Etiology of Myocardial Infarction - Research Paper Example

Myocardial Infarction Heart is the most vital organ in the body. It is the muscular pump that supplies blood to every organ and tissue to sustain life. Its own blood supply is however critical to life. The adequate function of heart depends upon the balance between its own metabolic demand and the supply of blood. An imbalance in this predisposes the heart muscle to ischemia, which means reduced blood flow. The tissue death as a result of ischemia occurs because of two reasons, reduced oxygen supply and the decreased delivery of nutrients, both of which are brought in by the flow of blood though the heart muscle. The area deprived of blood supply is said to have suffered ischemic injury. The ischemic injury, if severe enough to cause the complete block of oxygen and nutrients causes death of the heart tissue, which is termed as Myocardial Infarction (Guyton et al 200, Ganong 2005). Pathophysiology The blood vessels supplying the heart are called coronary arteries. There are three main coronary arteries which supply different areas of heart along with their branches. These are 1) Right coronary artery, 2) Left anterior descending artery, 3) Left circumflex artery. Above 90% cases of myocardial infarction occur as a result of coronary artery blockage, thus the disease is also referred to as coronary artery disease (CAD). The most common and dangerous cause of coronary artery obstruction, and thus MI is Atherosclerosis. Atherosclerosis refers to the narrowing of arteries because of accumulation of atherosclerotic plaques. These plaques are basically thrombi composed of lipid foam cells (cholesterol) and different cell components including smooth muscle, macrophages and collagen fibres. In most instances, the ischemic myocardial infarction is precipitated by the phenomenon called acute plaque change. Acute plaque change results from the rupture of pre-existing thrombi that partially occlude the lumen. The rupture exposes the underlying thrombogenic endothelium. The plaques are also termed as vulnerable plaques as they contain lipids in high amounts, along with collagen fibres and inflammatory cells. When ruptured, the reactivity of these components causes the inflammatory destabilization and result in the infarction (Libby P 2001). The acute phase reactant, C reactive protein (CRP) is thus found to be high during the acute myocardial infarction (Blake et al 2003). The infarction can occur in either of the two patterns, complete occlusion of a single coronary artery referred to as transmural infarct, which results in complete ischemia of the area supplied by that particular coronary artery. Subendocardial infarcts on the other hand occlude the arteries incompletely, and thus allow some perfusion. But since subendocardium is the least perused area of the myocardium, it is more prone to ischemic death. The aim of reperfusion is to save the viable muscle from necrosis (Huber et al 1996). The myocardial injury is reversible for up to 30 minutes after the ischemic attack, thereafter the injury becomes irreversible. The entire muscle becomes necrotic within six hours, if the collateral arteries are not well developed (Robbins et al 2005, Mohan 2007). Etiology of Myocardial Infarction The development of atherosclerotic plaques and pathogenesis of the process into the myocardial infarction is a complex one. It is a chronic disease taking years to evolve before it causes any modifiable consequences. The evolvement is subtle and the resultant damage is severe. The pathogenesis of the disease involves several factors. The balance among these factors in the long run determines the outcome of the condition. These factors can either be modifiable or non-modifiable. The modifiable factors are the ones that a person can control by bringing about certain changes. They include controlling the level of fats in diet, cessation of smoking, regular exercise and maintaining the blood pressure in the normal range (Manson et al 1996). The hyperlipidemias, i.e. elevated low density lipoproteins and cholesterol levels are solid risk factors for the development of atherosclerosis while high density lipoproteins are protective against the risk of atherosclerosis and ultimately the myocardial infarction. Packs of cigarette smoked per day are directly proportional to the risk of development of disease. Cigarette smoke causes the damage on both sides, to the smoker as well as indirectly as the other people around the smoker also suffer. Nicotine deranges the vascular reactivity and causes endothelial damage leading to vascular spasm (Fish et al 2007). Concomitant co-morbidities like diabetes mellitus also increase the risk. The non-modifiable factors, on the other hand are the ones that a person has no control on, like genetic, age, race and gender, etc. The risk of myocardial infarction rises with the increasing age. The risk is overall higher in men; however it rises in women after menopause. Cardiac diseases are known to run in families. They have genetic basis of predisposition. The individuals with a family history of cardiac disease are more prone to suffer and the onset of disease is also at an early stage in life (Mohan 2007, Robbins et al 2005). Diagnosis of Myocardial Infarction Diagnosis is done on the basis of laboratory tests, chest x- rays, electrocardiography (ECG) and magnetic resonance imaging (MRI). When cardiac muscle is damaged, certain enzymes leak out of it. The blood levels of these enzymes are measured to assess the level of damage done to the myocardium. The important ones measured in tests