Alterations in Left Ventricular Structure and Function in Type-1 Diabetics: A Focus on Left Atrial Contribution to Function - 17/08/11
†, ‡, ⁎ 
, Alan D. Waggoner, MHS ‡, Lisa de las Fuentes, MD ‡, Kenneth B. Schechtman, PhD §, Janet B. McGill, MD 
, Robert J. Gropler, MD, FACC ‡, ¶, Victor G. Dávila-Román, MD, FACC ‡ Cardiovascular Division, Washington University School of Medicine Division of Endocrinology and Metabolism, Washington University School of Medicine Reprint requests: Linda R. Peterson, MD, Washington University School of Medicine, 660 S Euclid Avenue, Campus Box 8086, St. Louis, MO 63110Résumé |
This study was designed to determine the effects of type 1 diabetes mellitus (T1DM) on left ventricular (LV) and particularly left atrial (LA) structure and function. We evaluated 88 non-obese subjects: 44 with T1DM, 44 age- and gender-matched normal controls (age 39 ± 11 years). LV and LA structure and function were quantified using two-dimensional echocardiography, pulse-wave Doppler, and tissue Doppler imaging, including early and late diastolic myocardial velocities (Em global and Am global, respectively). The T1DM subjects averaged higher heart rate, relative wall thickness, and ejection fraction, and lower indexed end-systolic volume than normal controls (P < .001, P < .05, P = .01, and P < .05, respectively). T1DM was related to A wave velocity, Am global, A wave integral, LA ejection fraction, and LA systolic ejection fraction (P < .01, P < .05, P < .0005, P < .001, and P < .0005, respectively). In multivariate analyses, T1DM was an independent predictor of the A wave integral, LA ejection fraction, and LA systolic ejection fraction (P < .01, P < .01, and P < .005, respectively). Thus, despite increased relative wall thickness, LV systolic function is increased and early diastolic filling is normal in T1DM subjects; however, they possess changes in LA transport function suggesting increased reliance on LA contribution to LV filling.
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| This work was supported by NIH grants R01HL58878, S10RR14778, K24HL67002, HL13581, AG154666, HL69100, RR00036 (General Clinical Research Center), and by a grant from the Barnes-Jewish Hospital Foundation to the Cardiovascular Imaging and Clinical Research Core Laboratory. |
Vol 19 - N° 6
P. 749-755 - juin 2006 Retour au numéro
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