Atherosclerotic involvement of the coronary arteries of adolescents and young adults

doi:10.1016/0021-9150(80)90238-5

Atherosclerosis

Volume 36, Issue 4, August 1980, Pages 449-460

https://doi.org/10.1016/0021-9150(80)90238-5 Get rights and content

Abstract

Coronary atherosclerotic plaques were revealed by light microscopy in 12% of adolescents and in 28% of young adults. All the plaques of adolescents and one-third of the plaques of young adults escaped recognition on ordinary gross inspection, even after Sudan staining. A centrifugal extension of plaques, from the branching areas to the proximal segment of the main coronary arteries took place, starting from adolescence. During early adulthood this centrifugal extension continued involving the intermediate segments of the anterior descending and right coronary arteries. In undistended vessels, the coronary atherosclerotic plaques narrowed the lumenal diameter up to 55%o in adolescents and up to 65% in young adults. Histologically, the mucoid type of plaque, rich in areas of edema, insudate and depolymerized ground substance, prevailed in the coronary arteries of adolescents; in young adults, the prevalent plaque was the lipid-rich variety, containing many clusters of lipid-filled and foam cells. In addition, necrotic plaques or atheromas have been revealed for the first time in young adults. A positive association appeared in our material between cigarette smoking and the presence of mucoid plaques in the proximal segment of the main coronary arteries of adolescents. On the other hand, no relation could be established between risk factors and the accumulation of lipid-filled and foam cells in the atherosclerotic plaques of young adults.

References (16)

D. Velican et al.
Study of fibrous plaques occurring in the coronary arteries of children
Atherosclerosis
(1979)
C. Velican et al.
Incidence, topography and light microscopic feature of coronary atherosclerotic plaques in adults 26–35 years old
Atherosclerosis
(1980)
M.D. Haust
The morphogenesis of potential and early atherosclerotic lesions in man
Hum. Path.
(1971)
C. Velican
Studies on the age-related changes occurring in human cerebral arteries,
Atherosclerosis
(1970)
C. Velican et al.
Intimal thickening in developing coronary arteries and its relevance to atherosclerotic involvement
Atherosclerosis
(1976)
C. Velican et al.
Histogenetic differences between parent and daughter vessels of human coronary arteries
Atherosclerosis
(1977)
C. Velican et al.
Heterogeneity in the composition and aggregation patterns of coronary intima acid mucopolysaccharides
Atherosclerosis
(1978)
C. Velican et al.
Some particular aspects of the microarchitecture of human coronary arteries
Atherosclerosis
(1979)

There are more references available in the full text version of this article.

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Excessive intimal hyperplasia in human coronary arteries before intimal lipid depositions is the initiation of coronary atherosclerosis and constitutes a therapeutic target
2016, Drug Discovery Today
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The following years brought numerous publications on coronary artery design in humans and large mammals. All of them unanimously confirmed the same facts: the tunica intima of coronary arteries of humans and large mammals invariably develops under physiologic conditions into normal intimal hyperplasia or DIT [24–47]. This arterial morphogenesis was particularly well described in great detail by French [25–27], Bálint [42], Velicans [28–40] and Cucu [46,47].
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The disease involves the development of atherosclerosis, which presents as deposition and accumulation of lipid molecules and macrophage foam cells in the artery wall [1]. Although patients with coronary artery disease often become symptomatic in their mid-forties, atherosclerotic conditions in the blood vessels are generally initiated earlier in life [2,3]. The prevalence of the disease varies from 17% (<20 years old) to 85% (≥50 years old), regardless of the presence of risk factors [4].
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Allograft vasculopathy (AV) has emerged as a major obstacle for long-term graft survival after cardiac transplantation. The shortage of donor hearts has meant fewer restrictions have been placed on acceptable hearts over the past few years resulting in an increase in the number of older hearts in the donor pool. This increase has subsequently led to the increase of donor hearts containing pre-existing disease. The importance of this pre-existing donor vascular disease in AV outcomes remains controversial.
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Citation Excerpt :
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Research paperAtherosclerotic involvement of the coronary arteries of adolescents and young adults

Abstract

Atherosclerosis

Atherosclerosis

Hum. Path.

Atherosclerosis

Atherosclerosis

Atherosclerosis

Atherosclerosis

Atherosclerosis

Research paper
Atherosclerotic involvement of the coronary arteries of adolescents and young adults