A detailed understating of the myocardial anatomy at the cellular level is of great importance to medical practitioners. As a major cause of death around the world, understanding the physiology of myocardial infarction at a cellular level goes a long way in creating awareness of its nature of the action (Braun, & Anderson, 2007). Primarily, these diseases manifest in the form of damaged heart muscles due to a decrease in the blood flow to all parts of the heart. At a cellular level, the disease comes about as a result of the spontaneous death of tissues of the heart muscle. The resultant outcome of this process is a thrombotic occlusion of a single or several coronary vessels (Skyschally, Schulz, & Heusch, 2008). According to Kumar and Cannon, the blockage of blood flow to heart muscles results in ionic and metabolic difficulties within the cells of the myocardium, an element that brings about decline in its systolic function (2009).
Prolonged blockage of blood flow sets in motion cardiomyocyte death which spans from the subendocardium through to the Subepicardium. Plaque rupture followed by platelet aggregation results in the propagation of the thrombus. Ideally, it spreads inside the blood vessel causing cellular damage within the subendocardial necrosed zone (Willis, Homeister, & Stone, 2014). Further on, the affected myocardium reaches the transmural necrosed zone where the most cells are dead, and neutrophils are present as a result of coagulation necrosis (Buerke, Lemm, Dietz, & Werdan, 2011; Frangogiannis, 2015). The buildup of neutrophils within the infarct results in the emergence of the granulation tissue on the edges of the infarct zone. The granulation tissue is primarily comprised of fibroblasts and Carophages. The accumulation of neutrophils and dead myocytes causes the granulation tissue to move inwards bringing about a scar tissue as a replacement of the dead tissue (Lilly, & Harvard Medical School, 2011; White, & Chew, 2008).
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References
Braun, C. A., & Anderson, C. M. (2007). Pathophysiology: Functional alterations in human health . Philadelphia: Lippincott Williams & Wilkins.
Buerke, M., Lemm, H., Dietz S. & Werdan, K. (2011). Pathophysiology, diagnosis, and treatment of infarction-related cardiogenic shock. Herz, 36 (2),73-83. doi: 10.1007/s00059-011-3434-7.
Frangogiannis, N. G. (2015). Pathophysiology of myocardial infarction. Comprehensive Physiology, 5 (4), 1841-1875. doi: 10.1002/cphy.c150006.
Kumar, A., & Cannon, C. P. (2009). Acute coronary syndromes: Diagnosis and management, part I. In Mayo Clinic Proceedings (Vol. 84, No. 10, pp. 917-938). London: Elsevier.
Lilly, L. S., & Harvard Medical School. (2011). Pathophysiology of heart disease: A collaborative project of medical students and faculty . Baltimore, MD: Wolters Kluwer/Lippincott Williams & Wilkins.
Skyschally, A., Schulz, R., & Heusch, G. (2008). Pathophysiology of myocardial infarction. Herz , 33 (2), 88-100.
White, H. D., & Chew, D. P. (2008). Acute myocardial infarction. The Lancet , 372 (9638), 570-584.
Willis, M. S., Homeister, J. W., & Stone, J. R. (2014). Cellular and Molecular Pathobiology of Cardiovascular Disease . London: Elsevier.
