Coronary artery spasm and vasoconstriction. The case for a distinction.

It is now generally accepted that an episodic increase of the vasomotor tone of epicardial coronary arteries not only is the cause of variant angina but also may represent a pathogenetic component in other, more common, anginal syndromes.1,2 The terms "spasm" and "coronary constriction" are often used interchangeably when referring to increases in coronary vasomotor tone. This generalization may find some justification in the common clinical indication for coronary vasodilator therapy that nonspecifically reduces smooth muscle tone but is confusing when trying to identify the actual causes of vasoconstriction and to develop specific forms of treatment against it. The degree of coronary constriction can vary. At one end of the spectrum of coronary constriction is the mild, physiological response to common constrictor stimuli normally observed in experimental animals and humans; at the other extreme is the severe, segmental constriction leading to total artery occlusion as typically observed in patients with variant angina. In between these two extremes are other forms of coronary constriction that do not cause total occlusion, which are observed in some patients with ischemic syndromes and in experimental conditions but cannot be considered physiological. To set the stage for a better understanding and classification of these conditions, it may be useful to clearly differentiate at least the extreme forms of constriction that can result in segmental vessel occlusion. We suggest some basic criteria for distinguishing the mechanisms of coronary constriction according to the intensity of the stimuli and the response of the vessel wall.