[Physiopathology of unstable angina].
The majority of cases of unstable angina and myocardial infarction have a common origin: rupture of an atheromatous plaque complicated by intracoronary thrombosis. The nature of these "high risk" plaques is now well known: they are excentric, moderately severe lesions, the voluminous lipid centres of which are covered only by a thin unstable fibrous layer. The triggering factor of the rupture of an unstable plaque may be an increase in wall stress (spastic vasoconstriction, rise in blood pressure), and/or an inflammatory or haemorrhagic phenomenon within the plaque itself. Once the plaque has ruptured, the outcome to unstable angina or myocardial infarction is determined by two factors: the size and rapidity of constitution of the thrombus and the quality of the collateral circulation.
Spaulding
C
C
Service de cardiologie, hôpital Cochin, Paris.
Cador
R
R
Ounnoughene
Z
Z
Ben Hamda
K
K
Weber
S
S
D000789:Angina, Unstable / Q000150:complications / Q000473:pathology / Q000503:physiopathology*; D003324:Coronary Artery Disease / Q000473:pathology / Q000503:physiopathology; D004730:Endothelium, Vascular / Q000473:pathology; D006801:Humans; D007249:Inflammation / Q000503:physiopathology; D009203:Myocardial Infarction / Q000209:etiology; D012307:Risk Factors
Physiopathologie de l'angor instable.