New insight into biology, molecular diagnostics and treatment options of unstable carotid atherosclerotic plaque: a narrative review

Indications for intervention in hemodynamically relevant carotid artery stenosis (carotid endarterectomy or stenting) are primarily based on a degree of stenosis and symptomatology. To date the plaque vulnerability is rarely taken into account in clinical decision making although development of molecular imaging allows a better understanding of plaque biology and provides new techniques detecting potentially vulnerable plaque at risk. A significant number of reports describing the mechanisms of unstable plaque formation suggest that it is a multifactorial process. Inflammation, lipid accumulation, apoptosis, proteolysis, the thrombotic process and angiogenesis are among the main factors of carotid plaque destabilization. Although inflammation is a key process in development of plaque vulnerability, the hemostasis and neoangiogenesis should be regarded as equally important. Only a small group of asymptomatic patients may benefit from the invasive treatment and it remains a challenge to determine whether initially asymptomatic carotid plaque become unstable or vulnerable. Currently, the main task of research on atherosclerotic lesion imaging is focused on functional state of the plaque. The presence of one or more features such as stenosis progression, large plaque area, large juxta-luminal black area, plaque echolucency, intra-plaque hemorrhage, impaired cerebral vascular reserve and spontaneous embolization may indicate patients at higher risk for stroke suitable for revascularization. Treatment of carotid stenosis as one of the manifestations of generalized atherosclerosis requires a broad approach. Nowadays pharmacological treatment options for the atherosclerotic process are largely aimed at stimulating the plaque stabilization, but in symptomatic patients and selected asymptomatic patients, carotid plaque should be removed as a potential source of embolism.