the overall incidence of death as a result of ASCAD is 0.5 in 1000 and decreasing. However, ASCAD differs in frequency in subpopulations with the following risk factors:a.Age. The incidence of ASCAD increases progressively with age The risk of death is 1 .5 in 1000 individuals at age 50. b.Gender. ASCAD is more prevalent in men than in women. This difference is most marked in premenopausal women compared with men of similar age. By the time men reach the age of 50 years, they are affected five times more often than women of the same age, and the difference declines as age increases.c. Serum cholesterol. The incidence oi ~SCAD ncreascs with increasing total serum cholesterol levels, as shown in Figuie 1-10. (1)Total serum cholesterol is carried ~n the ~Iood b\ low-density iipoprotein (LDL)~ very tow.density lipoprotein and high-density lipoprotein (HDL). (a)The higher the percentage of total cholesterol carried by LDL in relation to HDL, the higher the risk oi ASCAD. Patients with LDL to-HDL ratios of greater than 4:1 are particularv. 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. B)It is desirable for the total cholesterol level to be less than 200 mg/dl. (i)The [DL Cholesterol level should be less than 1 30 mg/dl; in patients with known coronary disease, it should be less than 100 mg/dl. ii) The HDL cholesterol level should exceed 40 mg/dl. Several type of hyperlipidemia exist & many are associated with an increased incidence of coronary artery disease. Table 1 -2 presents an overview of thehyperlipidemias d- Smoking. Compared to nonsmokers, cigarette smokers are 60% more likely to develop ASCAD when other risk factors are controlled for statistically. Smoking increases carbon monoxide levels in the blood, which may. in turn, damage the coronary endothelium. Smoking also increases platelet adhesiveness and thus the likelihood of thrombotic coronary occlusion. e.Hypertension. The higher either the systolic or diastolic blood pressure, the more likely the development of ASCAD. This likelihood is apparent in both men and women and becomes more pronounced with advancing age.f.Diabetes meiiitus is associated with a 50% increase in the incidence of ASCAD in men and a 100% increase in women, explained in part by the increased platelet adhesiveness and increased serum cholesterol le\els associated with diabetes. In general, however, there is a poor correlation bett\een the severity of the diabetes and the severity of ASCAD. g.Family history. A familial predisposition to coronary artery disease exists in part due to inheritance of the above risk factors except smoking). However, family history is the only risk factor in about one-third of indi\ duals with ASCAD.h.Oral contraceptives are associated with an increased incidence of Ml, a clinical consequence of ASCAD. The incidence of Ml rises from 0.01% to 0.04% in nonsmoking women between the ages of 30 and 40 who use oral contraceptives and, more dramatcal \ from O.O60/o to O.25~/~ in similar women who also smokeI. Obesih. Recently, obesity has been recognized as an independent risk factor for ASCAD.j.Other risk factors. Gout, type A personality, premature arcus corneae, hypertriglyceridemia, and a diagonal ear lobe crease are other conditions associated with an increased risk of ASCAD 3. Pathogenesis. The previously mentioned risk factors do not constitute a known mechanism for ASCAD. The major theory of atherogenesis is the response to injury theory. a.This theory states that some injurious stimulus (e.g., hypertension or hypercholesterolemia) causes endothelial damage, resulting in the release of various growth factors. These growth factors cause smooth cell proliferation and migration of macrophages into the vessel wall. At the same time, the now injured endothelium becomes more permeable, admitting lipid and cholesterol into the intima. b.These changes result in plaque formation, which may eventually compromise the vessel lumen
enough to impede blood flow. If the plaque is disrupted, platelets are
activated, leading to thrombus formation and worsening obstruction. Stages of atheroma formation: -1- fatty strick: broke areas of artery with lipidsyellow spotsthis stage is reversible by cleaning of cells. 2- lipoidosis and fibrosis: difuse intimal thickening, it is covered by fibrous cup (atheroma formation) this stage is elative reversible but may be irreversible.3- complications: absolutely irreversible: thrombosis on the surface of the plaque-plaque unstable-necrotic changes or rupture of plaque- irreversible growing of collagenic factors infarction, stroke of vessels. 4- calcification and total scarring.Clinical symptoms: if localization in aorta so aorta loose elasticitynot compensate the activity of the heartsystolic isolated HTA aneurysm of aorta- dissection of aorta- thromboembolism- stenosis of the root of aorta. If present in cerebral arteries there is 2 variants: acute and chronic if chronic prolonged decrease blood circulation and dementia duptencephalitis. If renal arteries: if paque r growing slowly- narrowing of blood supply of kidney-> malignant Hta, renal failure. If mesenterial artery it leads to neurosis or peritonitis, if in peripheral arteries and extremities esp legs ischemia & gangrene occurs. If in coronary arteries MI, angina heart failure occurs. Prognosis. The prognosis of patients with coronary artery disease is determined primarily by three variables: age, the extent of coronary disease in terms of the number of vessels affected h\ the disease, and the extent of left ventricular damage present as a result of nrevious MIs. a. Patients with uncorrected main left coronary artery disease have approximately a 20% mortality rate in the first \ ear after its discovery. b.Patients with singlevessel coronary artery disease have approximately a 2% annual mortality rate, those with double vessel disease have approx 3-4% annual mortality rate and those with triple-vessel disease have approximately a 5o/~8% annual mortality rate. Proximal anterior descending disease also increases risk. c.The presence of significant left ventricular dysfunction (as identified by an ejection fraction of less than 40% appro\imately doubles the yearly mortality rate at each level of extent of coronarydisease.d. Revascularization improves the prognosis for patients with main left coronary disease, for those with triple-\essel disease associated with left ventricular dystunction, and for those with proximal left anterior descending disease.