2 research outputs found
Microvasculature and Cardiovascular Risk Factors in Childhood
__Abstract__
Cardiovascular disease is the leading cause of mortality, morbidity and hospitalization
worldwide, and is a major public health problem in adult populations. The developmental‐
origins hypothesis suggests that cardiovascular disease might originate from
early life. Adverse exposures, acting in different periods of fetal and early postnatal life
might lead to permanent adaptations in the cardiovascular system, which are beneficial
for short term survival, but increase the susceptibility of cardiovascular disease in later
life. This hypothesis is supported by experimental studies in animals showing that
growth restriction in early life leads to developmental adaptations in cardiovascular
structure and function, which leads to an increase in vulnerability to cardiovascular
disease.
In line with this hypothesis, large observational studies in humans have shown that
fetal growth restriction and rapid infant growth are associated with cardiac and vascular
changes in childhood and an increased risk of cardiovascular disease in adulthood.
Also, observational studies using more detailed adverse exposures during fetal life suggested
that, among other maternal factors, higher maternal blood pressure during
pregnancy and the presence of gestational hypertensive disorders are associated with
increased risks of fetal growth restriction and a higher blood pressure in childhood.
Postnatally, suboptimal infant nutrition and increased adiposity levels throughout childhood
are also shown to be associated with the development of cardiovascular disease in
later life. Thus, previous research suggests that a restricted nutritional in utero environment
and abundant postnatal environment may lead to cardiovascular disease in
later life.
The mechanisms relating adverse maternal, fetal and infant factors with an increased
risk of cardiovascular diseases in later life are not fully understood. Early microvasculature
adaptations, in response to adverse exposures in early life, might be part of the
underlying mechanisms in the development of cardiovascular disease. Animal studies
have shown that alterations in the microvascular structure and, hence, increased peripheral
resistance, precede the development of hypertension. In humans, the microvasculature
can non‐invasively be assessed by using retinal vascular imaging. Several
longitudinal studies among adults have shown that retinal arteriolar narrowing, likely
indicative of increased peripheral vascular resistance, is associated with increased risks
of hypertension and stroke in later life, whereas wider retinal venular caliber is associated
with an increased risk of metabolic syndrome and inflammation. Thus, these
studies suggest that alterations in retinal vessel calibers can be used as early markers of
cardio‐metabolic disease risk.
In summary, cardiovascular disease might already originate in early life. Identifying
risk factors and potential mechanisms influencing the development of cardiovascular
diseases from early life onwards, is important for future preventive strategies that aim
to improve cardiovascular health throughout the life course. Therefore, studies presented
in this thesis were designed to identify maternal, fetal and infant factors associated
with microvasculature alterations and cardiovascular healt