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Although no reflow is clearly associated with a poor prognosis, little guidance is available on the treatment of this phenomenon. The ideal therapeutic approach comprises drugs with multiple actions on the microvascular damage produced by ischaemia/reperfusion, as well as knowledge of the time course of events in order to optimise the timing of administration
Extensively studied both in the experimental and clinical setting, the no reflow phenomenon is clearly associated with unfavourable clinical outcome and prognosis.1 Despite the large body of evidence on the efficacy of different possible therapeutic approaches, clear guidelines on the treatment of no reflow have not been given; thus, the phenomenon is not consistently and uniformly treated in clinical practice. A possible reason for this apparent paradox may reside in the confusion generated by the multifactorial pathogenesis of no reflow, with consequent difficulty in the design of an adequate therapeutic strategy. Thus, there is a need for a pathogenetic classification of the phenomenon as an important premise for targeted forms of treatment.
STRUCTURAL AND FUNCTIONAL NO REFLOW: A NOVEL PATHOGENETIC CLASSIFICATION
By definition, no reflow is the inability to reperfuse a myocardial region after prolonged ischaemia, despite reopening of the infarct related artery. Based on morphological and functional studies,23 the phenomenon may be classified into two different forms: structural and functional. In structural no reflow, microvessels confined within necrotic myocardium exhibit irreversible damage of the cellular components of their wall; in functional no reflow, patency of anatomically intact microvessels is compromised because of spasm and/or microembolisation. The need for a classification of the no reflow phenomenon comes from the observation that the pathogenesis, time course, functional implications, and possible therapeutic approach of structural and functional no reflow are different. Studied in experimental preparations, structural no reflow is the result of the loss of integrity of endothelial …