Pursuing the goal to improve downstream myocardial tissue perfusion

Abstract

The coronary slow flow phenomenon is an angiographic finding characterized by delayed distal vessel opacification in the absence of significant epicardial coronary disease. Extensively studied both in the experimental and clinical setting, it was clearly associated with unfavourable clinical outcome and prognosis.1,2 Several hypotheses, including embolization of platelet-rich thrombi or atherosclerotic plaque debris that can ‘sludge’ the distal vessel, and release of vasoconstrictive substances causing intense vasospasm of the distal microcirculation, were advocated to justify this event in the context of percutaneous coronary intervention. If the principal mechanism of the slow flow phenomenon is vasoconstriction, this would explain the favourable response seen with intracoronary administration of calcium antagonists such as verapamil, or vasodilators such as nitroprusside, papaverine, and adenosine. Nicorandil, a nicotinamide ester, is a vasodilator agent approved as an antianginal agent, with a compound and balanced mechanism of action which relaxes coronary vascular smooth muscle by stimulating guanylyl cyclase and increasing cGMP levels as well as by a second mechanism resulting in activation of K+ channels and hyperpolarization.3 Potassium channel opening effects a titratable and sustained dilating action on both coronary artery conductance and resistance vessels. Kawai et al. have provided evidence that a prophylactic bolus of 6 mg of nicorandil administered i.v. immediately prior to percutaneous coronary intervention (PCI) reduces the incidence of the slow flow phenomenon without any side effects.4 Conceptually, this strategy improves coronary flow and myocardial perfusion by dilating those vessels with loss of endothelial integrity and reducing capillary and arteriolar blockages resulting from the presence of leukocytes … *Corresponding author. Tel: +39 0957436201, Fax: +39 095362429, Email: tambucor{at}unict.it