I have an uncle who recently died of heart disease; he was only 45 years of age. The doctors told us that his smoking of tobacco was responsible. I thought smoking caused lung cancer. Is there a connection between smoking and heart disease?
Cardiovascular disease is the most common cause of death in the developed world. More than half of these deaths result directly from coronary artery disease. Another approximately 20 percent are due to stroke. With such a large amount of disease related to cardiovascular disease, it is important to look at the reasons.
Risk Factors
The science of epidemiology (the study of disease patterns and causes) has led to an understanding of risk factors. A risk factor is a feature or tendency in a population or individual associated with an increased risk of developing disease(s). Some risk factors cannot be changed. These include heredity, gender, and age. In contrast, some risk factors are modifiable or changeable; smoking is one of these.
Cigarette smoking remains the most important changeable risk factor for coronary artery disease (CAD) in much of the world. Approximately 1 billion individuals worldwide now smoke; five million people die annually of causes (including heart disease) directly related to smoking. It is important to note that even nonsmokers who have passive exposure to cigarettes, cigars, or pipe smoke have an increased risk of CAD from this exposure.
The effects of smoking on coronary risk have been absolutely proved over the past 50 years. People who consume 20 or more cigarettes daily have a two to three times increase in total CAD than nonsmokers. In young women who take the contraceptive pill and smoke, there is an even greater increase in CAD because of the additive effects of these two entities.
Smoking increases the disease of coronary arteries (atherosclerosis). Consequently, there is a significant association between smoking and angina (chest pain because of narrowed coronary arteries), first-time heart attacks, as well as repeated heart attacks. Likewise, there is an increase in all forms of stroke associated with smoking.
Other Effects of Smoking
Smoking causes blood pressure to rise. It also decreases the amount of oxygen that gets to the heart muscle. The chemicals in cigarette smoke, including nicotine and carbon monoxide (a deadly poison in high doses), accelerate blood vessels’ damage through arterial disease. Apart from making the dangerous LDL cholesterol (low-density lipoprotein) more harmful and worsening arterial damage, smoking increases the blood’s tendency to form clots.
Another way in which smoking affects the heart is through the damage it causes to the lungs. As the lungs are altered by exposure to smoke, a change occurs in the circulation of the lungs that is normally a very low pressure system. Lung damage causes the pressure in the blood vessels of the lung to rise. This results in a strain on the right ventricle (pumping chamber) of the heart—which is designed to function with low pressures—and can cause permanent damage to the heart.
Another condition that is directly related to smoking is Buerger’s disease. In this disease, inflammation takes place in the small and medium-sized arteries and veins in the arms and legs. This occurs mostly in men under the age of 40 and more commonly in Asians and individuals of eastern European origin. The only specific treatment is for the patient to stop smoking.
The Most Important Strategy
Smoking has very negative effects on health generally and on the cardiovascular system specifically. Yet, the tobacco industry continues to aggressively target all populations—especially young adults. It is therefore imperative that preventing people from starting to smoke be the most important strategy. The message should also be clear that smoking cessation cuts the health risks; cutting down on smoking does not. Prevention is not only better than the cure—it is the cure!
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Peter M. Landless is the Director of the General Conference Health Ministries Department.
Reprinted with permission Adventist World-NAD, October 2006, p. 11.
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