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Tobacco and cardiovascular health
Published in ProCOR

Bernard Lown, MD

The scourge of smoking: tobacco and cardiovascular health

During a good part of my  life in medicine I have campaigned against the arms trade as one of the great threats to human life. In recent years I have come to realize that those promoting the global use of   tobacco have been far more destructive of life than the arms merchants.  In the USA smoking kills over a 1,000 people daily,  or 430,000 annually. (1)  The use of tobacco imposes on each  American  a hidden tax for health care of $221 per person per year irrespective whether they smoke, a  tax that adds up to $52 billion annually. 

While the adverse health effects of tobacco have been debated for at least 400 years, the fact that  cigarette smoking is a form of  severe drug addiction is just beginning to be appreciated.   The reason for this belated   recognition, is that unlike  other addictive drugs, the effects of tobacco  are slow in developing,  usually requiring decades of exposure before causing premature disability and death.  Furthermore cognitive performance remains unimpaired, social behavior is largely unaffected, and smoking does not predispose to violence.  While society criminalizes the use of addictive drugs, the law does not prohibit the sale of tobacco, though it claims far more lives than all drugs combined.

In developed countries smoking accounts for  2 million deaths annually. >From 1950 to the year 2,000 there will have been  60 million such fatalities, of these, two thirds will  occur  at ages 35-69  and one third in those older.   Middle aged people whose death is tobacco related will have lost on average 20-25 years of  non -smoker life expectancy. Most of those dying are not particularly heavy smokers, but have generally  started the habit as teenagers.    Peto et al (2)  have estimated that in developed countries during the 1990's, tobacco will cause 30% of all deaths among those 35 to 69 years of age; thereby making cigarette smoking  the single largest cause of premature death in the world.

In a number of countries smoking is now in substantial decline. Before the milestone Surgeon Generals Report in 1964,   about 40% of US adults smoked; by 1991 this number receded to 25.7%.  In Britain smoking has decreased by about 1% annually since 1972. (3)   Given the lethality of cigarettes, one can derive little comfort from these figures as  nearly a third  of British and American people  still continue to smoke.  Former Surgeon General of the US Public Health Service, C. Everett Koop,  identified smoking as the most important public health problem of our time, and the leading cause of preventable death  in industrialized countries.

To compensate for the loss of customers, the tobacco companies spend billions of dollars to make smoking appear as  a  glamorous, adventurous and pleasurable past time.  Prodigious resources are invested to target  audiences such as women and vulnerable children.  The decrease in the number of  male smokers in the US is now, in part, compensated by an increase in  female smokers. Tobacco consumption is nearly equal in the two groups, with 24 million men and 22 million women. (4) Teen-agers have proved  especially susceptible to the hype of advertising. Tobacco is far more injurious when the habit is initiated at a young age.  In the US, four out of five smokers start before the age of eighteen.  In 1995 one third of high school students reported smoking at least occasionally.  Once begun and continued,  about half of these young people will eventually be killed by tobacco, of these about  one-quarter will die during  middle age. The tobacco companies argue  that they are not legally liable for health injuring habits of  informed  adults.  Given  the deliberate focus to ensnare youngsters in a life long addiction, this is less an issue in exercise of free choice than exploiting callow youth and doing violence to children.

>From a global perspective the reality is even  more dismal.  The tobacco companies,  to compensate for  diminishing markets in industrialized countries, are investing enormous wealth to promote the use of cigarettes in the developing world. (More about this in a future commentary). They are succeeding and have already made up for the curtailed use of cigarettes  in the developed  countries by bloating the global consumption of tobacco. While the toll  from smoking is beyond  precise reckoning, indubitably,  it will dwarf the brutal human sacrifice of  all the wars in this bloody 20th century.  The annual number of fatalities  attributable to cigarettes will quadruple by 2030 and the bulk of these will be in developing countries. (5)  Peto has estimated that smoking will exact 10 million premature deaths annually during the next century. (6)

