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• W2016287772 abstract "When the Spanish and Portuguese began to send tobacco from South America to Europe in the sixteenth century and John Rolfe did the same from Virginia in the next century, profit was the laudable motive. These early entrepreneurs could not have foreseen how pervasively lethal their new plant would be through the next three centuries. It has been estimated that 325,000 to 350,000 deaths caused by cigarette smoking occur annually in the United States, “more than all other drug and alcohol abuse deaths combined, seven times more than all automobile fatalities per year, more than one hundred times all recorded deaths caused by the acquired immunodeficiency syndrome, and more than all American military fatalities in World War I, World War II, and Vietnam put together.”1Pollin W. The role of the addictive process as a key step in causation of all tobacco-related diseases.JAMA. 1984; 252: 2874-2875Crossref PubMed Scopus (27) Google Scholar Although there has been a decline over the past decade in the number of adults who smoke, progress in treating the Tobacco Dependency Disorder (TDD), code 305.1 of the Diagnostic and Statistical Manual (DSM-III), is still inadequate. Although 50 years ago Pearl2Pearl R. Tobacco smoking and longevity.Science. 1938; 87: 216-217Crossref PubMed Scopus (108) Google Scholar showed in a survey of 6813 subjects that smokers die prematurely and additional evidence has since accumulated to confirm that observation, about 60 million Americans keep smoking and adolescents assume the habit at high rates.3Kannel WB. Update on the role of cigarette smoking in coronary artery disease.Am Heart J. 1981; 101: 319-328Abstract Full Text PDF PubMed Scopus (253) Google Scholar Currently about 37% of the male population and 29% of the female population older than 17 years of age smoke. For 1980, when the total U.S. health care bill was $218 billion,4Prospective payment. International Health Services, Ltd, Concord, Mass1983Google Scholar Kannel3Kannel WB. Update on the role of cigarette smoking in coronary artery disease.Am Heart J. 1981; 101: 319-328Abstract Full Text PDF PubMed Scopus (253) Google Scholar estimated that the medical care costs of smoking tobacco were $8.2 billion and the lost earnings were $19 billion, totaling 12.5% of health expenditures. In 1984, when the same total medical care bill was about $355 billion, the above-mentioned costs of smoking, assuming the same share, were $13.4 billion and $31 billion, respectively, dwarfing the approximately $4.8 billion in tobacco taxes collected annually. More than 3000 components are present in cigarette smoke, many of which are carcinogens or tumor inducers (e.g., nitrosamines, hydrazine, vinyl chloride, N' -nitrosonornicotine, beta-naphthylamine, polonium, nickel, cadmium, and arsenic), cocarcinogens (e.g., pyrene, fluoranthene, naphthalenes, 1-methylindol), carcinogen and toxin combinations (e.g., hydrogen cyanide, acrolein, acetaldehyde, phenol, and cresols), or straight toxins (e.g., nicotine and carbon monoxide [CO]).5Wynder EL. Tobacco and health: A societal challenge.N Engl J Med. 1979; 300: 894-903Crossref PubMed Scopus (109) Google Scholar Since the early reports of Wynder and Graham6Wynder EL Graham EA. Tobacco smoking as a possible etiological agent in bronchogenic carcinoma: A study of six hundred and eighty-four cases.JAMA. 1950; 143: 329-336Crossref PubMed Scopus (786) Google Scholar and Doll and Hill7Doll R Hill AB. Smoking and carcinoma of the lung: Preliminary report.Br Med J. 1950; 2: 739-748Crossref PubMed Scopus (1279) Google Scholar linking cigarette smoking to lung cancer were published in the 1950s, evidence has steadily accumulated that confirms not only the carcinogenic properties of tobacco but also its injurious effects on the arterial system. This evidence is familiar to most surgeons, but discussion of the epidemiology and pathophysiology of smoking is lacking in current surgical literature despite the fact that cardiovascular surgery owes much of its growth in the last two decades as much to TDD as it does to improved perioperative management and technical innovation. Although the manufacture of tobacco products is no longer considered a growth industry, it has spawned another one: the medical and surgical care of the large segment of our population with cardiovascular occlusive, thrombotic, and aneurysmal disease. Thomas, in one of the few reviews in the recent surgical literature, has summarized much of the published