Myocardial Infarction as a Leading Death Cause

Abstract

Coronary heart disease is a condition caused by decreased blood flow to the heart muscle due to atherosclerotic plaque and deposition of different substances that lead to narrowing of the coronary arteries, the plaque or even clotting is because of obesity unhealthy lifestyle and genetic factors as well, this decrease in blood supply can cause myocardial infarction or heart attack which can lead to the death of an area of the heart, this damage is irreversible and some morphological changes occur and a scar is formed. The most dangerous part is the complications that can result like decrease cardiac output and the heart being unable to pump enough blood to the body (heart failure), also difficulty of breathing, pericarditis, cardiac rupture, ventricular fibrillation, septal defects and aneurysm. Treatment is mediated through avoiding smoking, sugars, soda drinks, alcohol and fats in diet, also regular exercising and fat loss. Also using beta-blockers, aspirin, nitroglycerin and cholesterol medications to dilate the arteries and improve blood supply to the heart, also surgeries if required like stent replacement and coronary bypass.

Introduction

Ischemic heart disease also known as coronary artery/heart disease is a disease or condition caused by narrowing of coronary arteries that cause reduced blood thus oxygen to be delivered to the heart muscle causing chest pain known as angina pectoris ,which can also lead to heart attack. Also some people may have an ischemia that’s silent meaning with no angina, which can lead to a sudden heart attack (with no precedent warning).

Aim of this work: is to discuss the causes or etiology of ischemic heart disease as well as the risk factors, clinical presentations, MI features, myocardial necrosis related complications.

Causes and risk factors of ischemic heart disease include:

1. The buildup of an atherosclerotic plaque in walls of coronary arteries which supply the heart and other parts of the body. Cholesterol depositions also other substances as well is was builds up the plaque and causes the arteries to narrowen and hinder blood flow, as shown in the illustrative figure below.
2. Other causes/risk factors that’s controllable like: Smoking and high blood pressure as they causes damage arteries endothelium and contribute to the buildup of plaque and blood clotting. Also high cholesterol levels contribute the plaque. In addition to age ,obesity, diabetes (high blood glucose) , stress and anxiety and drinking alcohol.
3. Family history and genetics. Coronary artery disease causing disorders (risk factors) can be hereditary as genetics influence the strength of blood vessels and even the communications of heart cells and specific proteins so the body deals with cholesterol and process it differently and therefore affect the risk of developing plaques, ischemic disease and heart attacks. Genetics pass from parents to their children in deoxyribonucleic acid (DNA) through the sperm and the egg and the genes are copied into every cell. Hence, if a family member got a condition of heart disease this gives more reason for the family members to check on their cardiovascular system integrity.

The clinical presentations: they are often not the same in men and women. It’s probably chest pain as a stable condition on angina, heart failure and acute coronary syndrome or maybe even sudden cardiac arrest. Scarcely symptoms are hidden and the only presentation is an abnormal cardiac electrocardiogram or echocardiogram ordered by coincidence for another reason.

Also acute myocardial infarction as ischemic heart disease is sometimes diagnosed when a patient presents with chest pain and acute infarction due to thrombosis and arterial occlusion.

Dyspnoea or difficulty in breathing also occurs and is called the angina equivalent. Mechanism is probably the same as angina, but central appreciation of the afferent stimuli is not the same. Hence dysponea is often associated with angina as the difficulty in breathy is accompanied by chest pain. Dyspnoea is also associated with ischemic left ventricle that results in pulmonary venous congestion that causes pulmonary edema.

The association of presentation of dyspnoea, fatigue, and edema happens in cardiac failure, as atherosclerosis is a common cause in some areas for cardiac failure.

Atrial fibrillation and ventricular tachycardia are also important presentation that may occur. Acute myocardial infarction and ventricular fibrillation can lead to sudden death as well. History of angina, physical examination and some investigations as electrocardiogram, x-ray on chest and blood tests are very important regarding diagnosis.

The morphology of a myocardial infarction develops as time goes by and shows the arterial damage and the healing, as ischemia causes coagulative necrosis accompanied by acute inflammation. The inflammatory infiltrate is later replaced by granulation tissue and fibrosis occurs. 

During the First 12 Hours, very simple histological changes in myocardium are noticed. After four hours of blockage myocardial edema occurs due to damaged endothelial cells and ruined capillaries and wavy-shaped fibers appear due to separation of cardiac myocytes by the edema’s fluid. Also contraction bands appear due to calcium influx and contraction of the fibers of these separated myocytes.

During the period from 12 to 72 hours, pallor and a frame of red ring appear in the infarcted tissue. Also coagulative necrosis  becomes more obvious. By around eighteen hours, neutrophils begin to infiltrate from the lesion's borders. A very acute inflammation starts by the 2nd day and reaches its peak by the 3rd. During the period of 4 to 10 days, lesion becomes increasingly soft and yellow, and macrophages replace neutrophils and phagocytosis and degradation of necrotic tissue stars which negatively affects the integrity of the myocardial structure and can cause myocardial rupture, also fibroblasts and new capillaries begin to reach the lesion from borders to create a zone of granulation tissue. During the period of 10 days to 8 weeks all dead tissue is removed by phagocytes and granulation tissue is reorganized into a scar.

Myocardial infarction can lead to some complication; as sudden death often because dysrhythmia and ventricular fibrillation. Dysrhythmias are the most common complication, though they are very dangerous to the patient’s life, they mostly get only self-limiting dysrhythmias with minimal haemodynamic consequences.The dysrhythmias that happen late which is after 48 hours are reflect the extent of ventricular damage. They indicate an adverse prognosis and may reoccur, while the early ones (24-48 hours) ,due to ischemia, are unlikely to reoccur and they don’t indicate the size of infarction.Also cardiogenic shock occur in fifteen percent of patients due to great damage to the myocardium that’s irreversible, those who lost more than 40% of functional myocardium are at major risk. The first 24 hours witness the most deaths.Early measure to treat dysrhythmias, and decrease the infarction may seem helpful.After these complications, Cardiac rupture is a major cause of death following the acute myocardial infarction, it complicates around 10% of acute infarctions in healing stages at five to nine days.Beta-blockers are used to decrease risk of death.Extensive infarction and hypotension also complicate the case more and increase risk of death, also heart failure is a very severe complication in 25-50% of the patients with acute infarction for myocardial infarction due to inability to provide enough cardiac output for the requirements of the body. Other complications are angina, thromboembolism, pericarditis, ventricular septal defect, ventricular aneurysm, dressler’s syndrome, Ruptured papillary muscles, Shoulder hand syndrome and depression.

Treatment is through changing lifestyle by eating healthy foods, exercising , losing fat and medications like aspirin as a blood thinner to help prevent clotting, nitroglycerin to expand blood vessels and improve heart blood supply and beta-blockers to decrease heart rate and reduce oxygen demand to protect the heart from heart attacks or calcium channel blockers instead. Surgeries are sometimes necessary like angioplasty or stent replacement by a wire with a balloon that expands to improve blood supply or coronary bypass.

Conclusion

Decreased blood supply to the heart is what causes coronary artery disease resulting in heart attacks, myocardial necrosis and different dangerous complications like heart failure. Treatment is through healthy lifestyle, medications or surgery if needed.

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