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JACC March 12, 2019

Volume 73, Issue 9

Heart Failure and Cardiomyopathies

Oral Contributions
Room 255-256-257
Monday, March 18, 2019, 8:51 a.m.-9:01 a.m.

Session Title: Highlighted Original Research: Heart Failure and Cardiomyopathies and the Year in Review 
Abstract Category: 13. Heart Failure and Cardiomyopathies: Clinical
Presentation Number: 908-10

Authors: Michael S. Sabbah, Ahmed Fayyaz, Barry Borlaug, Surendra Carter, Rickey Carter, Margaret Redfield, Mayo Clinic, Rochester,
Background: Comorbidity (CM) driven microvascular inflammation is posited as a unifying pathophysiologic mechanism for HFpEF.
Obesity is pro-inflammatory and common in HFpEF. We hypothesized that other CM variably associated with obesity result in unique
obesity-inflammation phenotypes in HFpEF which are associated with differences in HFpEF severity.
Methods: Patients (n=301) from the NEAT, INDIE, and RELAX HFpEF clinical trials were analyzed using multi-plexed (hsCRP, SAA, INFγ,
IL-1β, IL-6, IL-8, IL-10, IL-16, TNFα, VEGF, MCP-1, VCAM-1, and ICAM-1) immunoassays. Unsupervised hierarchical clustering with
obese status (yes/no) and inflammatory proteins as input variables was used and association of clusters with HFpEF severity measures
and cardiac fibrosis biomarkers (PIIINP, CITP, IGFBP-7) were tested. Standardized (z -score) variables were compared across phenotypes.
Results: Clustering revealed 3 obesity-inflammation phenotypes: Obese-High CRP (O-CRP, 98% obese), Non-Inflammatory (NI, 55%
obese) and Pan-Inflammatory (PI, 64% obese; Figure 1A). The PI phenotype had more CM and HF hospitalizations, higher left atrial
volume (LAVI), NT-proBNP and fibrosis biomarkers and lower glomerular filtration rate (eGFR). The NI phenotype had fewer CM and better
functional status (peak VO2, 6-min walk distance (6MWD) and hours active/day (HAPD), Figure 1B).
Conclusion: Unique obesity-inflammation phenotypes exist in HFpEF and are associated with differences in CM burden and HFpEF