title: No-reflow: a heterogeneous clinical phenomenon with multiple therapeutic strategies.
abstract: Previously defined as the failure to achieve uniform intramyocardial reperfusion after prolonged but reversible coronary occlusion, only recently has no-reflow phenomenon been characterized as a heterogeneous clinical condition. In fact, in about half of post-infarct patients that show no-reflow after 24 hours from coronary recanalization by either thrombolysis or PTCA, no-reflow phenomenon is spontaneously reversible. Reversible no-reflow is associated with favorable left ventricular remodeling even in the absence of significant improvement in regional contractile function. Thus, it may be a clinical marker of yet unknown mechanisms, which may favorably affect myocardial response to necrosis. Based on the pathogenesis and on the time-course of no-reflow, the phenomenon may be associated with lack of patency or with loss of anatomic integrity of microvessels, with the former being potentially reversible while the latter associated with definitive tissue damage. As a consequence, possible therapeutic strategies of no-reflow have to be designed according to not only the main target [microvessel patency or integrity], but also taking into account the timing of development of the damage. This "mini review" is focused on recent advances on the pathogenesis and clinical presentation on no-reflow. These data will give the opportunity to formulate novel interpretation and classification of the phenomenon and consequently, to propose adequate therapeutic strategies.
authors.affiliation: Institute of Cardiology, Catholic University of the Sacred Heart, Rome, Italy. lgaliuto@rm.unicatt.it
authors.forename: Leonarda
authors.initials: L
authors.lastname: Galiuto
authors.forename: Filippo
authors.initials: F
authors.lastname: Crea
mesh_terms: D000241:Adenosine / Q000627:therapeutic use; D000818:Animals; D002121:Calcium Channel Blockers / Q000627:therapeutic use; D002317:Cardiovascular Agents / Q000494:pharmacology / Q000627:therapeutic use*; D003326:Coronary Circulation / Q000187:drug effects*; D003331:Coronary Vessels / Q000187:drug effects / Q000503:physiopathology; D006801:Humans; D008279:Magnetic Resonance Imaging; D008833:Microcirculation; D017202:Myocardial Ischemia / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology; D015428:Myocardial Reperfusion Injury / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology; D020108:Nicorandil / Q000627:therapeutic use; D015221:Potassium Channels / Q000187:drug effects / Q000378:metabolism; D016032:Randomized Controlled Trials as Topic; D014654:Vascular Patency
chemical_list: D002121:Calcium Channel Blockers; D002317:Cardiovascular Agents; D015221:Potassium Channels; D020108:Nicorandil; D000241:Adenosine