CONCLUSION
Coronary artery disease is caused by plaque buildup in the wall of the arteries that supply blood to the heart
(called coronary arteries). Plaque is made up of cholesterol deposits. Plaque buildup causes the inside of the
arteries to narrow over time. This process is called atherosclerosis.
The heart muscle needs a constant supply of oxygen-rich blood. The coronary arteries, which branch
off the aorta just after it leaves the heart, deliver this blood. Coronary artery disease that narrows
one or more of these arteries can block blood flow, causing chest pain (angina) or a heart attack
(also called myocardial infarction, or (MI).Myocardial Infarction.
Coronary artery disease was once widely thought to be a man’s disease. On average, men develop it about
10 years earlier than women because, until menopause, women are protected by high levels of estrogen.
After menopause, coronary artery disease becomes more common among women. Among people
aged 75 and older, a higher proportion of women have the disease because women live longer.
RESEARCH ARTICLE
Prognosis in Chronic Obstructive Pulmonary Disease
N. R. Anthonisen , E. C. Wright , J. E. Hodgkin etal We recruited 985 patients with COPD but without
hypoxemia or other serious disease, treated them in a standard fashion, and followed them closely for nearly
3 yr. At the time of recruitment the patients were carefully characterized as to symptom severity, lung function,
exercise tolerance, and quality of life, and studies of lung function were repeated during follow-up. Overall
mortality was 23% in 3 yr of follow-up. Patient age and the initial value of the FEV1 were the most accurate
predictors of death; when FEV1 before bronchodilator was used, the response to bronchodilators was directly
related to survival, but this relationship became nonsignificant when postbronchodilator FEV1 was used as a
primary predictor. After adjustment for age and FEV1, mortality was related positively to TLC, resting heart rate,
and perceived physical disability, and related negatively to exercise tolerance. These relationships, though
significant, were relatively weak. When standardized for age and FEV1, mortality in the present series was less
than that of a previous series (4), and the same as that of hypoxemic patients with COPD who received continuous
home O2 therapy. Changes in FEV1 with time averaged −44 ml/yr, but the standard deviation was large. Patients
with low initial values of FEV1 showed relatively little further decline, probably indicating a survivor effect. In
patients with well-preserved initial FEV1, rate of decline correlated negatively with bronchodilator response,
symptomatic wheezing, and psychological disturbances