ASSOCIATION OF EOSINOPHILS WITH CARDIAC RUPTURE
ASSOCIATION OF EOSINOPHILS WITH CARDIAC RUPTURE
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DOI:
10.1016/s0046-8177(85)80105-2
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发表时间:
1985-01-01
期刊:
影响因子:
3.3
通讯作者:
VIRMANI, R
中科院分区:
文献类型:
--
作者:
ATKINSON, JB;ROBINOWITZ, M;VIRMANI, R
Cardiac rupture occurs in 10% of patients who die with acute myocardial infarction, but the pathogenesis remains unclear. Randomly selected patients (20) with cardiac rupture were reviewed retrospectively at autopsy, and the findings were compared with those of 20 age- and sex-matched control subjects who had died of acute transmural myocardial infarction without rupture. The times from the onset of chest pain to death were similar in the 2 groups (5.7 .+-. 5.8 days for patients with rupture vs. 4.2 .+-. 4.9 days for control subjects), and there were no differences in the incidences of systemic hypertension, diabetes mellitus, hypercholesterolemia, history of myocardial infarction, or angina pectoris. The severity of coronary atherosclerosis was different in the 2 groups, with 55% of the patients with cardiac rupture having single-vessel disease and 70% of the patients without cardiac rupture having disease in 3 vessels. The incidence of thrombosis was greater in patients with cardiac rupture than in those without. The inflammatory cell response in each patient was quantitated microscopically (number and type of leukocytes) in 10 high-power fields. The inflammatory response was greater in patients with cardiac rupture. The number of eosinophils in the inflammatory response was significantly (P < 0.01) greater in hearts associated with cardiac rupture (29.5 .+-. 4%) than in control hearts (11.7 .+-. 3.1%). Eosinophils rich in arylsulfatase B, peroxidase, glucuronidase, .beta.-glycerophosphatase, major basic protein and eosinophilic cationic protein may further weaken the necrotic myocardium and, in part, determine whether acute myocardial infarction will eventually result in cardiac rupture.