An Overview Of Myocardial Infarction Disease

Introduction

As we all know one of the most dangerous diseases which many people are complaining about it or may be passed away because of it, is heart diseases especially myocardial infarction (MI), which has high mortality rate. MI happens due to dying of the part of the cardiac muscles, because of occlusion one of the coronary arteries, and it leads to this part of cardiac muscle which supplied by this artery, does not get enough oxygen. There are many factors which contribute in increasing the chances of developing heart attack like (smoking, obesity, and psychological factors). In this essay I will talk about the myocardial infarction, how does it happen, and what are those organs are affected and the way of diagnosis of MI, and the surgical and medicinal treatments for heart attack, then I will talk about the types of the heart attack and the different between them and the way of diagnosing them, and finally I will talk about social impacts on patents with MI. 

Myocardial infarction

Myocardial infarction (is also called heart attack), is a disease which affects many organs in our body, these organs are (heart, coronary arteries and lungs). As we know our heart has four main arteries and two of them are large, branching arteries (coronary artery) that supply oxygenated blood to muscles of the heart (myocardium). Myocardial infarction happens when the heart muscles don’t get adequate level of oxygenated blood for long enough, this causes death of heart tissue, almost all heart attacks are ultimately a result of endothelial cell dysfunction. Endothelial cells responsible for slipper of this contents which is transported by the blood, because of dysfunction (may because tobacco, age or any other factors) leads to irritates or inflames the slippery inner lining of artery, and this place in which this dysfunction has occurred it would be the site of arthrosclerosis which is the type of coronary artery disease (CAD) in which the fat, cholesterol, calcium, WBCs and proteins build up and start to block the coronary artery. This amount of stuff is composed of two parts (soft interior and hard shell) and all of them is called plague, and usually it takes years to build up, and this plague often partially blocks the coronary artery, and in the site of the plague the rate of the blood flow would be increased because of the decrease in cross section of the artery (Bernoulli’s equation) and this is lead to rupturing the hard shell of the plague, after the plague rupture the soft interior of the plague (fat, cholesterol, etc.) is exposed to the blood and fat, cholesterol and other components of soft interior of plague are all thrombogenic which means when the encounter the blood they attract with monocytes and macrophages and platelets which means blood clot formation is formed via thromboses process, and because of this blood clot, now the entire coronary artery is blocked and this part of myocardium which supplied oxygenated blood by this blocked coronary artery, starts to die because this part of heart muscle doesn’t have enough oxygen and another nutrients so the mitochondria of which can produce ATP. But not all heart attacks is originated from arthrosclerosis it may happen when the provided oxygen is smaller than the oxygen demand or heart attack may be occurred by spasm of the coronary artery which is a temporary and sudden condition in which the tightening and the contraction of coronary arteries occur and may this tightening make the coronary artery block entirely and stop supplying blood to the heart, and if this last for long enough it would be the heart attack. As it's mentioned above the heart attack can affect the lungs In acute myocardial infarction (AMI), alveolar interstitial edema is generally related with disturbance hydrostatic. However, inflammatory burden and hemodynamic stimulation might harm the micro vascular endothelial, eliciting interstitial overflow and changing alveolar-capillary gas diffusion. The inflammatory burden carried by the lungs in the case of AMI or the neural/hormonal stimulation elicited by an abrupt coronary occlusion are putatively blamable to damage the micro vascular pulmonary endothelial barrier, which is critical in stopping interstitial fluid overflow and deterioration of alveolar-capillary gas diffusion. A prognostically severe complication of acute myocardial infarction (AMI), is currently interpreted as the result of an imbalance in hydrostatic forces by severe myocardial damage and left ventricular (LV) dysfunction and/or mitral insufficiency. A less striking form of pulmonary edema after AMI is a large amount of fluid move out from capillaries to the alveolar interstitial without alveolar space flooding. Patients with MI may have some symptoms including vomiting, dizziness, dispnea, looking pale, sweating, chest pain and faintness. 

Investigations

• ECG/EKG (electrocardiography) 

It is a series of electrical traces taken around the long and short axes of the heart that reveals heart rate and rhythm and conduction defects. In addition, it demonstrates the overall function of the right and left sides of the heart and points of dysfunction. Specific changes in the ECG relate to the areas of the heart that have been involved in a myocardial infarction. For example, a right coronary artery occlusion produces infarction in the area of myocardium it supplies, which is predominantly the inferior aspect; the infarct is therefore called an inferior myocardial infarction. The ECG changes are demonstrated in the leads that visualize the inferior aspect of the myocardium (namely, leads II, III, and aVF). 

