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Myocardial Infarction - The Most Common Cause of Death in The World

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The World Health Organization (WHO) has announced cardiovascular disease as the leading cause of death in the developed world. It is a broad term used for the conditions affecting the heart and blood vessels. Although it is a preventable and predictable disease to a large extent, it, along with stroke, claimed the lives of 15.2 million people in 2016 alone. Coronary artery disease is a spectrum of interrelated diseases: stable angina, unstable angina, diffuse coronary artery insufficiency, and myocardial infarction. In this essay, I will describe myocardial infarction (MI), how it develops, what parts of the body it affects, how a case of MI presents i.e. its clinical featuresand finally, what the risk factors and incidence rates between different groups of people are. I will also add a note on the differential diagnosis of MI and the modified effect of diabetes mellitus on patients with MI while simultaneously explaining the fatigue experienced by the patients. Before moving on to those points, however, I will mention the fundamental anatomy and physiology of the heart and coronary vessels to better understand the subject.


The heart is a muscular organ in the center of the chest, below the sternum, slightly tilted to the left. It is the central component of the cardiovascular system. It is about the size of a clenched fist, though it differs in its shape. The heart lies on the diaphragm, a skeletal muscle which separates the thoracic and abdominal cavities. It is easier to visualize the heart as a cone lying on its side. It pumps all the body’s blood to the lungs first, where the oxygen from the alveoli diffuse to the red blood cells, then to the entire body, including the heart itself. It transports this blood through a closed system of blood vessels, the first and most major one being the aorta. Two coronary arteries, the left and right coronary arteries, branch off from the ascending aorta and supply oxygenated blood to the cardiac muscles i.e. myocardium. The left coronary artery further divides into two major branches, the anterior interventricular branch (left anterior descending branch: LAD), and the circumflex branch. While the two major branches of the right coronary artery are the right marginal branch and posterior interventricular. These arteries circle the heart in such a way which resembles a crown, hence the name “coronary” arteries. Clinically, physicians use alternative names for the coronary vessels. The short left coronary artery is referred to as the left main stem vessel. One of its primary branches, the anterior interventricular artery, is termed the left anterior descending artery (LAD). Similarly, clinicians call the terminal branch of the right coronary artery, the posterior interventricular artery, the posterior descending artery (PDA). Now that we have gone over the basic anatomy of the heart and its simplified vasculature, we can move on to our own topic, our topic being the presentation of myocardial infarction, a heart disease. Coronary artery disease is one of the major causes of heart disease. As we mentioned, the coronary arteries supply the myocardium with oxygenated blood, so for the heart to function smoothly and correctly, we need the blood from these arteries to reach the muscles with no blockage or obstruction. Atherosclerosis is a disease of arteries where they become clogged with fat deposits called plaques, also known as atheroma. This causes the stenosis, narrowing of arteries, which as a result decreases the blood perfusion of the target tissues. This is a major, potentially life-threatening disease, especially when the artery which has been narrowed leads to a sensitive organ such as the heart or brain. Though at first, this disease rarely has any symptoms, if left untreated, it may develop into other fatal diseases such as coronary artery disease, which is a spectrum of diseases ranging from angina to unstable angina induced by ischemia, then myocardial infarction because of nearly complete obstruction of the coronary arteries.

Myocardial infarction (MI), or heart attack, is one of the most common causes of heart failure. A typical MI usually occurs when an atherosclerotic plaque ruptures and forms a blood clot that occludes a coronary supply vessel. The myocytes that were supplied blood by the occluded vessel have a few outcomes. The collateral channels may completely ease the effect of the stenosis. Sometimes, the collaterals may provide enough blood during inactivity, but fail to keep up during exertion. This usually results in angina, also called angina pectoris, which is a pressure, squeezing, tightness or pain in your chest. In the case of cardiac ischemia, or the reduced blood flow to the heart, the coronary arteries have narrowed. Myocardial ischemia is because of a combination of fixed vessel narrowing and endothelial obstruction. This leads to an imbalance between cardiac output and demand. There may be even be non-atherosclerotic causes to ischemia such as low perfusion due to low blood pressure, decreased blood-oxygen in cases of anemia and pulmonary disease, and significant increases in heart oxygen demand such as in cases of acute tachycardia and acute hypertension. The obstruction of both venous and arterial sides may lead to the necrosis of myocardial tissue. We call this infarction. There are three crucial factors determining the severity of ischemia, lowered perfusion of a tissue, and whether it will lead to infarction of the myocardium.

