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Myocardial scarring

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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.

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. An Ischemic event is defined as the restriction of blood flow to the body tissue.[4] Without blood flow to the myocardium, it is deprived of oxygen, causing tissue death and irreversible damage.[5] The damage caused by the myocardial infarction the later replaced by non- functioning fibrosis.[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]

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.[9][10] 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".[10]  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.[10] As part of the extracellular matrix, granulated tissue consisting of fibrin, fibronectin, laminin, and glycosaminoglycan is suspended in a collagen base.[10]  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.[10]

References

  1. ^ a b 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. ^ a b c d Fomovsky, Gregory M. (2010). "Evolution of Scar Structure, Mechanics, and Ventricular Function after Myocardial Infarction in the Rat". American Journal of Physiology. Heart & 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. ^ a b "ISCHEMIA". Merriam-Webster. Retrieved 2020-03-23.
  6. ^ a b c 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. ^ 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.
  10. ^ a b c d e 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.