Abstract 15919: Latent Trajectory Patterns of Left Ventricle Ejection Fraction Among Heart Failure Patients With Chronic Inflammatory Disease: Longitudinal Analysis of Electronic Health Records

Abstract

Background: Immune regulation and inflammation play a role in the pathogenesis and progression of acute and chronic heart failure (HF). While overt inflammatory cardiomyopathy is a well-described clinical entity marked by acute cardiac dysfunction and relatively high rates of recovery, trajectories in cardiac function among people with chronically heightened systemic inflammation are less clear. We hypothesized that there are differences in trajectories of left ventricular ejection fraction among HF patients with different chronic inflammatory diseases (CIDs): human immunodeficiency virus (HIV), systemic lupus erythematosus (SLE), systemic sclerosis (SSc), rheumatoid arthritis (RA), inflammatory bowel disease (IBD), or psoriasis. Methods: We analyzed serial echocardiographic data from people with CIDs and HF who had at least three echocardiograms (n=974) at a large academic medical center. We identified latent trajectories patterns of LVEF using latent class trajectory models, then described clinical differences across the different trajectories. We then used multinomial regression to test if CID type and other baseline variables were associated with different trajectories. Results: We observed three major LVEF trajectories which paralleled known HF subtypes: preserved/intermediate EF (HFp/iEF, 687, 70.5%), reduced EF (HFrEF, 255, 26.2%), and recovered EF (HFrecEF, 32, 3.3%). These trajectories corresponded closely to accepted clinical definitions. For example, 30/32 (94%) patients in the HFrecEF trajectory had LVEF <40% at baseline that increased ≥15% on ≥1 follow-up. We observed significant differences in associations of CID type, age, sex, and diabetes with a specific LVEF trajectory (Figure) that remained even after regression. Conclusions: Among people with HF and CIDs, different trajectories of LVEF are associated with different CIDs and clinical characteristics. This may have implications for therapy and prognosis of HF in CIDs.