LAUSR

In this issue of the Journal of Nuclear Cardiology, Johnsrud et al. have explored the correlation between different quantification methods of F-fluorodeoxyglucose (F-FDG) uptake and plaque inflammation in endarterectomy specimens of patients with severe carotid stenosis. It has been over a decade since the initial reports of F-FDG accumulation in unstable carotid plaques and its correlation with indices of plaque vulnerability. This has elicited great enthusiasm to investigate the role of F-FDG PET in risk stratification of patients with carotid artery disease. However, the clinical utilization of F-FDG PET in the management of atherosclerosis has been hampered by multiple factors, including striking technical variabilities in image acquisition and quantification protocols between various studies as well as metabolic and biological complexity of F-FDG uptake in the vessel wall. Despite the recent declines in the incidence and ageadjusted mortality rate, stroke has remained a major global health issue. In the United States, approximately 800,000 people suffer from a new (* 75%) or recurrent (* 25%) stroke every year; and about 130,000 people die from it, which puts stroke as the 5th leading cause of death. Carotid atherosclerosis is a common and a potentially preventable cause of ischemic stroke, accounting for * 15% of cases. Currently, atherosclerosis is suspected as a possible etiology of stroke if the patient has significant disease ([ 50% luminal stenosis) in a clinically relevant artery, in accordance with the Trial of Org10172 in Acute Stroke Treatment (TOAST) classification system. However, strokes caused by thromboembolic complications of unstable non-stenotic or mildly stenotic (\50%) plaques are not accounted for in this classification; and such cases may instead be classified as cryptogenic. This may result in an underestimation of the true contribution of carotid atherosclerosis as the etiology of ischemic stroke. It is now well established that a large number of acute coronary syndromes originate from acute complications (e.g., rupture or ulceration) of vulnerable, but mildly stenotic, plaques, which triggers the activation of thrombotic cascade and luminal occlusion. 7 It is plausible to assume similar pathophysiology may contribute to plaque vulnerability in patients with mild carotid stenosis, which by current management guidelines will not be candidates for invasive interventions. Traditionally, the decision to proceed with carotid intervention to prevent new or recurrent stroke has been primarily based on the patients’ symptoms and the extent of luminal stenosis, as detected by catheter angiography or non-invasive imaging. Large randomized clinical trials dating back to 1980s have shown that carotid interventions (endarterectomy and more recently stenting) reduce the risk of stroke compared to medical therapy in symptomatic or asymptomatic patients with severe stenosis ([ 70%) and in symptomatic patients with moderate stenosis (50%-70%). However, this approach has several shortcomings, for example: