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- GUSTO IV-ACS, global use of strategies to open occluded coronary arteries IV – acute coronary syndromes
- PCI, percutaneous coronary intervention
- SVG, saphenous vein graft
Coronary atherosclerosis is the underlying cause of nearly all cases of ischaemic heart disease, and superimposed thrombosis is the cause of the great majority of acute coronary syndromes.1,2 The pathogenesis of peripheral arterial disease and, to a great extent, ischaemic stroke is similar. Thus, “atherothrombosis” is the leading cause of severe disability and cardiovascular death.
In general, atherothrombotic plaques responsible for acute coronary syndromes are larger (hidden in positively remodelled arteries) and softer (contain more lipid, inflammation and thrombus and less calcification) than angina producing lesions.1,2 Plaques in aortocoronary saphenous vein grafts (SVG) are, in general, extraordinarily bulky, friable, and thrombus-rich, regardless of clinical presentation.3 Recent observations indicate that the atherothrombotic burden is a major determinant of coronary microembolisation, particularly when plaques are crushed and fragmented mechanically during percutaneous coronary interventions (PCI).
Saphenous vein graft lesions
Atherogenesis is notably accelerated in SVGs, and fatal atherothrombosis may develop within a few years after grafting (fig 1A).3,4 Compared to atherothrombosis in native coronary arteries, plaques in SVGs are generally much larger and contain more lipid, inflammation (foam cells), and thrombus and less calcification.3 Consequently, the atherothrombotic burden is larger and the plaques are much more friable (vulnerable), which explains the exceptionally high risk of distal embolisation, particularly when old SVGs are manipulated by surgeons’ hands or cardiologists’ devices.
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