What is acute no reflow?

Acute No-Reflow Phenomenon

Acute no-reflow is a condition characterized by inadequate myocardial perfusion despite successful mechanical opening of an occluded coronary artery, occurring in two distinct forms: interventional no-reflow caused by vasospasm and downstream embolization during PCI, and suboptimal reperfusion of an infarct artery due to endothelial injury, embolization, and vasospasm. 1

Definition and Diagnosis

Acute no-reflow is diagnosed through:

• Angiographic assessment showing TIMI flow <3, or TIMI flow 3 with myocardial blush grade 0-1 2
• Less than 70% ST-segment resolution within 4 hours of the procedure 2
• Additional diagnostic techniques include:
  • Coronary flow velocity measurement using Doppler guidewire
  • Non-invasive imaging: contrast echocardiography, single-photon emission tomography, PET, and contrast-enhanced MRI 2

Pathophysiology

The pathophysiology of no-reflow is multifactorial:

• Microvascular obstruction due to:
  • Vasospasm of small vessels
  • Distal embolization of atherothrombotic debris 2
  • Endothelial injury and dysfunction
  • Inflammatory activation with leukocyte plugging
  • Cellular and interstitial edema 3
  • Platelet aggregation and microthrombi formation

Clinical Significance

No-reflow has significant clinical consequences:

• Occurs in 10-40% of patients undergoing reperfusion therapy for STEMI 2
• Associated with myonecrosis and increased infarct size 1
• Leads to prolonged myocardial ischemia, severe arrhythmias, and hemodynamic deterioration 2
• Independently associated with increased risk of:
  • Malignant arrhythmias
  • Heart failure
  • In-hospital and long-term mortality 4

Treatment Approaches

The 2011 ACCF/AHA/SCAI guidelines recommend:

• Intracoronary vasodilators as reasonable treatment for PCI-related no-reflow (Class IIa recommendation, Level of Evidence B) 1
  • Adenosine
  • Calcium channel blockers (verapamil, nicardipine)
  • Sodium nitroprusside

Preventive Strategies:

• Use of glycoprotein IIb/IIIa inhibitors (particularly abciximab) during native coronary interventions 5
• Distal embolic protection devices for saphenous vein graft interventions 5
• Minimizing door-to-balloon time in STEMI patients 3

Clinical Pitfalls and Considerations

1. Differential diagnosis: It's essential to differentiate true no-reflow from:

   • Competitive flow from collateral channels
   • TIMI grade 2 flow after chronic total occlusion PCI 2
   • Mechanical obstruction due to dissection or thrombus

2. Treatment limitations:

   • No single agent has proven universally effective
   • Combination therapy may be more beneficial than monotherapy 4
   • Emergency CABG is unlikely to improve perfusion in no-reflow and may be harmful 2

3. Monitoring after treatment:

   • Patients require close hemodynamic monitoring as no-reflow can lead to hypotension, bradycardia, and hemodynamic collapse 5
   • Serial ECGs and cardiac biomarkers should be obtained to assess for myocardial injury

Despite evidence for beneficial effects of various agents (abciximab, adenosine, nicorandil, nitroprusside), their adoption into clinical practice has been limited due to variable effects on hard clinical endpoints such as infarct size and mortality 1.