data on occlusive peripheral arterial disease (OPAD).8Thomas M. Smoking and vascular surgery.Br J Surg. 1981; 68: 601-604Crossref PubMed Scopus (22) Google Scholar In one British study nonsmokers comprised only 1% of patients suffering from claudication.9Eastcott HHG. Arterial surgery.in: ed 2. Pitman Publishers Ltd, London1973: 3Google Scholar Other recent surveys revealed that the risk of claudication developing in men older than 45 years of age who smoke more than 15 cigarettes each day was nine times that of nonsmokers.10Hughson WG Mann JI Garrod A. Intermittent claudication: Prevalence and risk factors.Br Med J. 1978; 1: 1379-1381Crossref PubMed Scopus (260) Google Scholar Furthermore, smokers who stopped smoking had less rest pain, less arterial surgery, fewer amputations, and lower mortality over the 8-year period of observation.10Hughson WG Mann JI Garrod A. Intermittent claudication: Prevalence and risk factors.Br Med J. 1978; 1: 1379-1381Crossref PubMed Scopus (260) Google Scholar A report by Juergens, Barker, and Hines11Juergens JL Barker NW Hines EA. Arteriosclerosis obliterans: A review of 520 cases with special reference to pathogenic and prognostic factors.Circulation. 1960; 21: 188-194Crossref PubMed Scopus (230) Google Scholar confirmed these findings; over a 5-year period, 11.4% of smokers underwent amputation whereas no amputations were performed in those who had stopped smoking. A report by Quick and Cotton12Quick CRG, Cotton LT. The measured effect of stopping smoking on claudication. Br J Surg 69:524-6.Google Scholar also confirmed that former smokers frequently enjoyed a lengthening of their claudication distance. Examining OPAD from still another angle, Kannel3Kannel WB. Update on the role of cigarette smoking in coronary artery disease.Am Heart J. 1981; 101: 319-328Abstract Full Text PDF PubMed Scopus (253) Google Scholar of the Framingham Heart Study found a direct relation between OPAD and smoking if the average annual incidence of OPAD for each 1000 persons (age-adjusted) is plotted against the daily number of cigarettes smoked. The incidence was 0.22% for nonsmokers and 0.65% for smokers of more than 20 cigarettes each day, a risk ratio of 3.0 (t = 4.46). With regard to coronary arterial occlusive disease (CAD), every study published from the western world has reported a strong correlation between the morbidity and mortality of CAD and smoking cigarettes. Extensive long-range data have been accumulated by the Framingham Heart Study and others that have shown that cigarette smokers younger than 65 years of age in western countries have twice the death rate from CAD of nonsmokers; “sudden death” shows an especially strong correlation with smoking.3Kannel WB. Update on the role of cigarette smoking in coronary artery disease.Am Heart J. 1981; 101: 319-328Abstract Full Text PDF PubMed Scopus (253) Google Scholar It has even been found that, similar to claudication,10Hughson WG Mann JI Garrod A. Intermittent claudication: Prevalence and risk factors.Br Med J. 1978; 1: 1379-1381Crossref PubMed Scopus (260) Google Scholar a dose-response relationship exists: the larger the number of cigarettes smoked, the greater the risk of CAD; the upward slope of the curve is steeper for men than for women.3Kannel WB. Update on the role of cigarette smoking in coronary artery disease.Am Heart J. 1981; 101: 319-328Abstract Full Text PDF PubMed Scopus (253) Google Scholar Conversely, after 2 years of abstinence from smoking, ex-smokers reduce their risk of CAD by 50%, with a further decline to approximate the CAD mortality rate of nonsmokers after 20 years.3Kannel WB. Update on the role of cigarette smoking in coronary artery disease.Am Heart J. 1981; 101: 319-328Abstract Full Text PDF PubMed Scopus (253) Google Scholar Similar reductions in the incidence of peripheral arterial disease after cessation of smoking were found by Koch.13Koch A. Smoking and peripheral arterial disease. 1. Government Printing Office, 1977Google Scholar The correlation of heavy smoking with cardiovascular disease in general, cerebrovascular accident (CVA), and congestive heart failure in the Framingham study was less pronounced than for CAD but was nevertheless related to risk ratios of 1.7, 1.8, and 1.3, respectively, in men aged 45 to 74 years during the 20-year period. But the correlation with CVA was not clear relationship between smoking and death from CVA in several other studies, both American and international. Considerable attention has been given in recent years to the hazards of “passive smoking.” Its most pernicious form is fetal toxicity, the mechanism for which is probably ischemic. Maternal smoking during pregnancy is associated with increased rates of spontaneous abortion, stillbirths, and neonatal death: abruptio placentae and placenta previa account for half the mortality, which in turn shows a correlation with the total duration of the mother's smoking and the intensity of cigarette consumption during the pregnancy.15Naeye RL. Common environmental influences on the fetus.Monogr Pathol. 