Résumés
Résumé
Le remodelage ventriculaire survenant à la suite d’un syndrome coronarien aigu est complexe et multiforme. Il est le fait de la réponse du myocarde aux différentes agressions intervenant au cours de ces syndromes, principalement de l’ischémie et de la nécrose du territoire en aval de l’artère occluse. Il ne faut toutefois pas négliger la responsabilité des lésions liées à la reperfusion spontanée ou provoquée des tissus ou encore liées aux embolies dans la microcirculation coronaire de divers types de cellules et de débris responsables du phénomène d’absence de reperfusion (no-reflow). Le remodelage à la phase aiguë de l’infarctus est dominé par la dilatation précoce du ventricule qui conditionne largement le pronostic tardif, la détersion de la nécrose remplacée par une fibrose cicatricielle et l’hypertrophie compensatrice associée à la fibrose des zones non infarcies survenant parallèlement. Les mécanismes cellulaires et moléculaires de ces divers aspects du remodelage sont de mieux en mieux connus, permettant d’expliquer l’effet bénéfique de nombreuses molécules déjà disponibles et offrant aussi des cibles potentielles pour de nouvelles thérapeutiques. Une valorisation de ces connaissances associée à l’identification de facteurs de risque de remodelage et à une intervention thérapeutique toujours plus précoce devrait permettre de limiter encore plus les aspects délétères de ce processus, afin d’éviter ou retarder encore l’évolution vers l’insuffisance cardiaque.
Summary
Ventricular remodelling following acute coronary syndromes is both complex and multiform. It is due to the response of the myocardium to the different agressions associated with these syndromes, in particular the ischemia and necrosis downstream of the occluded artery. We must not however neglect the role of the remodelling of the lesions resulting from spontaneous reperfusion or provoked by the cells and tissues associated with coronary microcirculation embolisms and the no-reflow phenomenon. Acute post-infarct remodelling is dominated by early ventricular dilatation which largely affects late prognosis, necrosis elimination and its replacement by a fibrotic scar in parallel with a compensatory hypertrophy of the non-infarcted myocardium. The diverse cellular and molecular components of this remodelling are increasingly well-known, allowing us to better explain the beneficial effects of the currently available medications and providing us with new potential therapeutic targets. A grading of this knowledge associated with the identification of new risk factors and early therapeutic interventions should help us to further limit the deleterious aspects of this remodelling in the goal of preventing, or at least delaying, the devolution towards heart failure.
Parties annexes
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