Significance of adventitial inflammation of the coronary artery in patients with unstable angina: results at autopsy.

Abstract

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

Distribution of Inflammatory Cells in Adventitia Changed with Advancing Atherosclerosis of Human Coronary Artery

“…Since calcified lesions were not suitable for immunostaining and more advanced type and with calcification or vulnerable lesions would be highly prone to ischemic episodes with inflammatory responses around atherosclerotic lesions, these lesions were excluded from the present study. Therefore, it is unlikely that the cases used here included cases of ischemic heart diseases, such as acute myocardial infarction and angina pectoris, although episodes of angina pectoris and coronary spasms, which were reported to induce inflammatory responses in the adventitia, were not checked in the used cases 22) . The distribution of infiltrating inflammatory cells in subintimal regions was compatible with previous reports [3][4][5][6][7][8][9][10][11] .…”

Successful Treatment of Refractory Vasospastic Angina With Corticosteroids-Coronary Arterial Hyperreactivity Caused by Local Inflammation?-

“…11 Also, Kohchi et al reported that focal infiltration of inflammatory cells was seen in the adventitia of the coronary artery in patients with VSA. 12,13 Thus, local inflammation of the coronary arterial wall is likely to play an important role in the pathogenesis of coronary spasm.…”

Stromelysin-1 and Interleukin-6 Gene Promoter Polymorphisms Are Determinants of Asymptomatic Carotid Artery Atherosclerosis

“…14 Data from the Physicians Health Study suggest that this association is still present after an 8-year follow-up period, 15 implying that progression of atheroma may also be associated with raised inflammatory markers. Unstable angina is associated with activation of systemic circulating neutrophils 16 and with elevated inflammatory markers such as C-reactive protein and IL-6 levels. [17][18][19] The magnitude of this elevation predicts poor outcome and is not merely secondary to the presence of myocardial necrosis or ischemia.…”