No-reflow phenomenon refers to the inability to perfuse the myocardium after opening a previously occluded coronary artery. It results from endothelial damage, platelet and fibrin embolization, vasospasm, and tissue edema overwhelming the coronary microcirculation. Risk factors include thrombus presence, cardiogenic shock, increased reperfusion time, and hyperglycemia. Diagnosis involves contrast staining in the coronary artery and residual chest pain after angioplasty. Treatment aims to prevent no-reflow through optimal blood sugar control, statin use, anticoagulation, and intracoronary nitrates. Pharmacological therapies like adenosine, statins, and calcium inhibitors may also help. Measurement of treatment outcome can be

1. No Reflow Phenomenon
Dr Hafeesh Fazulu
PIMS
06-01-2021

2. Definition
• inability to perfuse myocardium after opening of a previously
occluded or stenosed epicardial coronary artery
• “distal microambolisation into the coronary microcirculation”
• suspected to result from a combination of endothelial
damage, platelet and fibrin embolization, vasospasm, and
tissue edema that overwhelms the coronary microcirculation
• Reperfusion-related injury is hypothesized to contribute to
no-reflow via infiltration of the microcirculation with
neutrophils and platelets

3. Incidence
• 0.6 – 2%
• Frequently seen when using STENTS, ATHERECTOMY, PCI in
saphenous vein grafts

4. Aetiology

5. Risk factors
• Presence of thrombus
• Cardiogenic shock
• Increased REPERFUSION time
• Hyperglycemia
• leukocytosis

6. Mechanisms
Four interacting mechanisms (distal
embolization, ischemia-related injury,
reperfusion related injury, and
individual susceptibility to microvascular
injury) are responsible for no-reflow
phenomenon. The individual
contribution of these mechanisms to
the pathogenesis of no-reflow is likely to
vary in different patients.

7. Diagnosis
• Contrast medium staining in the coronary artery (not washed away)
• Persistent chest pain after Plasty
• Residual of increase in ST elevation

9. DD’s
• Coronary spasm – I/C nitrate
• Coronary dissection
• Intracoronary occlusive thrombus
• Diffusion of coronary hematoma
• Distal coronary stenosis –
• guide catheter extension and CAG
• Microcatheter
• Thrombus aspiration catheter
• Visualization of the distal part of the coronary artery is precious

12. TIMI Frame Count
• TIMI frame count is a quantitative index calculating the number of
frames between two landmarks proximal and distal to the
interrogated coronary artery.

13. Myocardial blush
• Microcirculation evaluation
• corresponds to a densitometric method, assessing maximum intensity
of contrast medium in the microcirculation

16. Intracoronary DOPPLER

17. MANAGEMENT

18. Prevention – before the procedure
• Optimal blood sugar control before the
procedure
• Control of Hypertension – Animal studies suggest
hypertension maybe associated with increased risk of no
reflow.
• STATINS
• Reduction by 4.2% (meta-analysis)
• Probably by the pleotropic effects (platelet
adhesion inhibition and thrombosis,
improvement of endothelial function,

19. • It is unclear whether the benefit of
statin therapy is due to acute anti-
inflammatory effects, long-term
lipid-lowering effects, or both.

20. • Anticoagulation – to be given early
UFH – 70-100 IU/kg
• Intracoronary nitrates – early
• Second angiographic view
• Optimal Catheter selection
• To precent damping -> thrombus formation
• Regular catheter flushing
• GPIIb/IIIa inhibitor – TIROFIBAN
• Tirofiban infusion ??
Prevention – during the procedure

21. • Direct stenting in bulky atheroma
• Avoid predilatation
• During Rotational Atherectomy
• Perform short runs (15 seconds)
• With a pecking motion to preserve flow at a speed
rate of 140,000 rpm
• Avoid deceleration >5000 rpm
• Venous graft PCI
• More risk – no reflow in >10%
• Due to highly friable atherothrombotic debris of
venous graft lesion
• Use distal protection device during stent implantation

22. PAHRMACOLOGICAL THERAPIES

23. ADENOSINE
• IV Adenosine
• Reduces infarct size – AMISTAD I & II
Trial
• I/C Adenosine after thrombus
aspiration ----
• showed a significant improvement in STR,
with better 1-year left ventricular
remodelling and reduction in clinical
events compared with saline and
nitroprusside

25. STATINS
• High dose statins

26. Calcium inhibitors
• Verapamil, Diltiazem, Nicardipine

27. Nitroprusside (SNP)

29. Summary of treatment

30. Measurement of treatment outcome
• ECG
• Residual ST elevation – independent predictor of microvascular injury

31. • ECHO
• Myocardial contrast Echo (MCE)
• Microbubbles
• Myocardial uptake of microbubbles is
delayed in hyareas of “no-reflow” and
MVO

32. On late gadolinium enhancement, areas of microvascular obstruction are seen, hypoen-
hancement (so-called “dark zones”) within an avidly enhancing site of myocardial infarction
• CMR
• Non invasive gold standard to
asses MVO
• MVO extent ≥2.6% of LV was the
strongest independent
• predictor of death and heart
failure hospitalization

33. Conclusion
• Lack of optimal treatment for no reflow
• PREVENTION IS EFFECTIVE
• Diagnosis is challenging, if not recognised--- may lead to

34. THANK YOU