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Interventional cardiology
Thrombus management in the catheterisation laboratory in the setting of primary percutaneous coronary intervention: what is the current evidence?
  1. Surya Dharma1,
  2. Sasko Kedev2,
  3. J Wouter Jukema3
  1. 1 Department of Cardiology and Vascular Medicine, Faculty of Medicine, University of Indonesia, National Cardiovascular Center Harapan Kita, Jakarta, Indonesia
  2. 2 Department of Cardiology, University Clinic of Cardiology, University of St Cyril & Methodius, Skopje, Macedonia
  3. 3 Department of Cardiology, Leiden University Medical Center, Leiden, The Netherlands
  1. Correspondence to Professor J Wouter Jukema, Department of Cardiology, Leiden University Medical Center, PO Box 9600, Leiden 2300 RC, The Netherlands; j.w.jukema{at}lumc.nl

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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

Figure 1

Illustration of the hypothesis of distal embolisation. Distal embolisation of atherothrombotic material (red and blue circles) can ‘plug’ the microvasculature (a), promote local platelet adhesion (b), and cause spasm (c) that can lead to serious impairment of tissue reperfusion and the no reflow phenomenon. Arrows indicate the distal embolisation of thrombotic material into the microvasculature.

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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