Figure 1 is a specimen showing Myocardial Infarction. There is severe myocardial scarring due to ischemia in the apex of the heart, the left ventricle and the Interventricular septum. The scarred tissue has no contractile function (i.e. complete loss of function due to scar formation) therefore the left ventricle has reduced overall contractility resulting in a diminished cardiac output. The wall of the left ventricle has gone through significant hypertrophy.
The myocardium of the heart is functionally contractile and requires a good blood supply to maintain this function. When the blood flow to this tissue is impaired, it sets in motion a process referred to as Ischemic Cascade. In this process cells of the affected tissue are killed either by necrosis or apoptosis, after which the regeneration of the tissue and its function cannot occur (Keith L. Moore, 2010). Instead, through the process of healing, a fibrous scar is formed. The formation of this fibrous scarring can lead to arrhythmias in the heart. In the region of the enlarged ventricular wall the individual myocardial cells have undergone a process of hypertrophy in response to the increased load on these fibres. Hypertrophy is the enlargement of the muscle fibre cells due to an increase in Actin and Myosin protein numbers and produces increased strength of the muscle (Keith L. Moore, 2010).
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Myocardial infarction is primarily caused by the gradual formation of an atherosclerotic plaque in a blood vessel that feeds the myocardium of the heart such as the anterior descending branch of the left coronary artery (Peter Libby, Paul M. Ridker, & Attilio Maseri, 2002). As the atherosclerotic plaque increases in size and accumulates debris from the blood, it begins to occlude the vessel and becomes unstable. The atherosclerotic plaque is the main cause of myocardial infarction because if the plaque ruptures, it results in the formation of a blood clot (thrombus) which blocks the blood flow to the tissue hence rendering the tissue ischemic and thus leading to myocardial infarction (Peter Libby, Paul M. Ridker, & Attilio Maseri, 2002).
An atherosclerotic plaque formation results from a condition referred to an Atheroma. This is the swelling of arterial blood vessel walls due to the accumulation of cholesterol and other fatty materials in blood vessels and the thickening of the walls of the vessels (Peter Libby, Paul M. Ridker, & Attilio Maseri, 2002). The accumulation of low density lipoproteins (fatty materials) leads to an inflammatory response due to damage done to the arterial wall by the oxidized lipoproteins and involving a gathering of macrophages. These macrophages attempt and fail to process the damaging lipoproteins once they have phagocytised them, rupture themselves thus releasing cholesterol and further enhancing the inflammatory response (Peter Libby, Paul M. Ridker, & Attilio Maseri, 2002).The muscle fibres grow in size and form a hard cover in response to the cholesterol plaque which results in the narrowing and hardening of the arterial blood vessel.
When an atherosclerotic plaque ruptures it generates a thrombus. A thrombus is the product of the haemostasis process and specifically the blood coagulation step (Peter Libby, Paul M. Ridker, & Attilio Maseri, 2002). The mechanism of how a thrombus generates is through platelet aggregation which forms a platelet plug (Peter Libby, Paul M. Ridker, & Attilio Maseri, 2002). It is this thrombus that occludes the blood vessel, preventing blood flow to the tissue and hence resulting in myocardial infarction of that tissue due to ischemia.
The myocardial infarction is damaging to the heart as it reduces the functional capacity of myocardium in the affected areas (Keith L. Moore, 2010). Due to the loss of blood flow and the essential nutrients and oxygen that it brings, the cells affected will experience irreversible cell injury if this is maintained for a long enough period of time. When cells suffer irreversible cell injury, they undergo cell death either by necrosis or, depending whether the cell has sufficient energy or time, apoptosis (Peter Libby, Paul M. Ridker, & Attilio Maseri, 2002). Following the death of the myocardial cells and the subsequent inflammatory response, the tissue undergoes the process of healing. This involves the cleaning up of the cellular debris due to necrosis and the subsequent organisation of the tissue into granulation tissue. This turns the injured tissue into stable tissue which is then converted into a fibrous scar once vessels have regressed and the collagen fibres have reorganised (Peter Libby, Paul M. Ridker, & Attilio Maseri, 2002).
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This scarring has a physiological effect through arrthymias. Two arrthymias that the scarring causes is ventricular fibrillation and ventricular tachycardia. Ventricular fibrillation is the uncoordinated, chaotic contraction of the ventricle. These contractions are ineffective in pumping the blood and can result in sudden cardiac death (Keith L. Moore, 2010). Ventricular tachycardia is the rapid beating of the ventricle which has reduced cardiac output and can lead to ventricular fibrillation (Keith L. Moore, 2010).
The inflammatory response is central to the formation of atherosclerotic plaques which in themselves can lead to myocardial infarction. Therefore, the risk of myocardial infarction is related to the degree of the inflammatory response and its intensity. In epidemiological studies it has been found that individuals with a higher prevalence of pro-inflammatory polymorphisms and a low incidence of anti-inflammatory polymorphisms have a genetic predisposition to myocardial infarction (Incalcaterra E, 2010).
The most frequent symptom associated with acute myocardial infarction is chest pain localised to the chest but pain can spread to the left arm and lower jaw (Prof KAA Fox, 2002). Other symptoms are shortness of breath which is a consequence of the damaged myocardium and hence reduced cardiac output (Prof KAA Fox, 2002). Shortness of breath usually arises with minimum exertion.
Methods for making a diagnosis for acute myocardial infarction include carrying out an Echo Cardiogram (ECG) to investigate arrthymias that could be present with myocardial infarction and to provide information of the location of the infarction (Prof KAA Fox, 2002). A coronary angiogram can be carried out which depicts the obstruction of the coronary artery that feeds the damaged tissue (Prof KAA Fox, 2002).
The primary goal in treating acute myocardial infarction is to restore blood flow. This can be achieved by treatment of anti-platelet agents which interferes with platelet adhesion in the thrombus that occludes the coronary artery (Prof KAA Fox, 2002). Patients with acute myocardial infarction are given supplement oxygen to try to maintain erythrocyte oxygen saturation which usually is reduced due to the lowered cardiac output (Prof KAA Fox, 2002). If it is an emergency situation, patients can undergo surgical revascularization which involves Coronary Artery Bypass Grafting to restore blood flow (Keith L. Moore, 2010).
The in-hospital risk of mortality after acute myocardial infarction is around 15 to 20%, but this can vary according to age, lifestyle choices and previous medical history such as diabetes (Achuff, 1981).