Tobacco Documents Online

C December 20, 1983 TO: FROM: W.T. Hoyt r'j Leonard S. Zahn SUBJECT: American Heart Association Anaheim, CA, Nov. 14-17, 1983 CC: WDH RFG SCS RCH It was AHA's biggest. meeting ever -- more than 1,700 presen- tations (:selected fromisome 5,000!abstracts that had.been submit- ted) before a record turnout of physicians from around the country. If the number of smoking-related papers and~posters didn't set a record for an AHA meeting, it was close. Further attention to, smoking and heart disease was sought by the AHA when its press . people arranged to pipe into the press room the press conference held in Washington on November 17 by the Surgeon Generali an~d issued a statement on its "reactions" to the SG's report. This event was live at 8 a.m. California time before some two dozen writers; after that session ended, the AHA held its own press conference with a panel of "experts," but attendance was somewhat sparse. Copies of the Surgeon General's Report were available on request. (I obtained a copy the prior weekend.) Press turnout in Aniaheimiwas quite extensive, but attention to the various smoking reports apparently was not, at least inithe lay media. Reporters fromithe major media (wire services, news maga zines, New York Times, etc.) left coverage of the Surgeon General's report to their Washington bureaus and I don't believe any of them filed any supporti.zg material from Anaheim. However, a few writers appear to be working on smoking-related stories for future publica- tion. (For example, a reporter for the news section of the Journal of the American Medical Association has been investigating the possibility, of an article onithe mechanism(s) of smoking inicardio- vascular diseases.) Conisiderable excitement was stirred by several reports that a human protein -- tissue plasminogen activator (TPA) -- had been, used successfully to dissolve clots in seven heart attack vilctims. Continuing,to attract interest were reports on coronary angio- plasty, the use of balloons at the end of catheters to ream out arterial lesions. The highlights: ~ . W 1. "Consumption of 'low-yield' cigarettes: its frequency and W relationship to serumithiocyanat.e" -- AARON FOLSOM, Minneapolis. W;b . ~! A study was done to assess the use and possible health risks N of low-yieldicigarettes (15 mg,tar or less). Cigarette brands and ~ serum thiocyanate (SCN) levels were determined in 2,561 adulit smok- eonard ahn andAs PUBUC RELATIONS COUNSEL sa iateSlnr, 13 LINCOLN ROAD •P-O. BOX 223 •GREAT NECK, N.Y. 11022 •(51!6)482-5715

2. ers (aged 25-74 years) who were among 9,10'6 persons participating in two heart disease risk factor surveys in seven upper Midwestern communities in 1,980-82. Brands were coded according,to Federal Trade Commission ratings for tar, nicotine and'carbon monoxide. The findings: Compared to 198'0 data (from the Nationial Center for Health Statistics) for the country as a whole, a greater pro- portion of smokers in these communities smoked low-yield brands. These brand~ were more popular with women than with men, and were smoked more by those with higher educational levels. Lower-yield brands are "toulted" as safer and probably appeal more to better- educated smokers and to women. Data show that there's no relationship between the number of cigarettes smoked daily and tar-nicotine yield. However, smokers of low-yi.eld brands compensate by altering their puffing patterns and depth of inahalation. SCN levels were only weakly re1'ated to brand ratings and tar-nicotine content. Even smokers of ultra low-yield brands had much hig,her SCN levels than nonsmokers. This suggests their disease susceptibility may not be reduced appreciably. "The public should know that cigarette adivertisments claiming, that low-yield'brands are less hazardous are misleading and, there- fore, switching to low-yield! brands is not an acceptable alter- native to total cessation."1 Overall, 32% of the study population smoked cigarettes con- taining,less than 15% mg of tar. More than 50% of adult smokers in, the U.S. smoked high-tar brands. In the study sample, 15% smoked cig,arettes with less than 5 mg tar, and 3% with less than 1 mg. 2. "Serumithiocyanate as a measure of disease risk among pipe and cigar smokers" -- Folsom gave this paper for co-worker TERRY PECHACEK, who was absent. (HENRY BLACKBURN also was a co-author.) Many pipe and cigar smokers, especially those who formerly smoked cigarettes, have higher risks of developing lung cancer and heart disease because they inhale. "Pipe and cigar smokers exhale much of the smoke, but then deeply inhale a blend of air and the samll' amount of smoke left in the mouth." Pipe and cigar smoke is "much more diense" than cigarette smoke and contains significant amounts of damaging chemicals even wheniit's diluted. These "find'ings" came from the same study population cited above and covered 114 cigar, cigarillo or pipe smokes who had~never smoked cigarettes and 194 who had. The former cigarette smokers were found to have higher SCN levels because they were more Likely to smoke four or more pipe bowls or cigars daily, which is equi- valent to smoking,10 cigarettes. 03734625 "Smokers of four or more pipe bowls or cigars per day, regard- less of whether they previously had smokedicigarettes, had quite high levels of thiocyanate, and therefore probably have an elevated risk of disease.".