The speed of onset is a major factor: If the obstruction is rapid, the effects are far more severe than if it is gradual. Another factor is the extent of obstruction. The more the percentage of occlusion, the more serious the effects. The last factor is the time the arteries have had to form collateral channels, so the age of the person is a good determinant of the intensity of the effects of ischemia i.e. the older the patient, the more time they have had to form collaterals, hence the higher the likelihood of suffering less damage. When a portion of the cardiac muscles die, they get replaced with fibrous tissue, sometimes called scar tissue. This fibrotic portion is rigid and doesn’t work in harmony with the myocardium therefore, it reduces cardiac contractility. The heart is a tough organ. Even though it suffers a lot of damage, it may still survive. Moving on to MI’s risk factors and its prevalence in certain groups, epidemiologists divide them into three groups of factors: major static risk factors, major modifiable risk factors, and contributing risk factors. Age is a major factor. The bulk of people dying by heart attacks are aged 65 or older. Gender is also an important static factor, since males are more likely to suffer a heart attack than females are. Females without hormonal imbalances suffer from MI after they have reached menopause, which on average is 51. The last non-modifiable factor is genetic: Children of patients of MI are more likely to suffer from it. There is also a pattern of inheritance in different races e.g. African Americans have higher blood pressure and are more likely to suffer from heart disease than Caucasians. Moving on to major modifiable factors, a strong and prominent one being smoking cigarettes. The risk that smokers will develop a coronary artery disease is much more than that of nonsmokers. Cigarette smoking also interacts with other risk factors to worsen the effects of both. Smoke from cigarettes will affect anyone who inhales it, including nonsmokers. Hyperlipidemia, another amendable factor, is the abundance of fat in the blood. A higher than normal level of cholesterol and triglyceride increases the risk of coronary heart disease. Another factor of the same category is high blood pressure. High blood pressure increases the work the heart must do, which causes it to become thicker and stiffer. This causes the abnormal functioning of the heart. A sedentary lifestyle also increases the chances of MI since when the body’s activity levels are high, the blood cholesterol levels drop, and it may even lower the blood pressure. One other factor is diabetes. Diabetes is a major risk to developing heart disease even when the blood-glucose levels are under control. The risk is even greater if the blood-glucose levels aren’t controlled. Obese and overweight people should work to change their lifestyles to lose weight, which may be through exercise and or eating better. The contributing factors include stress, alcohol, nutrition and diet, all of which are secondary and minor influences.

When talking about the manifestation of heart attacks in patients, the most symbolic presentation is the clenched fist over the center of the chest signifying the intense, crushing retrosternal pain they are experiencing. The most cardinal symptom of MI is chest pain accompanied by fatigue, but breathlessness, vomiting, and collapse or syncope are common features. The pain occurs in the same location as angina but is usually more severe and lasts longer; patients often describe it as a constriction in the chest. Typical MI cases have chest discomfort and an all-around uneasy feeling of illness prior to the heart attack. The chest pain experienced in MI is dull, non-localized, and vague, meaning the patient cannot pinpoint the exact origin of the pain. It is typical for the pain to be in the center of the chest, however, this pain may radiate to the left upper arm and shoulder, lower neck, jaws, and rarely the lower arm and back. In some cases, it may only show up in the radiated areas and not the chest itself. The cardiac pain is usually induced by exertion, exercise, stress, and heavy meals. The pain is mostly relieved by rest after a few minutes of severe discomfort. In contrast to cardiac pain, the pleural or pericardial pain is described as a sharp sensation which is worsened by breathing, coughing, or moving. Pain associated with a specific movement (bending, stretching, and turning) is likely to be musculoskeletal. MI commonly takes a few minutes to develop. Similarly, angina builds up gradually in proportion to the intensity of exertion. Pain that occurs after, rather than during, exertion is most likely to have originated from the musculoskeletal system or a psychological abnormality.

Other than the symptoms and signs, there are constitutional effects that accompany infarctions of any significant extent. Fever is one of these effects, and another one being the release of enzymes by the necrotic tissue into the bloodstream, which may be of diagnostic help.

A small infarct triggers short- and long-term compensatory mechanisms simultaneously. Short-term events help maintain output until the long-term pathways have had time to fully activate. There are both local and central short-termed reflexes. Interruption of blood flow to the myocytes causes interstitial metabolite levels (e.g., adenosine, potassium cation, carbon dioxide, lactate) to rise. All resistance in the immediate vicinity dilate reflexively through local vascular control mechanisms. Collaterals are normally constricted normally, but they also take part in the vasodilatory response because of rising metabolite levels. Blood flow through collaterals may allow areas peripheral to a focal infarct to survive the initial ischemic event. Death of myocytes impairs myocardial contractility, which reduces the left ventricular stroke volume and cardiac output. Mean arterial pressure (MAP) falls as a result. If the infarct is small, these pathways may be enough to restore MAP.