1981; 22: 52-66PubMed Google Scholar The resultant increase of fetal death ranges from 30% to 50%.16Landesman-Dwyer S Emanuel I. Smoking during pregnancy.Teratology. 1979; 19: 119-125Crossref PubMed Scopus (64) Google Scholar The causation appears to be mediated by placental vascular abnormalities, because ischemic necrosis at the edge of the placenta is more frequent in smokers than in nonsmokers.15Naeye RL. Common environmental influences on the fetus.Monogr Pathol. 1981; 22: 52-66PubMed Google Scholar Moreover, fetal and neonatal deaths caused by congenital malformations and reduced birth weight and length are also associated with maternal smoking, as is anencephaly, which has a frequency in the offspring of smoking mothers 17 times that of normal offspring.16Landesman-Dwyer S Emanuel I. Smoking during pregnancy.Teratology. 1979; 19: 119-125Crossref PubMed Scopus (64) Google Scholar The ill effects do not end with delivery; long-range studies, conducted over the first 5 to 11 years in about 40,000 children, have revealed deficiencies in reading, mathematical, perceptual skills, intelligence quotient testing, and social adjustment.16Landesman-Dwyer S Emanuel I. Smoking during pregnancy.Teratology. 1979; 19: 119-125Crossref PubMed Scopus (64) Google Scholar Behavioral disorders, including hyperactivity, are also more frequent.16Landesman-Dwyer S Emanuel I. Smoking during pregnancy.Teratology. 1979; 19: 119-125Crossref PubMed Scopus (64) Google Scholar For adults, the data relating passive smoking to illness are mixed, largely because of flawed methods to measure the degree of exposure to the toxic agents. A simple estimate of the spouse's smoking habit is not enough. No studies are yet available, probably for logistic and ethical reasons, in which blood analyses of tobacco smoke end products (e.g., thiocyanate, cotinine, or carboxyhemoglobin [COHb]) have been made. There are, however, sufficient data to indicate that passive smoking is harmful for people with angina pectoris, asthma, and chronic pulmonary insufficiency. Although the process by which atherosclerosis begins and advances is complex and incompletely analyzed, the broad mechanisms have been fairly well described. These include abnormally high blood lipids, injury to the endothelium, abnormal proliferation of fibroblasts and smooth muscle cells, intimal platelet deposition, accumulation of lipids in the intima and media, and impairment of the vasa vasorum. Nicotine appears to be the principal agent in tobacco smoke that accelerates the injury. Atherosclerosis begins in early life with “preclinical lesions,” which take the form of “fatty streaks.” However, because the segment most affected by the streaks in infancy (i.e., the thoracic aorta), is not the most heavily affected in adult life, a controversy continues over their role as precursors of atherosclerosis. Young adults from populations with a high incidence of atherosclerosis have fatty streaks with the features of early plaques: lipids, excess smooth muscle cells, necrosis, and fibrosis. Growth of such lesions into fibrous plaques, to the point where they impede or obstruct arterial flow, occurs at widely variable rates, but it is not clear why the plaques chiefly affect the coronary arteries, the abdominal aorta, and the iliofemoropopliteal arterial segments. Most authors agree that the progression of atherosclerosis depends on several risk factors, the most important of which are age, sex, hypercholesterolemia, hypertension, smoking, and diabetes. The place of smoking in the causation of atherosclerosis is prominent. Grundy,17Grundy SM. Atherosclerosis: Pathology, pathogenesis, and role of risk factors.DM. 1983; 29: 1-58PubMed Google Scholar in a recent comprehensive review, summarized the pathogenesis of atherosclerosis by dividing it into two phases. 