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Coronary intimal thickening in newborn babies and <or=1-year-old infants
José Milei1, Daniel R Grana, Carlos Navari
1Instituto de Investigaciones Cardiológicas (ININCA), University of Buenos Aires - Conicet, Buenos Aires, Argentina. ininca@fmed.uba.ar
Insights
Early coronary artery intimal thickening, characterized by smooth muscle cell infiltration, is present in infants. These initial changes suggest a crucial role for smooth muscle cells in early atherogenesis.
Area of Science:
- Cardiovascular Pathology
- Developmental Biology
- Histology
Background:
- Coronary artery disease (CAD) has early origins.
- Understanding initial atherogenesis in infants is crucial for prevention.
Purpose of the Study:
- To morphologically characterize early intimal thickenings in infant coronary arteries.
- To investigate the role of smooth muscle cells (SMCs) in initial coronary atherogenesis.
Main Methods:
- Examination of coronary artery specimens from 67 infants (first year of life).
- Histological staining (hematoxylin-eosin, Azan, Alcian blue, acetic orceine).
- Immunophenotyping for CD68, CD34, and alpha-smooth muscle (SM) actin.
Main Results:
- Substantial intimal changes found in approximately 1 in 3 infants.
- Lesions ranged from mild focal myointimal thickening to diffuse moderate thickening.
- SMCs infiltrated the subendothelium, often with internal elastic lamina rupture and no neoangiogenesis.
Conclusions:
- Early-life intimal thickenings are present in coronary arteries.
- Smooth muscle cells play a significant role in the initiation of coronary atherogenesis.
Abstract:
We performed a morphological characterization of intimal thickenings in coronary arteries in the very early stages of life to obtain insights into initial coronary atherogenesis. We examined specimens from 67 infants who had died of noncardiac causes within their first year of life. Serially cut sections were stained with hematoxylin-eosin, Azan, Alcian blue, acetic orceine, and immunotypified for CD68, CD34, and alpha-smooth muscle (SM) actin. Substantial changes were detected in about 1 of 3 participants. Alterations ranged from focal areas with mild myointimal thickening to diffuse moderate thickening. In those lesions, smooth muscle cells (SMCs) showed loss of polarity, infiltrating the subendothelium, mostly with rupture of the internal elastic lamina and without neoangiogenesis. Morphometrically, in musculoelastic intimal thickenings, neointimal thickness averaged 58.3 +/- 17.8 microm, affecting 46% of the internal elastic membrane perimeter; lumen stenosis averaged 13.7% +/- 5.0%. These lesions can be present very early in life and SMCs seem to play an essential role.
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