Discussion:
HIV-infected patients have an increased risk of developing coronary
artery disease (CAD), yet short-term prognosis after cardiovascular
events remains unclear (5). HIV-related Coronary heart disease risk
factors were described in literature, including Antiretroviral therapy,
HIV disease parameters, female gender and HCV co-infection (6). CAD
etiology in HIV-infected patients is the result of a number of
interactions causing inflammation, endothelial dysfunction, and
coagulation disorders, ultimately leading to atherosclerosis (7). The
severity of HIV-related immunosuppression is correlated with some
abnormalities which account for the observed hypercoagulability in
HIV-infected patients. This correlation is measured by CD4+ cell counts
and the presence of concurrent infectious or neoplastic diseases. These
abnormalities include the presence of decreased levels of natural
anticoagulants/heparin co-factor dimer, antiphospholipid
antibodies/lupus anticoagulant, elevated factor VIII coagulant activity,
activated protein C resistance, increased platelet activation and
hyperhomocysteinemia (8,9). In our patient, ECG showed Significant ST
segment elevation from v1 to v6 and mild elevation in lead 2, 3 and aVF
which was confirmed by positive serum troponin as Late Extensive ST
segment elevation Myocardial infarction. Myocardial infarction was our
initial working hypothesis, yet we included many possible underlying
pathologies. At first we excluded HIV opportunistic infections, because
myocardial infarction in HIV patients is usually a presentation of the
elderly, 50 years of age and more according to studies, unlike our 30
years old previously healthy patient(7). But on our routine out-patient
HIV testing program in the emergency department that was done before the
urgent coronary Angiography, ICT result for HIV turned out positive and
was confirmed with ELISA, which showed a high viral load of 22.4 AU/ml
(10-12). After management of myocardial infarction and stabilization of
the patient, he suddenly developed stroke. In addition to the
traditional risk factors, HIV is associated with other factors that
increase the risk of stroke, including immunosuppression and high
viremia, as in our patient. The etiology of stroke in people living with
HIV is multifactorial, including Atherosclerosis of the large arteries,
small vessel disease, cardio embolism, central nervous system (CNS)
infections, coagulation disorders, and non-atherosclerotic vasculopathy,
yet the triggering mechanism for stroke remains unclear (13). A possible
explanation of the presentation at this age is that the myocardial
infarction was directly related to HIV chronic inflammation and immune
activation independent of other risk factors (6). Two cohort studies
found a strong association of HIV with a 44% to 48% increased risk of
Myocardial Infarction, independent of traditional risk factors, such as
age, race, socioeconomic status, and substance abuse (14,15). To our
knowledge and available literature, this is the first case ever to
present with atypical HIV presentation as an ST-elevation Myocardial
Infarction complicated by stroke in such young age.