Analysis of Myocardial Infarction - Essay Example

MYCARDIAL INFARCTION By 20 March Myocardial Infarction Introduction Myocardial infarction is often cited among the leading causes of human death. Caused by the death of a heart muscle, myocardial infarction (or, simply, heart attack) usually reflects in chest pain and the feeling of chest pressure. Timely identification and diagnosis of myocardial infarction in all groups of patients is the basic prerequisite for saving thousands of lives. Timely and proper diagnosis, however, is possible only with the detailed knowledge of myocardial infarction etiology, pathogenesis, and with continuous monitoring of the disease progression. Thus, scientists do their best to make it possible to reveal the danger of myocardial infarction in patients timely in order to save their lives. This paper will seek to discuss the topic of myocardial infarction in detail, including prevention/ treatment options and recommendations for future research. Etiology Myocardial infarction can be defined as “the irreversible damage of myocardial tissue caused by prolonged ischemia and hypoxia. In simpler terms, myocardial infarction is caused by the death of one of the heart muscles which, in its turn, leads to irreversible changes in the heart function and, in many cases, to death” (Sharis & Cannon 2003). Professionals in cardiac studies usually link myocardial infarction etiology to complete focal blockage of one of the coronary arteries or their branches. The latter reflects in and leads to impaired contractility of one of the heart muscles but does not extend beyond the affected heart segment (Sharis & Cannon 2003). The myocardial ischemia begins in the inner lining of the heart, called endocardium and then spreads to the outer heart lining (epicardium); the risks of irreversible heart damage significantly increase if the complete blockage lasts 15-20 minutes (Sharis & Cannon 2003). Irreversible damage covers the affected segment and occurs within the first 2 or 3 hours following the infarction (Sharis & Cannon 2003). Restoration of the blood flow and heart activity is associated with the salvation of the heart muscle, and the earlier the salvation occurs the better the heart and blood flow will be. The size of the affected area is the determining factor of death of infarction, and increased oxygen supply to the site of blockage is believed to be a more effective instrument of salvaging the heart muscle, compared to reducing oxygen demand (Sharis & Cannon 2003). A whole set of modifiable risk factors contributes to the development of myocardial infarction risks in different population groups – smoking, diabetes, obesity and inactivity, and hypertension are, probably, the most important factors to consider in the discussion of myocardial infarction. Pathogenesis The onset of acute myocardial infarction usually occurs in the morning, shortly after waking up, due to the increased adrenergic activity, increased blood fibrinogen levels, and increased blood cell adhesiveness – these are the basic features in pathogenesis of Q-wave myocardial infarction (Sharis & Cannon 2003). In case of non-Q-wave myocardial infarction, the initial stages of pathogenesis are basically similar, including coronary occlusion and vasoconstriction (Sharis & Cannon 2003). Yet, there are significant differences in the pathogenesis between these two forms of myocardial infarction. First, the incidence of complete coronary occlusion in non-Q-wave infarction patients in no more than 20-30%, compared to 80-90% in Q-wave (Sharis & Cannon 2003). Second, the size of a non-Q-wave infarction is much less than that of Q-wave infarction (Sharis & Cannon 2003). Non-Q-wave infarction is connected with high incidence of reperfusion-induced contraction necrosis, but acute mortality rates for this type of infarction are only 2-3 percent, against potential 10 percent for Q-wave infarction (Sharis & Cannon 2003). Despite these differences, the progress and the symptoms of myocardial infarction are mostly the same: the loss of viable myocardium negatively affects the quality of global cardiac function, leading to reduced cardiac output and, in case of severe damage, to cardiogenic shock (Sharis & Cannon 2003). Impaired left ventricular function reflects in edema and pulmonary congestion, while abnormal cardiac rhythms continue threatening the heart function and increase death risks (Sharis & Cannon 2003). Reduced cardiac output and the changes in arterial pressure result in the development of the so-called baroreceptor reflexes, which activate sympathetic nerves and neurohumoral compensatory mechanisms: that is why patients with diagnosed myocardial infarction experience pain, anxiety, and fear (Sharis & Cannon 2003). The latter activate the sympathetic nervous system, causing cardiac stimulation and vasoconstriction that manifest through tachycardia and hypertension (Sharis & Cannon 2003). It should be noted, that sympathetic activation during acute myocardial infarction helps patients to maintain arterial pressure but, simultaneously, increases myocardial oxygen demand, leads to myocardial hypoxia, precipitates arrhythmias, and can even enlarge the area affected by the infarction (Sharis & Cannon 2003). That myocardial infarction patients sweat is also the result of the sympathetic activation (Sharis & Cannon 2003). Epidemiological aspects In the current state of health and medicine, coronary heart diseases are the most usual reason of death in the world, and the average incidence of myocardial infarction for the population groups aged between 30 and 70 is about 610 per 100,000 of men and 230 per 100,000 of women (Thygesen, Alpert & White 2007). The incidence of myocardial infarction increases with age, and elder populations face higher risks of mortality and morbidity with their infarcts. Age is the determining risk factor followed by gender, family history, and premature menopause in women (Roger 2007). Ethnicity is also one of the significant factors in the development of acute myocardial infarction – Asians and blacks face higher risks of myocardial infarction (Roger 2007). A whole set of modifiable risk factors contributes to the development of myocardial infarction risks in different population groups – smoking, diabetes, obesity and inactivity, and hypertension are, probably, the most important factors to consider in the discussion of myocardial infarction. When discussing myocardial infarction epidemiology, special attention should be paid to the new definition of the disease, offered by the American College of Cardiology and the European Society of Cardiology in 2000. The new definition implies that myocardial infarction is “the rise and fall of biochemical markers of myocardial necrosis with any of the following conditions: ischemic symptoms, ECG changes, and coronary intervention” (Roger 2007). Insignificant at first glance, these changes in the definition of myocardial infarction produce dramatic effects on how the disease and its complications are being diagnosed; as a result, the general epidemiology picture becomes more objective and complete. For many years epidemiological investigations of myocardial infarction did not account for a broad range of acute coronary syndromes, as far as the latter did not meet valid infarction criteria (Roger 2007). Having myocardial infarction redefined, epidemiologists will have to incorporate the new criteria in their surveillance procedures. Nevertheless, in the current state of knowledge about coronary syndromes and myocardial infarction these syndromes will not display any significant epidemiology variations, compared with those that have been discovered and diagnosed until present. Strategy and methods used to establish the diagnosis in clinical contexts When the new definition was created, alterations have been also made in standardized approaches to diagnosing myocardial infarction in clinical contexts. Generally, clinicians use a combination of clinical events and the results of laboratory tests to establish and confirm the presence of myocardial infarction in patients (Thygesen, Alpert & White 2007). The clinical diagnosis cannot be established, unless both laboratory tests and a specific combination of clinical events support the assumption. Today, troponin is the basic biomarker applied to establish the presence of myocardial infarction in all groups of people (Antman 2001; Thygesen, Alpert & White 2007). Typical changes on ECG and history must support troponin test results (Thygesen, Alpert & White 2007). “The 99 percentile of the upper reference limit (URL) of normal for blood measurement of troponin should be exceeded in order for the clinician to diagnose an acute MI” (Thygesen, Alpert & White 2007). Clinicians may also use non-invasive imaging tests, and even if required ECG changes are absent, a ventricular wall abnormality and the characteristic elevation of troponin values can altogether confirm the presence of myocardial infarction (Antman 2001). Despite recent scientific developments, almost one-third of myocardial infarctions go unrecognized (Sigurdsson et al 1995). The problem is in that clinical manifestations of coronary heart diseases vary considerably, and clinicians find it difficult to account for all changes and symptoms that could support the presence of myocardial infarction in patients. In most cases, troponin values and ECG changes can suffice to define the presence of acute myocardial infarction, but clinicians must be willing to apply to imaging tests and patient history, because the information about patient’s prognosis and the chances for full recovery require more than the mere statement that the patient has myocardial infarction (Thygesen, Alpert & White 2007). Progression and monitoring The electrocardiogram is still one of the basic means of monitoring patients with myocardial infarction (Mizelle & Goldstein 1999). Compared to ECG, laboratory plays secondary role in monitoring myocardial infarction progress. In clinical contexts, the use of ECG creates conditions necessary to timely identify and address health abnormalities, and to identify patients at increased risks for ventricular arrhythmias and sudden death (Mizelle & Goldstein 1999). The presence of AV block, QT prolongation, an increase in resting heart rate to 90 beats per minutes and higher, and intraventricular conduction defects are the basic markers used by clinicians to track progression of myocardial infarction (Mizelle & Goldstein 1999). Non-sustained ventricular tachycardia is another nonspecific factor of risk in postmyocardial infarction populations – for example, NSVT that takes place within 3 hours after acute myocardial infarction has serious implications for early mortality (Mizelle & Golstein 1999). The results of ECG must be supported by the results of laboratory and imaging tests, but ECG is still the central and the basic source of information about progression of myocardial infarction in all groups of patients. Treatment/ prevention Given the multitude of MI risk factors, prevention of myocardial infarction risks involves lifestyle changes and lifestyle approaches to health. Smoking cessation, physical activity, appropriate diet, and regular monitoring are likely to reduce the risks and predisposition to myocardial infarction and related coronary complications. But in