C 3. Inhalation of tobacco smoke is what kills smokers. "The thio- cyanate data suggest that the amount of smoke that actually goes into the lungs of pipe andi cigar smokers is surprisingly high." Cigarette smokers should not be encouraged to switch to pipes or cigars as an alternative to cessation of smoking. "Some doctors are starting to notice cases of lung cancer in people who quit smoking cigarettes 15 or 20 years ago but continue to smoke pipes or cigars." Because changing from cigarettes to pipes or cigars is a relatively recent trend, it will be years before a large number of lung cancer cases shows up in death statistics. "We think it's wrong to wait for those statistics before warning cigarette smokers that switching to piipes and cigars may not lower their risk of disease." 3. "Effect of cigarette smoking on electrical stability of ventricular myocardium in man. A study using programmed ventricular stimulationiandirepetitive ventricular responise" -- VINOD JIVRAJKA, Lexington, KY. For the first time, Jivrajka claimed,, a technique is available for studying the electrical stability of the myocardiium. It in- volves programmed ventricullar stimulationiandelectrograms of certainiheart muscle fibers (,the His bundle) that are major factors in imparting rhythm to the ventricles. Heart block results when the rhythm is interrupted. A study was done on 22 smokers, aged'32-70, who had'coronary artery disease. Electrode catheters were inserted and various measurements were made before and'within 15 minutes of smoking one reference cigarette at the rate of'four puffs per minute for a total of about 10 puffs. One measurement dealt with repetitive ventricular response (RVR), a suggested marker for sudden coronary death. Also measured were levels of blood'carboxyhemoglobin and nicotine concentrations. The findings: Smoking significantly increased the incidence of RVR' and!decreased the time in which the myocardium's activity re- turned to normal. The higher incidence of RVR after smoking sug- gests that smoking acutely affects the heart's rhythm in a manner that's independent of the atherogenic effect of smoking. 4. "Effects of cigarette smoking on coronary hemodynamics in coronary artery disese" -- C.V.R. REDDY, Brooklyn, NY. 03"734fi'26 Few previous studies have'provided evidence that smoking impairs the performance of the heart already damaged!by coronary artery disease, Reddy said in giving some background' to his in- vestigationlof 7 subjects with severe triple vessel disease. Hee noted there are few and conflicting data on the acute effects of smoking on coronary blood flow. Further, there have beenino de- tailed studies on the acute effects of smoking on coronary hiemo- dynamics, myocardial oxygen and lactate metabolism. Most of the

