Medicine:Cardiotoxicity

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Cardiotoxicity is the occurrence of heart dysfunction as electric or muscle damage, resulting in heart toxicity.[1] This can cause heart failure, arrhythmia, myocarditis, and cardiomyopathy,[2] resulting in a weakened heart that is not as efficient at pumping blood. While some of these effects are reversible, others can cause permanent damage, requiring further treatment. Cardiotoxicity may be caused by chemotherapy (a usual example is the class of anthracyclines)[3][4] treatment and/or radiotherapy;[5] complications from anorexia nervosa; adverse effects of heavy metals intake;[6] the long-term abuse of or ingestion at high doses of certain strong stimulants such as cocaine;[7] or an incorrectly administered drug such as bupivacaine.[8]

Mechanism

Many mechanisms have been used to explain cardiotoxicity. While many times, differing etiologies share the same mechanism, it generally depends on the agent inducing cardiac damage. For example, the primary mechanism is thought to be oxidative stress on cardiac myocytes.[8] It is thought that reactive oxygen species (ROS) overwhelm the antioxidant defenses of cardiac cells, causing direct cellular damage. This oxidative damage can disrupt mitochondrial function, therefore disrupting energy production in the heart muscle itself, leading to energy depletion via depleted ATP and promoting cell death through apoptosis or necrosis.[9]

Other mechanisms of cardiotoxicity include inflammatory,[10] DNA damaging, and disrupted cell signaling. DNA damage and disrupted cellular signaling are the proposed mechanism for many cardiotoxic chemotherapeutics.[11]

Regardless of the mechanism, clinical manifestations include heart failure, arrhythmia, myocarditis, and cardiomyopathy that can be permanent.[2] These conditions can greatly alter mortality and morbidity in patients meaning careful monitoring is necessary in patients exposed to cardiotoxic agents.

Inciting agents

The list of inciting agents is vast and involves various classes of medication as well as environmental agents. The effects of the cardiotoxic substances vary and are not all identical.

Chemotherapy drugs

Source:[12]

Other medications

Environmental toxins

Abused substances

Source:[17]

  • Alcohol: chronic heavy consumption leading to alcoholic cardiomyopathy
  • Recreational drugs: cocaine, methamphetamine

Others

  • Biological toxins such as diphtheria toxin[18]
  • Radiation therapy is known to cause radiation-induced heart disease (RIHD) [19]

These agents can lead to varying degrees of cardiotoxicity, and their effects may be dose-dependent and influenced by individual factors such as pre-existing cardiovascular disease and genetic predispositions that can foster greater sensitivity to any cardiac damage.

Treatment

The most likely effective treatment is to stop exposure to the inciting agent as soon as possible whether a pharmacologic or environmental agent. While some may fully recover from cardiotoxicity caused from exposure, many are left with permanent damage that may need further management. The management varies on the damage sustained, but generally follows guidelines for each condition such as heart failure, arrhythmias, and myocarditis.[20]

Patients taking anthracyclines can take dexrazoxane as a cardioprotective agent to prevent extensive cardiac damage.[21]

