ASCAD is the focal narrowing of the large and medium sized coronary arteries due to intimal proliferation of smooth muscle cells and the deposition of lipids. The basic lesion is called a plaque, the chief components. It include:
(i) Intimal smooth muscle cells, which are caused to proliferate due to endothelial damage.
(ii) Lipids (cholesterol esters and crystals), which are deposited at the center of the plaque and also accumulate within smooth muscle cells.
Currently in the United States the incidence of death due to ASCAD is 3 in 1000 and decreasing. However, ASCAD occurs with different frequencies according to the following risk factors:
(i) Age: The incidence of ASCAD in the United States increases progressively with age and is approximately 150 in 100,000 individuals at age 50.
(ii) Sex: ASCAD is more prevalent in men than in women. This difference is most marked in premenopausal women compared to men of similar age; men in this age group are affected five times more commonly than women.
(iii) Serum Cholesterol: The incidence of ASCAD increases with increasing total serum cholesterol levels. Total serum cholesterol is carried in the blood by low density lipoprotein (LDL), very low density lipoprotein (VLDL), and high density lipoprotein (HDL). The higher the percentage of total cholesterol carried by LDL in relation to HDL, the higher the risk of ASCAD. Patients with LDL to HDL ratios of greater than 5:1 are particularly prone to ASCAD. Conversely, high levels of HDL seem to be protective. One theory is that HDL may allow for elution of cholesterol out of the coronary vessel.
(iv) Smoking: Cigarette smokers are 60% more likely to develop ASCAD than nonsmokers when other risk factors are controlled. Smoking increase carbon monoxide levels in the blood, which may in turn damage the coronary endothelium. Smoking also increase platelet adhesiveness and thus the likelihood of thrombotic coronary occlusion.
(v) Hypertension: The higher either the systolic or diastolic blood pressure, the more likely the development of ASCAD. This likelihood is noted in both men and women and becomes more pronounced with advancing age.
(vi) Diabetes Mellitus is associated with a 50% increase in the incidence of ASCAD in men and a 100% increase in women. This correlation may be explained in part by the increased platelet adhesiveness and increased serum cholesterol levels associated with diabetes. In general, however, there is a poor correlation between the severity of the diabetes and the severity of ASCAD.
(vii) Family History: A familial predisposition to coronary artery disease exists and is partially due to the fact that the above risk factors (except smoking) also are inherited.
(viii) Oral Contraceptives are associated with an increased incidence of myocardial infarction from 0.01% to 0.04% in nonsmoking women aged 30-40 years who use oral contraceptives, the increase is more dramatic (0.06% to 0.025%).
(ix) Other Risk Factors: Gout, type A personality, premature arcus senilis, obesity, hypertriglyceridemia, and a diagonal ear lobe crease also are associated with an increased risk of ASCAD.
There are three major theories of atherogenesis exits:
(i) The Insudation Theory was developed from the constant observation that high levels of serum cholesterol and LDL are associated with ASCAD. This suggests that increased levels of these substances lead to their increased deposition in the vessel walls.
(ii) The Damage Thrombosis Theory postulates that intermittent damage to the vessel (e.g., from hypertension or carbon monoxide) leads to platelet activation and thrombus deposition. This in turn leads to smooth muscle cell proliferation and genesis of a plaque. The damage also may increase the permeability of the vessel to cholesterol, which could increase cholesterol deposition.
(iii) The Neoplasia Theory: Smooth muscle cells in atherosclerotic plaques in women have the same glucose-6-phosphate dehydrogenase isoenzyme, suggesting a monoclonal origin of all these cells. This theory postulates that a stimulus - perhaps vessel wall injury - leads to cell proliferation.
(1) Supply-Demand Relationship: The oxygen needs of the myocardium can be roughly approximated by the product of heart rate and left ventricular systolic pressure. As these variables increase (e.g., with exercise), myocardial oxygen consumption rises. This increased demand is met in normal individuals by auto regulated increases in coronary blood flow.
