To the Editor:
We read with particular interest the article by Connor et al1 in view of our approximately concurrent publication on the same topic2 that was not cited. Our study population was very different, the most pertinent aspects being black race, heterosexual HIV infection, and the fact that our series was relatively devoid of opportunistic infection. Our conclusions were similar, however, in that no evidence of a vasculitic process was found on the available angiographic investigations, which included 10 HIV stroke patients. Rather, large-vessel occlusive patterns were noted on catheter and MR angiography in the middle and posterior cerebral and internal carotid arteries. Our repertoire of prothrombotic tests was not extensive enough to permit diagnostic accuracy for a hypercoagulable state. We suggested a vascular bed–specific hemostasis as the most likely pathomechanism. The postmortem study by Connor et al also suggested a hypercoagulable state or as-yet undefined microemboli or covert HIV-induced vasculopathy. We think the similar conclusions in these 2 diverse HIV populations, 1 antemortem heterosexual HIV infection with a paucity of superinfection and 1 postmortem largely with opportunistic infection, deserve mention.
- Copyright © 2001 by American Heart Association
We appreciate the interest and comments of Hoffmann and colleagues regarding our recent articleR1 and have read with interest their recently published findingsR2 in a heterosexual South African population. Our study was designed to specifically exclude opportunistic infection, lymphoma, or embolic sources, and described patients with pathological evidence of cerebral infarction unrelated to these conditions. Both studiesR1 R2 therefore included patients without opportunistic infection. The absence of vasculitis in both a clinical seriesR2 and an autopsy series with clinical correlationR1 highlights our suspicion that cerebral vasculitis unrelated to opportunistic infections or lymphoma is rare in HIV-infected individuals. The exact mechanism of cerebral infarction remains unclear, and we agree with Hoffmann et al that altered vasoreactivity or altered vascular bed–specific hemostasis as well as microemboli, a hypercoagulable state, or covert HIV-induced vasculopathy are all possible—but unproven—pathological mechanisms.
Connor MD, Lammie GA, Bell JE, Warlow CP, Simmonds P, Brettle RP. Cerebral infarction in adult AIDS patients: observations from the Edinburgh HIV Autopsy Cohort. Stroke. 2000;31:2117–2126.
Hoffmann M, Berger JR, Nath A, Rayens M. Cerebrovascular disease in young HIV infected black Africans in the KwaZulu Natal Province of South Africa. J Neurovirol. 2000;6:229–236.