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.