The Enemy of Primary PCI

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The Enemy of Primary PCI

Chaim Lotan

Dr Chaim Lotan, Hadassah Medical Center (Jerusalem, Israel) discussed the clinical challenge of ‘no-reflow’ in primary PCI. Angioplasty is associated with improved epicardial flow, greater reperfusion rate and improved survival, when compared with thrombolytic therapy.⁷ However, despite TIMI 3 flow, optimal myocardial reperfusion is probably only achieved in one third of patients.⁸ This phenomenon is known as slow flow or no-reflow and characterised by ‘slow flow’ in the affected vessel and lack of contrast uptake (‘blush’) by the subtended myocardium, which is associated with a poor prognosis.^9,10 The pathophysiology of no reflow is described in Figure 4.¹¹ It is a multifactorial condition and is caused by four interacting mechanisms: ischaemic injury, reperfusion injury, distal embolisation and susceptibility of the microcirculation to injury.¹² The timing of distal embolisation varies and can affect outcomes: distal embolisation before PCI is visible in 5 % of angiograms before PCI and in 15–17% after PCI.^13,14 Thrombus composition and size is also related to outcomes. Fresh thrombus that can be aspirated typically only represents 30 % of the total thrombus load. The plaque represents 24 % and organised thrombus accounts for 47 %.¹⁵ Furthermore, angiography underestimates residual thrombus after aspiration; this can be demonstrated by optical coherence tomography (OCT).¹⁶

The MGuard EPS prevents post stenting protrusion of the remaining thrombus, commonly seen with conventional stent, as the micronet seals (“jails”) the thrombus against the vessel wall.