DOI:10.2214/AJR.05.0190
AJR 2006; 187:236-241
© American Roentgen Ray Society
Imaging of Cerebrovascular and Cardiovascular Disease in AIDS Patients
Peter D. Corr1
1 Department of Radiology, Nelson Mandela Medical School, University of KwaZulu
Natal, Private Bag 7, Congella, Durban, KZN, South Africa 4013.
Received February 9, 2005;
accepted after revision April 27, 2005.
Address correspondence to P. D. Corr
(corr{at}ukzn.ac.za).
Abstract
OBJECTIVE. The purpose of this article is to show the imaging
findings in patients who have cerebrovascular and cardiovascular complications
caused by AIDS.
CONCLUSION. Detection of multifocal aneurysms, unexplained
cardiomyopathy, and venous thrombosis in high-risk patients should suggest the
possibility of AIDS.
Keywords: AIDS cardiovascular disease cerebrovascular disease conventional angiography infectious diseases
Introduction
Vascular disease in patients with AIDS is not commonly recognized unless
the patient presents with a stroke or vascular thrombosis. Detection of
multifocal aneurysms, unexplained cardiomyopathy, and venous thrombosis in
high-risk patients should suggest the possibility of AIDS.
Vascular disease in patients with AIDS is uncommon. Vasculopathy often
remains asymptomatic until a complication, such as the rupture of an aneurysm
or a stroke, occurs. Both medium-size arteries and veins are involved with the
development of aneurysms, vessel occlusion, embolic disease, and venous
thrombosis. In this article, I describe the pathologic, clinical, and
radiologic findings of cerebrovascular and cardiovascular disease in AIDS
patients.
Pathology
Calabrese [1] first
described vasculopathy from HIV as at least seven pathologic processes. The
most common of these processes are infective vasculitis, necrotizing systemic
arteritis (nodosalike polyarteritis), hypersensitivity vasculitis, and
large-vessel vasculopathy. Vascular injury can be caused directly by the HIV
virus itself and also by the associated vasculitis of a chronic HIV viral
infection. The actual mechanism of vascular injury is unknown
[2]. Possible mechanisms
include direct invasion of endothelial cells by the HIV virus, associated
injury from cytokine release from perivascular lymphocytic infiltrates, or,
less likely, from recurrent opportunistic infections
[2]. The presence of
vasculopathy in association with high viral loads and the detection of gp41
capsular antigens in the wall of aneurysms suggest that the direct effect of
the HIV virus is the most likely cause for this vasculopathy
[3].
A characteristic vasculopathy involving both large elastic arteries and
smaller muscular arteries has been described in adults with AIDS
[4,
5]. The disease causes
aneurysms, vessel occlusion, and arterial and venous thrombosis. No evidence
of atherosclerosis is apparent in these patients while blood cultures are all
negative [4]. There is chronic
inflammation of all three layers of the artery wall with evidence of a
vasculitis of the vasa vasorum of the artery wall, as well as fragmentation of
both muscle and elastic fibers with calcification and fibrosis
[4]. An autopsy study has shown
intracerebral small-vessel vasculopathy in the brains of AIDS patients dying
from cerebrovascular disease
[6]. These patients' small
arteries have hyaline thickening and mineralization of the wall with
lymphocyte infiltration and widening of the perivascular spaces with pigment
deposition (Fig. 1). The
pathologic findings of intracerebral vasculopathy probably represent a
breakdown of the blood-brain barrier with exudation of plasma proteins into
the perivascular spaces.

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Fig. 1 Histologic section (H and E) through cerebral vessel of
patient with neuro-AIDS showing vasculopathy with marked hyaline thickening of
vessel wall with lymphocyte and macrophage infiltrate in perivascular
space.
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CNS
Up to 70% of patients with AIDS eventually develop neurologic signs during
their illness [7]; however,
patients presenting with strokelike syndromes are uncommon, occurring in less
than 5% [8]. Patients present
with stroke or subarachnoid or intracerebral hemorrhage. An autopsy study
found that cerebral infarction was present in only 5.5% of patients once
inflammatory causes were excluded
[6]. In children,
cerebrovascular disease was detected in 11 of 567 HIV-positive children (2.6%)
in a retrospective study [9].
The most common lesions detected in that study were ischemic infarcts and
cerebral aneurysms [9].