In  the public mind the major hazard of cigarettes is the predisposition to cancer especially of the lung, but far more victims are  claimed by cardiovascular sequelae.  As long ago as 1940, a  relation between cigarettes and coronary heart disease (CHD) was reported from the Mayo Clinic. (7)  It has since been voluminously  documented that smoking substantially increases the risk of cardiovascular disease including stroke, sudden death,  myocardial infarction,  peripheral vascular disease and aortic aneurysm.   Smoking increases the risk for developing coronary disease and enhances the occurrence of events among those with the disease. About one fifth of cardiovascular deaths in the US are attributable to smoking.  In a study of British doctors, a strong dose-response relation was observed in men younger than 65 years between duration and extent of smoking and death rate from ischemic heart disease. (8)  Similar trends have been noted in female smokers. (9)  Women who smoked as few as one to four cigarettes  daily had a 2.5  fold increased risk of fatal coronary heart disease and nonfatal myocardial infarction. 

The experience of the Coronary Artery Surgery Study (CASS) is relevant.  Among those who continued to smoke during the six years while enrolled in the study, the relative risk for cardiac death and for myocardial infarction was 1.7 and 1.5 respectively, as compared to those who gave up cigarettes the year before enrollment and thereafter abstained.  This relation held irrespective of age. (10)  When smokers and non-smokers were matched for coronary disease  severity and subjected to Holter monitoring, the smokers had three times as many ischemic episodes and  the duration of the episodes was twelve  times longer. (24min vs. 2min /24hrs.) (11)  Not only does smoking provoke more  active myocardial ischemia during ordinary daily life activities,  it also accelerates coronary progression and new lesion formation when  assessed by serial quantitative coronary arteriography.   Compared to a control group of non-smokers, mean luminal narrowing in coronary arteries  more than doubled among smokers  during a short  period of two years. (12)  This effect has also been reported in the carotid arteries of  identical twins who were  discordant for cigarette smoking. The total area of carotid plaques was 2.3 times larger in smoking twins than their non-smoking siblings. (13)

There is no dearth of possible  pathogenic mechanism to account for smoking induced atherogenesis and for the progression of ischemic heart disease. Components of cigarettes have been shown to damage vascular endothelium, the  antecedent lesion to atherosclerotic plaque formation. Carbon monoxide, one of the most poisonous by-products of cigarette smoke,  makes up approximately 2.7 to 6.0% of smoke. It is known to   damage endothelium and thereby enhance the deposition of cholesterol in plaques. Carbon monoxide, additionally  increases blood viscosity, fibrinogen levels, and prothrombotic state.  Smoking also increases platelet aggregability, thromboxane formation, plasma viscosity and  vasomotor reactivity. (14, 15) Furthermore smokers have higher total LDL cholesterol levels and lower HDL than control subjects. The degree of the adverse lipid profile alteration is a function of the daily cigarette consumption. (16)

Some of the cardiovascular adverse effects also relate to the nicotine, a potent stimulator of catecholamine release, which  thereby increases oxygen demand, accelerates heart rate and raises blood pressure.  Indeed smokers demonstrate an increased rate pressure product both at rest and during exercise.(17).  This occurs in a setting where carboxyhemoglobin decreases oxygen delivery. Additionally  smoking promotes coronary spasm and impairs coronary vasoreactivity. It is to be expected that this type of combination of factors would lower the vulnerable threshold for ventricular fibrillation (VF).   Halstrom and colleagues (18)  have, in fact, reported smoking to be a risk factor for recurrence of cardiac arrest among CHD patients who had been resuscitated from VF.  Further implicating nicotine as a major smoke component affecting the adrenergic system is the report that propranolol largely abolishes the deleterious effects of smoking on mortality following an initial heart attack. (19)

With the discovery that environmental tobacco smoke (ETS) is a source of indoor contamination, one can no longer argue that smoking is a private and individual matter.  In 1986 the National Research Council estimated that 3,000 lung cancer cases  per year were attributable to ETS among persons who never smoked.(20) However, the risk of ETS  appears far greater for ischemic heart disease.  In the US, environmental cigarette smoke is believed to account for 35,000 to 40,000 cardiac ischemic deaths annually among those who have never smoked but have been living with a current or former smoker.  (21)   It is currently  estimated that non-smokers have a 30 percent excess risk for acquiring coronary artery disease when living with smokers. In response to the emerging information on ETS, the American Heart Association affirmed, "A smoke-free environment  in the home, public buildings and work place should be the goal of society" (22)

In industrialized societies a public increasingly educated about the hazards of tobacco, has shaped  an anti-tobacco political climate.  Smoking is no longer deemed a  matter of personal choice or a transcendent individual right. The jurisdiction permissible to smokers is ever constricted  and is illegal in public  buildings, transport vehicles such as busses, trains or planes  and in many restaurants. Tobacco companies are increasingly beleaguered. Exposed for the first time are their campaigns of lies about the adverse health  effects of smoking that they had already documented decades ago.

