Essay Sample on Myocardial Infarction: Causes, Effects & Treatment

Introduction

Myocardial infarction can be described as a sudden ischemic death of myocardial tissue (Frangogiannis, 2011). In the clinical perspective, a myocardial infarction occurs as a result of thrombotic constriction of coronary arteries or veins by rupture of an atherosclerotic plaque (Frangogiannis, 2011). Ischemia invokes profound metabolic and ionic trepidations in the affected myocardium and causes a rapid depression of systolic functions. An adult heart has the tiny reformative capacity, therefore, the infarcted myocardium heals through the formation of a scar. The healing of Myocardial Infarction is reliant on an inflammatory cascade, stimulated by alarmins secreted by dying cells (Frangogiannis, 2011). Clearance of dead cells and matrix debris by infiltrating white blood cells triggers anti-inflammatory lanes leading to suppression of cytokine, and chemokine signaling (Frangogiannis, 2011). The essay will discuss the pathophysiology of myocardial infarction.

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Myocardial Infection is classified into five types hellbent on its pathophysiology, prognostics, and clinics. Type 1: Spontaneous MI: can be described as atherosclerotic plaque discomfort resulting in the formation of thrombus, and reduced myocardial blood flow (Tibaut et al.,2016). Type 11: MI parallel to ischemic unevenness. The disparity between myocardial oxygen supply, and /or demand due to other situations e.g. coronary endothelial dysfunction, embolism, anemia, hypotension (Tibaut et al., 2016). Type 111: Myocardial infarction results in death when biomarker values are not available. Type 1Va: Myocardial infarction associated with percutaneous coronary intervention (PCI) (Tibaut et al., 2016). Type IVb: Myocardial infarction connected to stent thrombosis. Type V: Myocardial infarction related to coronary artery bypass grafting (CABG) (Tibaut et al., 2016).

Intraplaque Hemorrhage

Interplaque hemorrhage could cause rapid plaque expansion, and ACS, however, that is rarely the cause. Mostly, intraplaque hemorrhages can lead to continuous stepwise blocking of corona arteries. Firstly, neovessels develop under the influence of many growth factors and angiogenic proteins which are unreasonably evident in the lacerations (Tibaut et a., 2016).

Atherosclerosis

Atherosclerosis is a severe, inflammatory, fibro-proliferative illness of Myocardial Infarction on large and medium-sized vessels. It involves numerous pathophysiological features; retention, and adjustment of lipoproteins, development of monocytes, and T-lymphocytes, and the accumulation of excessive fibrous tissue. The establishment and advancement of atherosclerosis rely on several risk factors, including male gender, history of a patient with diabetes, hypertension, smoking, augmented cholesterol levels, and sedentary lifestyle.

Development of Atherosclerosis

In areas where there is low shear stress, the intima is thickened apparently as a physical adaptation. The subendothelial proteoglycan-rich layer, and a deeper muscculoelastic layer with flexible fibers, and smooth muscle cells (SMC) begin to form. These purported intimal thickenings are atherosclerosis prone regions. Apo B-encompassing lipoproteins accumulate in the proteogylcan-rich layer. Fat droplets are then subject to enzyme and oxidative radical change and when oxidized, they will serve as a proinflammatory mediator that invokes the synthesis of endothelial adhesion molecules, and chemokines emanated from macrophages. After these macrophages phagocytes are oxidized they form an appearance of foam cells. The foam cells coagulate in the inflamed intina and lead to the formation of yellow fatty droplets. These fatty streaks are described as harmless, and entirely reversible stages of atherosclerosis present in infants in the first 6 months of living. On an individual is aged between 20-30 years, the lipoproteins accumulated in fatty streaks, lipid pools will begin to form beneath the layer of foam cells, albeit no disruption of vascular intimal structure will be seen.

Postinfarction Left Ventricular Remodelling

The severe loss of myocardium results in a sudden amass of loading conditions that invoke a unique pattern of remodeling including the infarcted edge zone, and far-flung noninfarcted myocardium (Sutton & Sharpe, 2000). Myocyte necrosis and the resultant increase in load induces a cascade of biochemical intracellular signaling processes that introduce and subsequently modulates reparative modifications, which includes dilatation, the development of a discrete collagen scar, and hypertrophy (Sutton & Sharpe, 2000). Ventricular rehabilitation will progress for weeks or months until the inflating forces are equally balanced by the ductile strength of a collagen scar. The myocardium has 3 combined parts; myocytes, extracellular matrix, and the capillary microcirculation that acts as the contractile unit assembly (Sutton & Sharpe, 2000). The integration of all the 3 components offers significant insights into the restoration process and a rationale for future medicinal strategies. The cardiomyocyte is gravely differentiated and develops tension by shortening. Further, the extracellular matrix offers a stress-tolerant, viscoelastic scaffold involving type 1 and type 111 collagen that merges myocytes, and balances the spatial relations between the myofilaments, and their capillary microcirculation (Sutton & Sharpe, 2000). The collagen framework adjoins adjacent myocytes by intracellular struts that align myofilaments to improve force development, disseminate force evenly to the ventricular wall, and prevent sarcomeric distortion (Sutton & Sharpe, 2000).

Acute myocardial infection occurs when there is fissuring or erosion of atherosclerosis plaque. If a coronary obstruction persists for more than half an hour, unalterable damage to the myocardium happens (Basso & Thiene, 2006). Progressive coronary blockage results in a persistent increase of the infarct size with a wavefront transmural extension from the endocardium towards the epicardium (Basso & Thiene, 2006).

Conclusion

The paper has examined and analyzed the pathophysiology of myocardial infarction. In the clinical context, a myocardial infarction occurs as a result of thrombotic constriction of coronary arteries or veins by rupture of an atherosclerotic plaque. Four forms of myocardial infarction have been discussed in the paper, and they include; Spontaneous MI, MI parallel to ischemic unevenness, Myocardial infarction results in death when biomarker values are not available, Myocardial infarction associated with the percutaneous coronary intervention, and Myocardial infarction related to coronary artery bypass grafting (CABG) (Tibaut et al., 2016).

References

Basso, C., & Thiene, G. (2006). The pathophysiology of myocardial reperfusion: a pathologist's perspective. Heart, 92(11), 1559-1562. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1861239/

Frangogiannis, N. G. (2011). Pathophysiology of myocardial infarction. Comprehensive Physiology, 5(4), 1841-1875. Retrieved from https://onlinelibrary.wiley.com/doi/abs/10.1002/cphy.c150006

Sutton, M. G. S. J., & Sharpe, N. (2000). Left ventricular remodeling after myocardial infarction: pathophysiology and therapy. Circulation, 101(25), 2981-2988. Retrieved from https://www.ahajournals.org/doi/full/10.1161/01.cir.101.25.2981

Tibaut, M., Mekis, D., & Petrovic, D. (2016). Pathophysiology of myocardial infarction and acute management strategies. Cardiovascular & Hematological Agents in Medicinal Chemistry (Formerly Current Medicinal Chemistry-Cardiovascular & Hematological Agents), 14(3), 150-159. Retrieved from https://www.researchgate.net/profile/Miha_Tibaut/publication/311792200_Pathophysiology_of_Myocardial_Infarction_and_Acute_Management_Strategies/links/5a152302a6fdccd697bc06e3/Pathophysiology-of-Myocardial-Infarction-and-Acute-Management-Strategies.pdf