Transcript Current Perspective No

Current Perspective
No-Reflow Phenomenon
By
Rezkalla and Kloner
Circulation 2002 February 5th
Overview
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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)
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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
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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
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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
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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