Otvaranje koronarne arterije u primarnim PCI ne znači uvek i optimalni protok i najpovoljniji ishod za bolesnika - tretman 'no reflow' fenomena

Abstract

Microvascular obstruction (MVO) commonly occurs following percutaneous coronary interventions (PCI), may lead to myocardial injury, and is an independent predictor of adverse outcome. Severe MVO may manifest angiographically as reduced flow in the patent upstream epicardial arteries, a situation that is termed 'no-reflow.' The no-reflow phenomenon was originally observed in experimental models of acute myocardial infarction (MI) and was described as a failure to restore normal myocardial blood flow despite removal of the coronary obstruction. Defined angiographically, no-reflow manifests as an acute reduction in coronary flow (TIMI grade 0-1) in the absence of dissection, thrombus, spasm, or high-grade residual stenosis at the original target lesion. Lesser degrees of flow impairment (TIMI grade 2) are generally referred to as 'slow-flow'. However, studies of acute MI patients have reported that scintigraphic evidence for no-reflow may occur in the absence of angiographic slow-flow, suggesting that microvascular injury may be angiographically inapparent in some patients. The mechanisms and mediators responsible for noreflow remain speculative, but the end result appears to be severe microvascular dysfunction. Potential mechanisms of microvascular dysfunction include vasospasm, distal embolization of thrombus or other debris, oxygen free radical mediated endothelial injury, capillary plugging by erythrocytes and neutrophils, and intracellular/interstitial edema with intramural hemorrhage. Microvascular obstruction can be broadly categorized according to the duration of myocardial ischemia preceding PCI. In 'interventional MVO' (e.g., elective PCI), obstruction typically involves myocardium that was not exposed to acute ischemia before PCI. Conversely 'reperfusion MVO' (e.g., primary PCI for acute myocardial infarction) occurs within a myocardial territory that was ischemic before the coronary intervention. Interventional and reperfusion MVO have distinct pathophysiological mechanisms and may require individualized therapeutic approaches. Interventional MVO is triggered predominantly by downstream embolization of atherosclerotic material from the epicardial vessel wall into the distal microvasculature. Reperfusion MVO results from both distal embolization and ischemia-reperfusion injury within the subtended ischemic tissue. Randomized clinical trials have studied strategies for prevention of MVO and no-reflow; however, the efficacy of measures for reversing MVO once no-reflow has been demonstrated angiographically is unclear. New approaches for prevention and treatment of MVO will require a better understanding of intracellular cardioprotective pathways such as the blockade of the mitochondrial permeability transition pore.