Chapter 1: OVERVIEW
1.1. Background of hypertrophic cardiomyopathy and cardiac dysfunction in
fetuses of diabetic mothers.
Diabetes in pregnancy is divided into 2 groups: pre-gestational diabetes and
gestational diabetes. According to the International Diabetes Federation,
Vietnam is one of the countries with the highest rates of diabetes in the world. In
addition, the prevalence of gestational diabetes increased significantly from 2,1
to 39% according to different diagnostic criteria. Diabetes in pregnancy has
many consequences for the mother and fetus. Fetal HCM due to diabtetic mother
is a common complication, accounting for about 33,3% of well-controlled
diabetic mothers and up to 75% in uncontrolled diabetic mothers. Fetal cardiac
dysfunction is also a frequent complication in these fetuses with mainly reduced
diastolic function at the rate of 15 - 40% and 5% systolic heart failure.
Fetal HCM related to diabetic pregnancy is an abnormal thickening of the
ventricular walls or interventricular septal (IVS) due to maternal hyperglycemia
without other cardiomyopathic etiologies in the fetus. Pathogenesis mechanisms
through four main pathways: increased fetal blood insulin, changes in the signaling
pathway to the target heart gene, overproduction of oxidative reagents and
increased fetal growth factors. Histopathological damage of fetal cardiomyopathy
due to diabetic mother is glycogen deposition, increases protein synthesis mainly
myosin, leading to an increase in myocardial cells size especially in IVS.
According to the recommendations of the American College of Cardiology and
the American Heart Association on the diagnosis of HCM, the diagnosis of fetal
HCM when the thickness of any cardiac walls or IVS is measured at the end of
diastole on time mode ultrasound is more than 2 time of standard deviations from
the mean of normal fetuses at the same gestational age. HCM in the fetus due to
diabetic mother has a number of specific characteristics such as: common in the
last 3 months of pregnancy, most hypertrophy of the IVS, the severity of
hypertrophy is usually moderate, less likely to obstruct the output of the ventricle,
may present transiently in the fetus and especially must occur in the fetus whose
mother was diagnosed with diabetes during pregnancy. Fetal cardiac dysfunction
due to diabetes is often discreet diastolic function. However, in order to diagnose
fetal anomaly in diabetic mother still need to eliminate other HCM etiologies in fetus,
so the diagnosis and monitoring after birth in these fetuses are very important.
1.2. Characteristic of structure and function of normal fetal heart and the role
of echocardiography in assessing fetal cardiac thickness and function.
The physiology of the fetal circulation is really different from after birth. The
fetal myocardium has inefficient contraction due to immature myocardial cells,
underdeveloped T-duct system, metabolism dependent on lactate metabolism
with low energy source, myocardium contains many protein components less
differentiated, large intracellular matrix makes fetal myocardium less dilated and
low elasticity, leading to reduced "inherent" physiological diastolic function in
the fetus. During pregnancy, fetal myocardial cells gradually improve in quality
and increase in size, reduce intracellular matrix, arrange and differentiate the
structure into a 3-layer pattern as in adulthood, thereby fetal cardiac function
gradually matures and improves. With the existence of internal and external
cardiac flows, the impact of preload and afterload on fetal cardiac performance is
also different from that of adulthood. Therefore, the assessment of fetal cardiac
function must be consistent with the development stage of the fetus.
