The heart and maternal diabetes mellitus

The heart and maternal diabetes mellitus

Congenital heart disease (CHD) affects 4–10 per 1000 live births. The cause of CHD may be either genetic or environmental, but is usually a combination of both.

Gestational diabetes (GDM) and pregestational diabetes (PGDM; ie, type 1 or type 2) are well known antenatal risk factors for defects of the cardiovascular, central nervous, genitourinary and musculoskeletal systems. Maternal obesity is another important maternal risk factor for CHD and is usually associated with diabetes mellitus. A recent study, published in Current Diabetes Reports, found that thirty percent of infants born to mothers with GDM and pre-existing diabetes present with cardiac malformations (2). Infants of diabetic mothers from all causes of GDM also are predisposed to later-life risk of obesity, diabetes, and cardiovascular disease so they need to be evaluated with a long-term follow-up through both traditional echocardiographic methods, as 2-dimensional ultrasonography and conventional Doppler, and the new methods as tissue doppler, speckle-tracking, 3-dimensional and 4-dimensional ultrasonography, arterial stiffness and laser doppler imaging.

Recently, we started a study to investigate time course and predictive value of regional microvascular alterations in normal newborns and neonates with severe lung or cardiac diseases through the assessment of skin microcirculation by real time laser doppler imaging (LDI), using an Aimago device.

Although the mechanism underlying the associations of diabetes mellitus with CHD is poorly understood, it is clear that epigenetic damages and an altered regulation of apoptosis play a critical role in determining fetal development disorders, especially during embryogenesis. One of the most important regulatory factors of apoptosis is the Caspases system. In our study we explored the potential role of Clivated-Caspase 3 (CC3) as oxidative and epigenetic damage marker evaluating Caspase 3 and CC3 in the cord blood cell both of a control group of 20 neonates and in a group of 30 neonates born by gestational diabetes pregnancy. We found Caspase3 inall enrolled patients; CC3 was instead found only in 9 neonates of the gestational diabetes group : 7 of these 9  neonates showed echocardiographic evidence of a interatrial septal defect (3).

Our results show a potential role of CC3 as a marker of the oxidative stress due to maternal diabetes. Further studies are necessary in order to define the association between maternal diabetes and specific damage marker as CC3, microdeletions, microduplications and DNA polymorphisms in the origin of fetal heart diseases.

 

References

  1. Ariane J. Marelli, MD; Andrew S. Mackie, MD, SM; Raluca Ionescu-Ittu, MSc et al.  Congenital Heart Disease in the General Population Changing Prevalence and Age Distribution. Circulation 2007;115:163-172.
  2. William W. Hay Jr. Care of the Infant of the Diabetic Mother.Curr Diab Rep (2012) 12:4–15.
  3. S.Troiani,P.Guccione,F.Tarquini,R.Tiribuzi,L.Crispoltoni,B.Cappuccini,E.Torlone, S.Arnone,G. Coata ,F.Pauselli ,A.Orlacchio ,G.Barboni,G.C.Di Renzo. Cardiac damage in neonates born by women with pregestational and gestational diabetes :
    potential role of Clivated-Caspase 3. XLI Congresso Nazionale della Società Italiana di Cardiologia Pediatrica. Bari 2011.