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Cardiology2099 papers

Toxic dilated cardiomyopathy

Last edited: 27 days ago

Overview

Dilated cardiomyopathy (DCM) is a heterogeneous group of myocardial disorders characterized by left ventricular dilation and systolic dysfunction, leading to heart failure and increased risk of arrhythmias and sudden cardiac death 111. It affects approximately 1 in 2500 individuals and is a significant cause of morbidity and mortality worldwide 111. The condition can arise from genetic mutations, toxic exposures, metabolic disorders, and other etiologies, making it crucial for clinicians to consider a broad differential diagnosis 21228. Understanding the nuances of DCM is essential for timely intervention and improved patient outcomes in day-to-day practice 111.

Pathophysiology

The pathophysiology of DCM involves complex interactions at molecular, cellular, and organ levels. At the molecular level, genetic mutations, particularly in genes encoding sarcomeric proteins like TTN, LMNA, and MYH7, disrupt the structural integrity of the sarcomere, leading to impaired contractility 23428. These mutations can also affect calcium handling proteins such as phospholamban (PLN) and ryanodine receptor 2 (RYR2), resulting in dysfunctional calcium cycling and energy metabolism 22224. Cellular dysfunction manifests as myocyte hypertrophy, apoptosis, and fibrosis, which collectively contribute to ventricular dilation and systolic dysfunction 11026. Organ-level changes include alterations in ventricular geometry, impaired diastolic function, and neurohormonal activation, further exacerbating heart failure symptoms 11545. Additionally, environmental factors like toxic exposures (e.g., doxorubicin) and metabolic disturbances (e.g., primary aldosteronism) can induce similar pathological changes, highlighting the multifaceted nature of DCM 11131.

Epidemiology

DCM exhibits variable incidence and prevalence rates globally, with estimates ranging from 0.2 to 15 cases per 100,000 population annually 111. The condition predominantly affects adults, with a median age of onset around 50 years, though it can occur at any age 111. There is a slight male predominance, though this varies by specific etiologies 118. Geographic and ethnic variations exist, with certain populations having higher frequencies of specific genetic mutations 11858. Over time, there has been an increasing recognition of genetic contributions, leading to improved diagnostic capabilities but also highlighting the complexity in identifying non-genetic causes 11258.

Clinical Presentation

Patients with DCM typically present with symptoms of heart failure, including dyspnea, fatigue, and exercise intolerance 1. Acute presentations may involve palpitations, syncope, or signs of cardiogenic shock due to arrhythmias or sudden cardiac death 116. Red-flag features include unexplained weight loss, edema, and signs of systemic congestion such as jugular venous distension and hepatomegaly 115. Atypical presentations can occur, especially in pediatric patients, where symptoms might be less specific and include growth retardation and developmental delays 79. Early recognition of these symptoms is crucial for timely intervention and management 17.

Diagnosis

The diagnostic approach to DCM involves a combination of clinical evaluation, imaging, and genetic testing. Key diagnostic criteria and tests include:

  • Clinical Evaluation: Detailed history and physical examination focusing on symptoms and signs of heart failure.
  • Echocardiography: Essential for measuring left ventricular ejection fraction (LVEF ≤35%) and assessing ventricular dilation and wall motion abnormalities 116.
  • Cardiac MRI: Utilized for detailed assessment of myocardial structure and function, including late gadolinium enhancement (LGE) patterns and T1 mapping for fibrosis quantification 192252.
  • Genetic Testing: Recommended for patients with familial DCM or unexplained cases, focusing on genes like TTN, LMNA, MYH7, and others 23428.
  • Blood Biomarkers: Natriuretic peptides (BNP/NT-proBNP) can help assess disease severity and prognosis 115.
  • Electrocardiography (ECG): Useful for identifying conduction abnormalities and arrhythmias 1749.

    • Differential Diagnosis:

  • Hypertrophic Cardiomyopathy (HCM): Distinguished by asymmetric septal hypertrophy on imaging.
  • Coronary Artery Disease (CAD): Presence of significant coronary stenosis on angiography or stress testing.
  • Valvular Heart Disease: Identified by echocardiography showing valve abnormalities.
  • Pericardial Disease: Pericardial effusion or constrictive pericarditis on imaging and clinical findings.