• Chest radiography 

It shows the hearts size and the chambers of the heart are narrow or not. Careful observation of the lungs will demonstrate excess fluid (pulmonary edema), which builds up when the left ventricle fails and can produce marked respiratory compromise and death unless promptly treated. 

• Blood tests

The heart releases enzymes during myocardial infarction, namely lactate dehydrogenase (LDH), creatine kinase (CK), and aspartate transaminase (AST). These plasma enzymes are easily measured in the hospital laboratory and used to determine the diagnosis at an early stage. Further specific enzymes termed isoenzymes can also be determined (creatine kinase MB isoenzyme [CKMB]). recent tests include an evaluation for troponin (a protein of the heart muscles), which is excreted into the blood when cardiac cells die during heart attack. 

• Exercise testing

Patients are connected to an ECG monitor and exercised on a treadmill. It shows you those regions of your heart which didn’t get enough blood supply, and shows you the occlusion of coronary arteries as well. 

• Nuclear medicine

Thallium (a radioactive X-ray emitter) and its derivatives are potassium analogs. They are used to determine areas of coronary ischemia. If no areas of myocardial uptake are demonstrated when these substances are administered to a patient the myocardium is dead. 

• Coronary angiography

Small arterial catheters are maneuvered from a femoral artery puncture site through the femoral artery and aorta and up to the origins of the coronary vessels. X-ray contrast medium then is added to show the coronary vessels and its branches. If there is any narrowing (stenosis), angioplasty may be carried out. In angioplasty tiny balloons are passed across the narrowed areas and inflated to reopen the vessel and so prevent more coronary narrowing and heart attack. 

Common heart attack treatments

We have two types of treatments for MI which are:

Surgical:

-Coronary angioplasty

It is the procedure by which the narrowed coronary arteries would be opened, first the thin tube(catheter) is inserted into an artery and pass it into the narrowed artery using x-ray imaging then inject an amount of dye through the catheter to the artery to find out any blockages on the x-ray images and then doctors insert another catheter with the balloon on the tip is then inserted through the first catheter and transmitted to the heart, when the second catheter reaches the blockage artery in the heart, the doctors inflate the balloon to reopen the artery and improve the blood flow, after that the doctor insert anther catheter with stent (is used for preventing re-narrowing the artery)after that the catheter will be removed. 

• Artificial heart valve surgery

It is a procedure one of the valves of the heart is removed by surgery and replaced by artificial one. 

• Bypass surgery

It is the procedure in which we leave that blockage artery in place but we go beyond that blockage and feed that artery with the new inlet for fresh blood supply. 

• Cardiomyoplasty

It is the surgical procedure where skeletal muscle mainly (latissimus dorsi muscle) is transformed to make the myocardium stronger. 

• CABG (coronary artery bypass graft)

It is transporting blood from aorta to blockage artery through a thin, small tube in order to provide blood to heart. 

Medications:

• Anticoagulant (like heparin and warfarin)

These drugs are used to slow down the process of thrombogenesis. 

• Thrombolytic (like streptokinase)

It dissolves this blood clot which have formed inside the arteries, like it is mentioned above that blood clot is the main cause of Myocardial infarction, So thrombolytic is very useful medication for this condition. 

• Antiplatlets (like aspirin)

This drug works like a barrier because it prevents the platelets to sticking to each other. 

• Beta blocker

These medication works like an inhibitor which inhibits the adrenaline receptor by which it prevents adrenaline and noradrenalin to do their works (increase the rate of the heart and its output). The heart beats are decreased by beta blockers, by which the blood pressure is also decreased. 

• Calcium channel blocker

One of the most important ions for muscle contraction is calcium, and it blocks the calcium channel to transport calcium to myocytes of heart and blood vessels in the result. It decreases the cardiac pumping strength and relaxes the blood vessels. 

• Cholestrol lowering medications

Like it is name, it lowers the cholesterol concentration in the blood, and it decreases the ratio of forming plague in the vessels. 

