CoChat
Sign Up
Cited by 184Viral Infections and Immunology ResearchCardiomyopathy and Myosin StudiesCardiovascular Effects of Exercise

Genetic Architecture of Acute Myocarditis and the Overlap With Inherited Cardiomyopathy

Open access
Lota, Amrit S., Hazebroek, Mark R., Theotokis, Pantazis, Wassall, Rebecca, Salmi, Sara, Halliday, Brian P., Tayal, Upasana, Verdonschot, Job +29 more·2022·Circulation
DOI 10.1161/circulationaha.121.058457PMC PMC9555763
Open this paper in CoChat — free accountOpen PDF

Abstract

Background: Acute myocarditis is an inflammatory condition that may herald the onset of dilated cardiomyopathy (DCM) or arrhythmogenic cardiomyopathy (ACM). We investigated the frequency and clinical consequences of DCM and ACM genetic variants in a population-based cohort of patients with acute myocarditis. Methods: This was a population-based cohort of 336 consecutive patients with acute myocarditis enrolled in London and Maastricht. All participants underwent targeted DNA sequencing for well-characterized cardiomyopathy-associated genes with comparison to healthy controls (n=1053) sequenced on the same platform. Case ascertainment in England was assessed against national hospital admission data. The primary outcome was all-cause mortality. Results: Variants that would be considered pathogenic if found in a patient with DCM or ACM were identified in 8% of myocarditis cases compared with <1% of healthy controls ( P =0.0097). In the London cohort (n=230; median age, 33 years; 84% men), patients were representative of national myocarditis admissions (median age, 32 years; 71% men; 66% case ascertainment), and there was enrichment of rare truncating variants (tv) in ACM-associated genes (3.1% of cases versus 0.4% of controls; odds ratio, 8.2; P =0.001). This was driven predominantly by DSP -tv in patients with normal LV ejection fraction and ventricular arrhythmia. In Maastricht (n=106; median age, 54 years; 61% men), there was enrichment of rare truncating variants in DCM-associated genes, particularly TTN -tv, found in 7% (all with left ventricular ejection fraction <50%) compared with 1% in controls (odds ratio, 3.6; P =0.0116). Across both cohorts over a median of 5.0 years (interquartile range, 3.9–7.8 years), all-cause mortality was 5.4%. Two-thirds of deaths were cardiovascular, attributable to worsening heart failure (92%) or sudden cardiac death (8%). The 5-year mortality risk was 3.3% in genotype-negative patients versus 11.1% for genotype-positive patients ( P adjusted =0.08). Conclusions: We identified DCM- or ACM-associated genetic variants in 8% of patients with acute myocarditis. This was dominated by the identification of DSP -tv in those with normal left ventricular ejection fraction and TTN -tv in those with reduced left ventricular ejection fraction. Despite differences between cohorts, these variants have clinical implications for treatment, risk stratification, and family screening. Genetic counseling and testing should be considered in patients with acute myocarditis to help reassure the majority while improving the management of those with an underlying genetic variant.

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1161/circulationaha.121.058457

Cites

Statistics

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • Genotype-positive patients had worse prognosis and increased 5-year mortality.

    “these genotype-positive patients had worse prognosis and increased 5-year mortality.”

    From Autoimmune Myocarditis, Old Dogs and New Tricks. (2024) · cites this paper as [219]

    The Clinical Outcomes results report a higher estimated 5-year mortality risk for genotype-positive than genotype-negative patients (11.1% versus 3.3%), but the adjusted comparison was not statistically significant (P=0.08). The Discussion describes worse outcomes as a tendency and says there were no significant differences in clinical outcomes by genotype status, so the claim overstates the certainty of a worse prognosis. (LLM, conf=0.88)

    Experimental — accuracy not yet measured

  • In that cohort, mutations in DCM genes (e.g., TTN) and arrhythmogenic cardiomyopathy genes (e.g., DSP) were identified.

    “Mutations in both DCM genes (eg, TTN ) and arrhythmogenic cardiomyopathy genes (eg, DSP ) were identified”

    From Autoimmune Myocarditis, Old Dogs and New Tricks. (2024) · cites this paper as [219]

  • There is an overlap between certain genetic cardiomyopathies and myocarditis.

