Background-Obesity predisposes to left ventricular (LV) dysfunction and heart failure; however, the risk of these complications has not been assessed in patients with a normal body mass index (BMI) but increased body fat content (normal-weight obesity, NWO). We hypothesized that LV performance in NWO may be impaired and sought to investigate potential contributors to cardiac functional abnormalities. Methods and Results-One hundred sixty-eight subjects (age, 38Ϯ7 years) with BMI Ͻ25kg/m 2 and no history of any disease affecting the myocardium were classified on the basis of body fat content into 2 groups: with NWO and without NWO. Echocardiographic indices of LV systolic and diastolic function, including myocardial velocities and deformation, serological fibrosis markers, indicators of proinflammatory activation, and metabolic control, were evaluated. Subjects with NWO demonstrated impaired LV systolic and diastolic function, increased fibrosis intensity (assessed by procollagen type I carboxy-terminal propeptide [PICP]), impaired insulin sensitivity, and increased proinflammatory activation as compared with individuals with normal body fat. The independent correlates of LV systolic and diastolic function variables were as follows: for strain, PϽ0.006

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In patients with stable CAD and preserved LV systolic performance, plasma levels of TNF-alpha and IL-6 are elevated and there is association between immunoinflammatory activation reflected by plasma levels of cytokines and LV diastolic dysfunction.

Endothelial progenitor cells (EPCs) play a key role in angiogenesis and vascular repair, although their exact functions are still disputable. The impact of EPC on left ventricular ejection fraction (LVEF) during acute myocardial infarction (MI) in patients treated with primary percutaneous coronary intervention (PCI) is also under investigation. The aim of this study was to assess the impact of different populations of EPC on LVEF during and 6 months after acute MI treated with primary PCI. The study included 34 patients with documented acute anterior wall MI. The control group consisted of 19 apparently healthy subjects. Blood for EPC assessments was obtained during the first 24 hours after MI and at 7 days and 6 months after PCI. CD34⁺/CD133⁺/CD45⁻, CD34⁺/CD31⁺/CD45⁻, CD34⁺/CD105⁺/CD45⁻, and CD31⁺/CD133⁺/CD45⁻ cell types were studied by flow cytometry. Echocardiography has been performed simultaneously with the EPC measurements. We observed a significant elevation of CD34⁺/CD133⁺/CD45⁻, CD34⁺/CD105⁺/CD45⁻, and CD31⁺/CD133⁺/CD45⁻ EPC at 7 days after PCI in comparison with 24 hours and 6 months after the MI. Patients with preserved LVEF at 7 days after PCI had also higher levels of CD31⁺/CD133⁺/CD45⁻. Acute anterior wall MI treated with primary PCI is followed by enhanced mobilization of EPC among which a high level of CD31⁺/CD133⁺/CD45⁻ subtype was strongly associated with the most preserved LVEF for up to 6 months after the index event. These data may provide some insight for future therapeutic strategies.

Using multiple biomarkers may contribute to the better prediction of LV dysfunction progression and the risk of adverse cardiac events in patients with STEMI. CystC may improve this evaluation, especially with regard to the development of echocardiographic features of elevated LV filling pressure.

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