• Vasodilator

These treatments relax the smooth muscles of blood vessels specifically; because of this the diameter of blood vessel and the blood flow increase while the heart workload and the blood pressure decreased. 

Social impacts of cardiac diseases

The effects of cardiovascular disease (CVD) are not restricted in physical health only, but also affect social life of the patient as well. Because of the cardiovascular diseases (CVD) are chronic diseases, may make the patient feel anxiety and worried about his/her future. And this diseases especially cardiovascular disease (CVD) may put some barriers on those actions which patient had previously been used to. And this restrictions like (physical, social, mood) limitations, and maybe these limitations would be make the patient become depressed. Many studies have shown that most of the patients who have heart diseases, have depression and also show that heart disease have a large effect on mental health as well as physical health. And maybe patients also afraid about surgery or go back to the hospital again or maybe worried about his/her parents or maybe they have afraid or death. 

Types of MI

We have three major types of MI which are (STEMI, unstable angina (UA), NSTEMI):

• STEMI

It stands for ST elevation of myocardial infarction, and also known as a classic heart attack. STEMI is serious type of heart attack because in this type the arteries are completely blocked with the plague, and in STEMI the ST segment in ECG is not flat (while in the ECG of normal person the ST segment is flat), but it will be elevated and also the Q wave will progressed, and the level of the troponin and creatine kinase will be elevated, and it is the most common type of myocardial infarction. 

• NSTEMI

It stands for non-ST elevation of myocardial infarction, and it is less serious than STEMI because the artery is not blocked completely but partially, in NSTEMI the ST segment in ECG is depressed (the T wave is not inversed) or the T wave is inversed (the ST segment is flat), but there is no progression in Q wave, like STEMI the troponin and creatine kinase concentration in blood are elevated. 

STEMI and NSTEMI can’t be distinguished by symptoms because their symptoms are the same. The only way is ECG. 

• Unstable angina

It is another type of myocardial infarction, like NSTEMI the artery is blocked partially, because of that they are very similar to each other but we can distinguish them by concentration of the troponin and creatine kinase in blood somehow in the unstable angina there will be no elevation cardiac troponin and creatin kinase. 

Conclusion

Myocardial infarction is a heart disease in which cardiac muscles die, due to they don’t get enough blood supply to perform their normal job, this happened because the plaque and blood clot block the coronary arteries and don’t let the blood to reach the heart. We have three types of myocardial infarction which are (STEMI, NSTEMI and unstable angina). In STEMI the coronary artery is completely blocked, but in NSTEMI the coronary artery is partially blocked as well as unstable angina, but the difference between NSTEMI and unstable angina is those enzymes concentration in blood which is released by dead cardiac myocytes. Myocardial infarction can be diagnosed by many mechanisms, and the most common ones are (ECG in which the electrical impulses of the heart change during the myocardial infarction, blood tests, catheter and exercise test), and myocardial infarction is treated by two ways, one of them is (surgical operations) like (angioplasty, bypass surgery and CABG), and another one is (medicinal treatments) like (anticoagulant, Antiplatelet and beta blocker drugs), finally heart attack can affect our social life through avoid us from many things, and this can lead to depression and restriction. 

References

• Тiranjan. o. cardiovascular diseases: myocardial infarction, Boston, 2019
• Saleh, M. , & Ambrose, J. A. , understanding myocardial infarction, an francisco, 3 sep 2018
• Burak. p, managment of myocardial infarction, myocardial infarction, Istanbul, turkey, 2019
• Maurizio D. G. , Evolving changes in lung interstitial fluid content after acute myocardial infarction: mechanisms and pathophysiological correlates, milano, 8 jan 2008
• Romagnoli E, et al. : Radial versus femoral randomized investigation in ST-segment elevation acute coronary syndrome: the RIFLE-STEACS (Radial Versus Femoral Randomized Investigation in ST-Elevation Acute Coronary Syndrome) study, J Am Coll Cardiol 60:2481–2489, 2012. 
• Salim Yusuf, MRCP, DPhil; Janet Wittes, PhD; Lawrence Friedman, MD, clinical cardiology, Treatments Following Myocardial Infarction, canada, Herbert J. Levin, 1988
• Shirly J, ECG Success: Exercises in ECG Interpretation, 1st ed, F. A. Davis Company, 2007