[The early and late complications after percutaneous balloon coronary angioplasty]

The coronary arteries from the hearts of 7 patients, 6 male and 1 female, age ranging from 39 to 69 years (mean 56), who died early or in the mid term from percutaneous transluminal coronary angioplasty (PTCA), were investigated by histology, immunohistochemistry and electron microscopy. Atherosclerotic coronary artery disease was present in all: single vessel disease in 2 and double vessel disease in 5. Indication to PTCA was stable angina in 1 patient, unstable angina in 2, postinfarction angina in 2 and acute myocardial infarction in the remaining 2. Thrombolysis was an associated procedure in 3 cases. Time interval between PTCA and death was less than 48 hours in 6, and 4 months in 1. Cause of death was myocardial infarction due to coronary occlusion complicating PTCA in 3 patients, and myocardial infarctions preceding PTCA in 4 patients. 9 coronary segments underwent dilatation: 5 in the anterior descending coronary artery, 3 in the right coronary artery and 1 in the left circumflex artery. Angiographically, the PTCA had been effective (decrease of stenosis > or = 40%) in 5 and failed in 4. Basically, the atherosclerotic plaques were eccentric in 3 and concentric in 6; the histotype was fibrotic in 4, atheromatous in 4 and fibro-atheromatous in 1. Only one case did not show any complication and the dilatation was effective as a consequence of plaque compression and stretching of the underlying tunica media. Complications observed in the other cases with early death consisted of: a) plaque cracks with intimal flaps and hematomas in all 6; b) laceration of the tunica media, even of the disease-free wall, with dissecting hematoma in 2; c) occlusive thrombosis in 3 and d) atheroembolism in 1. The 4 coronary segments, which appeared occluded angiographically soon after PTCA, were clinically interpreted as dissection in 3 and thrombosis in 1, whereas at histology the closing mechanism was an intimal hematoma with flap in 2, occlusive thrombosis in 1, and medio-adventitial dissecting hematoma with thrombosis in 1. Only ruptures of atheromatous plaques were complicated by thrombosis. The patient who died at 4 months exhibited a pattern of restenosis due to intimal smooth muscle cell proliferation. In conclusion, our postmortem study shows that PTCA may be associated with severe damage of the coronary artery consisting of plaque crack and laceration even of the disease-free wall, intimal and medial hematomas, thrombosis and atheroembolism.(ABSTRACT TRUNCATED AT 400 WORDS)