Sex and gender differences in myocarditis and dilated cardiomyopathy: An update
Open accessAbstract
In the past decade there has been a growing interest in understanding sex and gender differences in myocarditis and dilated cardiomyopathy (DCM), and the purpose of this review is to provide an update on this topic including epidemiology, pathogenesis and clinical presentation, diagnosis and management. Recently, many clinical studies have been conducted examining sex differences in myocarditis. Studies consistently report that myocarditis occurs more often in men than women with a sex ratio ranging from 1:2–4 female to male. Studies reveal that DCM also has a sex ratio of around 1:3 women to men and this is also true for familial/genetic forms of DCM. Animal models have demonstrated that DCM develops after myocarditis in susceptible mouse strains and evidence exists for this progress clinically as well. A consistent finding is that myocarditis occurs primarily in men under 50 years of age, but in women after age 50 or post-menopause. In contrast, DCM typically occurs after age 50, although the age that post-myocarditis DCM occurs has not been investigated. In a small study, more men with myocarditis presented with symptoms of chest pain while women presented with dyspnea. Men with myocarditis have been found to have higher levels of heart failure biomarkers soluble ST2, creatine kinase, myoglobin and T helper 17-associated cytokines while women develop a better regulatory immune response. Studies of the pathogenesis of disease have found that Toll-like receptor (TLR)2 and TLR4 signaling pathways play a central role in increasing inflammation during myocarditis and in promoting remodeling and fibrosis that leads to DCM, and all of these pathways are elevated in males. Management of myocarditis follows heart failure guidelines and there are currently no disease-specific therapies. Research on standard heart failure medications reveal important sex differences. Overall, many advances in our understanding of the effect of biologic sex on myocarditis and DCM have occurred over the past decade, but many gaps in our understanding remain. A better understanding of sex and gender effects are needed to develop disease-targeted and individualized medicine approaches in the future.
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Few females progress to DCM in humans or autoimmune/viral myocarditis animal models.
“Few females progress to DCM in humans or autoimmune/viral myocarditis animal models. 64,124”
From COVID-19, Myocarditis and Pericarditis (2023) · cites this paper as [64]
Section 6 reports that in an autoimmune/viral CVB3 myocarditis model, all (100%) female BALB/c mice progressed to DCM—contrary to the claim that few females do so in such models. Section 3 reports that DCM is less common in women than men, but does not establish how many women with myocarditis progress to DCM. No page numbers are available in our copy. (LLM, conf=0.90)
Checked by a reasoning model — may be wrong.
Experimental — accuracy not yet measuredMyocarditis occurs predominantly in male patients aged 12 to 40 years regardless of whether the cause was virus-like SARS-CoV-2 or associated with a vaccine.
“Importantly, the findings highlight that myocarditis occurs predominantly in male patients aged 12 to 40 years regardless of whether the cause was due to a virus-like SARS-CoV-2 or associated with a vaccine-a demographic that has been reported before COVID-19.”
From COVID-19, Myocarditis and Pericarditis (2023) · cites this paper as [64]
Section 3 (page not supplied) reports that myocarditis occurs more often in men under 50 and was most prevalent at ages 16–20 in several large studies, supporting the broad demographic pattern before COVID-19. It does not establish the claimed 12–40 age range or show that this pattern holds specifically for both SARS-CoV-2-related and vaccine-associated myocarditis. (LLM, conf=0.86)
Experimental — accuracy not yet measuredUpregulation of complement and TLRs including TLR4 are key immune pathways that promote myocarditis in the autoimmune-CVB3 animal model.
“We have published previously that upregulation of complement and TLRs including TLR4 are key immune pathways that promote myocarditis in the autoimmune-CVB3 animal model”
From COVID-19, Myocarditis and Pericarditis (2023) · cites this paper as [64]
Section 6 reports that male BALB/c mice in the autoimmune-CVB3 model have a dominant immune response marked by upregulation of complement and TLR4, and links TLR4 signaling to inflammatory responses and remodeling. It does not establish that upregulation of complement or TLRs generally promotes myocarditis across the model; the reported finding is specifically in males and identifies TLR4. (LLM, conf=0.82)
Experimental — accuracy not yet measuredMyocarditis typically occurs more often in young men aged 16 to 30 years, and the sex ratio for COVID-19 studies is typically observed to be 60% men to 40% women.
“Myocarditis typically occurs more often in young men aged 16 to 30 years, and the sex ratio for COVID-19 studies is typically observed to be 60% men to 40% women.”
From COVID-19, Myocarditis and Pericarditis (2023) · cites this paper as [64]
Section 3, “Sex differences in epidemiology” (page not provided), says myocarditis is more common in men and that several large studies found it most prevalent in males aged 16–20, not the stated 16–30 range. The passages found do not support a typical 60% men/40% women ratio for COVID-19 studies; the review instead gives a female-to-male ratio of 1:2–4 for myocarditis studies generally. (LLM, conf=0.86)
Experimental — accuracy not yet measuredMen develop more scar tissue and dilated cardiomyopathy (DCM) than women.
“with men developing more scar tissue and dilated cardiomyopathy (DCM) than women. 64,124,131”
From COVID-19, Myocarditis and Pericarditis (2023) · cites this paper as [64]
Section 3 (Sex differences in epidemiology; page unavailable) reports that DCM occurs more often in men than women. Section 6 (Sex differences in the pathogenesis of myocarditis and DCM; page unavailable) describes stronger profibrotic responses in male mice, but does not establish that men develop more cardiac scar tissue than women. (LLM, conf=0.83)
Experimental — accuracy not yet measured
Virus-negative lymphocytic myocarditis may have alternative pathogenesis such as autoimmunity, hypersensitivity, or medication usage.
“suggesting potential alternative pathogenesis such as autoimmunity, hypersensitivity, or medication usage.”
From Autoimmune Myocarditis, Old Dogs and New Tricks. (2024) · cites this paper as [150]
Section 2 (Definitions; page unavailable) says lymphocytic myocarditis can be autoimmune, supporting one proposed alternative pathogenesis. The passages do not link that explanation specifically to virus-negative cases or identify hypersensitivity or medication use as causes; searches for those terms found no supporting passage. (LLM, conf=0.83)
Experimental — accuracy not yet measuredIn some cases of lymphocytic myocarditis, viruses test negative while heart-specific autoantibodies are present.
“Notably, in some cases of lymphocytic myocarditis, these viruses tested negative, while autoantibodies specific to the heart were present”
From Autoimmune Myocarditis, Old Dogs and New Tricks. (2024) · cites this paper as [150]
The Definitions section (page unavailable) says lymphocytic myocarditis can be autoimmune, and the Sex differences in epidemiology section reports myocarditis cases with confirmed heart autoantibodies. Neither passage says that viruses tested negative in those cases, so the claimed combination of findings is not established by this source. (LLM, conf=0.82)
Experimental — accuracy not yet measuredMyocarditis presents sex differences, with males showing higher prevalence and mortality rate, observed in both human and animal models.
“Myocarditis is a well-known disease presenting sex differences, with males showing a higher prevalence and mortality rate, observed in both human and animal models. 150”
From Autoimmune Myocarditis, Old Dogs and New Tricks. (2024) · cites this paper as [150]
Section 3 (Sex differences in epidemiology; page unavailable) reports that myocarditis occurs more often in men and gives a higher worldwide mortality rate for men aged 35–39. Section 6 (Sex differences in the pathogenesis of myocarditis and DCM; page unavailable) reports worse myocarditis in male mice, but does not establish higher male prevalence or mortality in animal models; one model had no deaths in either sex. (LLM, conf=0.87)
Experimental — accuracy not yet measuredPre-COVID myocarditis occurs more often in young men under 50 years, with a sex ratio of 2 to 4:1 men to women.
