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Histological evaluation of coronary plaque in patients with variant angina: relationship between vasospasm and neointimal hyperplasia in primary coronary lesions

^a Department of Cardiology, Juntendo University School of Medicine, Tokyo, Japan
^* the Department of Cardiology, The Cardiovascular Institute, Tokyo, Japan

View larger version (101K): [in a new window]   Figure 1 Cineangiograms of focal coronary spasm occurring at the site of significant atherosclerosis (Patient No. 10). Left, coronary angiogram of the right coronary artery in left anterior oblique view shows severe coronary stenosis with a 75% reduction of lumen diameter in the midportion. Middle, results of the acetylcholine provocation test were positive with the lumen diameter decreasing from a 75% to a subtotal occlusion by the superimposed focal coronary spasm. Right, luminal dilatation of the right coronary artery with a residual fixed coronary lesion of approximately 50–75% stenosis was observed after the administration of intracoronary isosorbide dinitrate. Unfortunately, this patient died suddenly of his disease. Autopsy studies were conducted.

View larger version (132K): [in a new window]   Figure 2 Photomicrographs obtained at autopsy of the coronary arterial site responsible for variant angina in patient No. 10. Histological examination of the affected segment of the right coronary artery shows a focal obstructive fibrous plaque with a superimposed thrombus. There are two distinct intimal layers in the plaque. The inner, light-colored layer, is a myxedematous area of the neointima with an abundance of stellate smooth muscle cells and a considerable amount of extracellular matrix. The outer layer, dark-colored layer, consists of so-called "old" plaque that is mainly composed of relatively hypocellular dense fibrous connective tissue (upper). Neointimal hyperplasia with inflammatory cell infiltration is observed in the inner layer, and resembles the histological features in the atherectomy specimens obtained from 14 other patients with variant angina in the present study. Intimal hemorrhage (arrow) is also observed (lower). (Upper; elastica von Gieson stain, x4. Lower; hematoxylin and eosin stain, x60.)

View larger version (120K): [in a new window]   Figure 3 Progressive narrowing of the lumen of the coronary artery in patient No. 2 after 6 months. Coronary angiogram of the left coronary artery (in left cranial view) shows mild coronary stenosis with a 25% reduction in lumen diameter in the proximal portion after the intracoronary administration of isosorbid. Occlusive vasospasm was found at the same site at that time (upper). Six months later, rapid progression from a 25% to a 90% fixed coronary stenosis was observed at the previously spastic segment after the intracoronary administration of isosorbide in the follow-up angiogram (lower).

View larger version (130K): [in a new window]   Figure 4 Photomicrograph of atherectomy specimens obtained from the patient No. 2. The proliferation of characteristic spindle-shaped smooth muscle cells (neointimal hyperplasia) is observed in a fibrous plaque (hematoxylin and eosin, x40).