1.Injury—from hyperlipidemia (lipid influx), hypertension (hemodynamic mechanical injury), smoking (toxic products that induce hypoxia, such as nicotine and CO), and diabetes mellitus2.Response to injury—with platelet thrombosis, cellular proliferation (of smooth muscle and foam cells), phagocytosis, necrosis, secretion of connective tissue elements, and neovascularization. Many studies of blood cholesterol levels comparing smokers with nonsmokers have been made, which in the aggregate have yielded mixed, inconclusive results; either the differences were small or nonexistent,18McGill Jr, HC. Potential mechanisms for the augmentation of atherosclerotic disease by cigarette smoking.Prev Med. 1979; 8: 390-403Crossref PubMed Scopus (42) Google Scholar so that the conclusion has been reached that smoking does not universally increase serum cholesterol or beta-lipoprotein. However, after the discovery that cholesterol is transported in two different lipoproteins, low-density (LDL) and high-density (HDL), and after measurement of the two forms, differences were detected in smokers, who were found (in at least three surveys)19Hulley SB Cohen R Widdowson G. Plasma high-density lipoprotein cholesterol level. Influence of risk factor intervention.JAMA. 1977; 238: 2269-2271Crossref PubMed Scopus (143) Google Scholar, 20Goldbourt V Medelic JH. Characteristics of smokers, nonsmokers and ex-smokers among 10,000 adult males in Israel. II. Physiologic, biochemical, and genetic characteristics.Am J Epidemiol. 1977; 105: 75-86PubMed Google Scholar, 21Arntzenius AC van Gent CM van der Voort H Stegerhoek CI Styblo K. Reduced high density lipoprotein in women aged 40-41 using oral contraceptives.Lancet. 1978; 1: 1221-1223Abstract PubMed Scopus (58) Google Scholar to have a lower HDL level than nonsmokers (two studies did not show a difference).22Gordon T Castelli WP Hjortland MC Kannel WB Dawber TR. High density lipoprotein as a protective factor against coronary heart disease. The Framingham Heart Study.Am J Med. 1977; 62: 707-714Abstract Full Text PDF PubMed Scopus (4089) Google Scholar, 23Mjøs OD Thelle DS Førde OH Vik-Mo H. Family study of high-density lipoprotein cholesterol and the relation to age and sex.Acta Med Scand. 1977; 201: 323-329Crossref PubMed Scopus (70) Google Scholar This finding was particularly interesting because it had also been shown that reduced death rates from CAD are associated with high HDL levels, or low ratios of total cholesterol to HDL. A more recent study by Brooks et al.24Brooks SH Blankenhorn DH Chin HP Sanmarco ME Hanashiro PK Selzer RH Selvester RH. Design of human atherosclerosis studies by serial angiography.J Chronic Dis. 1980; 33: 347Abstract Full Text PDF PubMed Scopus (14) Google Scholar roughly quantified the progression of femoral atherosclerosis in 54 men, aged 45 to 50 years, by densitometry on arteriograms performed 10 to 34 months apart. Low levels of HDL and high levels of LDL were associated with more rapid rates of progression and smoking was also directly related to the degree of atherosclerosis in upper and middle femoral artery segments. In the study by Miller et al.25Miller NE Hammett F Saltissi S Rao S Van Zeller H Coltart J Lewis B. Relation of angiographically defined coronary artery disease to plasma lipoprotein subfractions and apolipoproteins.Br J Med. 1981; 282: 1741-1744Crossref PubMed Scopus (399) Google Scholar of coronary arteriograms a similar correlation was found; low levels of one form of HDL cholesterol (HDL2) were associated with more severe disease. Small increases of leukocyte counts and of hematocrit levels have been found in smokers, but there is no apparent causative link with increased risk of CAD, except for women who smoke and use oral contraceptives in whom there is a much greater leukocytosis and a greater risk of CAD.26Fisch IR Freedman SH. Smoking, oral contraceptives, and obesity. Effects on white blood cell count.JAMA. 1975; 234: 500-506Crossref PubMed Scopus (50) Google Scholar With regard to platelet function, several studies have reported increased adhesiveness and aggregation, but explanations for these changes did not appear until prostaglandins, especially prostacyclin (PGI2) and thromboxane (TxA2), were shown to be affected by smoking: production of PGI2 by the microvasculature is decreased and production of TxA2 is increased; both events favor platelet aggregation.27Hillis LD Hirsh PD Campbell WB Firth BG. Interactions of the arterial wall, plaque, and platelets in myocardial ischemia and infarction.Cardiovasc Clin. 1983; 14: 31-44PubMed Google Scholar Age, hypertension, and lipid peroxides also decrease PGI2 production, and hypercholesterolemia and emotional stress increase TxA2 production, so that other common risk factors may act synergistically with smoking to promote platelet clumping. These changes in blood components are augmented by several abnormalities of the arterial wall, which, according to a longstanding hypothesis that is supported by increasing evidence, begins with intimal injury and continues with progression of the atherosclerotic plaque. The rate of mitotic activity in endothelium is normally low, with a correspondingly low cellular turnover rate. The endothelial turnover rate in adult rats, with thymidine labeling, is 60 to 300 days.28Benditt EP Goun AM. Atheroma: The aterial wall and the environment.Int Rev Exp Pathol. 1980; 21: 55-118PubMed Google Scholar There are important species differences in such turnover rates and even differences in the rates among territories of the arterial tree.28Benditt EP Goun AM. Atheroma: The aterial wall and the environment.Int Rev Exp Pathol. 1980; 21: 55-118PubMed Google Scholar Because of the limited ability of endothelium to repair itself, with implications for the genesis of atherosclerosis, much experimentation has been done with various forms of injury, including balloon catheter abrasion, high cholesterol feeding, and smoking. The latter model has confirmed that nicotine injures endothelium. Whether given orally or intravenously to rats, nicotine, even in low doses (12.5 μg/kg) has an endothelial desquamating effect,29Hladovic J. Endothelial injury by nicotine and its prevention.Experientia. 1978; 34: 1585-1586Crossref PubMed Scopus (49) Google Scholar which has also been found in human beings. After 10 test subjects (11 controls) smoked two cigarettes within 15 minutes, the number of circulating endothelial cell carcasses increased by 50%.30Prerovsky I Hladovic J. Suppression of the desquamating effect of smoking on the human endothelium by hydroxy-ethylrutosides.Blood Vessels. 1979; 16: 239-240PubMed Google Scholar On the other hand, CO has not yet been proved decisively to have an atherogenic effect, although it does act in other injurious ways on the cardiovascular system. Platelets assist in intimal repair by forming pavement over denuded areas, which provides a temporary surface during endothelial proliferation. An important element in the repair is PGI2 generated by the intima of aorta, and mesenteric, coronary, fetal, and uterine arteries, as well as endocardium.27Hillis LD Hirsh PD Campbell WB Firth BG. Interactions of the arterial wall, plaque, and platelets in myocardial ischemia and infarction.Cardiovasc Clin. 1983; 14: 31-44PubMed Google Scholar Another secondary result of intimal injury and platelet adherence is the proliferation of smooth muscle cells stimulated by platelet-derived growth factor (PDGF). PDGF induces growth of smooth muscle cells in tissue culture and may have the same effect in vivo.17Grundy SM. Atherosclerosis: Pathology, pathogenesis, and role of risk factors.DM. 1983; 29: 1-58PubMed Google Scholar Whether the smooth muscle cells grow from the same monoclonal line, thus comprising a neoplasm as suggested by Benditt and Goun,28Benditt EP Goun AM. Atheroma: The aterial wall and the environment.Int Rev Exp Pathol. 1980; 21: 55-118PubMed Google Scholar their infiltration of the subendothelial layers contributes substantially to the “raised lesions,” or fibrous plaques, not only from their cellular mass but also from their surrounding collagen and ground substance. The latter is comprised of many large polymers, which are termed glycoaminoglycans (GAGs) plus mucopolysaccharides. Grundy17Grundy SM. Atherosclerosis: Pathology, pathogenesis, and role of risk factors.DM. 1983; 29: 1-58PubMed Google Scholar has speculated that GAG may be especially important in atherosclerosis because it can trap and bind LDL as it diffuses through the arterial wall. Other important constituents of the plaque are the foam cells. Although their origin is still not clear, they probably arise either from smooth muscle cells or from macrophages and are repositories for LDL cholesterol from pathways that are not mediated by LDL receptors, the so-called nonreceptor-mediated pathway,17Grundy SM. Atherosclerosis: Pathology, pathogenesis, and role of risk factors.DM. 1983; 29: 1-58PubMed Google Scholar through which lipoproteins move when the normal LDL-receptor pathway becomes saturated and insufficient. Although the manner in which nicotine, CO, or other components of tobacco smoke affect this process is unclear, it is presumed that lower levels of HDL and higher levels of VLDL somehow act to accelerate the process. The importance of vasa vasorum