See also

References

  1. ↑ Sishi, Balindiwe J. N. (2015-01-01), Hayat, M. A., ed., "Chapter 10 - Autophagy Upregulation Reduces Doxorubicin-Induced Cardiotoxicity" (in en), Autophagy: Cancer, Other Pathologies, Inflammation, Immunity, Infection, and Aging (Amsterdam: Academic Press): pp. 157–173, doi:10.1016/b978-0-12-801033-4.00010-2, ISBN 978-0-12-801033-4, https://www.sciencedirect.com/science/article/pii/B9780128010334000102, retrieved 2022-07-06 
  2. ↑ 2.0 2.1 Herrmann, Joerg (August 2020). "Adverse cardiac effects of cancer therapies: cardiotoxicity and arrhythmia" (in en). Nature Reviews Cardiology 17 (8): 474–502. doi:10.1038/s41569-020-0348-1. ISSN 1759-5002. PMID 32231332. 
  3. ↑ Huang, C.; Zhang, X.; Ramil, J. M.; Rikka, S.; Kim, L.; Lee, Y.; Gude, N. A.; Thistlethwaite, P. A. et al. (2010). "Juvenile Exposure to Anthracyclines Impairs Cardiac Progenitor Cell Function and Vascularization Resulting in Greater Susceptibility to Stress-Induced Myocardial Injury in Adult Mice. Cardiotoxins are the second most toxic venom while neurotoxins are the first.". Circulation 121 (5): 675–83. doi:10.1161/CIRCULATIONAHA.109.902221. PMID 20100968. 
  4. ↑ "Anthracycline Cardiotoxicity: Prevalence, Pathogenesis and Treatment". Curr Cardiol Rev 7 (4): 214–220. 2011. doi:10.2174/157340311799960645. PMID 22758622. 
  5. ↑ Suchorska, Wiktoria M. (2020-01-01). "Radiobiological models in prediction of radiation cardiotoxicity" (in en). Reports of Practical Oncology & Radiotherapy 25 (1): 46–49. doi:10.1016/j.rpor.2019.12.001. ISSN 1507-1367. PMID 31889920. 
  6. ↑ Nigra, Anne E; Ruiz-Hernandez, Adrian; Redon, Josep; Navas-Acien, Ana; Tellez-Plaza, Maria (2016). "Environmental Metals and Cardiovascular Disease in Adults: A Systematic Review beyond Lead and Cadmium". Current Environmental Health Reports 3 (4): 416–433. doi:10.1007/s40572-016-0117-9. ISSN 2196-5412. PMID 27783356. 
  7. ↑ Pergolizzi, Joseph V; Magnusson, Peter; LeQuang, Jo Ann K; Breve, Frank; Varrassi, Giustino (2021). "Cocaine and Cardiotoxicity: A Literature Review". Cureus 13 (4). doi:10.7759/cureus.14594. ISSN 2168-8184. PMID 34036012. 
  8. ↑ 8.0 8.1 "[Cardiotoxicity of local anesthetics]". Cahiers d'Anesthésiologie 41 (6): 589–598. 1993. PMID 8287299. 
  9. ↑ Huang, Mei-Zhou; Li, Jian-Yong (January 2020). "Physiological regulation of reactive oxygen species in organisms based on their physicochemical properties" (in en). Acta Physiologica 228 (1). doi:10.1111/apha.13351. ISSN 1748-1708. PMID 31344326. https://onlinelibrary.wiley.com/doi/10.1111/apha.13351. 
  10. ↑ Tousif, Sultan; Singh, Anand P.; Umbarkar, Prachi; Galindo, Cristi; Wheeler, Nicholas; Toro Cora, Angelica; Zhang, Qinkun; Prabhu, Sumanth D. et al. (2023-02-03). "Ponatinib Drives Cardiotoxicity by S100A8/A9-NLRP3-IL-1β Mediated Inflammation" (in en). Circulation Research 132 (3): 267–289. doi:10.1161/CIRCRESAHA.122.321504. ISSN 0009-7330. PMID 36625265. 
  11. ↑ Babiker, Hani M; McBride, Ali; Newton, Michael; Boehmer, Leigh M.; Drucker, Adrienne Goeller; Gowan, Mollie; Cassagnol, Manouchkathe; Camenisch, Todd D. et al. (June 2018). "Cardiotoxic effects of chemotherapy: A review of both cytotoxic and molecular targeted oncology therapies and their effect on the cardiovascular system" (in en). Critical Reviews in Oncology/Hematology 126: 186–200. doi:10.1016/j.critrevonc.2018.03.014. PMID 29759560. https://linkinghub.elsevier.com/retrieve/pii/S1040842817303566. 