“Myocarditis pre-COVID is known to occur more often in young men under the age of 50 years, with a sex ratio of 2 to 4:1 men to women”
From COVID-19, Myocarditis and Pericarditis (2023) · cites this paper as [64]
Women are more likely to develop myocarditis after menopause.
“while women are more likely to develop myocarditis after menopause, which is reviewed in previous studies. 64,113-117”
From COVID-19, Myocarditis and Pericarditis (2023) · cites this paper as [64]
Proposed mechanisms for sex differences include more proinflammatory and profibrotic immune profiles in the heart of males compared with females, potentially attributed to differences in sex hormones.
“Proposed mechanisms include more proinflammatory and profibrotic immune profiles in the heart of males compared with females, potentially attributed to differences in sex hormones. 150”
From Autoimmune Myocarditis, Old Dogs and New Tricks. (2024) · cites this paper as [150]
Pre-COVID pericarditis occurs more often in young men under 50 years with a sex ratio of around 2:1.
“Similar to myocarditis, preCOVID pericarditis occurs more often in young men under the age of 50 years with a sex ratio of around 2:1. 64,95,118”
From COVID-19, Myocarditis and Pericarditis (2023) · cites this paper as [64]
Section 3, “Sex differences in epidemiology,” reports that myocarditis is more common in men under 50, with female-to-male ratios ranging from 1:2 to 1:4. Searches for pericarditis found a study title in the References and a mention of myopericarditis in section 7, but no passage giving the claimed age pattern or 2:1 ratio for pre-COVID pericarditis. (LLM, conf=0.75)
Experimental — accuracy not yet measuredThe accuracy of cMRI depends on the amount of scar tissue present.
“The accuracy of cMRI depends on the amount of scar tissue present”
From COVID-19, Myocarditis and Pericarditis (2023) · cites this paper as [64]
The Definitions section discusses cMRI criteria and differing views on its diagnostic certainty, and separately mentions fibrotic scar tissue. It does not say that cMRI accuracy depends on the amount of scar tissue present. Searches for cMRI accuracy, fibrosis, and scar-tissue amount found no passage establishing that relationship; page numbers were unavailable in our copy. (LLM, conf=0.72)
Experimental — accuracy not yet measured
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Self-citationAnimal Models for Autoimmune Myocarditis and Autoimmune Thyroiditis
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Self-citationSex-Specific Mortality Risk by QRS Morphology and Duration in Patients Receiving CRT
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COVID-19, Myocarditis and Pericarditis
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Self-citationReconstituted Extracellular Vesicles from Human Platelets Decrease Viral Myocarditis in Mice
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Self-citationDeterminants of COVID-19 vaccine-induced myocarditis
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Self-citationImmunomodulating and Immunosuppressive Therapy for Virus-Negative Immune-Mediated Myocarditis
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Myocarditis Related to the Use of Mesalazine
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Understanding long COVID myocarditis: A comprehensive review
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Estrogen attenuates stiffness-driven fibrotic signaling via transcriptional regulation
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Sex Differences in Heart Failure: A Step Forward
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Cardiomyocyte β-arrestins mediate inflammation and cGAS-STING activation in CVB3 viral myocarditis
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Advanced Cardiac Imaging and Women’s Chest Pain: A Question of Gender
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Sex differences in left-ventricular strain in a murine model of coxsackievirus B3 myocarditis
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A murine model of Trypanosoma brucei- induced myocarditis and cardiac dysfunction
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Donor-dependent heterogeneity in therapeutic effects of adipose tissue extracellular vesicles
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Self-citationGenetic factors contributing to viral myocarditis
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Trends in age and sex-specific dilated cardiomyopathy mortality in Italy, 2005–2017
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Sex differences in coronavirus disease 2019 myocarditis
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Self-citationA descriptive review on the real-world impact of Moderna, Inc. COVID-19 vaccines
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Clinical features, myocardial injury and systolic impairment in acute myocarditis
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Acute Myocarditis According to Age: Presentation, Management and Early Outcomes
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Modeling the interplay of sex hormones in cardiac hypertrophic signaling
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Exploring the Genetic Architecture of Myocarditis and Inherited Cardiomyopathies
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Sex and Age Specific Genetic Risk Across the Dilated and Arrhythmogenic Cardiomyopathy Spectrum
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A viral-specific CD4+ T cell response protects female mice from Coxsackievirus B3 infection
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Does female sex matter in a chronic intermittent hypoxia mouse model?
