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PP 3.35
Large vessel damage due to accelerated atherosclerosis observed during HIV
disease. Life-threatening rupture of an aortic aneurism in an HIV-infected patient
Roberto Manfredi, Sergio Sabbatani
Infectious Diseases, University of Bologna, Italy
Introduction
Accelerated atherosclerosis and its multiform clinical correlates are of increasing concern
among HIV-infected patients (p) undergoing HAART.
Case report
A 55-year-old HIV-infected heterosexual male had HIV infection known since four years,
and started antiretroviral therapy 19 months before with associated ddI-ABC-EFZ. Save a
moderate dyslipidemia disclosed after 6 months of HAART (maximum serum cholesterol
level 255 mg/dL with LDL cholesterol 147 mg/dL, and maximum triglyceride levels 474
mg/dL), controlled by alternate statins-fibrates, no risk factors for heart-large vessel
diseases were present, with a mute personal-family history, no tobacco-alcohol
consumption, arterial hypertension, diabetes mellitus, and overweight. Eleven months
after HAART initiation (8 month ago), abdominal pain and a pulsating mass at palpation
led to a ultrasonography and CT-scan diagnosis of a thoracic-abdominal type III aortic
aneurism; at that time, plasma HIV viremia was undetectable, and CD4+ lymphocyte
count was 253 cells/µL. An endoprosthesis was positioned, and complications were
carefully excluded by imaging and functional techniques. Seven months later, a sudden
abdominal pain was due to the rupture of an abdominal-suprarenal aortic aneurism, which
deserved immediate positioning of an endoprothesis type Talent between the older
thoracic graft and the suvrarenal aortic prosthesis, and the revascularization of renal and
upper mesenteric arteries. As repeatedly checked by doppler-ulstrasonography and
CT-MRI scans, no sequelae occurred, and a normal kidney, gut, liver, and heart function
were maintained. HAART was successfully continued (with undetectable viremia and a
CD4+ count of 317 cells/µL), daily gemfibrozil was given for hypertriglyceridemia (232
mg/dL) together with ticlopidine, while beta-blockers were suspended three months after
surgery.
Discussion
Asymptomatic, symptomatic, and ruptured aortic and large vessel aneurisms were
anecdotally described in HIV-infected p (around 30 reported cases), but a double
intervention after rupture of a pre-treated aortic aneurism has no precedents. While in the
HAART era mycotic aneurysms followed the drop of opportunism, the increasing life
expectancy, the dysmetabolism, and the endothelial dysfunction due to possible direct
effects of HIV and multiple drug-related variables (especially when multiple-recurring
aneurisms occur), could represent risk factors for an increased morbidity of large vessel
vasculopathy. Clinicians should not underestimate these disorder, while therapeutic
guidelines should be the same of non-HIV-infected p [J Endovasc Ther 2005;12:405].
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