    “Recent data strongly suggest an overlap between certain genetic cardiomyopathies and myocarditis.”

    From Autoimmune Myocarditis, Old Dogs and New Tricks. (2024) · cites this paper as [219]

  • In a population-based cohort study of 336 consecutive patients with myocarditis, pathogenic mutations for well-characterized cardiomyopathy-associated genes were identified in 8% of cases compared with <1% of healthy controls (P=0.0097).

    “In a ­ population-based cohort study of 336 consecutive patients with myocarditis from 2 institutions, pathogenic mutations for well-characterized cardiomyopathy-­ associated genes were identified in 8% of myocarditis cases compared with &lt;1% of healthy controls ( P =0.0097).”

    From Autoimmune Myocarditis, Old Dogs and New Tricks. (2024) · cites this paper as [219]

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

No citation lists for this paper

No citation lists for this paper yet — checked again daily.

References 49 · Cited by 184

Research works printed but not linked: 43

  1. [1]Cooper LT Keren A Sliwa K Matsumori A Mensah GA. The global burden of myocarditis, part 1: a systematic literature review for the Global Burden of Diseases, Injuries, and Risk Factors 2010 study. Glob Heart. 2014; 9: 121– 129. doi: 10.1016/j.gheart.2014.01.007 25432122 · DOI
  2. [2]Grun S Schumm J Greulich S Wagner A Schneider S Bruder O Kispert EM Hill S Ong P Klingel K. Long-term follow-up of biopsy-proven viral myocarditis: predictors of mortality and incomplete recovery. J Am Coll Cardiol. 2012; 59: 1604– 1615. doi: 10.1016/j.jacc.2012.01.007 22365425 · DOI
  3. [3]Doolan A Langlois N Semsarian C. Causes of sudden cardiac death in young Australians. Med J Aust. 2004; 180: 110– 112. doi: 10.5694/j.1326-5377.2004.tb05830.x 14748671 · DOI
  4. [4]Portig I Wilke A Freyland M Wolf MJ Richter A Ruppert V Pankuweit S Maisch B. Familial inflammatory dilated cardiomyopathy. Eur J Heart Fail. 2006; 8: 816– 825. doi: 10.1016/j.ejheart.2006.02.010 16713338 · DOI
  5. [5]Piriou N Marteau L Kyndt F Serfaty JM Toquet C Le Gloan L Warin-Fresse K Guijarro D Le Tourneau T Conan E. Familial screening in case of acute myocarditis reveals inherited arrhythmogenic left ventricular cardiomyopathies. ESC Heart Fail. 2020; 7: 1520– 1533. doi: 10.1002/ehf2.12686 32356610 PMC7373927 · DOI
  6. [6]Kissopoulou A Fernlund E Holmgren C Isaksson E Karlsson JE Green H Jonasson J Ellegard R Arstrand HK Svensson A,. Monozygotic twins with myocarditis and a novel likely pathogenic desmoplakin gene variant. ESC Heart Fail. 2020; 7: 1210– 1216. doi: 10.1002/ehf2.12658 32301586 PMC7261567 · DOI
  7. [7]Poller W Haas J Klingel K Kuhnisch J Gast M Kaya Z Escher F Kayvanpour E Degener F Opgen-Rhein B,. Familial recurrent myocarditis triggered by exercise in patients with a truncating variant of the desmoplakin gene. J Am Heart Assoc. 2020; 9: e015289. doi: 10.1161/JAHA.119.015289 32410525 PMC7660888 · DOI
  8. [8]Ader F Surget E Charron P Redheuil A Zouaghi A Maltret A Marijon E Denjoy I Hermida A Fressart V,. Inherited cardiomyopathies revealed by clinically suspected myocarditis: highlights from genetic testing. Circ Genom Precis Med. 2020; 13: e002744. doi: 10.1161/CIRCGEN.119.002744 32522011 · DOI
