Coronary Artery Spasm

Allan Burns (1809) {1}, medical school dropout and brilliant autodidact, was the first to propose that angina during exercise was due to myocardial ischemia. He believed that diseased coronary arteries acted as constricted rigid tubes which limited blood supply to the myocardium and generated a state in which the heart’s “energy supply and its energy expenditure do not balance each other”. According to this concept it is an increased work load on the heart that precipitates myocardial ischemia and anginal symptoms. However, already Herber-den (1772) {2} had recognized that angina may occur at rest, often during the night, a phenomenon that cannot be readily explained on the basis of Burns’ mechanism. During the 19th century, many authors felt that anginal pain was triggered by some distention of the aorta or left ventricle. Such cardiovascular dis-tentions were sometimes thought to occur as a result of peripheral constrictor responses, a syndrome that had been outlined by Nothnagel (1867) {3} under the name “angina pectoris vasomotoria”. Latham (1876) {4} and others believed that angina might reflect a cramp or spasm of the heart, but such a mechanism was not widely accepted, since it was thought that a cramp of the heart was not compatible with survival {5}. In the first edition of his textbook, Osier (1892) {6} discussed the possiblity that cardiac pain “resulted from the great stretching and tension of the nerves in the muscular substance”. He added that “a modified form of this view is that there is a spasm of the coronary arteries with great increase in the intracardiac pressure”. Osier was still under the influence of the mechanistic hypotheses of the 19th century. However, in his second Lumleian lecture on angina pectoris 18 years later (1910) {7}, his “modified view” became explicit. He discussed the possible role of coronary artery spasm at great length, and indicated that angina may be associated with other vasomotor disturbances such as Raynaud disease or migraine. On the basis of his clinical observations, he concluded that there was “evidence that sclerotic arteries are specially prone to spasm”. Also, he speculated that coronary vessels might be affected by a “perverted internal secretion which favours spasm of the arteries”. Therefore, the 19th century, era of speculations and controversies, generated two seemingly contradictory “coronary theories”: Burns’ rigid arteries, an example of insufficient vasomotion, and Osler’s atherosclerotic vasospasm, an example of excessive vasomotion.