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Preventing Heart Failure in Inflammatory and Immune Disorders.

ABSTRACT: Patients with chronic inflammatory diseases are at increased risk for heart failure due to ischemic heart disease and other causes including heart failure with preserved ejection fraction. Using rheumatoid arthritis and treated HIV infection as two prototypical examples, we review the epidemiology and potential therapies to prevent heart failure in these populations. Particular focus is given to anti-inflammatory therapies including statins and biologic disease modifying drugs. There is also limited evidence for lifestyle changes and blockade of the renin-angiotensin-aldosterone system. We conclude by proposing how a strategy for heart failure prevention, such as the model tested in the Screening To Prevent Heart Failure (STOP-HF) trial, may be adapted to chronic inflammatory disease.

SUBMITTER: Serhal M

PROVIDER: S-EPMC4548924 | biostudies-literature | 2014 Jun

REPOSITORIES: biostudies-literature

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Preventing Heart Failure in Inflammatory and Immune Disorders.

Serhal Maya M Longenecker Chris T CT

Current cardiovascular risk reports 20140601 8

Patients with chronic inflammatory diseases are at increased risk for heart failure due to ischemic heart disease and other causes including heart failure with preserved ejection fraction. Using rheumatoid arthritis and treated HIV infection as two prototypical examples, we review the epidemiology and potential therapies to prevent heart failure in these populations. Particular focus is given to anti-inflammatory therapies including statins and biologic disease modifying drugs. There is also lim ...[more]

PMID: 26316924

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Project description:BackgroundComorbidity-driven microvascular inflammation is posited as a unifying pathophysiologic mechanism for heart failure with preserved ejection fraction (HFpEF). Obesity is proinflammatory and common in HFpEF. We hypothesized that unique obesity-inflammation HFpEF phenotypes exist and are associated with differences in clinical features, fibrosis biomarkers, and functional performance.MethodsPatients (n=301) from 3 HFpEF clinical trials were studied. Unsupervised machine learning (hierarchical clustering) with obese status and 13 inflammatory biomarkers as input variables was performed. Associations of clusters with HFpEF severity and fibrosis biomarkers (PIIINP [procollagen III N-terminal peptide], CITP [C-telopeptide for type I collagen], IGFBP7 [insulin-like growth factor-binding protein-7], and GAL-3 [galectin-3]) were assessed.ResultsHierarchical clustering revealed 3 phenotypes: pan-inflammatory (n=129; 64% obese), noninflammatory (n=83; 55% obese), and obese high CRP (C-reactive protein; n=89; 98% obese). The pan-inflammatory phenotype had more comorbidities and heart failure hospitalizations; higher left atrial volume, NT-proBNP (N-terminal pro-B-type natriuretic peptide), and fibrosis biomarkers; and lower glomerular filtration rate, peak oxygen consumption, 6-minute walk distance, and active hours/day (P<0.05 for all). The noninflammatory phenotype had the most favorable values for all measures. The obese high CRP phenotype resembled the noninflammatory phenotype except for isolated elevation of CRP and lower functional performance. Hierarchical cluster assignment was independent of CRP genotype combinations that alter CRP levels and more biologically plausible than other clustering approaches. Multiple traditional analytic techniques confirmed and extended the hierarchical clustering findings.ConclusionsUnique obesity-inflammation phenotypes exist in HFpEF and are associated with differences in comorbidity burden, HFpEF severity, and fibrosis. These data support comorbidity-driven microvascular inflammation as a pathophysiologic mechanism for many but not all HFpEF patients.

Dataset Information

Preventing Heart Failure in Inflammatory and Immune Disorders.

Publications

Preventing Heart Failure in Inflammatory and Immune Disorders.

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