© 2004 by BMJ Publishing Group & British Cardiac Society
EDITORIAL
Optimal therapeutic strategies in the setting of post-infarct no reflow: the need for a pathogenetic classification
Correspondence to:
Correspondence to:
Leonarda Galiuto
MD, PhD, Institute of Cardiology, Catholic University of the Sacred Heart, Policlinico A. Gemelli, Largo A. Gemelli, 8, 00136 Rome, Italy; lgaliuto@rm.unicatt.it
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
Keywords: microvascular dysfunction; no reflow
| The first 150 words of the full text of this article appear below. |
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.
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
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