in the clearance or deposition of lipoprotein in the arterial wall has recently received considerable attention and it has been postulated that defects, or underdevelopment, of the arterial, venous, or lymphatic channels comprising the vasa vasorum might impair lipoprotein clearance, with vasoconstriction by nicotine as one probable mechanism. On the other hand, the vasa vasorum supply to atherosclerotic arteries is often overabundant, suggesting that there may be a perverse effect with an increased deposition of lipids in the diseased media and intima.17Grundy SM. Atherosclerosis: Pathology, pathogenesis, and role of risk factors.DM. 1983; 29: 1-58PubMed Google Scholar In addition to its influence in building atheromata, smoking has other, more general, adverse effects on cardiovascular function. The physiologic effects of nicotine are similar to those of the sympathoadrenal system, because nicotine stimulates catecholamine release from sympathetic ganglia and nerve endings, the adrenal medulla, and other chromaffin tissues. Several animal studies have shown that nicotine may have both contractile and relaxant effects when directly applied to arterial strips.31Su C. Actions of nicotine and smoking on circulation.Pharmacol Ther. 1982; 17: 129-141Crossref PubMed Scopus (55) Google Scholar Su31Su C. Actions of nicotine and smoking on circulation.Pharmacol Ther. 1982; 17: 129-141Crossref PubMed Scopus (55) Google Scholar has pointed out that the neuroexcitatory effects of nicotine on vascular segments have complex mechanisms that probably depend on the functional importance of the constrictor or dilator nerves, their sensitivity to nicotine, and the degree of preexisting muscle tone. The effects of nicotine's acute sympathomimetic influence on the cardiovascular system are manifold: transient increase of heart rate and stroke volume (therefore of cardiac output), blood pressure, myocardial work (therefore of myocardial oxygen demand and consumption), increased coronary blood flow, and increased susceptibility to arrhythmias. In the process of smoking, the effects of nicotine are of course accompanied by those of CO. The final common result of the latter is the hypoxia that results from COHb and carboxymyoglobin (COMb). Cigarette smoke contains from 300 to 600 ppm of CO and is the most abundant source of inhaled CO. Cigars and pipe tobacco burn at lower temperatures and thus produce a CO content two to three times greater. (The California Department of Public Health has established an air quality allowable standard of only 30 ppm.) After inhalation and dilution by ambient air, cigarette smoke averages about 400 ppm of CO. At a consumption rate of 35 to 40 cigarettes each day, the alveolar concentration of CO is about 50 ppm.32Turino GM. Effect of carbon monoxide on the cardiorespiratory system. Carbon monoxide toxicity: Physiology and biochemistry.Circulation. 1981; 63: 253A-259APubMed Google Scholar Normal nonsmokers have mean COHb levels of about 0.5%; smokers of one pack each day, about 2%; and smokers of two packs each day, about 3%.32Turino GM. Effect of carbon monoxide on the cardiorespiratory system. Carbon monoxide toxicity: Physiology and biochemistry.Circulation. 1981; 63: 253A-259APubMed Google Scholar An increase of COHb in exercising subjects lowers oxygen-carrying capacity of the blood, which is compensated for by increased cardiac output, increased oxygen extraction, and a lower venous oxygen tension. These are facile adjustments for people who have normal cardiac function, but they are more difficult for patients with coronary occlusive disease, who are unable to augment their coronary flow, myocardial oxygen uptake, and myocardial work.32Turino GM. Effect of carbon monoxide on the cardiorespiratory system. Carbon monoxide toxicity: Physiology and biochemistry.Circulation. 1981; 63: 253A-259APubMed Google Scholar Anderson et al.33Anderson EW Andelman RJ Strauch JM Fortuin NJ Knelson JH. Effect of low-level carbon monoxide exposure on onset and duration of angina pectoris.Ann Intern Med. 1973; 79: 46-50Crossref PubMed Google Scholar showed that men with stable angina pectoris had major reductions in the time intervals to onset of angina and depression of ST segments during treadmill exercise when exposed to 50 to 100 ppm of CO. When administered alone (i.e., without nicotine) at 150 ppm, CO increased left ventricular end-diastolic pressure and decreased left ventricular pressure, stroke work index, cardiac index, and coronary sinus, arterial, and venous oxygen tension, without changing blood pressure or heart rate, thereby creating a negative inotropic effect.34Aronow WS Cassidy J Vangrow JS March H Kern JC Goldsmith JR Khemka M Pagano J Vawtor M. Effect of cigarette smoking and breathing carbon monoxide on cardiovascular hemodynamics in anginal patients.Circulation. 