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Fig. 2B 25-year-old HIV-positive woman with known cytomegalovirus
(CMV) retinitis who presented with stroke. MR angiography shows focal
irregularity of left middle cerebral artery with occlusion of distal branches
in keeping with vasculopathy.
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The many causes for cerebral infarction include embolic causes from HIV
cardiomyopathy; thrombotic and infective endocarditis; infective vasculitis
from cytomegalovirus (Figs. 2A
and 2B); tuberculosis
(Fig. 3); and HIV vasculopathy,
hypercoagulopathy, cerebral opportunistic infections, neoplasms such as
lymphoma, or cocaine or heroin abuse. Both CT and MRI can be used to identify
cerebral infarcts; however, it is essential that a contrast agent be given to
detect focal cerebral and meningeal inflammatory lesions. Vasculopathy can be
identified both on MR and digital angiography as caliber variation and
irregularity of vessels (Fig.
4). A dilating vasculopathy with intracerebral aneurysm formation
has been described in both adults and children presenting with ischemic stroke
and subarachnoid hemorrhage [9,
10]. The aneurysms tend to be
fusiform in shape and involve both major arteries of the circle of Willis and
second- and third-order branches, which differentiates these aneurysms from
berry aneurysms (Figs. 5 and
6). An association exists
between varicella-zoster infection and the presence of intracerebral aneurysms
in children [9,
11]. This may represent a
synergistic interaction between HIV and varicella-zoster viruses that causes
CNS vasculopathy [9].

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Fig. 4 27-year-old HIV-positive woman with stroke. Digital
subtraction angiogram of left middle cerebral artery territory shows HIV
vasculopathy with caliber variation of vessels and small peripheral
aneurysm.
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Extracranial Arteries
Aneurysm formation occurs in the thoracic and abdominal aorta; extracranial
carotid arteries; and subclavian, iliac, femoral, and popliteal arteries.
Common sites are the ascending aorta, carotid and aortic bifurcations, and the
superficial femoral artery. The aneurysms can be either saccular or fusiform
in shape. They tend to be multiple and occur in unusual locations. It is
important to consider this possibility in patients with advanced disease and
high viral loads. Patients present with a pulsatile mass or symptoms of
rupture or compression of surrounding structures such as nerves. Imaging
investigation includes Doppler sonography, CT angiography, MR angiography, and
angiography (Figs. 7,
8,
9,
10,
11). The sonographic features
are those of a false aneurysm with a defect in the wall and marked thickening
and echogenicity of the surrounding wall
[12].
Cardiac Disease
HIV infection may involve any layer of the heart. HIV infects myocytes
causing myocarditis and subsequent dilating cardiomyopathy
[13]. Pericardial effusion is
common, occurring in 22% of asymptomatic HIV-infected adults in one study
[14]. Often no cause can be
found, although opportunistic infection, such as tuberculosis, or malignancy
must be excluded. Endocarditis is especially common in HIV-positive patients
who are IV drug abusers. Usually the tricuspid and pulmonary valves are
involved [13]. Thrombotic
endocarditis occurs in 3-5% of patients who have a hypercoagulable state or
malignancy [15]. Pulmonary
hypertension, although uncommon, occurs in 1 in 200 HIV-positive patients
(Figs. 12A and
12B). HIV infects alveolar
macrophages resulting in cytokine release and pulmonary endothelial
proliferation and hypertension
[16]. Both Kaposi's sarcoma
and lymphoma can involve the heart.

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Fig. 12B 30-year-old HIV-positive man with shortness of breath.
High-resolution CT of lungs shows ground-glass infiltrates in both lungs from
lymphoid interstitial pneumonitis and prominent hila from pulmonary
hypertension.
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Venous Disease
Patients with advanced disease develop a hypercoagulable state. The
presence of antiphospholipid antibodies and lupus coagulant and deficiencies
of protein C, protein heparin cofactor II, and antithrombin with increased
levels of von Willebrand's factor and D-dimers predispose to a
hypercoagulable state [17].
Patients present with thromboembolic complications including deep venous
thrombosis, dural sinus thrombosis (Figs.
13A and
13B), and pulmonary
embolus.

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Fig. 13A 20-year-old HIV-positive man with headaches and confusion.
Contrast-enhanced CT (A) and T1-weighted MR (B) images show
occlusion of superior sagittal sinus at torcula and ring-enhancing tuberculoma
in left frontal lobe.
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Fig. 13B 20-year-old HIV-positive man with headaches and confusion.
Contrast-enhanced CT (A) and T1-weighted MR (B) images show
occlusion of superior sagittal sinus at torcula and ring-enhancing tuberculoma
in left frontal lobe.
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In conclusion, HIV-related cerebrovascular and cardiovascular disease is an
important cause of morbidity in patients with AIDS. Vascular disease is
especially common in those patients with advanced HIV disease. Radiologists
may have a potential role in screening asymptomatic patients with advanced
disease for CNS vasculopathy, especially if it can be shown that
antiretroviral drugs can arrest the progression of the vasculopathy.
Radiologists should consider the possibility of HIV infection in patients who
present with atypical multifocal vascular disease.
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