Prevention of myocardial stunning during percutaneous coronary interventions: novel insights from pre-treatment with glucagon-like peptide-1.

P atients undergoing high-risk percutaneous coronary interventions (PCIs) are at increased hazard of persistent hypotension and left ventricular (LV) dysfunction as a result of myocardial stunning. With the development of stunning, support devices and inotropes are frequently called upon to support the patient during and after procedures. Myocardial stunning is defined as the persistence of LV dysfunction after ischemia, in the absence of irreversible damage (1). Its duration is variable, but it often persists beyond 30 min, and repeated balloon occlusions prompt additional LV dysfunction (2). The mechanism of this persistent dysfunction is not known; proposed mechanisms include generation of oxygen-derived free radicals (3) or calcium overload (4). To date, no medications have proven effective in preventing this transient but potentially serious deterioration in function. The discovery that glucagon-like peptide-1 (GLP-1) provides myocardial protection has generated significant scientific interest. GLP-1 is a 30 amino acid peptide produced in the intestinal epithelium in response to food intake (5). It is rapidly metabolized by dipeptidyl peptidase-IV (DPP-4) to its primary metabolite GLP-1(9-36), and the half-life of GLP-1 in plasma is 2 to 3 min (6). The primary action of GLP-1 is to stimulate insulin secretion and inhibit glucagon secretion, and it appears to regulate appetite and food