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Phenotypic Presentations of Heart Failure Among Patients With Chronic Inflammatory Diseases
Daniel L Underberg1, Adovich S Rivera1, Arjun Sinha1
1Division of Cardiology, Department of Medicine, Chicago, IL, United States.
Insights
Heart failure (HF) phenotypes vary significantly across chronic inflammatory diseases (CIDs). Patients with systemic sclerosis (SSc) showed a higher prevalence of right-sided HF, while those with HIV and lupus (SLE) exhibited more left ventricular systolic dysfunction.
Area of Science:
- Cardiology
- Rheumatology
- Immunology
Background:
- Chronic inflammatory diseases (CIDs) are linked to increased heart failure (HF) risk.
- HF phenotypes across diverse CIDs remain poorly understood.
- Manual adjudication of HF phenotypes across a CID spectrum has not been previously studied.
Purpose of the Study:
- To characterize incident heart failure (HF) phenotypes in patients with various chronic inflammatory diseases (CIDs).
- To compare HF phenotypes across different CIDs and non-CID controls.
Main Methods:
- Screened patients with and without CIDs for possible HF using administrative codes.
- Hand-adjudicated HF endpoints using standardized criteria.
- Compared clinical, demographic, and HF phenotypic characteristics between CID patients and controls.
Main Results:
- Of 192 definite/probable HF patients, significant HF phenotype differences were observed across CIDs.
- Isolated right-sided HF was most common in SSc patients (27.8%).
- Left ventricular systolic dysfunction was prevalent in HIV and SLE patients; HIV and multiple CID patients had higher rates of coronary artery disease.
Conclusions:
- Distinct CIDs manifest unique HF phenotypes, possibly due to differing inflammatory pathophysiologies.
- Further research, including larger studies and mechanistic investigations into immunoregulatory factors, is warranted.
- Findings suggest a need for tailored approaches to HF management in CID patients.
Objective:
Characterize incident heart failure (HF) phenotypes among patients with various chronic inflammatory diseases (CIDs).
Background:
Several CIDs are associated with increased HF risk, but differences in HF phenotypes across CIDs are incompletely understood. No prior studies to our knowledge have manually adjudicated HF phenotypes across a CID spectrum.
Methods:
We screened for patients with-and controls without-CIDs who had possible HF, then hand-adjudicated HF endpoints. Possible HF resulted from a single HF administrative code; HF was deemed definite/probable vs. absent using standardized, validated criteria. We queried adjudicated HF patients' charts to define specific HF phenotypes, then compared clinical, demographic, and HF phenotypic characteristics for HF patients with specific CIDs vs. non-CID controls using Fisher's exact test.
Results:
Out of 415 possible HF patients, 192 had definite/probable HF. Significant differences in HF phenotypes existed across CIDs. Isolated right-sided HF was present in 27.8% of patients with SSc and adjudicated HF, which is more than twice as common as it was in any other CID. Left ventricular systolic dysfunction was most common in patients with HIV and lupus (SLE); mean LVEF was 45.0% ± 18.6% for HIV and 41.3% ± 17.1% for SLE, but was 57.7% ± 10.7% for SSc. Those with HIV and multiple CIDs were most likely to have coronary artery disease.
Conclusions:
Different CIDs present with different phenotypes of physician-adjudicated HF, potentially reflecting different underlying inflammatory pathophysiologies. Larger studies are needed to confirm these findings, as are mechanistic studies focused on understanding specific immunoregulatory contributors to HF.
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