Systemic and cardiac hemodynamics in acute heart failure
Five to 10% of patients presenting with acute myocardial infarction develop cardiogenic shock. Despite the early myocardial revascularization, optimal pharmacological treatment and the use of short-term mechanical circulatory support, the mortality of cardiogenic shock complicating acute myocardial infarction remains abnormally high. Insights into cardiogenic shock’s pathophysiology remain crucial to the development of new therapeutic approaches. In this context, large animal models may provide a heuristic methodology to test pathophysiological hypotheses and thus new therapies. Our group developed a stable and reproductible closed chest sheep’s model of severe cardiogenic shock due to myocardial infarction. Percutaneous closed-chest models present the advantage to profoundly limit the huge trauma of thoracotomy, thus respecting cardiac and whole-body physiology and favouring recovery. Consequently, our model presents a high rate of survival after the induction of CS. Our experimental set-up could lead to a better understanding of mechanical interaction between short-term mechanical circulatory support and an acutely failing ventricle. The potential usefulness or harmfulness of vasoactive and inotropic drugs in patients assisted with those devices might also be explored in this model. Moreover, the impact of ventricular support on early remodelling of non-ischemic territory could be more fully investigated.