A quantitative analysis of adventitial inflammation of the coronary artery with intimal lesions is described in 12 patients who suffered coronary death and had had unstable angina (crescendo angina) at rest (group 1). After autopsy in these patients we examined epon-embedded cross sections by light and electron microscopy, paying particular attention to the adventitia, and compared these results with those in six patients who had had angina but died of noncardiac causes (group 2) and those in 22 patients who did not have angina (group 3). Of the 132 segments from group 1 patients, 39 (30%) were narrowed 76% to 100% by atherosclerotic plaque (group 2, 27%; group 3, 1%), and 23 (17%) had occlusive thrombi. Of the 264 sections (two from each segment) from group 1 that were examined, 98 (37%) (group 2, 15%; group 3, 9%) revealed clustered infiltration of inflammatory cells in the adventitia, half of which were associated with vascular nerve involvement. These findings in the adventitia may be related to the vasospastic component of unstable angina. Circulation 71, No. 4, 709-716, 1985. THE SIGNIFICANCE of coronary artery spasm in patients with ischemic heart disease has been emphasized recently, as diagnostic techniques and methodology have improved.' Previously reported morphologic results obtained at autopsy in patients with coronary artery disease have been mainly concerned with the effects of the intimal lesions, such as the degree of luminal narrowing,4 thrombus,5 and rupture of atheroma.6 The once-emphasized inflammatory lesions in the adventitia of atherosclerotic coronary arteries7 have recently been largely ignored. However, they may have a significant role in causing coronary artery spasm because the coronary adventitia is richly innervated with autonomic fibers. In this report 12 patients with unstable angina culminating in sudden death or acute myocardial infarction were studied at autopsy as a representative sample of vasospastic angina in the waxing phase. The coronary artery of each was examined, with particular attention to the adventitia, with light and electron

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Light and electron microscopic examinations were performed on 20 coronary artery sites from nine patients who had undergone percutaneous transluminal coronary angioplasty. Twelve successfully dilated sites without prior thrombosis showed evidence of a tear in the luminal surface (with or without fracture of an atheroma) even at 140 days after angioplasty. The tear split through a relatively undistensible intima in 9 (75%) of the 12 sites. Two successfully dilated sites with prior thrombosis showed an intraintimal tear with a widely lacerated fibrous cap and thin mural thrombus. After dilation, the occluded prior nonthrombosed site showed marked protrusion of a separated plaque. An occluded prior thrombosed site after dilation revealed intraintimal canal-like hematoma. Four sites that occluded after balloon passage revealed a dissecting hematoma in three and plaque disruption in the other.

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Objective-To evaluate changes in coronary artery spasticity in patients with vasospastic angina who had been stable for years under continuous drug treatment. Methods-Follow up coronary angiography was performed under intracoronary ergonovine provocation in 27 well controlled patients with vasospastic angina and no organic stenosis; the tests were done > 24 months after the initial coronary angiography, in which occlusive spasm had been induced by the same regimen of ergonovine provocation. Results-The mean (SD) follow up period was 47.2 (21.6) months. All patients had been free from angina attack for more than 24 months under treatment with antianginal drugs. During this follow up period, organic stenosis developed in only one case. Occlusive spasm was observed during follow up coronary angiography in 23 patients. Spasm with 90% narrowing was observed in three other patients, and diVuse significant narrowing was seen in the final patient. No significant diVerence was found in spasticity (p = 0.75) between the initial and the follow up tests. Conclusions-Repeated ergonovine provocation during coronary angiography after a controlled period of several years showed that coronary spasm remains inducible in most patients. Discontinuance of drug treatment during the remission from anginal attacks achieved by medication may put the patient at high risk. (Heart 1999;81:528-532)