The Impact of Connective Tissue Diseases on the Inpatient Outcomes of Congestive Heart Failure Patients.

Background Rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE) are autoimmune diseases with chronically elevated inflammatory activity. Treatments typically have been aimed at decreasing inflammation. While RA and SLE are known to have a high incidence of congestive heart failure (HF), the mechanism behind this remains elusive. We sought to assess the outcomes of HF patients with either RA or SLE as opposed to HF patients without RA or SLE. Methods We conducted a retrospective analysis of the Healthcare Utilization Project - National Inpatient Sample Database from 2010 to 2015 (third quarter). Patients with a primary admitting diagnosis of HF were queried, and those with or without a diagnosis of either SLE or RA were separated into two groups. In-hospital mortality, total charges (TOTCHG), and length of stay (LOS) were analyzed with a multivariate regression model adjusted for demographical and comorbidity variables, using generalized linear models with family binomial, gamma, and negative-binomial, respectively. A p-value smaller than 0.05 was deemed statistically significant. All the statistical analyses were performed in R 3.5.5 (R Core Team, 2013, http://www.R-project.org/). Results  The in-hospital mortality (3.4% v/s 4.43%), mean TOTCHG ($46k v/s $51k), and mean LOS (5.79 v/s 6.12 days) were significantly lower in HF patients with RA/SLE when compared with HF patients without RA/SLE. A younger age (70.5 v/s 72.6 years) and a female preponderance (75% v/s 51%) were evident in the RA/SLE group. Both groups consistently showed a significant disparity in the rates of hospitalization, which was inversely related to household income. p-value was less than 0.001 for all the above outcomes. Conclusions  RA/SLE patients are associated with better in-hospital outcomes of HF. The underlying mechanism is unclear in terms of this paradox. Given the fact that the majority of RA/SLE patients are treated with agents aimed at decreasing inflammation, this may shed light on the role of inflammation being an important contributor to HF and implicate a future therapeutic direction.