treating myocardial infarction that has already occurred, the current practice relies on the use of thrombolytic drugs, which should be given within a half an hour of the person’s arrival to the hospital (Gershlick & More 1998). “Thrombolytic drugs have reduced mortality in patients with acute myocardial infarction, current treatments have limited success in achieving immediate vessel patency and in maintaining this in the longer term” (Gerschlick & More 1998), but accelerated tissue plasminogen activator is often used as an effective form of thrombolytic treatment of myocardial infarction patients (Montalescot 2001). Yet, the specific effects and safety of antithrombin drugs and antiplatelet treatments are yet to be discovered (Boden & Mackay 2001). Despite the relative effectiveness of thrombolytic drugs, they can hardly compare to the benefits of coronary angioplasty. Angioplasty results in 95% improved vessel patency, compared with 80% improvements for thrombolytic drugs (Stone, Grines & O’Neill 1997). Unfortunately, only a few patients have a chance to use the benefits of angioplasty, as far as most hospitals that admit myocardial infarction patients do not have necessary interventional facilities (Gerschlick & More 1998). Angioplasty should serve a viable option to those, who have contraindications to thrombolysis, or who face high mortality risks and can be easily transferred to a hospital with the equipment and staff needed to perform angioplasty. Recommendations for future research Timely identification and diagnosis of myocardial infarction in all groups of patients is the basic prerequisite for saving thousands of lives. Timely and proper diagnosis, however, is possible only with the detailed knowledge of myocardial infarction etiology, pathogenesis, and with continuous monitoring of the disease progression. This paper proves a simple thesis that the state of knowledge about myocardial infarction constantly evolves, while the rates of mortality and morbidity associated with myocardial infarction slowly, but steadily decrease. Yet, there is still much room for improvement, and much time will pass before myocardial infarction is no longer the primary cause of human death. Despite recent scientific developments, almost one-third of myocardial infarctions go unrecognized (Sigurdsson et al 1995). The problem is in that clinical manifestations of coronary heart diseases vary considerably, and clinicians find it difficult to account for all changes and symptoms that could support the presence of myocardial infarction in patients. For many years epidemiological investigations of myocardial infarction did not account for a broad range of acute coronary syndromes, as far as the latter did not meet valid infarction criteria (Roger 2007) Having myocardial infarction redefined, epidemiologists will have to incorporate the new criteria in their surveillance procedures. Nevertheless, in the current state of knowledge about coronary syndromes and myocardial infarction these syndromes will not display any significant epidemiology variations, compared with those that have been discovered and diagnosed until present. Taking into account the multitude of MI risk factors, prevention of myocardial infarction risks involves lifestyle changes and lifestyle approaches to health. Smoking cessation, physical activity, appropriate diet, and regular monitoring are likely to reduce the risks and predisposition to myocardial infarction and related coronary complications. Attention should be paid to how myocardial infarction is diagnosed in clinical contexts: despite recent advancements, clinicians still face difficulties in the process of interpreting the symptoms of acute coronary diseases in patients. Treatment and prevention is another issue of professional concern – obviously, thrombolytic drugs alone cannot suffice to reduce the risks of complications and mortality in postmyocardial infarction patients. Finally, the benefits of technology should be applied to improve the state of monitoring myocardial infarction progression in patients, to make sure that clinicians can timely react to the emerging abnormalities and complications. References Antman, EM 2001, ‘Troponin measurements in ischemic heart disease: More than just a black and white picture’, American College of Cardiology, vol. 38, no. 4, pp. 987-990. Boden, WE & Mackay, RG 2001, ‘Optimal treatment of acute coronary syndromes – An evolving strategy’, New England Journal of Medicine, vol. 344, no. 25, pp. 1939-1942. Gerschlick, AH & More, RS 1998, ‘Recent advances: Treatment of myocardial infarction’, BMJ, no. 316, pp. 280-284. Mizelle, KM & Goldstein, B 1999, ‘Advances in intensive care ECG and cardiac event monitoring’, Cardiac Electrophysiology Review, vol. 3, no. 4, pp. 245-248. Montalescot, G 2001, ‘Platelet glycoprotein inhibition with coronary stenting for acute myocardial infarction’, New England Journal of Medicine, vol. 344, no. 5, pp. 1895-1903. Roger, VL 2007, ‘Epidemiology of myocardial infarction’, Med Clin North Am, vol. 91, no. 4, pp. 537-545. Sharis, PJ & Cannon, CP 2003, Evidence-based cardiology, Lippincott Williams & Wilkins. Sigurdsson, E, Thorgeirsson, G, Sigvaldason, H & Sigfusson, N 1995, ‘Epidemiology, clinical characteristics, and the prognostic role of angina pectoris: The Reykjavik study’, Annals of Internal Medicine, vol. 122, no. 2, pp. 96-102. Stone, GW, Grines, CL & O’Neill, WW 1997, ‘Primary coronary angioplasty versus thrombolysis’, New England Journal of Medicine, vol. 337, pp. 1168-1180. Thygesen, K, Alpert, JS, & White, HD 2007, ‘Universal definition of myocardial infarction’, European Heart Journal, vol. 28, pp. 2525-2538. Read More