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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

Current PerspectiveNo-Reflow Phenomenon

By

Rezkalla and Kloner

Circulation 2002 February 5th

overview
Overview
  • Introduction
  • Historical Perspective
  • Pathophysiology
  • Diagnosis
  • Clinical Presentation
  • Management
    • Advantages
    • Measures
    • Treatments
  • Conclusion
introduction
Introduction
  • Epicardial verses microvasculature
  • No-Reflow
  • Low-Reflow
historical perspective
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
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
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
Pathophysiology 3
  • Leukocytes
    • ? Neutropenia, CD18 Ab, Free radiacl scavenging
  • Microemboli
    • Atherosclerotic debris in thrombolysis, angioplasty, rotablation and stenting – more common in vein graft interventions
slide8

Reperfusion

Ischaemia

No

Reflow

Atheroembolism

slide9

Coronary occlusion

Reperfusion

Atheroembolism

Endothelial damage

Tissue oedema

Platelet/fibrin

Oxygen/free radicals

Leukocytes

Tissue contracture

No reflow

diagnosis 1
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
Diagnosis 2
  • Coronary doppler
  • Serial ECGs
  • PET
  • MRI
  • Myocardial contrast echocardiography
clinical presentation
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
Management advantages
  • May not decrease infarct size
  • Speed healing of necrotic area
  • Reduce infarct expansion and aneurysm formation
  • Help collateral circulation
management measures
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
Management treatments
  • Calcium channel blockers eg Verapamil
  • Adenosine
  • ATP K+ channel opener eg Nicorandil
  • Papaverine
  • Urokinase no good
  • Cardioplegia and transplant
conclusion
Conclusion
  • Previous 2 decades concentrated on epicardial arteries, next decade will concentrate on microvascular perfusion