NO REFLOW PHENOMENON

Definition No reflow is a phenomenon in which myocardial ischemia and reduced antegrade flow occur despite the absence of proximal stenosis, spasm, dissection, or embolic cut off of major distal branches.1 In another word no reflow phenomenon means failure of restoration of myocardial flow despite removal of epicardial coronary obstruction.2 The incidence is 2% with plain balloon angioplasty (PTCA), 7% in patients undergoing rotational atherectomy, 12% for primary percutaneous coronary intervention (PCI), and much higher at 42% for PCI of degenerated Saphenous Vein Graft (SVG).3 No reflow is a strong predictor of mortality after PCI. The mortality of patients who developed no reflow has been estimated to be 8% Predictors of no reflow include a higher plaque burden, thrombus, lipid pools by intra vascular ultra sonography (IVUS), higher lesion elastic membrane cross sectional area, preinfarction angina and thrombolysis in myocardial infarction (TIMI) flow grade 0 on the initial coronary angiogram. Mechanism The cause is mainly embolization of atheromatous material (gruel). Particles are composed of cholesterol clefts, lipid rich macrophages, fragments of fibrous cap, necrotic lesion core and fibrin. This is aggravated by microembolization of platelet-rich thrombi that release vasoactive agents (e.g., serotonin and thromboxane A2), leading to intense arteriolar vasopasm in the distal vasculature. In the animal laboratory, experimental no reflow has been shown to be due to the plugging of capillaries by red blood cells and neutrophils, myocyte contracture and local intracellular and interstitial edema.4,5 A loss of capillary autoregulation and severe microvascular dysfunction are the ultimate physiologic consequences of these microscopic anatomic alterations. Debris of varying sizes of particulate has variable effects on microcirculatory plugging. The effect of particle size on microvascular dysfunction has been mostly investigated during rotablation. Rotational atherectomy mostly creates particle size less than 6 micron. These smaller particles pass through the capillary circulation in the same manner as red blood cells. Larger particles, which comprises about 20% of the rotational atherectomy debris or particle load, are trapped in the microcirculation and contribute to slow flow and Creatine kinase (CK) elevations from this procedure5. Some of the more common mechanisms of no reflow is shown in Table 1. Table 1. Proposed Mechanisms of No Reflow Microvascul