Concurrent Carotid Inflammation in Acute Coronary Syndrome as Assessed by 18F-FDG PET/CT: A Possible Mechanistic Link for Ischemic Stroke

Abstract

Patients with acute coronary syndrome (ACS) are prone to ischemic stroke (IS) especially during the early phase. ACS patients are more likely to have concurrent complex carotid plaques which, when destabilized, may serve as a source of distal embolism. This study investigated whether inflammatory activity in carotid artery was increased in ACS survivors compared to chronic stable angina (CSA) patients. We prospectively enrolled 74 patients with ACS or CSA (39 ACS patients versus 35 CSA patients), and fluorodeoxyglucose positron emission tomography/computed tomography ((18)F-FDG PET/CT) was performed within 1 week after diagnosis. Carotid PET signal was quantified as standardized uptake value (SUV) and target-to-background ratio (TBR, carotid SUV/jugular venous SUV). Baseline characteristics were similar between groups. TBRs and SUVs were significantly higher in the carotid arteries of ACS patients than those of CSA patients (P < .001). Systemic inflammatory biomarker correlated significantly with carotid FDG uptake (high-sensitivity C-reactive protein versus average SUV: r = .361, P = .002), and the presence of cardiovascular risk factors was also related to inflammation activity. During follow-up, 3 cerebrovascular events occurred in ACS patients (including 1 early IS in a patient with severe baseline carotid inflammation), whereas none in CSA patients (P = .057). This study provided in vivo evidence that ACS survivors might experience concurrent carotid arterial inflammation. Our findings supported the role of systemic immune activation contributing to multiarterial instability in symptomatic atherosclerosis as a possible mechanistic link between ACS and IS.