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Current Perspective No-Reflow Phenomenon By Rezkalla and Kloner Circulation 2002 February 5th Overview • • • • • • Introduction Historical Perspective Pathophysiology Diagnosis Clinical Presentation Management – Advantages – Measures – Treatments • Conclusion Introduction • Epicardial verses microvasculature • No-Reflow • Low-Reflow Historical Perspective • Initially found in brain • Occurs in heart, skin, skeletal muscle and kidney • In hearts, mainly subendocardial myocardium • EM shows swollen endothelium, intra luminal endothelial protrusions occasional platelets, fibrin, and oedema • PTCA and emergency CABG Pathophysiology 1 • Prolonged cessation of epicardial blood flow results in damage to microcirculation, which prevents restoration of normal flow • Inadequate cardiac scar • Process NOT an immediate event on reperfusion • NO-Reflow area increases with time Pathophysiology 2 • Endothelial swelling and intra luminal protrusions occlude microvasulature – ? Why dexamethasone and Mannitol help • Intravasular plugging fibrin and platelets – Ibuprofen, PG E1, heparinised saline, platelet depletion Pathophysiology 3 • Leukocytes – ? Neutropenia, CD18 Ab, Free radiacl scavenging • Microemboli – Atherosclerotic debris in thrombolysis, angioplasty, rotablation and stenting – more common in vein graft interventions Reperfusion Ischaemia No Reflow Atheroembolism Coronary occlusion Endothelial damage Tissue oedema Platelet/fibrin Oxygen/free radicals Leukocytes Atheroembolism Tissue contracture No reflow Reperfusion Diagnosis 1 • Angiography • TIMI flow (thrombolysis in myocardial infarction) – – – – Grade 0 no flow Garde 1 fails to opacify whole artery Grade 2 opacification of coronaries but slow Grade 3 normal • Quantify further using TIMI frame count Diagnosis 2 • • • • • Coronary doppler Serial ECGs PET MRI Myocardial contrast echocardiography Clinical Presentation • Cath Lab post angioplasty • CCU after thrombolysis – Preinfact angina reduces chance of no-reflow • No-Reflow linked to – – – – Ventricular arrhythmias Early CCF Cardiac rupture Death • Post CABG – Decreased EF despite completely successful revasculisation Management advantages • May not decrease infarct size • Speed healing of necrotic area • Reduce infarct expansion and aneurysm formation • Help collateral circulation Management measures • Retrieval of debris in vein grafts and after atherectomy • IABP • GP IIb/IIIa clinical and lab evidence • Anti-leukocyte Abs and complement inhibitors Management treatments • • • • • Calcium channel blockers eg Verapamil Adenosine ATP K+ channel opener eg Nicorandil Papaverine Urokinase no good • Cardioplegia and transplant Conclusion • Previous 2 decades concentrated on epicardial arteries, next decade will concentrate on microvascular perfusion