  9. [9]Belkaya S Kontorovich AR Byun M Mulero-Navarro S Bajolle F Cobat A Josowitz R Itan Y Quint R Lorenzo L,. Autosomal recessive cardiomyopathy presenting as acute myocarditis. J Am Coll Cardiol. 2017; 69: 1653– 1665. doi: 10.1016/j.jacc.2017.01.043 28359509 PMC5551973 · DOI
  10. [10]Kontorovich AR Tang Y Patel N Georgievskaya Z Shadrina M Williams N Moscati A Peter I Itan Y Sampson B. Burden of cardiomyopathic genetic variation in lethal pediatric myocarditis. Circ Genom Precis Med. 2021; 14: e003426. doi: 10.1161/CIRCGEN.121.003426 34228484 PMC8373803 · DOI
  11. [11]Seidel F Holtgrewe M Al-Wakeel-Marquard N Opgen-Rhein B Dartsch J Herbst C Beule D Pickardt T Klingel K Messroghli D,. Pathogenic variants associated with dilated cardiomyopathy predict outcome in pediatric myocarditis. Circ Genom Precis Med. 2021; 14: e003250. doi: 10.1161/CIRCGEN.120.003250 34213952 PMC8373449 · DOI
  12. [12]Tirón C Campuzano O Fernández-Falgueras A Alcalde M Loma-Osorio P Zamora E Caballero A Sarquella-Brugada G Cesar S Garcia-Cuenllas L,. Prevalence of pathogenic variants in cardiomyopathy-associated genes in myocarditis. Circ Genom Precis Med. 2022; 101161: circgen121003408. doi: 10.1161/circgen.121.003408 35522179 · DOI
  13. [13]Law YM Lal AK Chen S Cihakova D Cooper LT Jr Deshpande, S Godown J Grosse-Wortmann L Robinson JD Towbin JA. Diagnosis and management of myocarditis in children: a scientific statement from the American Heart Association. Circulation. 2021; 144: e123– e135. doi: 10.1161/CIR.0000000000001001 34229446 · DOI
  14. [14]Ware JS Li J Mazaika E Yasso CM DeSouza T Cappola TP Tsai EJ Hilfiker-Kleiner D Kamiya CA Mazzarotto F,. Shared genetic predisposition in peripartum and dilated cardiomyopathies. N Engl J Med. 2016; 374: 233– 241. doi: 10.1056/NEJMoa1505517 26735901 PMC4797319 · DOI
  15. [15]Ware JS Amor-Salamanca A Tayal U Govind R Serrano I Salazar-Mendiguchia J Garcia-Pinilla JM Pascual-Figal DA Nunez J Guzzo-Merello G,. Genetic etiology for alcohol-induced cardiac toxicity. J Am Coll Cardiol. 2018; 71: 2293– 2302. doi: 10.1016/j.jacc.2018.03.462 29773157 PMC5957753 · DOI
  16. [16]Garcia-Pavia P Kim Y Restrepo-Cordoba MA Lunde IG Wakimoto H Smith AM Toepfer CN Getz K Gorham J Patel P,. Genetic variants associated with cancer therapy-induced cardiomyopathy. Circulation. 2019; 140: 31– 41. doi: 10.1161/CIRCULATIONAHA.118.037934 30987448 PMC6613726 · DOI
  17. [17]Tanawuttiwat T Sager SJ Hare JM Myerburg RJ. Myocarditis and ARVC/D: variants or mimics? Heart Rhythm. 2013; 10: 1544– 1548. doi: 10.1016/j.hrthm.2013.06.008 23773988 · DOI
  18. [18]Zegkos T Panagiotidis T Parcharidou D Efthimiadis G. Emerging concepts in arrhythmogenic dilated cardiomyopathy. Heart Fail Rev. 2021; 26: 1219 – 1229. doi: 10.1007/s10741-020-09933-z 32056050 · DOI
  19. [19]Calabrese F Basso C Carturan E Valente M Thiene G. Arrhythmogenic right ventricular cardiomyopathy/dysplasia: is there a role for viruses? Cardiovasc Pathol. 2006; 15: 11– 17. doi: 10.1016/j.carpath.2005.10.004 16414451 · DOI
  20. [20]Pieroni M Dello Russo A Marzo F Pelargonio G Casella M Bellocci F Crea F. High prevalence of myocarditis mimicking arrhythmogenic right ventricular cardiomyopathy differential diagnosis by electroanatomic mapping-guided endomyocardial biopsy. J Am Coll Cardiol. 2009; 53: 681– 689. doi: 10.1016/j.jacc.2008.11.017 19232901 · DOI
  21. [23]Cooper LT Jr Čiháková D. Do genes influence susceptibility to myocarditis? JACC Basic Transl Sci. 2021; 6: 593– 594. doi: 10.1016/j.jacbts.2021.06.003 34368508 PMC8326289 · DOI
