Myocardial scarring

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Inferior left ventricle wall scar, short axis echocardiography view Heart inferior wall scar.jpg
Inferior left ventricle wall scar, short axis echocardiography view

Myocardial scarring is the accumulation of fibrous tissue resulting after some form of trauma to the cardiac tissue. [1] [2] Fibrosis is the formation of excess tissue in replacement of necrotic or extensively damaged tissue. Fibrosis in the heart is often hard to detect because fibromas, scar tissue or small tumors formed in one cell line, are often formed. [3] Because they are so small, they can be hard to detect by methods such as magnetic resonance imaging. [1] A cell line is a path of fibrosis that follow only a line of cells.

Contents

Causes

Myocardial infarction

A myocardial infarction, also known as a heart attack, often result in the formation of fibrosis. [2] A myocardial infarction is an ischemic event, or a restriction of blood flow to body tissue, such as by atherothrombosis. [4] Without blood flow to the myocardium, it is deprived of oxygen, causing tissue death and irreversible damage. [5] The tissue destroyed by the infarction is replaced with non-functioning fibrosis, restoring some of the structural integrity of the organ but resulting in impaired myocardial function. [6]

Coronary heart disease

Coronary heart disease, also known as coronary artery disease, is one of the most common causes of myocardial damage, affecting over three million people in the United States. [7] In coronary heart disease, the coronary arteries narrow due to the buildup of atheroma or fatty deposits on the vessel walls. The atheroma causes the blood flow of the arteries to be restricted. [6] By restricting the blood flow, the tissue is still receiving some oxygen, but not enough to sustain the tissue over time. [5] The accumulation of the fibrotic tissue is much slower in coronary heart disease compared to an infarction because the tissue is still receiving some oxygen. [6]

Birth defect repairs

Another form of myocardial scarring results from surgical repairs. [2] Surgical repairs are often necessary for a person born with a congenital defect of the heart. [8] While surgical laparoscopy still leaves myocardial scarring, the trauma seems to be less damaging then naturally occurring scarring. [2]

Excessive exercise

Excessive exercise, particularly in endurance athletes, has been linked to myocardial scarring, a condition where fibrous tissue in the heart muscle forms. Intense, prolonged physical activity can lead to repetitive stress on the myocardium, causing micro-injuries that may trigger inflammation and subsequent scarring. This is especially prevalent in individuals engaging in extreme endurance sports, such as marathons or ultra-marathons, very long bicycle racing, where sustained high cardiac output can strain the heart. Studies have shown that some athletes develop focal myocardial fibrosis, detectable via cardiac imaging (cardiac MRI, etc), which may increase the risk of arrhythmias or reduced cardiac function over time. While exercise is generally beneficial for heart health, excessive and prolonged exertion without adequate recovery may contribute to pathological changes in susceptible individuals - genetic tendency toward cardiac fibrosis, undiagnosed heart issues, or a reduced ability to recover from exercise-induced inflammation or micro-injuries. [9] [10] [11] [12]

Hypertension

Chronic hypertension can lead to myocardial scarring by imposing persistent high pressure on heart walls. This stress causes left ventricular hypertrophy, increasing oxygen demand and potentially leading to micro-ischemia. Over time, these changes may result in fibrosis as the heart attempts to repair damaged tissue, impairing cardiac function. [13]

Cardiomyopathies

Cardiomyopathies, such as dilated or hypertrophic cardiomyopathy, are associated with myocardial scarring. These conditions alter heart muscle structure and function. Scarring may contribute to heart failure or arrhythmias. [14]

Myocarditis

Myocarditis, inflammation of the heart muscle often caused by viral infections, can result in myocardial scarring. The inflammatory response damages cardiac tissue, triggering repair processes that replace necrotic cells with fibrous tissue. This scarring may increase the risk of arrhythmias. [15] [16]

Cardiac toxins

Exposure to cardiotoxic substances, such as chemotherapy drugs (e.g., anthracyclines), alcohol, or recreational drugs like cocaine, can cause myocardial scarring due to free radical damage, strand breakage of DNA in cardiomyocytes. [17] These toxins induce direct damage to heart muscle cells, leading to inflammation and fibrosis as the body attempts to repair the injured tissue. [18] [19] [20]

Aging

Aging is a natural contributor to myocardial scarring. Over time, cumulative stress from oxidative damage, low-grade inflammation, and microvascular changes can lead to gradual fibrosis in the heart. This age-related scarring may reduce cardiac elasticity and contribute to diastolic dysfunction in older individuals. [21] [22]