Some patients with MI feel fatigued all the time. Fatigue is a condition characterized by a diminished capacity for work and reduced productivity, usually accompanied by a feeling of lethargy and tiredness. Chronic fatigue is more or less associated with having had a myocardial infarction or having a heart condition in general. Studies on this subject divide the fatigue into smaller constituents such as general fatigue, mental fatigue, reduced motivation, and reduced activity. Fatigue also forms part of an adaptive range with tiredness and exhaustion as beginning and end points respectively, with each state being a response to stimulants. To identify the underlying causes of post-myocardial infarction tiredness, we need to look at it from many points of view. It could have physiological bases because of illness, raised cardiac enzymes, damaged heart muscle, altered electrical and neural transmissions and a threatened immune system.

As diabetes is a major modifiable risk factor for MI, we should also talk about the presentation of diabetes in patients to further expand our diagnostic capabilities. Diabetes mellitus (derived from the Greek word diabetes, meaning to go through, and the Latin word mellitus, meaning sweet or honeyed) is the disease in which the human body lacks the proper resources to store and use glucose, an energy-producing monosaccharide within cells. This causes the blood-glucose levels to sky-rocket. Insulin is the hormone responsible for the storage of glucose as glycogen, the stored form of glucose. Glycogen is a multi-branched polymer of glucose which is amassed in response to insulin and broken down in the presence of glucagon. Glucagon’s antagonistic hormone is insulin. Insulin facilitates the entry of glucose into cells, because glucose cannot enter cells alone without special transporters. Specialized cells called beta islet cells within the pancreas produce insulin. Any problem with these cells will cause the inappropriate amount of insulin to flow within the bloodstream. There are two types of diabetes; type 1 and type 2. Type 1, also known as the insulin-dependent diabetes, occurs when an autoimmune reaction in which the patient’s own immune system attacks the insulin-secreting cells in the pancreas, destroying them. This causes the complete nonexistence of insulin in the circulation. Type 1 is not related to genetics, can’t be controlled by a diet, and usually occurs at a young age. Type 2 diabetes, known as the insulin-independent diabetes, is the diabetes related to obesity. It mostly affects middle-aged people. It is caused by the insufficient amount of insulin within the bloodstream. It is associated with obese and overweight people. It is also passed on through genetics. Before type 2 diabetes is diagnosed, some patients may be put into a prediabetes group, meaning their blood-glucose is too high to be normal but not high enough to be classified as diabetic. Moving on to diabetes’ clinical manifestation, patients with diabetes typically present with increased thirst, hunger, and urination. Some cases also experience blurred vision, nausea, drowsiness, and decreased stamina during exertion. In diabetes type 1, the symptoms usually appear abruptly and intensely e.g. diabetic ketoacidosis is a serious condition in which excess acid builds up within the body. Initially, the symptoms of diabetic ketoacidosis include nausea, vomiting, fatigue, and abdominal pain. These symptoms occur alongside the increased thirst, hunger, and urination mentioned before. If left untreated, diabetic ketoacidosis may quickly develop into a coma or death. In type 2 diabetes, the cases are typically that of overweight, obese, or of people with sedentary lifestyles. Diabetes mellitus also decreases sensation by damaging nerves, a condition known as autonomic neuropathy. Silent infarction, a condition in which patients with diabetes have a heart attack and not notice it because of their senses having been weakened by the effects of high blood-glucose. Diabetic cases with MI may have a typical or an atypical presentation. Typical includes the normal features of heart attacks such as chest pain, breathlessness, and fatigue, while atypical includes cases may have no chest pain, the main symptom. Therefore, patients of diabetes are a highly risky group for MI because of their more difficult diagnosis, causing the mortality of diabetic patients with MI to be higher than typical cases.


To summarize, heart attacks are the death of a part of the cardiac muscle. They are responsible for the most deaths in the world. According to the World Health Organization (WHO), ischemic heart diseases with stroke took 15.2 million live in 2016 alone. Although there are many major risk factors which worsen and or speed-up the attack, some of them are static such as age and gender. Realistic approaches to reduce the chances of a myocardial infarction include changing one’s lifestyle into a healthier one and or quitting smoking cigarettes. Diabetics are also a risky group. Diabetes is the disease in which the simple sugar, glucose, cannot be stored or transported into the cells in which they are changed into energy through complex pathways known as cellular respiration. When a diabetic patient has an atypical presentation of MI: neck pain, sweating, easily fatigued, etc…, we should suspect a case of myocardial infarction. 

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