    • Management

    First-Line Treatment

  • Medications:
    • - Angiotensin-Converting Enzyme Inhibitors (ACE-I) or Angiotensin Receptor Blockers (ARBs): Initiate to reduce afterload and improve survival (e.g., enalapril 10 mg daily, losartan 50 mg daily) 115. - Beta-Blockers: Standard therapy to improve survival and reduce hospitalizations (e.g., carvedilol 6.25 mg twice daily, metoprolol succinate 25 mg nightly) 115. - Aldosterone Antagonists: Consider in NYHA class III-IV heart failure (e.g., spironolactone 25 mg daily) 115. - Diuretics: Manage fluid overload (e.g., furosemide 20-40 mg daily) 115.

    Second-Line Treatment

  • Inotropes: For advanced heart failure (e.g., dobutamine infusion titrated to effect) 115.
  • Device Therapy:
    • - Implantable Cardioverter Defibrillator (ICD): Recommended for primary prevention in patients with LVEF ≤35% and appropriate risk factors (e.g., LVEF ≤35%, NYHA class II-III symptoms) 11757. - Cardiac Resynchronization Therapy (CRT): Consider in patients with LVEF ≤35%, QRS duration ≥130 ms, and NYHA class III-IV symptoms 2157.

    Refractory / Specialist Escalation

  • Heart Transplantation: Consider for end-stage refractory cases 59.
  • Advanced Therapies: Investigational treatments such as gene therapy (e.g., AAV-TNNI3 for specific mutations) and novel pharmacological agents (e.g., danicamtiv for myosin activation) 144454.

    • Contraindications:

  • ACE-I/ARBs in bilateral renal artery stenosis.
  • Beta-blockers in decompensated heart failure without prior use.

    • Complications

    Acute Complications

  • Arrhythmias: Ventricular tachycardia, atrial fibrillation, and sudden cardiac death 11649.
  • Heart Failure Exacerbation: Fluid overload, pulmonary edema, and systemic congestion 115.

    • Long-Term Complications

  • Cardiomyopathy Progression: Continued ventricular dilation and worsening LVEF 115.
  • Renal Dysfunction: Secondary to neurohormonal activation and fluid retention 115.
  • Thromboembolic Events: Increased risk due to atrial fibrillation and mural thrombi 115.

    • Management Triggers:

  • Frequent monitoring of electrolytes, renal function, and BNP levels.
  • Early intervention with device therapy (ICD, CRT) and optimized medical management.

    • Prognosis & Follow-Up

    The prognosis of DCM varies widely, influenced by factors such as LVEF, genetic background, and response to therapy. Prognostic indicators include:
  • LVEF: Lower LVEF correlates with worse outcomes 115.
  • T1 Mapping: Elevated T1 values on CMR indicate increased fibrosis and poorer prognosis 52.
  • Arrhythmias: Presence of ventricular arrhythmias significantly worsens prognosis 116.

    • Recommended Follow-Up:

  • Regular Echocardiograms: Every 6-12 months to monitor LVEF and ventricular dimensions.
  • Cardiac MRI: Annually to assess myocardial fibrosis and structure.
  • Electrocardiograms: Every 6 months to monitor arrhythmias.
  • Blood Biomarkers: BNP/NT-proBNP levels every 3-6 months to assess disease progression.

    • Special Populations

    Pediatric Patients

  • Management: Includes LVAD support in severe cases (e.g., Berlin Heart EXCOR) 7.
  • Prognosis: Generally better than adults, but requires close monitoring for growth and development 7.

    • Elderly Patients

  • Considerations: Increased comorbidities and polypharmacy; careful titration of medications 115.
  • Device Therapy: ICDs and CRT may have different efficacy profiles 2157.

    • Genetic Variants

  • Specific Mutations: Tailored genetic counseling and monitoring based on specific mutations (e.g., TTN, LMNA) 23428.

    • Key Recommendations

  • Initiate ACE-I or ARB in all patients with symptomatic DCM to improve survival (Evidence: Strong) 115.
  • Prescribe beta-blockers as standard therapy to reduce mortality and hospitalizations (Evidence: Strong) 115.
  • Consider ICD implantation for primary prevention in patients with LVEF ≤35% and appropriate risk factors (Evidence: Strong) 11757.
  • Evaluate and consider CRT in patients with LVEF ≤35%, QRS ≥130 ms, and NYHA class III-IV symptoms (Evidence: Moderate) 2157.
  • Perform genetic testing in familial DCM or unexplained cases to guide management (Evidence: Moderate) 23428.
  • Regular follow-up with echocardiography every 6-12 months to monitor LVEF and ventricular dimensions (Evidence: Expert opinion) 1.
  • Monitor BNP/NT-proBNP levels every 3-6 months to assess disease progression and response to therapy (Evidence: Moderate) 115.
  • Consider heart transplantation for end-stage refractory DCM (Evidence: Expert opinion) 59.
  • Evaluate for and manage comorbidities such as atrial fibrillation and renal dysfunction (Evidence: Moderate) 115.
  • Tailor management based on specific genetic mutations to optimize therapy and prognosis (Evidence: Moderate) 23428.

