P950LV function abnormalities in patients with normal weight obesity: contribution of android fat deposit, increased fibrosis and proinflammatory activation

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Obesity predisposes to left ventricular (LV) dysfunction and heart failure.Pts with normal BMI,but increased body fat content (normal weight obesity,NWO) have not been assessed so far with respect to the risk of these complications.We hypothesized that LV performance in NWO may be impaired and sought to investigate potential contributors to cardiac functional abnormalities.Methods: We included 168 pts (age 38±7 yrs) with BMI <25 and no history of any cardiac disease.Each study participant underwent body composition evaluation by X-ray absorptiometry,echo study with measurement of LV systolic function (strain and tissue S velocity,Sm),diastolic function (tissue E velocity,Em and E/e' ratio) and myocardial reflectivity (calibrated integrated backscatter,cIB),and serum procollagen type I carboxy-terminal propeptide (PICP,marker of fibrosis),CRP and IL-18 assessment.Results: NWO was identified in 73 enrolees.Subjects with NWO demonstrated impaired LV systolic and diastolic function and cIB,and increased PICP and CRP as compared with individuals with normal body fat content (Table).In multivariable analysis,among the independent associates of LV function parameters were:for strain – IL-18 (β=-0.17, p<0.006),CRP (β=-0.20, p<0.002) and android fat deposit (AFD, β=-0.20, p<0.003)), for Sm -PICP (β=-0.21, p<0.002) and AFD (β=-0.43, p<0.0001),for Em AFD (β=-0.30, p<0.0001) and PICP (β=-0.31, p<0.0001), and for E/e' -PICP and IL-18 (both β=0.18, p<0.01).Conclusion: In patients with NWO, subclinical disturbances of LV systolic and diastolic function are independently determined by the extent of android fat deposit, enhanced fibrosis and proinflammatory activation.

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