Adiponectin, leptin, and resistin in patients with aortic stenosis without concomitant atherosclerotic vascular disease

INTRODUCTION: Early stages of atherosclerosis and aortic stenosis (AS) are similar. Advanced coronary artery disease is characterized by altered profile of circulating adipocytokines. We hypothesized that plasma profile of adipocytokines is associated with the severity of AS. OBJECTIVES: The aim of the study was to evaluate the relationship between AS and adipocytokines. PATIENTS AND METHODS: In 74 patients with AS without atherosclerosis and left ventricular ejection fraction above 50% (57 men, 17 women, aged 58 ±9.1 years) and 74 controls, resistin, leptin, and adiponectin levels were determined by the Bio‑Rad Luminex system. Aortic valve area indexed to body surface area (AVAI) as well as the mean and peak transvalvular pressure gradients (PG) were assessed by echocardiography. RESULTS: We observed similar adiponectin and leptin levels in patients with AS and controls (20.8 ±7.9 vs. 20.4 ±3.9 μg/ml, P = 0.67 and 17.0 ±6.4 vs. 16.4 ±5.9 ng/ml, P = 0.52, respectively). Twenty‑one patients had mild, 21 moderate, and 32 severe AS. After adjusting for age and the body mass index, adiponectin levels were 20.3 ±0.5 μg/ml in controls, 26.7 ±0.9 μg/ml in mild, 20.2 ±0.9 μg/ml in moderate, and 17.5 ±0.7 μg/ml in severe AS (P <0.001). Leptin levels were 16.4 ±0.7 ng/ml in controls, 21.1 ±1.3 ng/ml in mild, 16.9 ±1.3 ng/ml in moderate, and 14.4 ±1.1 ng/ml in severe AS (P = 0.003). Adiponectin and leptin correlated with the AVAI (r = 0.70, P <0.001; r = 0.37, P = 0.001; respectively), mean PG (r = –0.72, P <0.001; r = –0.27, P = 0.009; respectively), and peak PG (r = –0.67, P <0.001; r = –0.23, P = 0.03; respectively). In a multivariable analysis, the mean PG was the only independent echocardiographic predictor of adiponectin levels (P <0.001), while the AVAI was the only independent echocardiographic predictor of leptin levels in AS patients (P = 0.049). CONCLUSIONS: Lower levels of adiponectin and leptin, but not resistin, are associated with severe AS, suggesting that adipocytokines may be involved in the progression of AS, and especially adiponectin, which plays a protective role in this process.