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Clonal Hematopoiesis of Indeterminate Potential From a Heart Failure Specialist's Point of View

Maurits A Sikking1, Sophie L V M Stroeks1, Olivia J Waring2

  • 1Department of Cardiology Cardiovascular Research Institute Maastricht (CARIM), Maastricht University Medical Center (MUMC) Maastricht the Netherlands.

Journal of the American Heart Association
|July 25, 2023
PubMed

Insights

Clonal hematopoiesis of indeterminate potential (CHIP), driven by mutations, fuels inflammation that worsens cardiovascular disease and heart failure. Targeting these inflammatory pathways offers a promising new therapeutic strategy for heart failure patients.

Area of Science:

  • Cardiovascular Medicine
  • Hematology
  • Immunology

Background:

  • Clonal hematopoiesis of indeterminate potential (CHIP) arises from age-related DNA mutations in bone marrow.
  • CHIP generates proinflammatory immune cells that contribute to cardiovascular disease progression.
  • Inflammatory pathways, including IL-1 and IL-6, play a key role in CHIP-associated cardiac issues.

Purpose of the Study:

  • To explore the mechanisms by which CHIP exacerbates cardiovascular disease and heart failure.
  • To investigate the role of inflammation, particularly inflammasome-dependent responses, in CHIP-induced cardiac pathology.
  • To assess the association of CHIP with cardiovascular mortality and its role in different heart failure subtypes.

Main Methods:

  • Review of existing literature on CHIP, cardiovascular disease, and heart failure.
  • Analysis of the role of proinflammatory macrophages and inflammasome pathways.
  • Examination of evidence linking CHIP to heart failure outcomes and pathophysiology.

Main Results:

  • CHIP-induced inflammation, mediated by immune cells, worsens atherosclerosis and can induce or accelerate heart failure.
  • Intracardiac inflammation from CHIP can lead to decreased cardiac function and fibrosis, independent of atherosclerosis.
  • CHIP is linked to increased cardiovascular mortality in heart failure with reduced ejection fraction and contributes to heart failure with preserved ejection fraction.

Conclusions:

  • CHIP represents a significant risk factor and potential driver of heart failure development and progression.
  • Targeting CHIP and its associated inflammatory pathways presents a novel therapeutic avenue for heart failure.
  • Clinical trials investigating anti-inflammatory therapies for CHIP in heart failure are emerging, signaling a new treatment era.

Keywords:
atherosclerotic cardiovascular diseaseclonal hematopoiesisheart failureinflammation

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