Atherosclerosis: Incidence and risk factors.

Currently in the United States,

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.