Author + information
- Received August 14, 2019
- Revision received December 8, 2019
- Accepted January 6, 2020
- Published online March 16, 2020.
- Sean P. Murphy, MB, BCh, BAOa,
- Rahul Kakkar, MDb,
- Cian P. McCarthy, MB, BCh, BAOc and
- James L. Januzzi Jr., MDc,∗ (, )@JJheart_doc
- aDepartment of Medicine, Massachusetts General Hospital, Boston, Massachusetts
- bDivision of Cardiology, Department of Medicine, Brigham and Women’s Hospital, Boston, Massachusetts
- cDivision of Cardiology, Department of Medicine, Harvard Medical School, Boston, Massachusetts
- ↵∗Address for correspondence:
Dr. James L. Januzzi Jr., Massachusetts General Hospital, 55 Fruit Street, Boston, Massachusetts 02114-2696.
• Inflammation contributes to the pathogenesis of HF and may be a biotarget for therapy.
• Although clinical trials of anti-inflammatory therapies have failed, targeting inflammation in specific sub-phenotypes may yet prove successful.
• Potential anti-inflammatory targets include inhibition of IL-1β, IL-6, and galectin-3.
It has long been observed that heart failure (HF) is associated with measures of systemic inflammation. In recent years, there have been significant advancements in our understanding of how inflammation contributes to the pathogenesis and progression of HF. However, although numerous studies have validated the association between measures of inflammation and HF severity and prognosis, clinical trials of anti-inflammatory therapies have proven mostly unsuccessful. On this backdrop emerges the yet unmet goal of targeting precise phenotypes within the syndrome of HF; if such precise definitions can be realized, and with better understanding of the roles played by specific inflammatory mediators, the expectation is that targeted anti-inflammatory therapies may improve prognosis in patients whose HF is driven by inflammatory pathobiology. Here, the authors describe mechanistic links between inflammation and HF, discuss traditional and novel inflammatory biomarkers, and summarize the latest evidence from clinical trials of anti-inflammatory therapies.
Dr. Januzzi is supported in part by the Hutter Family Professorship; is a Trustee of the American College of Cardiology; has received grant support from Novartis Pharmaceuticals, Roche Diagnostics, Abbott, Singulex, and Prevencio; has received consulting income from Abbott, Janssen, Novartis, Pfizer, Merck, and Roche Diagnostics; and has participated in clinical endpoint committees/data safety monitoring boards for Abbott, AbbVie, Amgen, Boehringer Ingelheim, Janssen, and Takeda. Dr. Kakkar has served as a consultant for Corvidia Therapeutics; is an employee of Pandion Therapeutics; and owns equity in Corvidia Therapeutics and Pandion Therapeutics. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- Received August 14, 2019.
- Revision received December 8, 2019.
- Accepted January 6, 2020.
- 2020 American College of Cardiology Foundation
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