Abstract 17445: Human Immunodeficiency Virus (HIV)-Related Immunosuppression and Systolic Dysfunction Following Myocardial Infarction
Introduction: HIV+ persons have greater risks for myocardial infarction (MI) and heart failure than the general population. Immune dysfunction appears to underlie much of these elevated risks, but the extent to which it may affect myocardial healing and dysfunction after MI in HIV is largely unknown.
Hypothesis: Lower nadir CD4 counts are associated with lower left ventricular ejection fraction (LVEF) following MI for HIV+ persons.
Methods: Using an electronic cohort of patients (pts) who received care at our institution since 2000, we evaluated echo measures following MI for HIV+ persons. HIV+ pts were included if they had at least one CD4 count, an adjudicated diagnosis of MI, and no echo with LVEF<50% or diagnosis of heart failure prior to MI. Patients were split into 3 clinically relevant exposure groups: nadir CD4 count <200, 200-499, and ≥500 cells/mm3. Logistic regressions adjusted for age, sex, race, antiretroviral use, and protease inhibitor use were performed to evaluate odds of having LVEF<50% following MI by nadir CD4 count.
Results: Among 46 pts, nadir CD4 counts were <200, 200-499, and ≥500 for 18, 12, and 16 pts respectively. There were no significant differences between groups in demographic or clinical covariates. Mean LVEF following MI was 41.2%, 48.3%, and 54.5% for patients with nadir CD4 counts <200, 200-499, and ≥500, respectively (Figure 1; p=0.006). Compared with pts with nadir CD4 <200, pts with ≥500 were significantly more likely to have LVEF>50% after MI (adjusted OR 3.31; 95% CI 1.12-5.49); this was not the case for patients with nadir CD4 of 200-499 (adjusted OR 1.26; 0.70-3.22).
Conclusions: HIV+ patients with greater immunosuppression, as measured by lower nadir CD4 counts, had more systolic dysfunction following MI even after adjustment for demographics and cardiovascular risk factors. Future studies in larger cohorts are needed to confirm this finding and evaluate potential mechanisms of myocardial vulnerability to infarction in HIV.
Author Disclosures: P. Engel Gonzalez: None. D.M. Lloyd-Jones: None. M.J. Feinstein: None.
- © 2016 by American Heart Association, Inc.