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Recently, primary percutaneous coronary intervention (PPCI) has become the preferred option in the treatment of acute ST elevation myocardial infarction (STEMI) due to its rapid and effective re-establishment of epicardial coronary flow.1 ,2 w1 Randomised controlled trials have shown the superiority of PPCI with an overall 40% reduction of major adverse cardiovascular events (MACE) compared to fibrinolytic treatment.w2
One of the technical issues that arises in PPCI is how to prevent embolisation of atherothrombotic material, that occurs in 15% of the PPCI population3 and is a common cause of periprocedural complications. Once embolisation occurs, distal emboli can: (1) mechanically ‘plug’ the microvasculature, leading to continued ischaemic necrosis of the myocardium; (2) promote local in situ platelet adhesion and thrombosis, causing impairment of tissue reperfusion and a higher chance of the so called ‘no-reflow phenomenon’; and (3) may also provoke microvascular spasm and local inflammatory reactions that may further complicate recovery due to more extensive myocardial necrosis (figure 1).4 ,5
Indeed, distal embolisation of thrombus may result in occlusion of the microvascular bed, resulting in suboptimal reperfusion5 and impaired prognosis due to increased infarct size, reduced ventricular function, and a fivefold increase in 5 year mortality.w3−w6
Furthermore, STEMI patients with a large thrombus burden suffer from a higher incidence of infarct related artery stent thrombosis compared to patients with a small thrombus burden (8.2% vs 1.3%, p<0.001).6 Therefore, an appropriate and aggressive management of the thrombus is …
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