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Obesity has become an important public health issue in Western and developing countries, with well known metabolic and cardiovascular complications. In the last decades, evidence have been growing about the active role of adipose tissue as an endocrine organ in determining these pathological consequences. As a consequence of the expansion of fat depots, in obese subjects, adipose tissue cells develope a phenotypic modification, which turns into a change of the secretory output. Adipocytokines produced by both adipocytes and adipose stromal cells are involved in the modulation of glucose and lipid handling, vascular biology and, moreover, participate to the systemic inflammatory response, which characterizes obesity and metabolic syndrome. This might represent an important pathophysiological link with atherosclerotic complications and cardiovascular events. A great number of adipocytokines have been described recently, linking inflammatory mileu and vascular pathology. The understanding of these pathways is crucial not only from a pathophysiological point of view, but also to a better cardiovascular disease risk stratification and to the identification of possible therapeutic targets. The aim of this paper is to review the role of Adipocytokines as a possible link between obesity and vascular disease.

Objectives: To investigate by standard echocardiography and pulsed-tissue Doppler imaging (TDI) the course of systemic sclerosis (SSc) heart disease and its correlation with epidemiological, clinical, and serological features of the disease and drug treatment., Methods: A total of 74 consecutive patients (69 females, between the ages of 19 and 71 years, and disease duration 1-43 years) and 71 controls underwent cardiac assessment at baseline and at 3-year follow-up., Results: At baseline, compared to controls, patients showed post-Bonferroni correction, impaired left (LV) and right ventricular (RV) diastolic function (Em/Am 0.85 ± 0.4 vs 1.5 ± 0.7, p = 0.0003; Et/At 0.9 ± 0.3 vs 1.3 ± 0.4, p = 0.0003), subtle LV and RV systolic dysfunction (Sm 13.7 ± 2.7 vs 15.4 ± 3.2cm/s, p = 0.031; St < 11.5cm/s in 16/74 patients vs 0 controls, p = 0.0031), and higher pulmonary artery systolic pressure (sPAP) (26.1 ± 6.0 vs 24.1 ± 5.1, p = 0.040). At 3-year follow-up, SSc patients showed a further deterioration of biventricular diastolic and systolic function and a further sPAP increase. At multiple regression analysis of baseline data, Em/Am < 1 was detected in 55/74 patients vs 25/71 controls (p < 0.0001) and was associated with age (p = 0.030); Et/At < 1 was detected in 16/74 patients vs 7/71 controls (p < 0.0001), was associated with NYHA class ≥ II (p = 0.033), late capillaroscopic pattern (p = 0.029), and a baseline cardiac Medsger severity score ≥ 1 (p = 0.029). TDI evidence of new abnormalities in RV and/or LV diastolic function was associated with a baseline cardiac Medsger severity score ≥ 1 (p = 0.01). Neither diastolic or systolic abnormalities nor sPAP changes correlated with treatment., Conclusions: Our study confirms that SSc patients exhibit biventricular systolic and diastolic dysfunction and increased sPAP and reveals further deterioration at 3-year follow-up., (© 2013 Published by Elsevier Inc.)