A. Tabib et al., Accelerated coronary atherosclerosis and arteriosclerosis in young human-immunodeficiency-virus-positive patients, CORON ART D, 11(1), 2000, pp. 41-46
Objective To determine the type of lesions observed in young patients infec
ted with human immunodeficiency virus-1 (HIV-1),
Design Examination of coronary networks in corpses of 13 men and two women
who had died aged 23-32 years after having been infected with HIV-1 virus,
having been seropositive for 2-5 years. Causes of death were infectious com
plications (five cases), infection with cytomegalovirus leading to gastroin
testinal haemorrhaging (one case), infection with cytomegalovirus and Kapos
i's sarcoma (one case), overdoses of drugs (five cases) and sudden death (t
hree cases).
Methods The pathological analysis was carried out on the proximal and dista
l coronary networks, In order to characterize the lesions better, the cells
and the cytokines involved were characterized by immunohistochemistry.
Results In all 15 cases we observed thickening of intima in the proximal ne
twork at least as great as that of the media, caused by a proliferation of
secreting cells, phenotypically identified as smooth muscle cells, with exa
ggerated production of elastic fibres and in association with an increase i
n the expression of tumor necrosis factor-alpha and interleukin-1 alpha. In
nine cases, atherosclerosis had developed from and on the surface of this
proliferation and in four cases arteriosclerosis had an unusual appearance,
in the form of mamillated vegetations with endoluminal protrusions. A simi
lar proliferation was found in the distal network in four cases, but with a
significantly smaller proportion of elastic fibres
Conclusions The lesions we examined in these young HIV-1-infected patients
presented particular features and were intermediate between the lesions obs
erved during common coronary atherosclerosis and atherosclerosis associated
with chronic rejection of cardiac transplants, Coronary Artery Dis 11:41-4
6 (C) 2000 Lippincott Williams & Wilkins.