Thrombogenesis in acute coronary syndromes.
J Interv Cardiol
; 8(6 Suppl): 724-9, 1995 Dec.
Article
en En
| MEDLINE
| ID: mdl-10159763
It is well-established that intracoronary thrombosis, which may be associated with plaque fissure and enhanced coronary vasoconstriction, is the immediate cause of a sudden impairment of regional myocardial perfusion, which is transient in unstable angina and is, eventually, irreversible in acute myocardial infarction. It is also well-known that increased platelet reactivity, increased procoagulant activity, and reduced endogenous fibrinolysis are risk factors for acute coronary events. Nevertheless, the primary causes responsible for sudden intracoronary thrombosis and for coronary vasoconstriction causing acute coronary syndromes are still largely speculative. Recent studies have shown activated inflammatory cells both in the coronary arterial wall and in the systemic circulation of patients with unstable angina. Furthermore, the intensity of the inflammatory response is correlated with an adverse prognosis. This inflammatory component may have important pathogenetic and prognostic roles because an outburst of inflammatory cytokines has the potential to increase the sensitivity of platelets to agonists, to turn the anticoagulant and vasodilator physiological properties of the endothelium into procoagulant and vasoconstrictor properties, and to cause plaque fissure by the release of proteolytic enzymes.
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Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Trombosis Coronaria
/
Enfermedad Coronaria
Tipo de estudio:
Etiology_studies
/
Prognostic_studies
Límite:
Humans
Idioma:
En
Revista:
J Interv Cardiol
Asunto de la revista:
CARDIOLOGIA
Año:
1995
Tipo del documento:
Article
País de afiliación:
Italia
Pais de publicación:
Estados Unidos