1974; 50: 340-347Crossref PubMed Scopus (81) Google Scholar Other adverse cardiovascular effects of CO are increased vulnerability to arrhythmias, including ventricular fibrillation, reduced time interval until marked dyspnea in patients with chronic pulmonary insufficiency, and anatomic changes in rabbit myocardium.32Turino GM. Effect of carbon monoxide on the cardiorespiratory system. Carbon monoxide toxicity: Physiology and biochemistry.Circulation. 1981; 63: 253A-259APubMed Google Scholar In summary, while nicotine increases myocardial demand for coronary flow and oxygen by increasing blood pressure, cardiac output, and myocardial work, CO impairs myocardial performance by induced hypoxia. Where arteriosclerosis restricts coronary flow, CO-induced hypoxia compounds the insult in smokers. Although considerable progress has been made in defining the role of tobacco smoke in vascular disease, our understanding of the addictive process is rudimentary and has barely advanced from crude phenomenology. As defined by Pollin,1Pollin W. The role of the addictive process as a key step in causation of all tobacco-related diseases.JAMA. 1984; 252: 2874-2875Crossref PubMed Scopus (27) Google Scholar TDD is the “inability to discontinue smoking despite awareness of medical consequences.” The degree of addiction varies among its victims, but if the degree of addiction is expressed as a percentage of those unable to control their habit, tobacco is nearly eight times as addictive as alcohol.1Pollin W. The role of the addictive process as a key step in causation of all tobacco-related diseases.JAMA. 1984; 252: 2874-2875Crossref PubMed Scopus (27) Google Scholar What can be done? Wynder,5Wynder EL. Tobacco and health: A societal challenge.N Engl J Med. 1979; 300: 894-903Crossref PubMed Scopus (109) Google Scholar Pollin,1Pollin W. The role of the addictive process as a key step in causation of all tobacco-related diseases.JAMA. 1984; 252: 2874-2875Crossref PubMed Scopus (27) Google Scholar and Read35Read RC. Systemic effects of smoking.Am J Surg. 1984; 148: 706-711Abstract Full Text PDF PubMed Scopus (50) Google Scholar have emphasized that the medical profession must play a leading role in the reduction of smoking. Moreover, the most powerful figure influencing the individual patient will continue to be his or her physician. The vascular surgeon is in an especially advantageous position. Not only can he refer to all of the general health hazards, he can stress the abundant evidence that the patency of arterial reconstructions is adversely affected by smoking as he proceeds with treating disorders that threaten life or limb. This is especially true for carotid endarterectomy; Clagett et al.,36Clagett GP Rich NM McDonald PT Salander JM Youkey JR Olson DW Hutton JE. Etiologic factors for recurrent carotid artery stenosis.Surgery. 1983; 93: 313-318PubMed Google Scholar in a study of 29 patients with recurrent carotid artery stenosis, found that 95% of those with recurrence continued to smoke postoperatively compared with 24% of those who did not smoke. There was no significant difference between the two groups for any of the 13 other risk factors examined, except that women had a disproportionately high representation in the group with recurrent stenosis. Similar adverse effects have been found for arterial reconstructions in the legs. Myers et al.37Myers KA King RB Scott DF Johnson N Morris PJ. The effect of smoking on the late patency of arterial reconstructions in the legs.Br J Surg. 1978; 65: 267-271Crossref PubMed Scopus (97) Google Scholar reported a femoropopliteal graft patency at 4 years of 90% for aortoiliac reconstructions and 80% for femoropopliteal reconstructions in patients who smoked less than five cigarettes each day, but of only 79% and 61%, respectively, in those who smoked more than five. This study was criticized because it relied on the patient's testimony to determine smoking habits, but the difference in patency rates would probably have been even greater if an objective test, such as cotinine, thiocyanate, or COHb blood analysis, had been used. The nonsmoking group would probably have been contaminated by smokers claiming abstinence, not the reverse. To meet this objection, Greenhalgh et