Histopathological Findings of the No-reflow Phenomenon Following Coronary Intervention for Acute Coronary Syndrome

Abstract

SUMMARYAlthough no-reflow phenomenon may occur in patients that experience reperfusion after ischemia, there have been no reports describing the postmortem findings in these patients. We describe the findings of an autopsy in a 56-year-old man who experienced acute coronary syndrome with no-reflow phenomenon after coronary intervention. Macroscopic study demonstrated myocardial infarction with diffuse hemorrhage, and microscopic analysis revealed vascular damage and microembolization in the no-reflow area. In conclusion, coronary microembolization and damage to the small coronary artery may contribute to the pathogenesis of no-reflow phenomenon following coronary intervention in humans. ( 4,5) However, there has been only one report that describes the postmortem findings in patients with no-reflow phenomenon after PCI. We report findings of an autopsy in a 56-year-old man who experienced acute coronary syndrome with no-reflow phenomenon after coronary intervention.

Coronary no‐reflow phenomenon: From the experimental laboratory to the cardiac catheterization laboratory

“…Autopsy studies documented the occurrence of noreflow in humans with microscopic features similar to that of experimental canine studies [2]. The event encountered in the clinical setting where no-reflow plays a significant role is acute myocardial infarction [3], and prognosis consequential to an untreated noreflow event is guarded [4].…”

Microemboli and Microvascular Obstruction in Acute Coronary Thrombosis and Sudden Coronary Death

“…Microemboli are histopathologically associated with MVO, myocyte necrosis and edema, and endothelial cell sloughing within the intramyocardial capillaries (13,14). Polymorphonuclear leukocytes are the principal inflammatory cells seen in these regions, and capillary lumina show platelet and fibrin plugging.…”

Effect of Atorvastatin (Lipitor) on Myocardial Apoptosis and Caspase-8 Activation Following Coronary Microembolization

“…CME, as an independent predictor of poor long-term prognosis in patients with acute myocardial infarction [3], causes transient ''no blood flow'' or ''slow flow'' [1,2]. Animals' studies have shown that during the acute phase following CME, local myocardium exhibits microinfarction foci, necrosis and apoptosis of the myocardial cells, and a decline in cardiac function [8].…”

“…The incidence of CME is approximately 15-20%, increasing up to 30-45% during procedures such as great saphenous vein grafts or percutaneous coronary intervention (PCI). CME causes transient ''no blood flow'' or ''slow flow'' [1,2] and is an independent predictor of poor long-term prognosis in patients who have suffered from acute myocardial infarction [3]. Once CME occurs, intracoronary thrombolytics, nitroglycerin, or platelet glycoprotein GPIIb/IIIa receptor antagonists along with remedial measures of direct mechanical embolus removal cannot improve the short-or long-term prognosis of patients.…”