Literature DB >> 16278273

Increased periconceptual maternal glycated haemoglobin in diabetic mothers reduces fetal long axis cardiac function.

H M Gardiner1, L Pasquini, J Wolfenden, E Kulinskaya, W Li, M Henein.   

Abstract

OBJECTIVE: To compare ventricular long axis function in fetuses of diabetic mothers (FDM) with contemporaneously studied normal controls (N) and to assess the effect of pre-pregnancy diabetic control on these measurements.
DESIGN: Long axis function was compared in 41 FDM and 159 N fetuses in a cross sectional observational study.
SETTING: Fetal medicine unit. METHODS AND
RESULTS: Echocardiography confirmed structural normality. Pulsed wave valvar Doppler velocimetry, lengthening and shortening myocardial velocities, and amplitude of ventricular long axis movement were recorded at the base of the left and right ventricular free walls and septum. Periconceptual diabetic control was assessed by haemoglobin A1c (HbA1c) in early pregnancy. Doppler and myocardial velocities were negatively related and myocardial thickness was positively related with HbA1c. In both cohorts all variables except mitral and tricuspid late filling (A wave) velocities were dependent on gestational age. FDM gestational age related values were higher for most variables and robust analysis of covariance showed significantly different maturation patterns in mitral valve E:A ratio (p = 0.036) and pulmonary velocity (p = 0.04), late lengthening myocardial velocities (left p = 0.016 and right p = 0.066), left myocardial shortening velocities (p = 0.008), and left free wall (p = 0.03) and septal (p = 0.04) amplitude of motion. FDM septal thickness was significantly increased throughout gestation (p < 0.0001).
CONCLUSION: Periconceptual diabetic control influences fetal cardiac performance and myocardial hypertrophy but, unlike the pathophysiology of adult ventricular hypertrophy, is accompanied by functional adaptation. It is unlikely to explain the increased rate of late stillbirth observed in diabetic pregnancies.

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Year:  2005        PMID: 16278273      PMCID: PMC1861086          DOI: 10.1136/hrt.2005.076885

Source DB:  PubMed          Journal:  Heart        ISSN: 1355-6037            Impact factor:   5.994


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