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  • Selective association of el...
    Bhatt, Anish B.; Mulvey, Claire K.; Qasim, Atif N.; Nair, Jayamohan V.; Rickels, Michael R.; Prenner, Stuart B.; Iqbal, Nayyar; Reilly, Muredach P.

    Diabetes/metabolism research and reviews, October 2016, Letnik: 32, Številka: 7
    Journal Article

    Background We investigated the association of electrocardiographic (ECG) abnormalities with markers of insulin resistance and pancreatic beta‐cell dysfunction in a cross‐sectional study of type 2 diabetes patients. Methods Electrocardiographic criteria were evaluated in the Penn Diabetes Heart Study participants (n = 1671; 64% male; 61% Caucasian), including a sub‐sample (n = 710) that underwent oral glucose tolerance testing. The Matsuda Insulin Sensitivity Index and homeostasis model assessment of insulin resistance (HOMA‐IR) estimated insulin sensitivity; Insulinogenic Index and homeostasis model assessment of beta‐cell function assessed beta‐cell function. Multivariable regression modelling was used to analyse associations of ECG changes with these indices. Results In unadjusted analyses, subjects in the highest quartile of Matsuda index had the lowest prevalence of Q‐waves (6.3% versus 15.3%, p = 0.005). In adjusted models, an inverse association was seen between Q‐waves and log Matsuda index one standard deviation increase; OR = 0.59 (95% CI 0.43‐0.87 p = 0.001). In the full Penn Diabetes Heart Study, there was a direct association between Q‐waves and HOMA‐IR one standard deviation increase; OR = 1.43 (95% CI 1.13–1.81, p = 0.003). In adjusted models, left ventricular hypertrophy also was inversely associated with Matsuda index and directly with HOMA‐IR. Higher Insulinogenic Index scores were associated with a lower prevalence of nonspecific ST changes OR = 0.78 (95% CI 0.62–0.98, p = 0.032). Conclusions In type 2 diabetic patients, both oral glucose tolerance testing‐derived and HOMA‐derived measures of insulin resistance were associated with pathologic Q‐waves and left ventricular hypertrophy on ECGs. Copyright © 2016 John Wiley & Sons, Ltd.