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Current Perspective No-Reflow Phenomenon

Current Perspective No-Reflow Phenomenon. By Rezkalla and Kloner Circulation 2002 February 5 th. Overview. Introduction Historical Perspective Pathophysiology Diagnosis Clinical Presentation Management Advantages Measures Treatments Conclusion. Introduction.

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Current Perspective No-Reflow Phenomenon

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  1. Current PerspectiveNo-Reflow Phenomenon By Rezkalla and Kloner Circulation 2002 February 5th

  2. Overview • Introduction • Historical Perspective • Pathophysiology • Diagnosis • Clinical Presentation • Management • Advantages • Measures • Treatments • Conclusion

  3. Introduction • Epicardial verses microvasculature • No-Reflow • Low-Reflow

  4. 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

  5. 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

  6. 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

  7. Pathophysiology 3 • Leukocytes • ? Neutropenia, CD18 Ab, Free radiacl scavenging • Microemboli • Atherosclerotic debris in thrombolysis, angioplasty, rotablation and stenting – more common in vein graft interventions

  8. Reperfusion Ischaemia No Reflow Atheroembolism

  9. Coronary occlusion Reperfusion Atheroembolism Endothelial damage Tissue oedema Platelet/fibrin Oxygen/free radicals Leukocytes Tissue contracture No reflow

  10. 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

  11. Diagnosis 2 • Coronary doppler • Serial ECGs • PET • MRI • Myocardial contrast echocardiography

  12. 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

  13. Management advantages • May not decrease infarct size • Speed healing of necrotic area • Reduce infarct expansion and aneurysm formation • Help collateral circulation

  14. 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

  15. Management treatments • Calcium channel blockers eg Verapamil • Adenosine • ATP K+ channel opener eg Nicorandil • Papaverine • Urokinase no good • Cardioplegia and transplant

  16. Conclusion • Previous 2 decades concentrated on epicardial arteries, next decade will concentrate on microvascular perfusion

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