Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 3 complete abstracts (582 words), 9 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
Enlargement of the heart, usually indicated by a cardiothoracic ratio above 0.50. Heart enlargement may involve the right, the left, or both heart ventricles or heart atria. Cardiomegaly is a nonspecific symptom seen in patients with chronic systolic heart failure (heart failure) or several forms of cardiomyopathies.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Enlarged Heart; Heart, Enlarged; Heart Enlargement; Enlargement, Heart; Cardiac Hypertrophy; Cardiac Hypertrophies; Hypertrophies, Cardiac; Hypertrophy, Cardiac.
Where it fits in the MeSH classification
- Broader topics
- Heart Diseases; Hypertrophy
- Narrower topics
- Cardiomyopathy, Dilated; Hypertrophy, Left Ventricular; Hypertrophy, Right Ventricular
Related concepts
- Heart
- Heart Ventricles
- Heart Atria
- Heart Failure
- Cardiomyopathies
Research landscape
PubMed indexes 61,437 records tagged with the MeSH heading “Cardiomegaly” (counts retrieved 2026-10-29). 7,404 of them (12.1%) were published from 2020 onward, and the busiest period so far is through 1999 with 24,178 records.
Reviews account for 6,758 records (11.0%) and meta-analyses for 237. Randomized controlled trials number 1,248 (2.0%) as a share of all records on the topic.
Show the data
| Period | Records |
|---|---|
| through 1999 | 24,178 |
| 2000-2009 | 14,591 |
| 2010-2019 | 15,264 |
| 2020 onward | 7,404 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 6,758 | 11.0% |
| Meta-analyses | 237 | 0.4% |
| Randomized controlled trials | 1,248 | 2.0% |
Method: PubMed query "Cardiomegaly"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-29.
Reading the evidence in cardiovascular medicine
Cardiovascular medicine has an unusually large body of randomized trials, so the type of outcome matters: hard clinical events such as death, heart attack and stroke carry more weight than changes in blood pressure, cholesterol or imaging markers that only predict risk. Observational studies can show associations but are confounded by age, lifestyle and other illness. Check whether a result is about prevention or treatment, the baseline risk of participants, and the absolute rather than only the relative size of any benefit.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Left ventricular hypertrophy and myocardial fibrosis in heart failure with preserved ejection fraction: mechanisms and treatment | 2026 | Review article Design not recorded in structured metadata | 31 | cc by PMID 40892534 · DOI · PMC12765563 |
| Rac1 palmitoylation is required for cardiac stress adaptation and regulation of protein kinase A signaling | 2025 | Research article Design not recorded in structured metadata | 6 | cc by PMID 40924486 · DOI · PMC12581661 |
| Molecular determinants of cardiac lymphatic dysfunction in a chronic pressure-overload model | 2026 | Research article Design not recorded in structured metadata | 5 | cc by PMID 41381806 · DOI · PMC12808729 |
Left ventricular hypertrophy and myocardial fibrosis in heart failure with preserved ejection fraction: mechanisms and treatment [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Heart failure with preserved ejection fraction (HFpEF) accounts for nearly half of all heart failure cases and is characterized by phenotypical heterogeneity with a high prevalence of multiple, often overlapping cardiometabolic disorders.
- Closing excerpt
- This review elaborates on the pathophysiological role of fibrotic remodelling and LV hypertrophy in HFpEF, outlines contemporary diagnostic standards, and discusses emerging therapeutic strategies, aiming at directly modulating myocardial fibrosis and hypertrophy in HFpEF.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (199 words)
Heart failure with preserved ejection fraction (HFpEF) accounts for nearly half of all heart failure cases and is characterized by phenotypical heterogeneity with a high prevalence of multiple, often overlapping cardiometabolic disorders. Comorbidities such as hypertension, obesity, or diabetes are present in many HFpEF patients and are hypothesized to contribute to adverse cardiac remodelling and myocardial fibrosis through a variety of haemodynamic and metabolic impairments, with nearly half of all HFpEF patients exhibiting left ventricular (LV) hypertrophy or concentric remodelling. Myocardial fibrosis and its surrogate changes in LV structure and geometry lead to functional impairments such as increased diastolic stiffness and elevated filling pressures and are associated with reduced exercise tolerance and poor prognosis in patients with HFpEF. Despite recent therapeutic progress, there are currently no evidence-based therapies mechanistically focusing solely on myocardial fibrosis and LV hypertrophy in HFpEF. Recognizing myocardial fibrosis and LV hypertrophy as key features of the heterogeneous HFpEF pathophysiology may contribute to the development of promising targets for future clinical trials. This review elaborates on the pathophysiological role of fibrotic remodelling and LV hypertrophy in HFpEF, outlines contemporary diagnostic standards, and discusses emerging therapeutic strategies, aiming at directly modulating myocardial fibrosis and hypertrophy in HFpEF.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 40892534 · DOI · PMC12765563
Rac1 palmitoylation is required for cardiac stress adaptation and regulation of protein kinase A signaling [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Cardiac hypertrophy is a common adaptation to cardiovascular stress and often a prelude to heart failure.
