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William H. McMicken, M.D.
Suite 323
2600 Philmont Avenue
Huntingdon Valley, Pennsylvania 19006
Page 8

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).

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.


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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