Formation

Immediately after damage to the myocardium occurs, the damaged tissue becomes inflamed. Inflammation is the accumulations of neutrophils, macrophages, and lymphocytes at the site of the trauma. [23] [24] In addition, "inflammatory cells upregulate the release of a myriad of signaling cytokines, growth factors, and hormones including transforming growth factor β, interleukins 1, 2, 6, and 10, tumor necrosis factor α, interferon γ, chemokines of the CC and CXC families, angiotensin II, norepinephrine, endothelin, natriuretic peptides, and platelet-derived growth factors". [24] Both the necrotic cells and the inflamed myocardium secrete and activate matrix metalloproteinase. Metalloproteinase aids in the destruction and reabsorption of necrotic tissue. After several days, collagen accumulation at the site of injury begins to occur. [24] As part of the extracellular matrix, granulated tissue consisting of fibrin, fibronectin, laminin, and glycosaminoglycan is suspended in a collagen base. [24] The extracellular matrix acts as scaffolding for the fibrillar collagen to form. The fibrillar collagen is the main constitute of what will become the scar tissue. [24]

References

  1. 1 2 Guler, Gamze Babur (2011). "Myocardial Fibrosis Detected by Cardiac Magnetic Resonance Imaging in Heart Failure: Impact on Remodeling, Diastolic Function and BNP Levels". Anatolian Journal of Cardiology. 11 (1): 71–76. doi:10.5152/akd.2011.013. PMID   21220243.
  2. 1 2 3 4 Fomovsky, Gregory M. (2010). "Evolution of Scar Structure, Mechanics, and Ventricular Function after Myocardial Infarction in the Rat". American Journal of Physiology. Heart and Circulatory Physiology. 298 (1): 1–12. doi:10.1152/ajpheart.00495.2009. PMC   2806135 . PMID   19897714.
  3. ↑ "FIBROMA". Merriam-Webster. Retrieved 2020-03-23.
  4. ↑ Katz, Monica Y. (2014). "Three-Dimensional Myocardial Scarring along Myofibers after Coronary Ischemia-Reperfusion Revealed by Computerized Images of Histological Assays". Physiological Reports. 2 (7): 1–3. doi:10.14814/phy2.12072. PMC   4187547 . PMID   25347856.
  5. 1 2 "ISCHEMIA". Merriam-Webster. Retrieved 2020-03-23.
  6. 1 2 3 Liang, Cuiping (2019). "Influence of the Distribution of Fibrosis within an Area of Myocardial Infarction on Wave Propagation in Ventricular Tissue". Scientific Reports. 15 (1): 1–24. Bibcode:2019NatSR...914151L. doi: 10.1038/s41598-019-50478-5 . PMC   6775234 . PMID   31578428. S2CID   203626142.
  7. ↑ "CORONARY HEART DISEASE". Merriam-Webster. Retrieved 2020-03-23.
  8. ↑ CDC (2019-11-22). "What are Congenital Heart Defects? | CDC". Centers for Disease Control and Prevention. Retrieved 2020-03-23.
  9. ↑ Patil, Harshal R.; O'Keefe, James H.; Lavie, Carl J.; Magalski, Anthony; Vogel, Robert A.; McCullough, Peter A. (2012). "Cardiovascular damage resulting from chronic excessive endurance exercise". Missouri Medicine. 109 (4): 312–321. ISSN   0026-6620. PMC   6179786 . PMID   22953596.
  10. ↑ "Heart Risks Associated With Extreme Exercise". Cleveland Clinic. Retrieved 2025-05-29.
  11. ↑ O'Keefe, James H.; Patil, Harshal R.; Lavie, Carl J.; Magalski, Anthony; Vogel, Robert A.; McCullough, Peter A. (June 2012). "Potential adverse cardiovascular effects from excessive endurance exercise". Mayo Clinic Proceedings. 87 (6): 587–595. doi:10.1016/j.mayocp.2012.04.005. ISSN   1942-5546. PMC   3538475 . PMID   22677079.
