Myocardial Infarction, or heart attack, occurs when the coronary artery becomes blocked or occluded, resulting in damage to the heart muscle tissue. Patients often experience some degree of chest pain or discomfort, which may extend to the shoulders and arms, as well as the back, neck, and jaw. It is most often felt in the centre or left side of the chest and lasts several minutes or longer. Periodically, heartburn-like sensations may occur. Side symptoms such as shortness of breath, nausea, dizziness, a chilly sweat, and tiredness are all possible (Mythli and Malathi, 2015). Cardiovascular disease adversely affects both self-reported health and quality of life. Individuals with a cardiovascular problem were four times as likely as those without to report poor health, a rate that topped that of any other chronic illness, including diabetes. In the same vein, the primary objective of this article is to examine the ailment’s process and to establish how it might be prevented to a certain degree.
Myocardial ischemia occurs when the heart’s blood flow is compromised, depriving the heart muscle of enough oxygen. Reduced blood flow is typically caused by a partial or total blockage of an individual’s coronary arteries (coronary arteries) (Mythili and Malathi, 2015). Myocardial ischemia, sometimes referred to as cardiac ischemia, inhibits the heart muscle’s ability to pump blood. Myocardial ischemia occurs when the blood flow through one or more of an individual’s coronary arteries is diminished. Myocardial ischemia may occur gradually as arteries narrow over time. Alternatively, it might arise unexpectedly as a result of a clogged artery.
(Mythili and Malathi, 2015)
Ischemic cell injury occurs when a cell sustains damage as a result of a decrease in its blood supply. The process is characterised by hypoxia, which is caused, among other things, by a disruption in blood flow, nutritional deficiency, and the buildup of harmful metabolites (Okada et al., 2019). Depending on the length of ischemia, cell damage may be reversible or permanent. While it is feasible to restore blood flow and allow cells to recover after an ischemia event, reperfusion might result in harm to previously ischemic tissues. Reperfusion has the ability to induce cell death, often necrosis, by causing calcium excess, oxidative stress, and inflammatory processes involving immune cells, cytokines, and the complement system (among other variables) (Heusch, 2020). Ischemia risk is influenced by a variety of variables, including metabolic activity, the existence of collateral circulation, and the location of watershed regions. Ischemia is most dangerous to the brain. Additionally, the heart, kidneys, liver, and big intestine are all very vulnerable organs.
Ischemia has also been demonstrated to deplete cellular ATP by inactivating ATPases (e.g., Na+/K+ ATPase), lowering active Ca2+ efflux, and limiting calcium absorption by the endoplasmic reticulum (ER), resulting in calcium overload (Li et al., 2021). Following these changes, the mitochondrial permeability transition (MPT) hole is opened, further reducing the potential of the mitochondrial membrane and inhibiting ATP synthesis. Following these cellular changes in the heart, intracellular proteases (e.g., calpains) are activated, resulting in myofibril destruction, hypercontracture, and contracture band necrosis. Other biochemical responses occur during ischemia that do not directly result in ischemic damage, but when fed by the return of oxygen and newly formed components into the blood upon resumption of blood flow, trigger a cascade of events that exacerbate tissue damage.
After 15 minutes, ischemic damage advances from reversible to irreversible in the left ventricle’s most severely ischemic subendocardium and subsequently spreads in a wavefront pattern from subendocardium to subepicardium over the ischemic bed-at-risk (Hashmi and Al-Salam, 2015). With enough collateral blood flow, severe ischemia may be restricted to the inner half of the left ventricle. Acute myocardial infarction (AMI) progresses swiftly, with the majority of myocardial necrosis occurring within three hours after coronary blockage initiation.
Reperfusion is essential in deciding the outcome of an acute myocardial infarction (AMI). When treatment is initiated quickly, a transmural AMI is very improbable: necrosis is much decreased and restricted to the subendocardium. Nevertheless, some wounded cardiomyocytes along the wavefront’s edge survive permanent damage after reperfusion, resulting in a deadly component of reperfusion injury (Hashmi and Al-Salam, 2015). Myocardial stunning occurs when the revived myocardium has reduced contractile performance after reperfusion. The earlier reperfusion occurs, the less overall necrosis occurs from both ischemia and reperfusion, and contractile function recovers more quickly after acute shock.