    • References

    Showing 100 most recent of 1512 indexed papers.

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Journal of cardiovascular electrophysiology 2026. link 9 Panaioli E, Pontailler M, Gaudin R, Raisky O, Bonnet D, Khraiche D. Pulmonary artery banding as an adjunct to optimized medical therapy in infants and toddlers with severe dilated cardiomyopathy: A strategy to promote cardiac remodeling. International journal of cardiology 2026. link 10 Liu CF, Leon S, Tang WHW. Epigenetic Regulation in Dilated Cardiomyopathy. Heart failure clinics 2026. link 11 Abdul Jabbar AB, Javed MA, Mohammed SF. Dilated Cardiomyopathy-Related Mortality in the United States: Demographic and Regional Trends Over the Past 2 Decades. Circulation. Heart failure 2026. link 12 Weir RA, Millarvie C, Smith C, McGuire J, Simpson J, Petrie CJ. Determining aetiology in dilated cardiomyopathy - does the 'cardiomyopathy blood panel' ameliorate clinical assessment?. Acta cardiologica 2026. link 13 Yuan W, Gao Q, Liu X, Ying L, Zhang X, Fan X. 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Detection of Titin-Associated Electrocardiography Features in Dilated Cardiomyopathy Using Conventional and Deep Neural Network Analysis. JACC. Clinical electrophysiology 2026. link 18 Stroeks SLVM, Oko-Osi S, Arasu A, Hirst JE, Tayal UP. Sex Differences in Dilated Cardiomyopathy: Evidence Gaps and Future Directions. Journal of the American College of Cardiology 2026. link 19 Jia X, Zhao K, Dong Z, Ma X, Yang K, Yang S et al.. Subendocardium-involved late gadolinium enhancement in non-ischemic dilated cardiomyopathy improves risk stratification of sudden cardiac death. European heart journal. Cardiovascular Imaging 2026. link 20 Yang J, Li Y, Hou Y, Luo J, Li Y, Liu S et al.. Incremental Prognostic Value of Cardiac MRI-Based Right-to-Left Ventricular Blood Pool T2 Ratio in Patients With Dilated Cardiomyopathy. Journal of magnetic resonance imaging : JMRI 2026. link 21 Das A, Lakhani G. Left bundle branch area pacing or conventional cardiac resynchronization therapy: an Electrophysiology-guided tailored approach. Journal of interventional cardiac electrophysiology : an international journal of arrhythmias and pacing 2026. link 22 Zhang X, Wen T, Chen H, Jiang Z, Gu W, Yuan W et al.. Novel Compound Heterozygous Missense Variants in RPL3L Gene Associated With Neonatal Dilated Cardiomyopathy. American journal of medical genetics. Part A 2026. link 23 Yu Q, Shen Y, Barndt RJ, Sallam K, Tang Y, Brown CE et al.. Promoting Autophagy Mitigates Stress-Induced Remodeling in Patient iPSC-CMs with the Phospholamban R9C Mutation. Advanced science (Weinheim, Baden-Wurttemberg, Germany) 2026. link 24 Zhang N, Wang Y, Hou J, Zhang Y, Shan Y, Hu Y et al.. Generation of an induced pluripotent stem cell line (SSMCi002-A) from a pediatric dilated cardiomyopathy patient carrying heterozygous mutation in the TTN gene. Stem cell research 2026. link 25 Xie M, Xie B, Huang L, Chen Y, Lai X, Yan M et al.. MYBPC3 (c.194 C > T) mutation-mediated RyR2 dysfunction contributes to pathogenic phenotypes of DCM revealed by HiPSC modeling. Cellular and molecular life sciences : CMLS 2026. link 26 Wang J, Qi S, Chen S, Yu H. Effect of SGLT2 Inhibitors on Atrial Fibrillation in Patients With Type 2 Diabetes With Dilated Cardiomyopathy: A Cohort Study. Cardiovascular therapeutics 2026. link 27 Varlik T, Algan D, Sönmez Ö, Singh KK, Ülger Ö, Kubat GB et al.. Intravenous mitochondrial transplantation as an adjunctive therapy for dilated cardiomyopathy. Mitochondrion 2026. link 28 Wang L, Liu H, Zhao Q, Chen Y, Sun Y, Li R et al.. Identification of the non-canonical splice-disrupting variants of TTN in dilated cardiomyopathy. International journal of cardiology 2026. link 29 Angelotti A, Ponnusamy T, Kumar V, Passarelli GV, Malysz J, Mahesh B et al.. Phenotypes and mechanisms of dysfunctional cardiac T-lymphocytes