Verdonschot, Job A JFuster, Jose JWalsh, KennethHeymans, Stephane R B2024-12-182024-12-182024-10-17Eur Heart J . 2024 Oct 17;45(45):4797-4807.https://hdl.handle.net/20.500.12105/25906J.A.J.V. was supported by a Dekker clinical scientist grant from the Dutch Heart Foundation, and the Academic Funds of the Maastricht University Medical Center+. J.J.F. was supported by grant PLEC2021-008194, funded by MICIU/AEI/10.13039/501100011033 and by ‘European Union Next Generation EU/PRTR’; grant PID2021-126580OB-I00, funded by MICIU/AEI/10.13039/501100011033; and grant 202314-31, funded by Fundació ‘La Marató TV3’. He also received research funding from ‘la Caixa’ Foundation under the project code LCF/PR/HR22/ 52420011, and from Instituto de Salud Carlos III (ISCIII), co-funded by the European Union Next Generation EU/PRTR under the umbrella of the Partnership Fostering a European Research Area for Health (ERA4Health) (GA No 101095426 of the EU Horizon Europe Research and Innovation Programme). The CNIC was supported by ISCIII, the Ministerio de Ciencia e Innovación and the Pro CNIC Foundation, and is a Severo Ochoa Center of Excellence (grant CEX2020-001041-S funded by MICIN/AEI/10.13039/501100011033). K.W. receives funding from the National Institutes of Health (NIH)) grants AG073249, HL142650, and HL152174 and NASA grant 80NSSC21K0549. S.R.B.H. received funding from the European Union Commission’s Seventh Framework programme under grant agreement no. 305507 (HOMAGE); the IMI2-CARDIATEAM, from the Innovative Medicines Initiative 2 Joint Undertaking (JU) under grant agreement no. 821508, where the JU receives support from the European Union’s Horizon 2020 research and innovation programme and EFPIA; support by funding from the Pathfinder Cardiogenomics programme of the European Innovation Council of the European Union (DCM-NEXT pro ject); and further support from the Netherlands Cardiovascular Research Initiative, an initiative with support of the Dutch Heart Foundation, Dutch Cardiovascular Alliance Double Dosis, 2020-B005; ZonMW-Metacor.The increased sensitivity of novel DNA sequencing techniques has made it possible to identify somatic mutations in small circulating clones of haematopoietic stem cells. When the mutation affects a 'driver' gene, the mutant clone gains a competitive advantage and has the potential to expand over time, a phenomenon referred to as clonal haematopoiesis (CH), which is emerging as a new risk factor for various non-haematological conditions, most notably cardiovascular disease (e.g. heart failure). Dilated cardiomyopathy (DCM) is a form of non-ischaemic heart failure that is characterized by a heterogeneous aetiology. The first evidence is arising that CH plays an important role in the disease course in patients with DCM, and a strong association of CH with multiple aetiologies of DCM has been described (e.g. inflammation, chemotherapy, and atrial fibrillation). The myocardial inflammation induced by CH may be an important trigger for DCM development for an already susceptible heart, e.g. in the presence of genetic variants, environmental triggers, and comorbidities. Studies investigating the role of CH in the pathogenesis of DCM are expected to increase rapidly. To move the field forward, it will be important to report the methodology and results in a standardized manner, so results can be combined and compared. The accurate measurement of CH in patients with DCM can provide guidance of specific (anti-inflammatory) therapies, as mutations in the CH driver genes prime the inflammasome pathway.engVoRhttp://creativecommons.org/licenses/by-nc-sa/4.0/CHIPClonal haematopoiesisDilated cardiomyopathyHeart failureSequencingSomatic mutationsAttribution-NonCommercial-ShareAlike 4.0 International3941771045(45)4797-4807European Heart Journalopen access