Invasive sealing of vulnerable, high-risk lesions

Pioneering histology-based studies performed at the beginning of the last century have demonstrated that the culprit lesions responsible for sudden death have specific morphological characteristics [1-4]. More recently, Davies and Thomas have shown that plaque disruption was the main cause of coronary thrombosis and is associated with crescendo angina, myocardial infarction, and sudden death [5,6]. These landmark studies have attracted attention and efforts were made to identify features associated with plaque vulnerability. Today it is known that the high-risk lesions have a specific phenotype called thin cap fibroatheroma (TCFA) that exhibits an increased plaque burden, with a necrotic core that is covered by a thin fibrous cap and is rich in macrophages [7-10]. More recent evidence has shown that vulnerable lesions also have micro-calcifications and are rich in neo-vessels and cholesterol crystals [11-13].