(i) Increased Demand: In patients with ASCAD, stenosis of the coronary artery prevents the increase in coronary blood flow needed to compensate for an increased demand, resulting in oxygen demand exceeding oxygen supply. Myocardial ischemia is the end product of this imbalance.
(ii) Reduced Supply: The atherosclerotic stenosis was once viewed as a fixed obstruction to coronary blood flow. In fact, the diseased area of the coronary artery often remains dynamic, and the effective lumen of the artery undergoes constant change. Changes are produced by vasoconstriction of the coronary artery, by production and degradation of local thrombi at the site of stenosis, and by progressive enlargement of the atherosclerotic plaque. These changes may reduce the supply of coronary blood flow and, thus produce ischemia without an increase in demand.
(2) Myocardial Infarction:
(i) Although the cause of transmural infarction has been debated for much of the last century, recent studies demonstrate that most transmural myocardial infarctions are associated with early occlusion of a coronary artery by a thrombus. The thrombus usually is located adjacent to an atherosclerotic coronary stenosis. The initial events producing this thrombus are not clear. Acute lysis of the thrombus with agents such as streptokinase reestablishes coronary blood flow, relieves pain, reestablishes contractile function of the segment of myocardium supplied by the thrombosed artery, and may reduce myocardial damage. These observations confirm that the thrombus is not merely a coincident event in myocardial infarction but is central to its pathogenesis. Without therapeutic or natural recanalization, cell death ensues. The rapidity and extent of the infarction process are determined by the extent of reduction of blood flow to the area. In some cases, collateral flow may supply enough blood flow to prevent infarction despite a total coronary occlusion.
(ii) The pathogenesis of nontransmural infarction is less clear, but total coronary occlusion is significantly less common, occurring in less than 50% of cases.
Definition: Angina pectoris refers to chest pain or pressure produced by myocardial ischemia.
(i) Characteristics of Angina Pectoris.
(ii) Diagnosis of Angina Pectoris.
(iii) Therapy/Treatment of Angina Pectoris.
Definition: Myocardial infarction occurs when myocardial oxygen demand severely exceeds myocardial oxygen supply for a prolonged period of time. This usually is due to a severe reduction in coronary blood flow produced by coronary occlusion. The events leading to this sudden reduction are unclear. Coronary thrombosis recently has been implicated in most transmural myocardial infarctions, but the cause of this thrombosis is unknown. Coronary spasm with total occlusion of the vessel also may produce transmural myocardial infarction. The cause of nontransmural or subendocardial myocardial infarction remains unclear.
(i) Clinical Features of Myocardial Infarction.
(ii) Diagnosis of Myocardial Infarction.
(iii) Complications of Myocardial Infarction.
(iv) Therapy/Treatment of Myocardial Infarction.
(v) Reduction of Myocardial Infarction.
The prognosis of patients with coronary artery disease is primarily determined by two variables: the extent of coronary disease in terms of the number of vessels affected by the disease and the extent of left ventricular damage present due to previous myocardial infarctions.
(i) Patients with main left coronary artery disease have approximately a 20% mortality rate in the first year after its discovery.
(ii) Patients with single-vessel coronary artery disease have approximately a 2% annual mortality rate, those with double-vessel disease have approximately a 3%-4% annual mortality rate, and those with triple-vessel disease have approximately a 5%-8% annual mortality rate.
(iii) The presence of significant left ventricular dysfunction (as identified by an ejection fraction of less than 40%) approximately doubles the yearly mortality rate at each level of extent of coronary disease.
Note: Must consult your doctor for more information and proper treatment for the above described disease.
Click here to read more diseases relevant to atherosclerotic coronary artery disease (ASCAD).
|Congestive Heart Failure|
|♦||Ischemic Heart Disease|
|♦||Valvular Heart Disease|
|♦||Congenital Heart Disease in the Adults|
|♦||Venous Thrombosis and Pulmonary Embolism|
All the material
on this site is the property of abouthumanbody.com.