factor, which has an
additive, or even synergistic, effect with other risk
factors. An obese cigarette smoker has three times the risk
of heart attack than a thin non-smoker of comparable sex and
age (Heyden, et al, 1971).
The
immediate effects of the carbon monoxide and nicotine in the
cigarette smoke partially explain the increased incidence of
illness and heart attack in smokers. While cigarette smoke
contains many toxic substances, carbon monoxide is an
important factor in the increased risk of coronary heart
disease. Carbon monoxide has been shown to cause
atherosclerotic changes in laboratory animals. Carbon
monoxide may predispose one to increased risk of blood clot
formation, since it increases the adhesiveness of platelets.
Platelets are elements that help initiate the clotting
mechanism.
Carbon
monoxide displaces oxygen because it binds with hemoglobin
in the blood 200 times more readily than oxygen (Bass,
1982). Binding hemoglobin with carbon monoxide decreases the
amount of oxygen the blood can transport. During smoking,
carbon monoxide temporarily combines with hemoglobin in
about 20 percent of all circulating red blood cells. It may
convert up to 10 percent of available hemoglobin to
carboxyhemoglobin, which is then unable to carry oxygen. The
rate of release of oxygen from blood is markedly
reduced.
Lack
of oxygen to the heart muscle increases the likelihood of
cardiac arrhythmias, such as ventricular fibrillation and
cardiac arrest. This decreased oxygen release from
hemoglobin to heart muscle occurs even in patients with
open, normal, coronary arteries. With continued smoking, and
the development of lung disease also, risks due to decreased
oxygen supply are compounded. Strenuous exercise may
precipitate abnormal rhythms also, especially in a heart
with impaired oxygen supply due to high levels of carbon
monoxide. Strenuous exercise may not be a benefit to a
cigarette smoker, but a hazard. Exercise testing shows that
cigarette smokers generally cannot maintain maximal exertion
a long as nonsmokers (McHenry et al, 1977).
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In
addition to the effects of carbon monoxide,
nicotine contained in cigarette smoke also
increases abnormal rhythms, raises heart rate and
blood pressure, all of which increase coronary
risk. Nicotine also causes constriction of small
arteries, which aggravates peripheral vascular
disease associated with atherosclerosis.
Mortality
statistics demonstrate the effects of the
tobacco
epidemic.
Of the more than two million deaths in the United
States in 1990, smoking related illnesses accounted
for about 400,000 of them, and for more than a one
quarter of all deaths among those 35 to 64 years of
age. Statistically, each cigarette robs a regular
smoker of 5.5 minutes of life.
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In
the remainder of this article, the most important
arteriosclerotic disease entities will be presented. These
diseases include hypertension, coronary heart disease,
strokes, and peripheral vascular disease. The causes of
each, along with signs, symptoms and methods of diagnosis
will be discussed. Treatment will be described, both as to
prevention and medical therapy. Hypertension, or high blood
pressure, can be considered both as an arteriosclerotic risk
factor and a disease in itself. Coronary heart disease
includes in its manifestations angina, heart attack, and
congestive heart failure. Strokes may be due to thrombosis
(blood clots), or bleeding (hemorrhage). Peripheral vascular
disease results from sclerotic changes in arteries to the
extremities. Such changes can also occur in arteries to
specific vital organs, such as the brain and kidneys.
An abnormal level of
cholesterol or other fatty substances in the blood, called
hyperlipidemia or dyslipidemia, is also both a
treatable disease and a risk factor.
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8
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