al.38Greenhalgh RM Laing SP Colap V Cole PV Taylor GW. Progressing atherosclerosis following re-vascularization.in: Complications in vascular surgery. Grune & Stratton, Inc, New York1980: 39Google Scholar studied a group of 200 consecutive patients for 5 years, using COHb levels as an indicator of smoking. They found that those whose grafts failed had an average COHb level about 2.5 times that of those whose grafts remained patent, although the data were widely scattered. Robicsek et al.39Robicsek F Daugherty HK Mullen DC Masters TN Narbay D Sanger PW. The effect of continued cigarette smoking on the patency of synthetic vascular grafts in Leriche syndrome.J Thorac Cardiovasc Surg. 1975; 70: 107-112PubMed Google Scholar have also reported similar adverse effects on the patency of reconstructions for aortoiliac occlusive disease. For most patients who have undergone operation to avert disability or loss of a leg, cautionary notes about the threat of smoking, delivered with appropriate gravity by their vascular surgeons, should be very persuasive, and the surgeon should make the most of this opportunity. It is obvious that legislated prohibition of smoking or interdiction of supply would be just as ineffective and prone to unintended adverse consequences as the Volstead Act of 1919 or the current campaign against hard drugs. A much more aggressive effort should be made by the electronic and printed media, but for economic reasons, much of it relating to the huge sums of money spent on advertising by the tobacco industry, it is unlikely to occur soon.40Warner KE. Special report. Cigarette advertising and medical coverage of smoking and health.N Engl J Med. 1985; 312: 384-388Crossref PubMed Scopus (76) Google Scholar This inadequate performance is especially regrettable because the public, as Warner40Warner KE. Special report. Cigarette advertising and medical coverage of smoking and health.N Engl J Med. 1985; 312: 384-388Crossref PubMed Scopus (76) Google Scholar has reminded us, has been sensitive to antismoking messages in the past. After each one of the following events there was an important reduction of adult per capita smoking: the first “smoking-and-ill-health” scare resulting from the Reader's Digest article by Norr published in 1952,41Norr R. Cancer by the carton.Reader's Digest. 1952; 61: 7-8Google Scholar the first Surgeon General's report of 1964,42U.S Public Health Service. Smoking and health. Report of the Advisory Committee of the Surgeon General of the Public Health Service (Washington).in: 1964: 387Google Scholar closely followed by antismoking messages on television and radio, and the beginning of the nonsmokers' rights movement in the early 1970s. All of this resulted in annual declines in per capita smoking through the last 12 years, rather than a continuation of the upward slope of the 1950s and 1960s. In the meantime, tobacco addicts have rather limited means for cure, despite the fact that many forms of withdrawal continue to be employed. It has been found that about 90% of smokers would like to quit, but the recidivism rate in the smaller percentage who succeed continues to be very high. The “cold turkey” method, for those with a strong will appears to be the best method, but for those with less resolve, the group therapy techniques and slow-release nicotine chewing gum seem to be fairly effective. Hypnotism, despite much initial promise, has been widely disappointing.5Wynder EL. Tobacco and health: A societal challenge.N Engl J Med. 1979; 300: 894-903Crossref PubMed Scopus (109) Google Scholar In those cases in which the addict is incapable of abstinence, his only hope is a less toxic tobacco. Fortunately there is evidence, albeit mixed, that the incidence of death from CAD and from lung cancer is lower in people who use filtered cigarettes than in those who use nonfiltered brands.43Wynder EL Stellman SD. The impact of long-term filter cigarette usage on lung and larynx cancer risk: A case-control study.JNCI. 1979; 62: 471-477PubMed Google Scholar, 44Hammond EC Garfinkel L Seidman H Lew EA. Some recent findings concerning cigarette smoking.in: Origins of human cancer: Cold Spring Harbor Conferences on Cell Proliferation. vol 4. Cold Spring Harbor, New York1977: 101-112Google Scholar Probably the crucial advance will come only when the neurochemistry of addiction is sufficiently understood, so that chemical antagonists can defeat this bizarre, grim disorder." @default.
• W2016287772 created "2016-06-24" @default.
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