  12. ↑ Jain, Diwakar; Aronow, Wilbert (2019-01-01). "Cardiotoxicity of cancer chemotherapy in clinical practice" (in en). Hospital Practice 47 (1): 6–15. doi:10.1080/21548331.2018.1530831. ISSN 2154-8331. PMID 30270693. https://www.tandfonline.com/doi/full/10.1080/21548331.2018.1530831. 
  13. ↑ Li, Xiao-Qing; Tang, Xin-Ru; Li, Li-Liang (2021-10-19). "Antipsychotics cardiotoxicity: What's known and what's next". World Journal of Psychiatry 11 (10): 736–753. doi:10.5498/wjp.v11.i10.736. ISSN 2220-3206. PMID 34733639. 
  14. ↑ Goldstein, E. J. C.; Owens, R. C.; Nolin, T. D. (2006-12-15). "Antimicrobial-Associated QT Interval Prolongation: Pointes of Interest" (in en). Clinical Infectious Diseases 43 (12): 1603–1611. doi:10.1086/508873. ISSN 1058-4838. PMID 17109296. https://academic.oup.com/cid/article-lookup/doi/10.1086/508873. 
  15. ↑ Ferreira, Gonzalo; Santander, Axel; Chavarría, Luisina; Cardozo, Romina; Savio, Florencia; Sobrevia, Luis; Nicolson, Garth L. (October 2022). "Functional consequences of lead and mercury exposomes in the heart" (in en). Molecular Aspects of Medicine 87. doi:10.1016/j.mam.2021.101048. PMID 34785060. https://linkinghub.elsevier.com/retrieve/pii/S0098299721001084. 
  16. ↑ Georgiadis, Nikolaos; Tsarouhas, Konstantinos; Tsitsimpikou, Christina; Vardavas, Alexandros; Rezaee, Ramin; Germanakis, Ioannis; Tsatsakis, Aristides; Stagos, Dimitrios et al. (August 2018). "Pesticides and cardiotoxicity. Where do we stand?" (in en). Toxicology and Applied Pharmacology 353: 1–14. doi:10.1016/j.taap.2018.06.004. PMID 29885332. Bibcode: 2018ToxAP.353....1G. https://linkinghub.elsevier.com/retrieve/pii/S0041008X18302606. 
  17. ↑ Varga, Zoltán V; Ferdinandy, Peter; Liaudet, Lucas; Pacher, Pál (November 2015). "Drug-induced mitochondrial dysfunction and cardiotoxicity" (in en). American Journal of Physiology. Heart and Circulatory Physiology 309 (9): H1453–H1467. doi:10.1152/ajpheart.00554.2015. ISSN 0363-6135. PMID 26386112. 
  18. ↑ Sagar, Sandeep; Liu, Peter P; Cooper, Leslie T (February 2012). "Myocarditis" (in en). The Lancet 379 (9817): 738–747. doi:10.1016/S0140-6736(11)60648-X. PMID 22185868. 
  19. ↑ Slezak, Jan; Kura, Branislav; Ravingerová, Táňa; Tribulova, Narcisa; Okruhlicova, Ludmila; Barancik, Miroslav (September 2015). "Mechanisms of cardiac radiation injury and potential preventive approaches" (in en). Canadian Journal of Physiology and Pharmacology 93 (9): 737–753. doi:10.1139/cjpp-2015-0006. ISSN 0008-4212. PMID 26030720. http://www.nrcresearchpress.com/doi/10.1139/cjpp-2015-0006. 
  20. ↑ Fanous, Ibrahim; Dillon, Patrick (August 2016). "Cancer treatment-related cardiac toxicity: prevention, assessment and management" (in en). Medical Oncology 33 (8): 84. doi:10.1007/s12032-016-0801-5. ISSN 1357-0560. PMID 27372782. http://link.springer.com/10.1007/s12032-016-0801-5. 
  21. ↑ Chow, Eric J.; Aggarwal, Sanjeev; Doody, David R.; Aplenc, Richard; Armenian, Saro H.; Baker, K. Scott; Bhatia, Smita; Blythe, Nancy et al. (2023-04-20). "Dexrazoxane and Long-Term Heart Function in Survivors of Childhood Cancer" (in en). Journal of Clinical Oncology 41 (12): 2248–2257. doi:10.1200/JCO.22.02423. ISSN 0732-183X. PMID 36669148. 



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