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[Incidence of induced coronary artery spasm in recent acute transmural myocardial infarction].

A number of studies have suggested that coronary spasm may play a role in the genesis of myocardial infarction. We carried out a provocation test with 0,4 mg intravenous methylergometrine in 131 patients undergoing routine coronary angiography at least 6 weeks after transmural myocardial infarction. The 124 men and 7 women of equal mean age of 49,6 years underwent the investigation on average 27 +/- 9 days after the date of onset of myocardial infarction. Seventy four patients had anterior infarcts (antero septal, anterior, apical), 55 had inferior infarcts (inferior, diaphragmatic and true posterior) and 2 had lateral wall infarcts. Thirty two patients with anterior infarcts (45 p. cent) had a single vessel disease of the left anterior descending artery, 19 had double vessel disease (25 p. cent), 16 had triple vessel disease (21,6 p. cent). During the provocation test with methylergometrine, 13 patients (17,6 p. cent) developed a spasm, 6 on the left anterior descending, 6 on the right coronary and 1 on the left circumflex artery. The patients with insignificant coronary lesions (7 cases) did not develop focal spasm. Twenty seven patients with inferior infarcts (49 p. cent) had single vessel disease, 19 had double vessel disease (34,6 p. cent) and 9 patients had triple vessel disease (16,4 p. cent). The provocation test induced spasm in 14 of the 55 patients (25,5 p. cent). The spasm was localised on the right on the right coronary artery in 9 cases, on the left circumflex in 3 cases and the left anterior descending artery in 2 cases. Therefore, in the whole population studied, 27/131 patients (21 p. cent) developed focal spasm after methylergometrine. In 13 cases, the spasm was observed in the coronary artery presumed to be responsible for the infarct, and in 14 cases on a vessel which did not correspond to the infarcted territory. Resting angina preceded myocardial infarction in only 6 of these 27 patients. This study does not confirm that coronary spasm was the cause of myocardial infarction. It does show the presence of a certain degree of reactivity of the coronary vessels after recent myocardial infarction. Half of the cases of spasm occurred on the vessel presumed responsible for the infarct but the other cases occurred in another zone, which suggests the possibility of post-infarction angina or even a recurrent myocardial infarction. This would be an indication for prophylactic treatment with calcium antagonist drugs.