  22. [24]Lota AS Halliday B Tayal U Salmi S Shakur R Hammersley D Jones R Daubeney P Ware JW Cleland JG. Epidemiological trends and outcomes of acute myocarditis in the National Health Service of England. Circulation. 2019; 140: A11463. Abstract. doi: 10.1161/circ.140.suppl_1.11463 · DOI
  23. [25]Caforio AL Pankuweit S Arbustini E Basso C Gimeno-Blanes J Felix SB Fu M Helio T Heymans S Jahns R,. Current state of knowledge on aetiology, diagnosis, management, and therapy of myocarditis: a position statement of the European Society of Cardiology Working Group on Myocardial and Pericardial Diseases. Eur Heart J. 2013; 34: 2636– 48, 2648a. doi: 10.1093/eurheartj/eht210 23824828 · DOI · Paper page
  24. [26]Karczewski KJ Francioli LC Tiao G Cummings BB Alfoldi J Wang Q Collins RL Laricchia KM Ganna A Birnbaum DP,. The mutational constraint spectrum quantified from variation in 141,456 humans. Nature. 2020; 581: 434– 443. doi: 10.1038/s41586-020-2308-7 32461654 PMC7334197 · DOI · Paper page
  25. [29]Jordan E Peterson L Ai T Asatryan B Bronicki L Brown E Celeghin R Edwards M Fan J Ingles J. Evidence-based assessment of genes in dilated cardiomyopathy. Circulation. 2021; 144: 7– 19. doi: 10.1161/CIRCULATIONAHA.120.053033 33947203 PMC8247549 · DOI
  26. [31]Whiffin N Walsh R Govind R Edwards M Ahmad M Zhang X Tayal U Buchan R Midwinter W Wilk AE. CardioClassifier: disease- and gene-specific computational decision support for clinical genome interpretation. Genet Med. 2018; 20: 1246– 1254. doi: 10.1038/gim.2017.258 29369293 PMC6558251 · DOI
  27. [32]Frankel KA Rosser RJ. The pathology of the heart in progressive muscular dystrophy: epimyocardial fibrosis. Hum Pathol. 1976; 7: 375– 386. doi: 10.1016/s0046-8177(76)80053-6 939536 · DOI
  28. [33]Xiong D Lee GH Badorff C Dorner A Lee S Wolf P Knowlton KU. Dystrophin deficiency markedly increases enterovirus-induced cardiomyopathy: a genetic predisposition to viral heart disease. Nat Med. 2002; 8: 872– 877. doi: 10.1038/nm737 12118246 · DOI
  29. [34]Miles C Finocchiaro G Papadakis M Gray B Westaby J Ensam B Basu J Parry-Williams G Papatheodorou E Paterson C,. Sudden death and left ventricular involvement in arrhythmogenic cardiomyopathy. Circulation. 2019; 139: 1786– 1797. doi: 10.1161/CIRCULATIONAHA.118.037230 30700137 PMC6467560 · DOI
  30. [36]Smith ED Lakdawala NK Papoutsidakis N Aubert G Mazzanti A McCanta AC Agarwal PP Arscott P Dellefave-Castillo LM Vorovich EE,. Desmoplakin cardiomyopathy, a fibrotic and inflammatory form of cardiomyopathy distinct from typical dilated or arrhythmogenic right ventricular cardiomyopathy. Circulation. 2020; 141: 1872– 1884. doi: 10.1161/CIRCULATIONAHA.119.044934 32372669 PMC7286080 · DOI · Paper page
  31. [37]Scheel PJ 3rd Murray B Tichnell C James CA Tandri H Calkins H Chelko SP Gilotra NA. Arrhythmogenic right ventricular cardiomyopathy presenting as clinical myocarditis in women. Am J Cardiol. 2021; 145: 128– 134. doi: 10.1016/j.amjcard.2020.12.090 33460606 · DOI · Paper page
  32. [38]Bowles NE Ni J Marcus F Towbin JA. The detection of cardiotropic viruses in the myocardium of patients with arrhythmogenic right ventricular dysplasia/cardiomyopathy. J Am Coll Cardiol. 2002; 39: 892– 895. doi: 10.1016/s0735-1097(02)01688-1 11869858 · DOI