Yet, at this very moment, in other parts of the world, smoking is spreading as a veritable fire storm fanned by these same unprincipled and discredited tobacco corporations. This is especially deplorable as the demographic transition exposes for the first time large populations to the risk of ischemic heart disease. The ready availability of tobacco makes a cardiovascular epidemic inevitable.  Richard Doll, a giant in cardiovascular epidemiology, recently wrote,  "One of the great objectives of medicine is to enable people to live out the span of life to which they are biologically adapted."(23) This is beyond  a mere objective of medicine, far more it is  the  inalienable right of every living  human beings.  We members of the health profession can not stand idly by when this fundamental right is abridged.   We must speak loudly and without equivocation.  A single  global standard must be forged that strictly curtails the sale of tobacco until the weight of informed public opinion completely proscribes the use of  this poisonous weed.

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Bibliography


1.  Sullivan Louis Editorial. To thwart the tobacco companies JAMA  October  16, 1991 p2131  vol 2662.
2.  Peto R, Lopez AD, Boreham J, Thun M, Heath C Jr Mortality from tobacco in developed countries: indirect estimation from national vital statistics. Lancet 1992;239:1268-78.
3.  Office of Population Census and Surveys,. General Household Surveys       1988 London:HM Stationary Office, 1990.
4.  Cigarette smoking among adults - United States, 1991. MMWR Morb Mortality Wkly Rep 1993;42:230-3.
5.  Mackay J. Tobacco The Third World war.  Thorax 1991;46-:153-6
6.  Peto R.  World Conference on Tobacco and Health, Pert, Western Australia 1-5; April 1990
7.  English JP, Willius FA,  Berkson J.  Tobacco and coronary disease. JAMA 1940;115:1327-9.
8.  Doll R, Peto R. Mortality in relation to smoking: 20 years observations on male British doctors. BMJ 1976;2:1525-36.
9.  Willett WC et al  Relative and absolute excess risks of coronary heart disease among women who smoke cigarettes. NEJM 1987;317: 1303-9. 10.  Hermanson B et al. Beneficial six-year outcome of coronary  cessation in older men and women with coronary artery disease: results of the CASS Registry. NEJM 1988;319:1365-9
11.  Barry J et al Effects of smoking on the activity of ischemic heart disease JAMA 1989;261: 398-402.
12   Waters D, Lesperance J, Boccuzzi SJ et al Efects of cigarette smoking on the angiographic evolution of coronary atherosclerosis :a Canadian coronary atherosclerosis intervention trial (CCAIT) substudy  Circulation 1996;94:614-621.
13.   Haapanen A, Koshenvuo M, Kaprio J, et al. Carotid arteriosclerosis in identical twins discordant for  smoking. Circulation. 1989;80:10-6. 14.   Davis et al.  Passive smoking affects endothelium and platelts Archives int. Med 1989;76:6-14.
15.   McBride PE. The health consequences of smoking:cardivascular disease. Med  Clinics North Am. 1992;76:333-353.
16.   Muscat JE et al Smoking  and plasma cholesterol. Am Ht J 1991;121:141-147. 
17.   Aronow W.  Effect of passing smoking on angina pectoris New Eng J Med.1978;299:21-24
18.   Hallstrom AP, et al Smoking as a risk factor for recurrence of sudden cardiac arrest. NEJM 1986;314:271-5
19.   Jafri, Tilley BC, Peters R, et al. Effects of cigarette smoking and propranolol in survivors of acute myocardial infarction. AJC 1990:65:271-76. 20.   National Research Council. Environmental Tobacco  Smoke. Measuring  Exposure and Assessing Helath Effects. Washington, DC: National Academy  Press;1986.
21.   Steenland K. Passive smoking and the risk of heart disease JAMA 1992;267:94-99.
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