Epicardial and microvascular reperfusion with primary percutaneous coronary intervention.
Restoration of normal flow and tissue-level perfusion are key factors in the reduction of mortality in acute myocardial infarction. The goal of reperfusion during primary percutaneous coronary intervention (PCI) should be to restore not only epicardial patency and flow, but also downstream myocardial tissue perfusion. This review will focus on the techniques able to evaluate and quantify epicardial and microvascular perfusion and on the available therapeutic tools that may be useful in primary PCI. After primary PCI, rates of TIMI flow grade 3 of 80 to 100% have been reported. Furthermore, after stenting during primary PCI more than one third of patients have persistently abnormal corrected TIMI frame counts related to increased downstream resistance. Achievement of TIMI flow grade 3 is no longer sufficient to define an optimal result of primary PCI and restoration of normal tissue-level perfusion is also required. Coronary no/slow reflow and myocardial hypoperfusion after otherwise successful recanalization of infarct-related arteries may involve more than just classical non-reperfusion of the myocardium that is already dead: distal embolization of debris or microparticulate atheromatous material, capillary edema, inflammation, and neurohormonal reflexes and vasoconstriction may play a crucial role. Evolving treatments of the no-reflow phenomenon are directed toward the restoration of microvascular flow abnormalities because these either directly or indirectly contribute to cell death. Promising adjunctive therapies that may reduce microemboli include intensive antiplatelet therapy with aspirin and ticlopidine, platelet glycoprotein IIb/IIIa inhibitors, coronary vasodilators, and embolization protection devices. Therapy targeting microvascular vasospasm also appears promising. Finally a variety of interventional new approaches have been focused on the setting of primary PCI, like atherectomy and thrombectomy devices, distal protection devices, hypothermia and hyperoxemic therapy, that are under investigation in numerous trials before they can be used routinarily.
Bolognese
Leonardo
L
Department of Cardiovascular Diseases, Hospital ofArezzo, Arezzo, Italy. leonardobolognese@hotmail.com
Falsini
Giovanni
G
Liistro
Francesco
F
Angioli
Paolo
P
Ducci
Kenneth
K
D015906:Angioplasty, Balloon, Coronary / Q000379:methods*; D001783:Blood Flow Velocity / Q000502:physiology; D017023:Coronary Angiography; D003326:Coronary Circulation / Q000502:physiology*; D003331:Coronary Vessels / Q000503:physiopathology*; D006801:Humans; D008833:Microcirculation / Q000502:physiology; D009203:Myocardial Infarction / Q000000981:diagnostic imaging / Q000503:physiopathology / Q000628:therapy*; D010496:Pericardium; D016896:Treatment Outcome