  33. [39]Asimaki A Tandri H Duffy ER Winterfield JR Mackey-Bojack S Picken MM Cooper LT Wilber DJ Marcus FI Basso C. Altered desmosomal proteins in granulomatous myocarditis and potential pathogenic links to arrhythmogenic right ventricular cardiomyopathy. Circ Arrhythm Electrophysiol. 2011; 4: 743– 752. doi: 10.1161/CIRCEP.111.964890 21859801 PMC3203520 · DOI · Paper page
  34. [40]Badorff C Knowlton KU. Dystrophin disruption in enterovirus-induced myocarditis and dilated cardiomyopathy: from bench to bedside. Med Microbiol Immunol. 2004; 193: 121– 126. doi: 10.1007/s00430-003-0189-7 12920582 · DOI
  35. [42]Savvatis K Muller I Frohlich M Pappritz K Zietsch C Hamdani N Grote K Schieffer B Klingel K Van Linthout S. Interleukin-6 receptor inhibition modulates the immune reaction and restores titin phosphorylation in experimental myocarditis. Basic Res Cardiol. 2014; 109: 449. doi: 10.1007/s00395-014-0449-2 25344085 · DOI
  36. [43]Vikhorev PG Vikhoreva NN Yeung W Li A Lal S Dos Remedios CG Blair CA Guglin M Campbell KS Yacoub MH. Titin-truncating mutations associated with dilated cardiomyopathy alter length-dependent activation and its modulation via phosphorylation. Cardiovasc Res. 2022; 118: 241– 253. doi: 10.1093/cvr/cvaa316 33135063 PMC8752363 · DOI
  37. [44]Akhtar MM Lorenzini M Cicerchia M Ochoa JP Hey TM Sabater Molina M Restrepo-Cordoba MA Dal Ferro M Stolfo D Johnson R. Clinical phenotypes and prognosis of dilated cardiomyopathy caused by truncating variants in the TTN gene. Circ Heart Fail. 2020; 13: e006832. doi: 10.1161/CIRCHEARTFAILURE.119.006832 32964742 · DOI
  38. [45]Kyto V Sipila J Rautava P. The effects of gender and age on occurrence of clinically suspected myocarditis in adulthood. Heart. 2013; 99: 1681– 1684. doi: 10.1136/heartjnl-2013-304449 24064227 · DOI · Paper page
  39. [46]Gigli M Stolfo D Graw SL Merlo M Gregorio C Nee Chen S Dal Ferro M Paldino MA De Angelis G Brun F,. Phenotypic expression, natural history, and risk stratification of cardiomyopathy caused by filamin C truncating variants. Circulation. 2021; 144: 1600– 1611. doi: 10.1161/circulationaha.121.053521 34587765 PMC8595845 · DOI
  40. [47]Blanco-Dominguez R Sanchez-Diaz R de la Fuente H Jimenez-Borreguero LJ Matesanz-Marin A Relano M Jimenez-Alejandre R Linillos-Pradillo B Tsilingiri K Martin-Mariscal ML,. A novel circulating microRNA for the detection of acute myocarditis. N Engl J Med. 2021; 384: 2014– 2027. doi: 10.1056/NEJMoa2003608 34042389 PMC8258773 · DOI · Paper page
  41. [48]Claes GR van Tienen FH Lindsey P Krapels IP Helderman-van den Enden AT Hoos MB Barrois YE Janssen JW Paulussen AD Sels JW,. Hypertrophic remodelling in cardiac regulatory myosin light chain (MYL2) founder mutation carriers. Eur Heart J. 2016; 37: 1815– 1822. doi: 10.1093/eurheartj/ehv522 26497160 · DOI
  42. [49]O’Roak BJ Vives L Fu W Egertson JD Stanaway IB Phelps IG Carvill G Kumar A Lee C Ankenman K,. Multiplex targeted sequencing identifies recurrently mutated genes in autism spectrum disorders. Science. 2012; 338: 1619– 1622. doi: 10.1126/science.1227764 23160955 PMC3528801 · DOI · Paper page
  43. [50]Roberts AM Ware JS Herman DS Schafer S Baksi J Bick AG Buchan RJ Walsh R John S Wilkinson S. Integrated allelic, transcriptional, and phenomic dissection of the cardiac effects of titin truncations in health and disease. Sci Transl Med. 2015; 7: 270ra– 27276. doi: 10.1126/scitranslmed.3010134 PMC4560092 25589632 · DOI