are Cardiac Tropnin T (TnT) and Cardiac Troponin I (TnI), Creatine Kinase (CK-MB), Myoglobin and Lactate Dehydrogenase. These enzymes are the biomarkers to assess the myocardial injury. The most sensitive biomarkers are the troponins and the next is creatine kinase. Initially creatine Kinase was considered to be the Gold Standard, but with the fact that it is not just specific for mycardium and it is released from skeletal muscle injury as well, it has now been replaced by the troponins. The blood levels of these markers (rise and fall) at different time intervals reflect the time elapsed since the ischemic attack and thus help in the assessment of the extent of injury (Robbins et al 2005). The blood level of troponins starts rising within 2 to 4 hours after the initial ischemia and attain the peak level at about 48 hours. They remain elevated for about a week to 10 days after the attack. Creatine Kinase, on the other hand has a quick rise and fall pattern. It starts rising in 2 to 4 hours, attains a peak level in a day, and falls back to normal in about 3 days. Urine myoglobin levels rise in 1-4 hrs of injury which is sensitive, but yet again not specific. LDH rises in 1 to 5 days and lasts for up to 10 days. The ECG results revealed elevated ST segment in anterior lead, with inverted T wave (Otto et al 1994). Chest radiographs give an idea about the size of heart and concomitant chest diseases (Masuda Y et al 1984). Coronary angiography aids the decision of guiding the therapy by revealing the extent of the block. Echocardiography is another process through which myocardial infarction can be diagnosed. A research was carried out to find out the efficacy of echocardiography in comparison to ECG and it was found that the former one is more efficient. In Myocardial ischemia it is seen that the patient suffers from regional wall motion abnormality and this can be best detected with the help of echocardiography (Luotolahti 1999). Treatment Drug therapy revolves around three groups of drugs, 1) organic nitrates, 2) Beta Blockers, and 3) calcium channel blockers. Nitroglycerin is the prototype organic nitrate that gives immediate relief through sublingual absorption by relaxing the vascular smooth muscle tone. It causes dilation of the coronary blood vessels and thus increases the blood flow towards the heart. Apart from that, it also dilates the large veins, resulting in peripheral pooling of blood, thereby reducing the workload on heart (Finkel et al 2009). Beta Blockers reduce the oxygen demand of the cardiac muscle and are used in combination with organic nitrites to enhance exercise endurance. They are however contraindicated in asthmatics and diabetics. Calcium channel blockers (Nifedipine, verapamil) are vasodilators and work by lowering smooth muscle tone and resistance of vessels (Finkel et al 2009)). The lipid lowering drugs, Statins reduce the incidence and severity of the ischemic attacks (Katzung 1987, Ambrose et al 2002). Surgical interventions are available for the long term management of the condition. Percutaneous transluminal angioplasty (PTCA) and coronary artery bypass surgery/ graft surgery (CABG) are the most widely adopted. PTCA is the stenting procedure to recanalize the vessel by inflating the balloon. In coronary artery bypass graft surgery, the occluded segment of the artery is excised and a healthy artery or vein is grafted in its place to restore the flow of blood. This procedure is done when either there are extensive thrombi, large area of myocardium is at risk or when the conservative therapy fails. (Serruys PW et al 2001). The most commonly used vessel for the process of coronary grafting is saphenous vein of the leg. The vein is grafted on one end with the coronary artery cut end, while on the other end t is attached to the aorta for direct blood supply. The surgery is an open chest procedure and takes about four hours to complete. The long term results are very promising, as the average reported survival without complications is ten years. The grafts of Saphenous vein have 50% patency at 10 years (Safian 2002), while those of left internal mammary artery are above 90% patent around same time (Loop et al 1986). These interventions however have their failure rates as well; therefore proper care and follow up are necessary for the long term survival Conclusion Myocardial Infarction is an extensive pathological phenomenon that not only involves the physical factors but is also heralded by several psychological and behavioural factors. Stressful personality is one of the most important behavioural factors. Heart attack as it is commonly known as, is a distressing condition and puts a person in doubts about life ahead. People with type “A” personality develop cardiovascular disease at an early age (Contrada 1989). It is a condition which involves one of the vital organs of the body and should not be overlooked upon. References AMBROSE, J. A., & MARTINEZ, E. E. (2002). A New Paradigm for Plaque Stabilization. CIRCULATION. 105, 2000-2004. BLAKE, G. J., & RIDKER, P. M. (2003). C-reactive protein: a surrogate risk marker or mediator of atherothrombosis? American Journal of Physiology. 285, R1250-R1252. FINKEL, R., CLARK, M. A., CUBEDDU, L. X., COOPER, M., FLATT, C. T., & 'LEARY, L. (2009). Pharmacology: Lippincott's illustrated reviews. Philadelphia [etc.], Lippincott Williams & Wilkins. FISH, J., & BARTHOLOMEW, J. (2007). Cigarette smoking and cardiovascular disease. Current Cardiovascular Risk Reports. 1, 384-390 GANONG, W. F. (2005). Review of medical physiology. 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