in dilated cardiomyopathy patients. Journal of molecular and cellular cardiology 2026. link 30 Sun S, Yang X, Zhou Y, Yu R, Walther P, Teuteberg J et al.. Generation of two induced pluripotent stem cell lines from dilated cardiomyopathy patients carrying RBM20 mutations. Stem cell research 2026. link 31 Marzano L, Zoccatelli F, Friso S. Dilated cardiomyopathy in primary aldosteronism: A state-of-the-art of mechanistic insights, therapeutic strategies, and future perspectives. Trends in cardiovascular medicine 2026. link 32 Tomar N, Vennela AT, Mukhopadhyay S, Kondapi AK. Targeted nano delivery of p53 DNA and carvedilol for the treatment of dilated cardiomyopathy in a rat model. Nanomedicine (London, England) 2026. link 33 de Castro D, Fatkin D, Rodriguez-Rubio E, Haddad F, Hernández-Terciado F, Purohit A et al.. Truncating Variants in . Journal of the American Heart Association 2026. link 34 Wang H, Wang Y, Huang D, Jiang X, Li C, Xia X et al.. Potential Risk Factors and Therapeutic Targets for Dilated Cardiomyopathy Identified Through Mendelian Randomization Analysis. Journal of the American Heart Association 2026. link 35 Saha S, Singh P, Dutta A, Raj A, Rathore M, Jindal D et al.. A systems proteolipidomic approach identifies novel circulatory biomarkers for idiopathic dilated cardiomyopathy. American journal of physiology. Heart and circulatory physiology 2026. link 36 Ruan J, Guan Y, Le K, Zhang A, Tan P, Ran Y et al.. MYOM1 deficiency leads to dilated cardiomyopathy by disrupting the homeostasis of sarcoplasmic reticulum. Redox biology 2026. link 37 Yasufuku Y, Nishioka Y, Yasunaga H, Imamura T. Association of early cardiac rehabilitation on mortality in patients with dilated cardiomyopathy using national inpatient database. Scientific reports 2025. link 38 Mazarura GR, Hébert TE. 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Ethanol Ablation of Refractory Premature Ventricular Complex Originating from a Left Ventricular Summit Communicating Vein after Radiofrequency Catheter Ablation Failed in a Dilated Cardiomyopathy Patient. Internal medicine (Tokyo, Japan) 2025. link 50 Johnson R, Fletcher RA, Peters S, Ohanian M, Soka M, Smolnikov A et al.. Titin-related familial dilated cardiomyopathy: factors associated with disease onset. European heart journal 2025. link 51 Hanna AD, Chang T, Ho KS, Yee RSZ, Walker WC, Agha N et al.. Mechanisms underlying dilated cardiomyopathy associated with FKBP12 deficiency. The Journal of general physiology 2025. link 52 Berdibekov BS, Alexandrova SA, Bulaeva NI, Golukhova EZ. Prognostic value of myocardial tissue characterization by cardiac magnetic resonance imaging using T1 mapping in nonischemic dilated cardiomyopathy: a systematic review and meta-analysis. 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Sex Differences in the Clinical Presentation and Natural History of Dilated Cardiomyopathy. JACC. Heart failure 2024. link 87 Pérez-Serra A, Toro R, Martinez-Barrios E, Iglesias A, Fernandez-Falgueras A, Alcalde M et al.. Implementing a New Algorithm for Reinterpretation of Ambiguous Variants in Genetic Dilated Cardiomyopathy. International journal of molecular sciences 2024. link 88 Chen P, Aurich M, Greiner S, Maliandi G, Müller-Hennessen M, Giannitsis E et al.. Prognostic relevance of global work index and global constructive work in patients with non-ischemic dilated cardiomyopathy. The international journal of cardiovascular imaging 2024. link 89 Inciardi RM, Merlo M, Bellicini M, Setti M, De Luca A, Di Meo N et al.. Hepatic T1-time, cardiac structure and function and cardiovascular outcomes in patients with dilated cardiomyopathy. European journal of internal medicine 2024. link 90 Henkens MTHM, Raafs AG, Vanloon T, Vos JL, Vandenwijngaard A, Brunner HG et al.. 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    Original source

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