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INVITED REVIEW

Mechanisms leading to reversible mechanical dysfunction in severe CAD: alternatives to myocardial stunning

¹Centre de Recherche et d'Applications en Traitement de l'Image et du Signal, Unité Mixte de Recherche Centre National de la Recherche Scientifique 5515, Institut National de la Santé et de la Recherche Médicale Unité 630, Université Claude Bernard 1, Institut National de Sciences Appliquées; ²Centre d'Exploration et de Recherche Médicale par Emission de Positons-Imagerie du Vivant, Lyon; ³Université Claude Bernard; ⁴Hôspices Civils de Lyon; and ⁵Institut National de la Santé et de la Recherche Médicale Unité 226, Lyon, France

Patients with severe chronic coronary artery disease (CAD) exhibit a highly altered myocardial pattern of perfusion, metabolism, and mechanical performance. In this context, the diagnosis of stunning remains elusive not only because of methodological and logistic considerations, but also because of the pathophysiological characteristics of the myocardium of these patients. In addition, a number of alternative pathophysiological mechanisms may act by mimicking the functional manifestations usually attributed to stunning. The present review describes three mechanisms that could theoretically lead to reversible mechanical dysfunction in these patients: myocardial wall stress, the tethering effect, and myocardial expression and release of auto- and paracrine agents. Attention is focused on the role of these mechanisms in scintigraphically "normal" regions (i.e., regions usually showing normal perfusion, glucose metabolism, and cellular integrity as assessed by nuclear imaging techniques), in which stunning is usually considered, but these mechanisms could also operate throughout the viable myocardium. We hypothesize that reversion of these three mechanisms could partially explain the unexpected functional benefit after reperfusion recently highlighted by high-spatial-resolution imaging techniques.

stunned myocardium; hibernating myocardium; inotropic reserve; cardiac imaging; myocardial wall stress; ventricular remodeling