Myocardial Infarction: Heart Attack

The most common physiological process leading to a myocardial infarction is the occlusion of coronary arteries by a process known as atherosclerosis. In fact, atherosclerosis is present in more than 90% of persons with coronary heart disease.1

Nevertheless, there is an understandable and noticeable link between circulatory related diseases and lifestyle diseases, such as Coronary Heart Disease. Coronary heart disease can occur when fatty acids, such as cholesterol in an inadequate diet, build up in the walls of the coronary artery. These fatty deposits collect minerals and harden to become a plaque. Eventually, this plaque grows and can swells up, forming an aneurism. In some cases, this aneurism may burst leading to instant death. As it continues to grow and swell up, it finally blocks the artery completely and forms blood clots. This is known as coronary thrombosis. A myocardial infarction, or in other words as heart attack, occurs when no oxygen is able to reach the coronary artery and thus it is unable to fulfil its role in providing the heart muscle with a sufficient supply of blood. Heart attacks are very common in the society nowadays, especially occurring in smokers or obesity related diseases (Millar, June 2014)

Ischemia caused by coronary blood vessel obstruction as a result of vasospasm, thrombosis or atherosclerosis. Ischemia can also

Myocardial Infarction (MI) is more commonly referred as the heart attack. This typically occurs due to an interruption, albeit partial to some part of the heart, which causes the cells in the heart to die and as a result sends

Heart muscle died as a results of myocardial infarction (MI) which the main coronary arteries was blocked, and large part of the heart muscle was affected due to cellular death from lack of blood flow and oxygen. Cell death is one of the most crucial events in the evolution of MI. A heart attack or MI is usually caused by a blood clot (thrombosis) that forms inside a coronary artery, or one of its branches, which suddenly blocks and stops the blood flowing to a part of the heart muscle. When the blood flow is interrupted necrosis occurs ( McCance & Huether, 2014).

The coronary artery that was occluded in M.T.’s coronary circulation were the right coronary artery. When coronary blood flow is interrupted for an extended period, myocyte necrosis occurs. This results in MI. In the majority of MI, the decrease in coronary flow is the result of atherosclerotic CAD (McCance & Huether, 2014). M.T. is experiencing transmural MI. According to H. Michael Bolooki (2010), a transmural MI is characterized by ischemic necrosis of the full thickness of the affected muscle segment(s), extending from the endocardium through the myocardium to the epicardium. M.T. was exhibiting crushing substernal chest pain radiating down his left arm. He was complaining of dizziness and nausea. During M.T.’s physical exam, he

The heart is an organ that pumps blood from the body and maintains all the organs functioning to keep one alive; when one of the arteries that receive blood is blocked it can cause a heart attack or myocardial infarction (MI). “During a heart attack, the heart muscle (the myocardium) is damaged, and part of it die from lack of blood” (book, p. 429).

Myocardial infarctions are all too familiar in this day and age. Just about every person knows somebody who has either had a myocardial infarction. “About every 40 seconds, someone in the United States has a myocardial infarction (heart attack.” (American Heart Association, Inc., 2016). That means that roughly, in the ninety minutes of this class time, one hundred and thirty-five people have had heart attacks across the country. According to the CDC, “Every year, about 735,000 Americans have a heart attack. Of these cases, 525,000 are a first heart attack.” (CDC, 2015). So, what exactly is a myocardial infarction and what causes it to happen? There are several signs that could potentially alert an individual to

Typically the heart works aerobically, meaning the heart uses oxygen to function properly. The process of the heart converting from aerobic to anaerobic metabolism, meaning the heart no longer uses oxygen, during an MI causes the heart muscle to significantly decrease its contractility. When the conversion from aerobic to anaerobic metabolism takes place, changes to the structure of the myocardial cells develop within only a few minutes. The cells undergo glycogen depletion and experience mitochondrial swelling. If the cells are depleted of oxygen for an extended period of time, roughly twenty to forty minutes, permanent myocardial necrosis (tissue death) occurs (Grossman & Porth. 2014). Myocardial cells that are alive and functioning properly contain the enzymes and proteins creatine, kinase, troponin I and T, and myoglobin. When the heart tissue is deprived of oxygen during an MI, the myocardial cells cannot survive. When the cells die, their cell membranes become flexible, and the enzymes and proteins inside the cells leak out and move through the blood stream (Askari & Bolooki,

disease. Myocardium is the heart muscles. It's getting it's oxygen and nutrients through the coronary

Alike all muscle in the body the heart requires its own constant supply of oxygen and nutrients. Out of three coronary arteries, large two and branching arteries supply oxygenated blood to the cardiac muscle. Any sudden block of these arteries or its branches causes starvation of heart from oxygen and this condition called “cardiac ischemia”. When myocardial ischemia exceeds a critical inception and overthrows cardiac cellular repair mechanisms deliberate to maintain normal operating function and homeostasis. Ischemia at this critical limit for prolonged period causes permanent cardiac cell injury or

There are a couple of differences between the two. First I’ll tell you what a MI is. A MI is also known as a heart attack. A heart attack is when a blood clot causes a blockage of blood flow to the heart. If blood flow becomes blocked it prevents the tissue from receiving oxygen. If a part of the heart does not get the oxygen it needs it dies. Symptoms include tightness in the chest, pain in the arms, back, and neck. It can also cause fatigue, lightheadedness, and an abnormal heartbeat. If doctors believe you are having a MI your blood pressure will be taken. Then you’ll get a EKG. Along with the ECG you will also get some blood work done.

Farrell & Dempsey (2014) suggests that the main cause of myocardial infarction (MI) is the underlying coronary artery disease (CAD), such as atherosclerosis. Atherosclerosis, is the abnormal accumulation of lipids, fatty substances or fibrous tissue in the lining of arterial blood vessels. These deposits, called atheromas, cause a narrowing or blockage of the arterial lumen which reduces blood flow to the myocardium. If the atheroma becomes too large it may rupture or haemorrhage into a plaque. The ruptured plaque becomes a site for thrombus formation, and this thrombus may then obstruct coronary blood flow resulting in an AMI

A heart attack, also known as a myocardial infarction, usually occurs when a blood clot forms inside a coronary artery at the site of an atherosclerotic plaque. The blood clot severely limits or completely cuts off blood flow to part of the heart. In a small percentage of cases, blood flow is cut off when the muscles in the artery wall contract suddenly, constricting the artery. This constriction, called vasospasm, can occur in an artery that is only slightly narrowed by atherosclerosis or even in a healthy artery. Regardless of the cause of a heart attack, the oxygen deprivation is so severe and prolonged that heart muscle cells begin to die for lack of oxygen. About 1.1 million people in the United States have a heart attack every year;

We present an 85 year old non-diabetic and non-hypertensive patient admitted with acute inferior wall myocardial infarction. After successful coronary angioplasty patient had no reflow phenomenon which was treated with adenosine, nikorandil and nitroglycerine with TIMI 3 flow achieved at the end. This case report revisits one of the dreaded complications in cath-lab and its successful management