  12. ↑ "New research to better understand how heart scarring impacts veteran athletes". www.bhf.org.uk. Retrieved 2025-05-29.
  13. ↑ Saheera, Sherin; Krishnamurthy, Prasanna (2020). "Cardiovascular Changes Associated with Hypertensive Heart Disease and Aging". Cell Transplantation. 29: 963689720920830. doi:10.1177/0963689720920830. ISSN   1555-3892. PMC   7586256 . PMID   32393064.
  14. ↑ El Hadi, Hamza; Freund, Anne; Desch, Steffen; Thiele, Holger; Majunke, Nicolas (2023-02-11). "Hypertrophic, Dilated, and Arrhythmogenic Cardiomyopathy: Where Are We?". Biomedicines. 11 (2): 524. doi: 10.3390/biomedicines11020524 . ISSN   2227-9059. PMC   9953324 . PMID   36831060.
  15. ↑ Kang, Michael; Chippa, Venu; An, Jason (2025), "Viral Myocarditis", StatPearls, Treasure Island (FL): StatPearls Publishing, PMID   29083732 , retrieved 2025-05-29
  16. ↑ Shams, Pirbhat; Collier, Sara A. (2025), "Acute Myocarditis", StatPearls, Treasure Island (FL): StatPearls Publishing, PMID   28722877 , retrieved 2025-05-29
  17. ↑ Chong, Esther G.; Lee, Eric H.; Sail, Reena; Denham, Laura; Nagaraj, Gayathri; Hsueh, Chung-Tsen (2021-01-26). "Anthracycline-induced cardiotoxicity: A case report and review of literature". World Journal of Cardiology. 13 (1): 28–37. doi: 10.4330/wjc.v13.i1.28 . ISSN   1949-8462. PMC   7821007 . PMID   33552401.
  18. ↑ Morelli, Marco Bruno; Bongiovanni, Chiara; Da Pra, Silvia; Miano, Carmen; Sacchi, Francesca; Lauriola, Mattia; D'Uva, Gabriele (2022). "Cardiotoxicity of Anticancer Drugs: Molecular Mechanisms and Strategies for Cardioprotection". Frontiers in Cardiovascular Medicine. 9: 847012. doi: 10.3389/fcvm.2022.847012 . ISSN   2297-055X. PMC   9051244 . PMID   35497981.
  19. ↑ Mabudian, Leila; Jordan, Jennifer H.; Bottinor, Wendy; Hundley, W. Gregory (2022-09-27). "Cardiac MRI assessment of anthracycline-induced cardiotoxicity". Frontiers in Cardiovascular Medicine. 9. doi: 10.3389/fcvm.2022.903719 . ISSN   2297-055X. PMC   9551168 . PMID   36237899.
  20. ↑ Adão, Rui; de Keulenaer, Gilles; Leite-Moreira, Adelino; Brás-Silva, Carmen (2013-05-01). "Cardiotoxicity associated with cancer therapy: Pathophysiology and prevention". Revista Portuguesa de Cardiologia (in Portuguese). 32 (5): 395–409. doi:10.1016/j.repce.2012.11.019. ISSN   0870-2551.
  21. ↑ Horn, Margaux A.; Trafford, Andrew W. (April 2016). "Aging and the cardiac collagen matrix: Novel mediators of fibrotic remodelling". Journal of Molecular and Cellular Cardiology. 93: 175–185. doi:10.1016/j.yjmcc.2015.11.005. ISSN   1095-8584. PMC   4945757 . PMID   26578393.
  22. ↑ Wood, Colby; Salter, Wm Zachary; Garcia, Isaiah; Nguyen, Michelle; Rios, Andres; Oropeza, Jacqui; Ugwa, Destiny; Mukherjee, Upasana; Sehar, Ujala; Reddy, P. Hemachandra (2025-05-13). "Age-associated changes in the heart: implications for COVID-19 therapies". Aging. 17. doi:10.18632/aging.206251. ISSN   1945-4589. PMID   40372276.
  23. ↑ Radauceanu, Anca (2007). "Residual Stress Ischemia Is Associated with Blood Markers of Myocardial Structural Remodeling". European Journal of Heart Failure. 9 (4): 370–376. doi: 10.1016/j.ejheart.2006.09.010 . PMID   17140850. S2CID   2118209.
  24. 1 2 3 4 5 Richardson, William J.; Clarke, Samantha A.; Quinn, T. Alexander; Holmes, Jeffrey W. (2015-09-20). "Physiological Implications of Myocardial Scar Structure". Comprehensive Physiology. 5 (4): 1877–1909. doi:10.1002/cphy.c140067. ISSN   2040-4603. PMC   4727398 . PMID   26426470.
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