Objective-To assess the frequency of circulating cardiac specific auto
antibodies in HIV positive patients with and without echocardiographic
evidence of left ventricular dysfunction. Subjects-74 HIV positive pa
tients including 28 with echocardiographic evidence of heart muscle di
sease, 52 HIV negative people at low risk of HIV infection, and 14 HIV
negative drug users who had all undergone non-invasive cardiac assess
ment were studied along with a group of 200 healthy blood donors. Resu
lts-Cardiac autoantibodies detected by indirect immunofluorescence (se
rum dilution 1/10) were more common in the HIV positive patients (15%)
, particularly the HIV heart muscle disease group (21%), than in HIV n
egative controls (3.5%) (both p < 0.001). By ELISA (dilution 1/320), a
bnormal anti-alpha myosin autoantibody concentrations were found more
often in HIV patients with heart muscle disease (43%) than in HIV posi
tive patients with normal hearts (19%) or in HIV negative controls (3%
) (p < 0.05 and p < 0.001, respectively). Anti-alpha myosin autoantibo
dy concentrations were greater in HIV positive patients than in HIV ne
gative controls, regardless of cardiac status ((mean SD) 0.253 (0.155)
v 0.170 (0.076); p = 0.003). In particular the mean antibody concentr
ation was higher in the HIV heart muscle disease patients (0.291 (0.16
0) v 0.170 (0.076); p = 0.001) than in HIV negative controls. On follo
w up, six subjects with normal echocardiograms but raised autoantibody
concentrations had died after a median of 298 days, three with left v
entricular abnormalities at necropsy. This compared with a median surv
ival of 536 days for 21 HIV positive patients with normal cardiologica
l and immunological results. Conclusions-There is an increased frequen
cy of circulating cardiac specific autoantibodies in HIV positive indi
viduals, particularly those with heart muscle disease. The data suppor
t a role for cardiac autoimmunity in the pathogenesis of HIV related h
eart muscle disease, and suggest that cardiac autoantibodies may be ma
rkers of the development of left ventricular dysfunction in HIV positi
ve patients with normal hearts.