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Midkine Serum Levels in Inflammatory and Non-Inflammatory Dilated Cardiomyopathy
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Investigating pathological features of myocarditis-related sudden cardiac deaths in Egypt
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“Bridging the clinical, molecular and genetic perspectives on myocarditis in post-COVID-19 era”
Birla, S., Angural, A., Madathumchalil, A., Shende, R. V., Shastry, S. V., Shekar, P. K., Mahadevappa, M., Vishwanath, P. M., & Prashant, A. (2026) · International Journal of Cardiology Cardiovascular Risk and Prevention · doi:10.1016/j.ijcrp.2026.200576 · Cited by 1 · see citing works
MyoClass: A modular multimodal auto-classification system for myocardial tissue characterization
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Myocarditis after COVID-19 mRNA vaccination in Norway: a nationwide validation study
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Antiviral innate immunity in myocarditis: mechanisms and emerging therapeutics
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Clinical and echocardiographic spectrum of dilated cardiomyopathy: A single-center study
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Cytokines as Potential Novel Therapeutic Targets in Severe Inflammatory CardiomyopathyPreprint
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Self-citationDDX3X-mediated translation of structured cardiac mRNAs is essential for female heart developmentPreprint
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Focal myocarditis, an unusual imitator: Case report and short literature review
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Dilated cardiomyopathy in a green-winged saltator (Saltator similis)
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Etiopathogenetic factors of infective endocarditis in patients undergoing mitral valve surgery
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The effects of conditional loss of myosin binding protein H-like on cardiac functionPreprint
Burnham, H. V., Peña, A., Gandhi, S., Fritzmann, G. E., & Barefield, D. Y. (2024) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2024.10.07.617136
CHARACTERISTICS OF CLINICAL MANIFESTATIONS IN INFECTIVE ENDOCARDITIS WITH MITRAL VALVE INVOLVEMENT
Soltani, S. E., & Krikunov, A. A. (2024) · Актуальні проблеми сучасної медицини Вісник Української медичної стоматологічної академії · doi:10.31718/2077-1096.24.3.46
- Authors
- Fairweather, D., Beetler, D. J., Musigk, N., Heidecker, B., Lyle, M. A., Cooper, L. T., & Bruno, K. A.
- Affiliations
- Mayo Clinic (US)
- Humboldt-Universität zu Berlin (DE)
- Corresponding author
- Fairweather, DeLisa
- ORCID
- Venue
- Frontiers in Cardiovascular Medicine
- Publisher
- Frontiers Media SA
- Published
- 2023-03-02
- Volume
- 10
- Pages
- 1129348-1129348
- ISSN
- 2297-055X (ISSN-L)
- PMC
- PMC10017519
- OpenAlex
- W4322773336
- Cited by
- 124
- References
- 333
- Citations by year
- 2026: 29 · 2025: 32 · 2024: 44 · 2023: 19
- FWCI
- 6.60
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Frontiers in Cardiovascular Medicine (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Institutes of Health (R01 HL164520, R21 AI145356, R21 AI152318, R21 AI154927, TL1 TR002380, R21 AI163302, R01 HL135165)
- American Heart Association (20TPA35490415)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Viral Infections and Immunology Research
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiomyopathy and Myosin Studies
- Keywords
- sex differences, gender differences, myocarditis, dilated cardiomyopathy, sex ratio, postmenopausal women, heart failure biomarkers, soluble ST2, Toll-like receptor signaling, cardiac remodeling, heart failure treatment, personalized medicine
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