Reperfusion, on the other hand, may be harmed by the microvascular damage and occlusion that occur during the ischemia phase; this is known to as the no-reflow phenomena. Inside the first 6-24 hours after myocardial infarction, a huge burst of cell death occurs within the ischemic area (Hashmi and Al-Salam, 2015). Less cell death occurs in the peri-infarct zone initially as a result of residual ischemia but continues as a result of cardiac remodelling induced by the loss of contractile units in the infarct.
Acute myocardial infarction (MI) is defined by irreversible damage to cardiomyocytes, resulting in ischemia necrosis, which histologically is classified as ‘coagulative type’ necrosis. Another form of necrosis that is often seen during autopsy is called ‘contraction band necrosis,’ which is a characteristic of a variety of other types of cardiac damage and should be distinguished from this one.
The bloodstream may be used to detect myocardial cell death by checking for a variety of proteins secreted by damaged myocytes, including myoglobin, cardiac troponin T and I, creatine kinase, and lactate dehydrogenase (LDH) (Chan and NG, 2010). Myocardial infarction is diagnosed when sensitive and specific biomarkers such as cardiac troponin or CKMB levels in the blood rise in the presence of acute myocardial ischemia in the patient’s clinical scenario. Elevated levels of these biomarkers suggest the existence of myocardial necrosis, but do not reveal the cause of necrosis. As a result, if there are no clinical signs of ischemia and an increased cardiac troponin level, it is critical to rule out other potential causes of myocardial necrosis, including myocarditis, aortic dissection, pulmonary embolism, congestive heart failure, or renal failure (Chan and NG, 2010). Cardiovascular troponin (I or T) is recommended for use as a biomarker for myocardial necrosis because it has almost 100% myocardial tissue specificity and a high clinical sensitivity, enabling the detection of even tiny zones of myocardial necrosis in the heart (Park et al., 2017).
Conclusion
In summation, it can be understood that there are numerous reasons that can lead to MI as well as the progression of the same. It can also be seen that there are several mechanisms leading from reversible cell damage to permanent cell death. In due course of this process, immediate medical action can aid the patient but even a slight delay can prove to be fatal. Also, the biomarkers of the condition are discussed towards the end of the report which provides us with additional information toward understanding the condition.
References
Ahmadi, A., Leipsic, J., Blankstein, R., Taylor, C., Hecht, H., Stone, G.W. and Narula, J., 2015. Do plaques rapidly progress prior to myocardial infarction? The interplay between plaque vulnerability and progression. Circulation research, 117(1), pp.99-104.
Chan, D. and Ng, L.L., 2010. Biomarkers in acute myocardial infarction. BMC medicine, 8(1), pp.1-11.
Hashmi, S. and Al-Salam, S., 2015. Acute myocardial infarction and myocardial ischemia-reperfusion injury: a comparison. International Journal of Clinical and Experimental Pathology, 8(8), p.8786.
Heusch, G., 2020. Myocardial ischaemia–reperfusion injury and cardioprotection in perspective. Nature Reviews Cardiology, 17(12), pp.773-789.
Li, L.L., Ke, X.Y., Jiang, C., Qin, S.Q., Liu, Y.Y., Xian, X.H., Liu, L.Z., He, J.C., Chen, Y.M., An, H.F. and Sun, N., 2021. Na+, K+?ATPase participates in the protective mechanism of rat cerebral ischemia?reperfusion through the interaction with glutamate transporter?1. Fundamental & Clinical Pharmacology, 35(5), pp.870-881.
Mythili, S. and Malathi, N., 2015. Diagnostic markers of acute myocardial infarction. Biomedical reports, 3(6), pp.743-748.
Okada, Y., Numata, T., Sato-Numata, K., Sabirov, R.Z., Liu, H., Mori, S.I. and Morishima, S., 2019. Roles of volume-regulatory anion channels, VSOR and Maxi-Cl, in apoptosis, cisplatin resistance, necrosis, ischemic cell death, stroke and myocardial infarction. Current Topics in Membranes, 83, pp.205-283.
Park, K.C., Gaze, D.C., Collinson, P.O. and Marber, M.S., 2017. Cardiac troponins: from myocardial infarction to chronic disease. Cardiovascular research, 113(14), pp.1708-1718.
Yang, L., Wang, B., Zhou, Q., Wang, Y., Liu, X., Liu, Z. and Zhan, Z., 2018. MicroRNA-21 prevents excessive inflammation and cardiac dysfunction after myocardial infarction through targeting KBTBD7. Cell death & disease, 9(7), pp.1-14.
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