4.5 Article

Do diabetes, metabolic syndrome or their association equally affect biventricular function? A tissue Doppler study

Journal

HYPERTENSION RESEARCH
Volume 36, Issue 1, Pages 36-42

Publisher

NATURE PUBLISHING GROUP
DOI: 10.1038/hr.2012.137

Keywords

biventricular dysfunction; diabetes; heart failure; metabolic syndrome; tissue Doppler imaging

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Metabolic syndrome (MetS) and type 2 diabetes (T2DM) have been associated with an impairment of left (LV) and right ventricular (RV) function as well as an increased risk of heart failure (HF). However, it remains unclear whether these clinical entities or their associations promote a similar derangement of biventricular function. Overall, 345 patients without overt cardiovascular disease consecutively underwent routine blood chemistry including high-sensitivity C reactive protein (hs-CRP) and echocardiographical examination with conventional and tissue Doppler imaging (TDI) of both ventricles. According to the ATP III criteria and fasting glucose levels, the study population was stratified into four groups: (1) healthy controls (n = 120); (2) MetS without T2DM (n = 84); (3) T2DM without MetS (n = 49); and (4) MetS + T2DM (n = 92). The Myocardial performance index (MPI) of the RV and LV was obtained with a multi-segmental approach using TDI. Patients with MetS and T2DM exhibited a similar impairment of biventricular function compared with healthy controls, whereas a further decline was observed in patients having both MetS and T2DM. In addition to MetS markers, hs-CRP exhibited the strongest association with the MPI of both ventricles. Regression analyses indicated that individual MetS markers were inferior to MetS in identifying subtle cardiac dysfunction. Independent associations of MetS and T2DM with biventricular dysfunction were comparable, and the coexistence of MetS and T2DM exhibited the highest risk for biventricular dysfunction. Our findings emphasize the importance of MetS as an equivalent of T2DM and support a synergic effect of these clinical conditions on cardiac organ damage requiring more aggressive therapeutic strategies to prevent HF. Hypertension Research (2013) 36, 36-42; doi:10.1038/hr.2012.137; published online 6 September 2012

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