- Closing excerpt
- Taken together, this study suggests Rac1 S-palmitoylation dampens adrenergic drive and PKA-dependent modulation of the phospho-proteome in response to cardiovascular stress, revealing essential functions for S-acylated Rac1 in cardiac adaptation.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (205 words)
Cardiac hypertrophy is a common adaptation to cardiovascular stress and often a prelude to heart failure. We examined how S-palmitoylation of the small GTPase, Ras-related C3 botulinum toxin substrate 1 (Rac1), impacts cardiomyocyte stress signaling. Mutation of the Cys-178 palmitoylation site impaired activation of Rac1 when overexpressed in cardiomyocytes. Cardiomyocyte-specific Rac1 conditional knockin (Rac1cKI) mice expressing a Rac1C178S mutant protein exhibited normal cardiac structure and function but developed more severe cardiac hypertrophy in response to angiotensin II (AngII) infusion, cardiomyocyte-specific overexpression of AngII type 1 receptor (AT1R), and cardiac pressure overload. Moreover, pressure overload and AT1R overexpression evoked cardiac failure phenotypes in Rac1cKI mice not observed in controls. Mechanistically, Rac1cKI hearts and cardiomyocytes genetically resistant to Rac1 S-palmitoylation had a profound increase in protein kinase A (PKA) substrate phosphorylation in response to acute β-adrenergic stimulation, as did Rac1cKI hearts subjected to chronic AngII treatment, AT1R overexpression, or pressure overload that correlates with more advanced heart failure phenotypes. This was not associated with increased PKA enzymatic activity, suggesting potential deficits in phosphatase activity at PKA-regulated phospho-sites. Taken together, this study suggests Rac1 S-palmitoylation dampens adrenergic drive and PKA-dependent modulation of the phospho-proteome in response to cardiovascular stress, revealing essential functions for S-acylated Rac1 in cardiac adaptation.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 40924486 · DOI · PMC12581661
Molecular determinants of cardiac lymphatic dysfunction in a chronic pressure-overload model [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Cardiac lymphatic alterations and insufficient lymphatic drainage have been found in cardiovascular diseases (CVDs).
- Closing excerpt
- Our work provides tractable targets to restore lymphatic health in CVDs.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (178 words)
Cardiac lymphatic alterations and insufficient lymphatic drainage have been found in cardiovascular diseases (CVDs). To unravel the mechanisms underlying lymphatic dysfunction, we applied single-cell (sc) analyses in murine heart failure (HF) models. Transaortic constriction (TAC) in C57BL/6J and BALB/c mice modeled chronic pressure -overload-induced cardiac hypertrophy and HF, respectively. Cardiac lymphatic (LEC) and blood vascular endothelial cells (BEC) were analyzed by scRNAseq, and targets validated by immunohistochemistry and human LEC cultures. While LEC profiles were comparable between strains in healthy mice, we found expansion of lymphatic capillaries and loss of valves post-TAC only in BALB/c. Differentially expressed gene (DEG) analysis revealed a reduction post-TAC only in BALB/c of lymphatic junctional components. Conversely, LEC expression of immune cell cross-talk mediators was mostly preserved post-TAC. Interestingly, around 35% of DEGs identified in cardiac LECs post-TAC were similarly altered in interleukin (IL)1β-stimulated human LECs. In conclusion, loss of lymphatic valves and dysregulated lymphatic barrier may underlie poor drainage capacity during pressure-overload-induced HF, despite potent lymphangiogenesis and preserved LEC immune attraction. Our work provides tractable targets to restore lymphatic health in CVDs.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41381806 · DOI · PMC12808729
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Shared genetic pathways contribute to risk of hypertrophic and dilated cardiomyopathies with opposite directions of effect [4]
- Research article Metabolic mechanisms in physiological and pathological cardiac hypertrophy: new paradigms and challenges [5]
- Research article Dilated cardiomyopathy: causes, mechanisms, and current and future treatment approaches [6]
- Research article Left-ventricular hypertrophy and obesity: a systematic review and meta-analysis of echocardiographic studies [7]
- Research article Pathophysiology of Hypertensive Heart Disease: Beyond Left Ventricular Hypertrophy [8]
- Research article Acute myocarditis: aetiology, diagnosis and management [9]
References
- Peikert A, Fontana M, Solomon SD, Thum T. Left ventricular hypertrophy and myocardial fibrosis in heart failure with preserved ejection fraction: mechanisms and treatment. . 2026. PMID 40892534 · DOI · PMC12765563
- Teuber JP, Scissors RE, Subramani A, Madamanchi N, Brody MJ. Rac1 palmitoylation is required for cardiac stress adaptation and regulation of protein kinase A signaling. . 2025. PMID 40924486 · DOI · PMC12581661
- Heron C, Lemarcis T, Laguerre O, Bourgeois B, Thuilliez C, Valentin C, et al.. Molecular determinants of cardiac lymphatic dysfunction in a chronic pressure-overload model. . 2026. PMID 41381806 · DOI · PMC12808729
- Tadros R, Francis C, Xu X, Vermeer AMC, Harper AR, Huurman R, et al.. Shared genetic pathways contribute to risk of hypertrophic and dilated cardiomyopathies with opposite directions of effect. Nat Genet. 2021. PMID 33495596 · DOI · PMC7611259
- Ritterhoff J, Tian R. Metabolic mechanisms in physiological and pathological cardiac hypertrophy: new paradigms and challenges. Nat Rev Cardiol. 2023. PMID 37237146 · DOI
- Heymans S, Lakdawala NK, Tschöpe C, Klingel K. Dilated cardiomyopathy: causes, mechanisms, and current and future treatment approaches. Lancet. 2023. PMID 37716772 · DOI
- Cuspidi C, Rescaldani M, Sala C, Grassi G. Left-ventricular hypertrophy and obesity: a systematic review and meta-analysis of echocardiographic studies. J Hypertens. 2014. PMID 24309485 · DOI
- Nwabuo CC, Vasan RS. Pathophysiology of Hypertensive Heart Disease: Beyond Left Ventricular Hypertrophy. Curr Hypertens Rep. 2020. PMID 32016791 · DOI
- Lampejo T, Durkin SM, Bhatt N, Guttmann O. Acute myocarditis: aetiology, diagnosis and management. Clin Med (Lond). 2021. PMID 34507935 · DOI · PMC8439515
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-29.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.