Adipokines: a novel link between adiposity and carotid plaque vulnerability

Abstract

In patients with carotid stenosis, we prospectively investigated the association of novel adipokines, apelin and visfatin, with gray-scale median (GSM) score, a valid index of carotid plaque vulnerability. We also assessed the impact of atorvastatin therapy on the above biochemical and imaging markers. Seventy-four overweight [body-mass index (BMI) > 25 kg/m(2) , fat-mass > 30%], statin-free patients, with carotid stenosis, but without indications for intervention were enrolled. Thirty-eight age-, sex- and BMI-matched healthy subjects served as healthy controls (HC). All patients received gradual titrated (10-80 mg) atorvastatin therapy to target LDL-C < 100 mg/dL. GSM score, blood pressure (BP), fat-mass, lipid profile, and serum high-sensitivity C-reactive protein (hsCRP), apelin and visfatin levels were obtained at baseline and after 24 months. At baseline, patients with carotid atherosclerosis had worse lipid profile, lower apelin and higher systolic BP, hsCRP, visfatin levels compared with HC (P < 0·05). Notably, decreased apelin (P < 0·001) and GSM score (P = 0·010), while increased visfatin (P = 0·019) and hsCRP (P = 0·039) levels were found in symptomatic rather than asymptomatic patients. At baseline, GSM score correlated with fat-mass, BMI, LDL-C, visfatin and apelin (P < 0·05). Apelin, visfatin and fat-mass remained independent determinants of baseline GSM score (R(2) = 0·391, P = 0·007). In parallel, we found that apelin increment and LDL-C reduction were independently associated with the atorvastatin-induced GSM increase (R(2) = 0·411, P = 0·011). Increased fat-mass, low apelin and high visfatin serum levels seem to correlate with carotid plaque vulnerability in patients with carotid stenosis. The atorvastatin-induced modification of apelin and LDL-C may beneficially affect carotid plaque stability.