Étude des effets de l'adénosine sur le remodelage ventriculaire gauche survenant après un infarctus du myocarde

Mélanie Bousquenaud

    Research output: Types of ThesisDoctoral Thesis


    [Study of the effects of adenosine on left ventricular remodelling]
    Left ventricular (LV) remodeling can follow myocardial infarction (MI), an acute ischemic event which occurs after occlusion of a coronary artery. Remodeling allows maintaining and adapting cardiac function by geometric and functional changes of the myocardium. If this process becomes maladaptive, the patients? prognostic and life quality are impaired by the development of heart failure. Adenosine is an ubiquitous nucleoside with partially characterized effects on LV remodeling. These effects depend on the type of receptor activated. Previous in vitro studies from our laboratory have shown that adenosine regulates several key processes involved in LV remodeling. Here, we hypothesized that adenosine may have beneficial effects on LV remodeling after MI. First, we showed that positon emission tomography (PET) can accurately characterize MI severity and predicts subsequent LV remodeling in the rat model of MI induced by coronary occlusion. Using this technique, we described the case of a rat that survived after a massive infarct covering 70% of the left ventricle. Second, we showed that a chronic administration of adenosine preserves cardiac contractility in the border zone, two months after MI. This cardioprotective effect can be explained, in part, by the stimulation of angiogenesis involving a stimulation of the recruitment of endothelial progenitor cells to the heart. Then, we showed that the Monocyte Chemotactic Protein 3 stimulates the migration of endothelial progenitor cells and is thereby a potential therapeutic target after MI. Finally, we started the preclinical study of an A2A agonist / A3 antagonist, a promising candidate to prevent LV remodeling after MI
    Original languageFrench
    • Devaux, Yvan, Supervisor
    Award date18 Jul 2012
    Publication statusPublished - 18 Jul 2012

    Cite this