Authors
Lota, A. S., Hazebroek, M. R., Theotokis, P., Wassall, R., Salmi, S., Halliday, B. P., Tayal, U., Verdonschot, J., Meena, D., Owen, R., de Marvao, A., Iacob, A., Yazdani, M., Hammersley, D. J., Jones, R. E., Wage, R., Buchan, R., Vivian, F., Hafouda, Y., Noseda, M., Gregson, J., Mittal, T., Wong, J., Robertus, J. L., Baksi, A. J., Vassiliou, V., Tzoulaki, I., Pantazis, A., Cleland, J. G. F., Barton, P. J. R., Cook, S. A., Pennell, D. J., Garcia-Pavia, P., Cooper, L. T., Heymans, S., Ware, J. S., & Prasad, S. K.
Affiliations
  • Guy's and St Thomas' NHS Foundation Trust (GB)
  • Maastricht University Medical Centre (NL)
  • Imperial College London (GB)
  • London School of Hygiene & Tropical Medicine (GB)
  • National Heart &amp; Lung Institute (A.S.L., P.T., R.W., S.S., B.P.H., U.T., A.d.M., A.I., M.Y., M.J.H., R.E.J., R.W., R.B., M.N., J.L.R., A.P., J.G.F.C., P.J.R.B., D.J.P., J.S.W., S.K.P.), Imperial College London, UK.
  • University of East Anglia (GB)
  • National University of Singapore (SG)
  • Heart Failure and Inherited Cardiac Diseases Unit, Department of Cardiology, Hospital Universitario Puerta de Hierro, CIBERCV, Madrid, Spain (P.G.-P.).
  • Mayo Clinic (US)
Corresponding author
Prasad, Sanjay K.
ORCID
Venue
Circulation
Publisher
Ovid Technologies (Wolters Kluwer Health)
Published
2022-10-11
Volume
146
Issue
15
Pages
1123-1134
ISSN
  • 0009-7322 (ISSN-L)
  • 1524-4539
DOI
10.1161/circulationaha.121.058457
PMC
PMC9555763
OpenAlex
W4297226827
Cited by
184
References
49
Citations by year
2026: 51 · 2025: 48 · 2024: 48 · 2023: 35 · 2022: 2
FWCI
23.14
Type
journal article
Language
en
Open access
Licence
Locations
  • Circulation (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • Research Publications (Maastricht University) (publishedVersion, cc-by)
  • ENLIGHTEN (Jurnal Bimbingan dan Konseling Islam) (acceptedVersion, cc-by-sa)
  • LSHTM Research Online (London School of Hygiene and Tropical Medicine) (acceptedVersion)
  • UEA Digital Repository (University of East Anglia) (acceptedVersion)
  • Deposito Digital UFV (Francisco de Vitoria University) (submittedVersion, cc-by-nc-nd)
  • Lirias (submittedVersion, cc-by)
  • Spiral (Imperial College London) (submittedVersion, other-oa)
  • Research Publications (Maastricht University) (submittedVersion, other-oa)
Funders
  • Wellcome Trust (107469/Z/15/Z)
  • British Heart Foundation (FS/17/21/32712, FS/ICRF/21/26019, FS/CRTF/21/24167)
  • Rosetrees Trust (BHF2021 1)
Topics
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Viral Infections and Immunology Research
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiomyopathy and Myosin Studies
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Effects of Exercise
Keywords
acute myocarditis, dilated cardiomyopathy, arrhythmogenic cardiomyopathy, familial cardiomyopathy, genetic variants, DSP, titin, truncating mutations, all-cause mortality, sudden cardiac death, heart failure, genetic risk stratification, genotype-negative patients
MeSH terms
Adult, Cardiomyopathy, Dilated, Female, Heart, Humans, Male, Middle Aged, Myocarditis, Stroke Volume, Ventricular Function, Left

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review