Clonal haematopoiesis is associated with higher mortality in patients with cardiogenic shock

Scolari, Fernando Luís; Abelson, Sagi; Brahmbhatt, Darshan H.; Medeiros, Jessie J. F.; Fan, Chun‐Po Steve; Fung, Nicole L; Mihajlovic, Vesna; Anker, Markus S.; Otsuki, Madison; Lawler, Patrick R.; Ross, Heather J.; Luk, Adriana; Anker, Stefan D.; Dick, John E.; Billia, Filio

doi:10.1002/ejhf.2588

Cited by 33 publications

(33 citation statements)

References 31 publications

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“…al. 2022 [ 81 ] 341 patients with cardiogenic shock (mainly non-ischemic cause) vs. 345 patients with ambulatory heart failure 3-year follow-up Cardiogenic shock patients had a higher prevalence of CHIP (OR 1.5, 95% CI 1.0–2.1) Decreased survival among CHIP patients at different time points (30-days: HR 2.7; 95% CI 1.3–5.7; 90-days: HR 2.2; 95% CI 1.3–3.9; 3-years: HR 1.7; 95% CI 1.1–2.8) Several prospective and retrospective cohort analyses draw correlations of CHIP with a wide range of cardiovascular diseases, such as heart failure, cardiovascular disease, aortic valvular stenosis, CVD and stroke AS aortic stenosis, BMCs bone marrow cells, CAD coronary artery disease, CHIP Clonal hematopoiesis of indetermined potential, CI confidence interval, HF heart failure, HR hazard ratio, cHF chronic heart failure, PAH pulmonary artery hypertension …”

Section: Current Evidence For Clinical Relevance Of Chipmentioning

confidence: 99%

“…In line with this, Scolari et al observed a 1.5-fold increased prevalence of CHIP-mutations, particularly TET2 and ASXL1 , among patients with cardiogenic shock predominantly of non-ischemic origin, compared to HF patients (95% CI 1.0–2.1). At the same time, harboring a CHIP mutation was associated with a decrease of survival at multiple timepoints (30-days: HR 2.7; 95% CI 1.3–5.7, P = 0.006; 90-days: HR 2.2; 95% CI 1.3–3.9, P = 0.003; and 3-years: HR 1.7; 95% CI 1.1–2.8, P = 0.01), while individuals carrying a TET2 -mutation displayed elevated serum levels of SCD40L, IFNγ, IL-4 and TNFα [ 81 ].…”

Section: Current Evidence For Clinical Relevance Of Chipmentioning

confidence: 99%

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Clonal hematopoiesis and cardiovascular disease: deciphering interconnections

et al. 2022

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Cardiovascular and oncological diseases represent the global major causes of death. For both, a novel and far-reaching risk factor has been identified: clonal hematopoiesis (CH). CH is defined as clonal expansion of peripheral blood cells on the basis of somatic mutations, without overt hematological malignancy. The most commonly affected genes are TET2, DNMT3A, ASXL1 and JAK2. By the age of 70, at least 20–50% of all individuals carry a CH clone, conveying a striking clinical impact by increasing all-cause mortality by 40%. This is due predominantly to a nearly two-fold increase of cardiovascular risk, but also to an elevated risk of malignant transformation. Individuals with CH show not only increased risk for, but also worse outcomes after arteriosclerotic events, such as stroke or myocardial infarction, decompensated heart failure and cardiogenic shock. Elevated cytokine levels, dysfunctional macrophage activity and activation of the inflammasome suggest that a vicious cycle of chronic inflammation and clonal expansion represents the major functional link. Despite the apparently high impact of this entity, awareness, functional understanding and especially clinical implications still require further research. This review provides an overview of the current knowledge of CH and its relation to cardiovascular and hematological diseases. It focuses on the basic functional mechanisms in the interplay between atherosclerosis, inflammation and CH, identifies issues for further research and considers potential clinical implications.

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Section: Current Evidence For Clinical Relevance Of Chipmentioning

confidence: 99%

Section: Current Evidence For Clinical Relevance Of Chipmentioning

confidence: 99%

Clonal hematopoiesis and cardiovascular disease: deciphering interconnections

et al. 2022

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“…Prognosis is worse for patients with CHIP who have chronic ischemic heart failure, 129,130 severe aortic stenosis undergoing transcatheter aortic valve implantation, 131 or cardiogenic shock. 132,133…”

Section: Links With Other Cardiovascular and Noncardiovascular Outcomesmentioning

confidence: 99%

Genomic Aging, Clonal Hematopoiesis, and Cardiovascular Disease

Natarajan

2023

ATVB

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Chronologic age is the dominant risk factor for coronary artery disease but the features of aging promoting coronary artery disease are poorly understood. Advances in human genetics and population-based genetic profiling of blood cells have uncovered the surprising role of age-related subclinical leukemogenic mutations in blood cells, termed “clonal hematopoiesis of indeterminate potential,” in coronary artery disease. Such mutations typically occur in DNMT3A , TET2 , ASXL1 , and JAK2 . Murine and human studies prioritize the role of key inflammatory pathways linking clonal hematopoiesis with coronary artery disease. Increasingly larger, longitudinal, multiomics analyses are enabling further dissection into mechanistic insights. These observations expand the genetic architecture of coronary artery disease, now linking hallmark features of hematologic neoplasia with a much more common cardiovascular condition. Implications of these studies include the prospect of novel precision medicine paradigms for coronary artery disease.

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“…17 Better knowledge of pathophysiological mechanisms in cardiogenic shock is necessary. 6,18 Scolari et al 19 showed that patients with cardiogenic shock are more prone to present gene mutations related to clonal haematopoiesis, particularly TET2 and AXSL1 mutations which are associated with reduced survival and a dysregulation of inflammatory cytokines.…”

Section: Pathophysiology and Biomarkersmentioning

confidence: 99%