“In Greek translation, the word atherosclerosis means hard stuff in the arteries. This hard stuff, primarily cholesterol and lipids, accumulates in the arterial wall, decreases the luminal diameter of the artery and obstructs blood flow. An initial insult to the vascular endothelium is believed to result in atherosclerosis.
This may explain why atherosclerotic lesions tend to occur where arteries branch, and the blood flow is turbulent. In the early stages of atherosclerosis, endothelial cells take up and oxidize LDL cholesterol and transport it into the arterial wall. Macrophages ingest the oxidized LDL, becoming foam cells. Foam cells form the earliest lesions of atherosclerosis, called fatty streaks. However, not all fatty streaks lead to atherosclerosis. These lesions can get larger and thicker, eventually developing a tough, fibrous cap.
At this point, symptoms of myocardial ischemia due to inadequate blood flow can result in occlusion of the arterial lumen by the sclerotic plaque. Most cases of unstable angina (USA) and myocardial infarction (MI) are thought to occur when the fibrous cap ruptures, exposing the underlying cholesterol core to the blood stream. The subsequent activation of clotting factors causes an acute thrombosis, which blocks most or all of the blood flow through that artery. In patients with coronary artery disease (CAD), there can be stable plaques, causing reversible ischemia, and unstable plaques, in danger of rupturing and triggering thrombosis, complete occlusion and infarction.
In order for the heart to function properly, it requires a constant supply of oxygenated blood. Blood is supplied to the working heart muscle through the Right Coronary Artery (RCA), the Left Anterior Descending Coronary Artery (LAD), and the Left Circumflex Coronary Artery (LCX). Each of these arteries supplies blood to specific regions of the myocardium. Coronary artery disease can be defined as a condition hat reduced blood flow through the coronary arteries and the myocardium by a pathological process called atherosclerosis. As an atherosclerotic plaque forms over time in the arterial lumen, blood flow will be decreased.
The severity of the disease is a function of the size of the plaque. In patients with Chronic Stable Angina, the interior lumen is narrowed so that there may be adequate flow at rest, but during exercise, the myocardium can get all the blood it needs, resulting in myocardial ischemia. Ischemia typically causes chest pain, called angina pectoris. This ischemia subsides when the patient rests and the myocardial oxygen requirement is reduced. In some patients, this situation can deteriorate, with worsening angina at rest. This is called unstable angina. Although the anginal pain may be severe, it is a result of transient and reversible ischemia. However, with total loss of blood flow, myocardial cells die in an irreversible process known as infarction. If the infarction is large enough, the ventricle may be unable to function properly, and a greater burden of work is placed on the remaining viable myocardium. A myocardial infarction can limit the ventricle’s ability to contract with sufficient force.
If severe enough, this could potentially result in Congestive Heart Failure. The diastolic filling pressure causes the weakened ventricle to dilate. This results in a vicious cycle of stretching, dilation, progressively weaker contractions, declining ejection fractions, and worsening heart failure. The patient’s prognosis is serious, and could result in death.”
