and thrombotic lesions have long been known to cause myocardial ischemia and cardiac pain, the various transient or dynamic events that may also cause ischemia and pain have become better understood in the past 15 years. These can be classified into two broad categories: those that cause a dynamic reduction in the caliber of the coronary arteries and those that reduce the coronary vasodilatory reserve capacity. In the first group are myocardial compression or “bridging” of an artery; coronary vasoconstriction due to frank spasm or generalized arterial hypertonus, particularly at the site of atherosclerotic lesions; reduced arterial distending pressure and platelet aggregation which may transiently occlude a diseased arterial segment. The causes of inadequate coronary vascular reserve flow capacity can be either anatomic or functional. Among the former, the increased muscle mass to blood vessel ratio occurring in myocardial hypertrophy is most important. The functional causes of limited coronary vascular reserve include diastolic transmural compression and coronary “steal,” both of hemodynamic origin. In addition, arteriolar “unresponsiveness” or dysregula-tion caused by smoking, drugs or other unknown conditions may adversely affect coronary vascular reserve. Hence, myocardial ischemia may result from conditions that limit potential for increase in flow or from conditions that reduceflow from a preexisting level. These conditions, which are transient and dynamic in nature, may modify the threshold for ischemia, particularly in patients with fixed coronary obstructive disease.
This study was presented as the 18th Annual Laurence B. Ellis Lecture at Harvard Medical School (200th Anniversary), October 25, 1982
- Received November 9, 1982.
- Revision received December 7, 1982.
- Accepted December 13, 1982.
- American College of Cardiology Foundation