Factors influencing the presence or absence of acute coronary artery thrombi in sudden ischaemic death

Abstract

Sudden ischaemic death results either from an episode of acute myocardial ischaemia consequent upon coronary thrombosis or from an arrhythmia arising within a scarred left ventricle. Very different proportions of these two groups have been reported in both clinical studies in resuscitated subjects with out-of-hospital ventricular fibrillation, and in necropsy series. In 168 cases of sudden death due to ischaemic heart disease coming to necropsy 73 (43.5%) had mural intraluminal coronary thrombi, 50 (29.8%) had occlusive intraluminal thrombi, and 45 (26.7%) had no intraluminal thrombi, giving a ratio of 2.7:1 for those with and without coronary thrombosis. Single vessel disease, the presence of acute infarction at autopsy and prodromal symptoms were positively associated with the presence of coronary thrombosis. Conversely, the presence of old myocardial infarction at necropsy, a known clinical history of ischaemic heart disease and triple vessel disease were associated with the absence of acute thrombosis. The reported variation in the incidence of coronary thrombi in sudden ischaemic death can be largely explained by selection of subjects with those clinical characteristics which are positively or negatively associated with coronary thrombosis.

Intravascular Ultrasound Assessment of Ulcerated Ruptured Plaques

“…6,7 Recently, IVUS studies have demonstrated that ruptured plaques do not always cause ACS. 4,5 One IVUS study showed a high incidence of ruptured plaques (79%) in coronary segments remote from the culprit lesion of ACS patients.…”

“…5 Furthermore, pathological studies reported plaque ruptures in coronary arteries of patients with noncardiac death. 6,7 Thus, it is not clear why some plaque ruptures lead to clinical manifestations, whereas others remain asymptomatic and heal, perhaps leading to disease progression. Therefore, we undertook the present study to compare ruptured plaques in culprit lesions of ACS patients with ruptured plaques in nonculprit lesions of ACS patients and ruptured plaques in lesions of non-ACS patients.…”

Induction of Endothelial-Leukocyte Interaction by Interferon-γ Requires Coactivation of Nuclear Factor-κB

“…[8][9][10] Activated T lymphocytes and MHC-II-positive vascular smooth muscle cells (SMCs) are colocalized within atherosclerotic lesions, 11,12 and recent evidence suggests that T lymphocytes contribute to the development and rupture of atherosclerotic plaques. 13 Interestingly, IFN-␥, which is an inducer of IRF-1, cannot alone induce endothelial VCAM-1 expression or substantial monocyte adhesion to endothelial cells. In contrast, IFN-␥ potently stimulates VCAM-1 expression in SMCs.…”

Burgeoning Dilemmas in the Management of Diabetes and Cardiovascular Disease

“…After the seminal work of Falk and Davies et al, 23,24 it has become increasingly clear that morbidity and mortality associated with coronary artery disease are often associated with lesions that are not obstructive until they rupture and precipitate clinical events. Abluminal lesions are frequently present.…”