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Preliminary and early stages of atherosclerosis in childhood
1Children's Hospital, University of Helsinki, Finland.
Insights
Atherosclerosis begins in infancy, with endothelial cell damage and arterial thickening observed even in newborns. These early changes in coronary arteries predispose children to lipid accumulation and later plaque development.
Area of Science:
- Cardiovascular Pathology
- Developmental Biology
- Atherosclerosis Research
Background:
- Atherosclerosis is a progressive disease involving endothelial cell injury and lipid infiltration.
- Early life factors significantly influence the development of cardiovascular disease.
- Understanding the initial stages of atherogenesis is crucial for prevention.
Purpose of the Study:
- To investigate the presence and characteristics of early atherosclerotic changes in the coronary arteries of newborns and children.
- To correlate age-related changes in arterial intima with lipid accumulation.
- To explore potential triggers and genetic influences on early atherogenesis.
Main Methods:
- Histological examination of coronary arteries from newborns and children.
- Electron microscopy to detect endothelial cell damage.
- Quantification of intimal thickening and lipid deposition.
Main Results:
- Endothelial cell damage and thickened intima observed in newborns, with increased connective tissue.
- Cholesterol ester accumulation in the coronary intima begins in childhood, mirroring serum low-density lipoprotein composition with age.
- Fatty streaks appear during puberty, and fibrous plaques develop after age 20.
- Significant stenosis (up to 20%) due to myo-intimal thickening is present in infants under one week old.
- Intimal thickening can account for up to 57% of arterial narrowing.
Conclusions:
- Atherosclerosis initiates in early life, with significant arterial changes detectable at birth.
- Early endothelial injury and intimal thickening create a substrate for subsequent lipid deposition and plaque formation.
- Genetic and environmental factors likely contribute to the initiation and progression of early-life atherosclerosis.
Abstract:
According to the unified theory of atherosclerosis, endothelial cell injury and lipid infiltration play an important role in atherogenesis. Newborn babies may suffer endothelial cell damage, as may be detected by electron microscopy. Connective tissue elements are occasionally abundant already in newborns. Chondroitin sulfate A and C increase with age. The children may exhibit continuous accumulation of cholesterol esters in the intima of coronary arteries. Cholesteryl ester fatty acid composition, along with age, tends to approach that of serum low-density lipoproteins. Fatty streaks appear in coronary arteries in puberty, and fibrous plaques are recordable beyond the age of 20 years. The topography of myo-intimal thickenings, fatty streaks, and fibrous plaques is similar to complicated atherosclerotic lesions. Even newborn babies have obstructive myo-intimal thickenings in their coronary arteries. One fifth of all infants under one week of age suffer 20% stenosis, with percentile manifestation of stenosis in the arterial cross-section being established as ratio of intimal area to luminal area of a dilated coronary artery multiplied by 100. Occasionally, the intima is very thick, in our series initiating up to 57% of all narrowing. There are probably noxious factors which temporarily damage the endothelial cells and initiate a rapid, partially reversible thickening reaction. Some of this response of the intima to exogenous stimuli might be genetically determined. A thickened intima is susceptible to lipid deposition and atherosclerosis.