Exertion has been reported to acutely increase the risk of sudden coronary death, but the underlying mechanisms are unclear.
To determine the frequency of plaque rupture in sudden deaths related to exertion compared with sudden deaths not related to exertion.
Autopsy survey. Coronary arteries were perfusion fixed and segments with more than 50% luminal narrowing were examined histologically. Ruptured plaques were defined as intraplaque hemorrhage with disruption of the fibrous cap and luminal thrombus. Exertion before death was determined by the investigator of the death.
Medical examiner's office.
A total of 141 men with severe coronary artery disease who died suddenly, including 116 whose deaths occurred at rest (mean [SD] age, 51  years) and 25 who died during strenuous activity or emotional stress (age, 49  years).
The frequency and morphology of plaque rupture was compared in men dying at rest vs those dying during exertion. Independent association of risk factors (total cholesterol, high-density lipoprotein cholesterol, glycosylated hemoglobin, cigarette smoking) in addition to acute exertion with plaque rupture were determined.
The mean (SD) number of vulnerable plaques in the coronary arteries of men in the exertional-death group was 1.6 (1.5) and in the at-rest group was 0.9 (1.2) (P=.03). The culprit plaque in men dying during exertion was plaque rupture in 17 (68%) of 25 vs 27 (23%) of 116 men dying at rest (P<.001). Hemorrhage into the plaque occurred in 18 (72%) of 25 men in the exertional-death group and 47 (41%) of 116 men in the rest group (P=.007). Histological evidence of acute myocardial infarction was present in 0 of 25 in the exertion group and in 15 (13%) of 116 in the rest group. Men dying during exertion had a significantly higher mean (SD) total cholesterol-high-density lipoprotein cholesterol ratio (8.2 [3.0]) than those dying at rest (6.2 [ 2.7]; P=.002), and the majority (21/25) were not conditioned. In multivariate analysis, both exertion (P=.002) and total cholesterol-high-density lipoprotein cholesterol ratio (P=.002) were associated with acute plaque rupture, independent of age and other cardiac risk factors.
In men with severe coronary artery disease, sudden death related to exertion was associated with acute plaque rupture.
"Il s'agit surtout de la pratique occasionnelle d'une activité physique intense et d'un niveau de risque cardiovasculaire élevé avec un score coronaire élevé (voir ci-dessous)  . Ainsi, le risque relatif d'infarctus chez un sujet de plus de 35 ans, sédentaire, qui pratique brutalement un effort très intense est multiplié par 100 par rapport au repos . Pour comparaison, ce sur-risque chez le pratiquant régulier d'activité physique est inférieur à 5 . "
[Show abstract][Hide abstract] ABSTRACT: Non-traumatic sudden death related to sport is a rare but always dramatic event.
Its causes are mainly cardiovascular.
Prevention of sudden death depends on effective medical examination involving history, physical examination and resting ECG, as education of athletes who must follow the rules for safe sport practice and lastly training for emergency actions of the population.
Journal Europeen des Urgences et de Reanimation 10/2014; 26(3-4). DOI:10.1016/j.jeurea.2014.10.010
"The loss of integrity from the protective covering induces plaque ruptures or erosions. This disruption allows blood to come in contact with the highly thrombogenic contents of the necrotic core of the plaque and luminal thrombosis to occur.2)3) "
[Show abstract][Hide abstract] ABSTRACT: A 51-year-old man was being admitted to the emergency department with chest pains. He had a history of acute myocardial infarction (MI) on two prior occasions and was successfully treated with drug eluting stents. He was diagnosed with 3 consecutive events of acute MI in 3 different vessels. The consecutive events of acute MI in different vessels are a very rare case. He did not have risk factors, such as coagulation abnormality, clopidogrel resistance, patient's compliance and vessel abnormality, except for his cigarette smoking. We reported the first case with 3 consecutive events of acute MI in each 3 vessels during a long-term interval.
Korean Circulation Journal 10/2013; 43(10):694-698. DOI:10.4070/kcj.2013.43.10.694 · 0.75 Impact Factor
"Intraplaque hemorrhage is believed to arise from the disruption of thin-walled microvessels that are lined by a discontinuous endothelium without supporting smooth-muscle cells. Several studies have suggested that intraplaque hemorrhage and rupture of the fibrous cap are associated with an increased density of microvessels. Therefore, it is important to find a useful marker for detecting fragile microvessels. "
[Show abstract][Hide abstract] ABSTRACT: Microvascular proliferation is a major risk factor for plaque vulnerability in patients with carotid stenosis. There are several vascular endothelial markers such as CD31 and CD105, but it is unclear which marker is most sensitive for microvessels. This study sought to examine the correlations between CD31 and CD105 expression in microvessels on carotid plaques and clinical manifestations.
We studied 13 lesions in 12 patients. The patients underwent carotid endarterectomy and samples were stained for CD31 and CD105. The numbers of microvessels positive for these markers within a field of view were counted.
The average numbers of microvessels were 5.8 ± 5.4 for CD31 and 9.2 ± 9.3 for CD105 (P = 0.04). More microvessels were positive for CD105 than there were for CD31 in patients with diabetes mellitus (P = 0.04).
In patients with carotid artery stenosis, CD105 is more appropriate than CD31 for detecting microvessels in carotid plaques. In patients with diabetes mellitus, CD105 is significantly more highly expressed in microvessels than CD31.
Surgical Neurology International 09/2013; 4:132. DOI:10.4103/2152-7806.119081 · 1.18 Impact Factor
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