Rupture of atheromatous plaque as a cause of thrombotic occlusion of stenotic internal carotid artery.

Abstract

We analyzed the clinical profiles and autopsy findings of five patients who died shortly after developing cerebral infarction following thrombotic occlusion of the internal carotid artery. In all five cases, thrombotic occlusion was caused by rupture of the fibrous lining over the gruel of atheroma at the origin of the internal carotid artery showing tight stenosis of the lumen. The mean±SD shorter diameter of the lumen at the site of occlusion was 1.5±0.4 mm. Our results show that an internal carotid artery with tight stenosis of the lumen by atheroma containing gruel harbors a risk of thrombotic occlusion, which may give rise to cerebral infarction by artery-to-artery embolism or by reduced cerebral perfusion. there are only a few reports analyzing mechanisms of thrombotic occlusion of the ICA in patients who died shortly after the occlusion. 2 -3 Postmortem study, which enables us to examine the entire length of the extracranial and intracranial cervicocephalic arteries and the brain, is a golden opportunity to analyze plaque complication leading to thrombotic occlusion of the ICA and the mechanism for occurrence of stroke. We had previously reported a patient with recent thrombotic occlusion of a stenotic ICA due to rupture of the plaque. 2 We extensively reviewed all the autopsy cases in our hospital and found four more patients with recent thrombotic occlusion of the ICA, which urged us to report the clinical features and postmortem pathologic findings of the five patients to add to the body of knowledge that would influence the formulation of a treatment plan. Subjects and MethodsAmong 1,550 patients autopsied in the National Cardiovascular Center from 1977 to 1988, ICA occlusion was found in 48. Of the 48 patients, five died <60 days after developing thrombotic occlusion of an atherosclerotic ICA, 16 (including one with a recent thrombus on the other side [case 2 in this report]) had an atherosclerotic ICA occluded by organized thrombi, 26 had an ICA occluded by fresh or organized thromboemboli of cardiac origin, and two (one suffering from Behcet's syndrome and the other from aortitis syndrome) had an ICA occluded by organized thrombi. We analyzed the clinical profiles and autopsy findings of the five patients with recent thrombotic occlusion of the ICA. These patients comprised three men and two women aged 61-78 (mean 69) years (Table 1). At autopsy, the brain and extracranial arteries were removed and fixed in 10% formalin. After fixation, the arteries at the base of the brain and the extracranial arteries were decalcified in 45% formic acid in 10% sodium citrate solution for 2 days, then histologically examined at approximately 3-mm intervals with hematoxylin and eosin staining and other methods as needed.The clinical and pathologic features of case 5 have been reported previously.

Recently Occluded Intracranial and Extracranial Carotid Arteries

“…Fisher 6,7 suggested that atherosclerosis was the likely pathological cause of occlusive carotid sinus thrombosis, and he confirmed Chiari's earlier observation that thrombosis at this site is often preceded by plaque ulceration. 7 This concept has subsequently been confirmed by others, and carotid sinus plaque rupture has been associated with sites at which a thin, fibrous cap overlies a large necrotic core, 16 as in the coronary circulation. There are rather more data, although much conflicting, concerning nonocclusive carotid plaque morphology and its prognostic value regarding the development of neurological symptoms.…”

Source of Microembolic Signals in Patients With High-Grade Carotid Stenosis

“…[23][24][25][26] Harrison and Marshall 26 found thrombus in 66% of the 24 carotid plaques taken within 4 weeks of the most recent ischemic event but in only 21% of 28 plaques taken Ͼ1 month after. However, surface thrombus is also a common finding in asymptomatic patients, present in Ϸ30% to 56% of patients.…”

Inflammation, Statin Therapy, and Risk of Stroke After an Acute Coronary Syndrome in the MIRACL Study

“…15 The sources of emboli to consider would include the carotid arteries, aortic arch, or the heart. 3,4 Although in studies of selected patient groups, large or anterior myocardial infarction increases the risk of stroke, 18 -20 in the Northern Sweden MONICA study (a population study), only 20% of strokes within 1 month of a myocardial infarct were associated with left ventricular thrombus. 2 In the MIRACL study, troponin elevation related to the risk of stroke, suggesting that larger myocardial infarcts more likely serve as a source of cerebral emboli.…”

“…Plaques removed during carotid endarterectomy or at postmortem examinations of fatal carotid occlusions consistently show inflammatory cell infiltration, plaque rupture, and intraplaque hemorrhage. 3,4,9 Complex or ulcerated carotid plaques are more likely to demonstrate these inflammatory and hemorrhagic features than smooth carotid plaques. 8 The coronary arteries of patients with acute coronary syndrome also show wide-spread inflammation, as suggested by Berk and Buffon.…”

“…1,2 Intracranial arterial occlusion and emboli from atherosclerotic plaques in the carotid arteries and aortic arch can also cause stroke. 3,4 Patients with acute coronary syndromes have more prevalent complex plaques in the carotid arteries, 5 lesions more likely to lead to stroke and transient ischemic attack (TIA) than less complex plaques. 6,7 Like their coronary counterparts, complex carotid plaques exhibit more commonly plaque disruption and inflammation, with abundant accumulations of activated leukocytes and the expression of cellular adhesion molecules.…”