In treating thrombus-loaded lesions through percutaneous coronary intervention (PCI) in the settings of acute myocardial infarction (MI), saphenous vein grafts (SVGs) and acute coronary syndromes (ACS), distal embolisation is a recognised prevalent occurrence, adversely affecting reperfusion and mortality rates. Thus, efficient management of embolisation, in terms of both reduced occurrence and minimised impact, could significantly improve the long-term success of PCI procedures in acute settings of thrombus-containing lesions. This article reviews the prevalence of distal embolisation in these settings, its clinical implications and current strategies to prevent embolisation, and presents a new, innovative and promising approach to treat these lesions.
Distal Embolisation ├óÔé¼ÔÇ£ Clinical Consequences and Prevalence
There are two distinct sources within the affected artery for distal embolisation: the thrombus occluding the artery and the plaque residing on the lesion™s lumen. Both thrombus and plaque embolisation often cause a shower of emboli to be released into circulation, potentially leading to life-threatening intra- or postprocedural complications. The trigger to the embolisation process is the result of mechanical interference with the thrombus or the plaque by various devices during PCI, rendering the plaque layers unstable and causing crushing and fragmentation. However, embolisation may also be a consequence of a spontaneous rupture of plaque without any mechanical interference. In either case, it is clear that the atherothrombotic burden of the patient is a major determinant of embolisation.
The clinical effects of distal embolisation range in severity from small MIs to cardiogenic shock and death. The outcome depends on the extent of embolisation, the size of the vascular bed involved and the haemodynamic status and associated co-morbidities of the patient. Emboli released distally can block a capillary ├óÔé¼ÔÇ£ part of the microvasculature ├óÔé¼ÔÇ£ leading to a potential ischaemia in part of the epicardium, which, in turn, can lead to necrosis. In addition, it can cause a local inflammatory reaction at the blocked capillary due to platelet aggregation, further aggravating the thrombogenic microenvironment. This chain of events is associated with suboptimal perfusion, larger infarct size, lower ejection fraction and higher mortality rate.1 The suboptimal perfusion ranges from lower epicardial flow to an impaired flow (no re-flow) and occurs despite a full restoration of flow (TIMI 3) in the infarcted lesion through PCI.2 The clinical implications of suboptimal perfusion have been shown to significantly affect one-year mortality rates: 3.9% for a reduced perfusion and 4.5% for an absent perfusion, compared with 1.4% for a normal perfusion.3
A good indication for the high prevalence of embolisation in an acute MI setting can be deduced from the exceptionally high rate of suboptimal perfusion ├óÔé¼ÔÇ£ as high as 82%.3 Direct evidence of the presence of embolised debris through its retrieval from various embolic protection devices points to more than 70% of cases.4
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