4. studies have used high nicotine cigarettes and some have used more than one cigarette. -W His subjects, ranging in age from 41-67, were chronic smokers but had no evidence of'heart failure, obstructive airway disease, kidney or liver disease, or cardiac conductance problems. Various control measurements and blood samples were obtained from the subjects, alll of whom had cardiac catheters inserted. They were then stressed~on a treadmill until the onset of angina. After a rest period during which values returned to normal, each subject smoked~a low-yield cigarette (4 mg,tar, 0.4 mg nicotine). Repeat measuremenits were made immediately afterward. The subjects were then pacedianew unitil angina set in and measurements were again taken. The findings: The overall effect of smoking one cigarette was a decrease in coronary vascular reserve. The subjects developed angina earlier and at lower pacing rates. The mechanism seems to be a marked increase in coronary vascular tone that limites coronary blood flow; there was aparallel decrease in myocardial oxygen con- sumption. There also was a tendency for lactate production follow- ing smoking, indicating development of severe ischemia. Smoking produced negligible increases in myocardial metabollic demands. 5. "Acute effects of cigarette smoking on coronary vascular dynamics" --LLOYD KLEIN, New York. Klein reported two years ago that chronic cigarette smoking J.eads to changes in coronary artery reactivity, causing decreased coronary vascular reserve. From there, he and his colleagues went on to study the acute coronary hemodynamic response toismoking in patients with coronary artery disease (CAD) anid in normal subjects. His study group consisted~of 22 subjects (17 men, 5 women),, all of whom were former or current smokers. CAD was detected by coronary angiography in 16 subjects who were designated as Group I. These patients were further subdivided~into two groups on the basis of the lesion of greatest narrowing iniany region seenion angio- graphy: Group IA consisted of 7 patienits with severe proximal left coronary lesions, and Group IB' had!9 patients with significant distal lesions. The 6 normals were designated as Group II. With the use of cardiac catheters, blood flow was measured irn the coronary sinus (the terminal portion of the great cardiac vein) in all subjects immediately after they smoked one commercially available filter cigarette (16 mg tar, 1.0 mg nicotine)03'73462'7 The findings: Coronary sinus blood flow increased slightly overall in Group I patients compared to Group II patients. Coronary resistance increased overall iniGroup I but decreased in Group II. Patients in Group IA had a highly significant increase in coronary resistance as compared to Group IB. Coronary sinus blood flow tend- ed to decrease in Group IA and to increase in Group IB.

C 5. Conclusions: Smoking caused an increase in coronary resistance in patients with1CAD1. This had a greater impact in patients withia severe proxima,l narrowing than in those with a distal narrowing. "We propose that smoking,increases coronary tone at the site of the stenlosis (narrowing), limiting the coronary flow response pro- portionally to the size of the affected vascular bed." 6. "Effects of cigarette smoking on systemic and coronary sinus thromboxane (TX) and prostacyclin concentrations" -- JACK MARTIN, Philadelphia. Martin has previously reported work claiming that smoking de- creased coronary blood flow and increased coronary vascular resist- ance for an~y given level of myocardial oxygen demand. Smoking may increase platelet aggregation and~potentiate the release of TX, a potent indu~cer of platelet aggregation and a potent arterial con- strictor. Smoking has been reported to decrease the production of P, a potent inhibitor of platelet aggregation and a potent vaso- dilator. If a similar drop in P production occurs in the coronary circulation, then an imbalance between TX and P could potentially account for the acute coronary vasoconstrictive effects of smoking. A study was done to determine whether the acute coronary vaso- constrictive effects of smioking,wEre accompanied by an increase in intracoronary platelet activationiand~ a change in the balance be- tween TX and P production; also, to see what effects chronic smok- ing had on arterial and coronary sinu~s P concentrations. Subjects consisted of 8 lonig-time smokers, 6 men and 2'women. Four had more than 70% obstruction of at least one major branchiof the left cor- onary system; the other 4 hadionLy minor coronary irregularities. The subjects were tested while pacing on a treadmill before and after smoking. Conclusions: The acute coronary vasoconstrictive effects of smoking,were not associated with any detectable increase in intra- acoronary platelet activationior changes in the balance between TX and P production. However, smokers "may" have chronically reduced P production by vascular epitheliumiin bothicoronary and noncoronary tissues. Such reductions "may" predispose to the development of atherosclerosis or coronary thrombosis. 7. "Cigarette smoking: what is the evidence that cessation of smoking,is beneficial in coronary artery disease?" -- WILLIAM'. FRIEDEWALD, Bethesda, MD. Friedewal!d spoke at a symposium on clinical approaches to risk factor modification in patienits with heart disease. He presented no new data, but reviewed familiar material that he summed up as "powerful evidence," especially in regard' to smoking as a risk factor in heart disease. 03734628 Most of the dataihe cited were from well-known sources: the American Cancer Society, U.S. Veterans Administrationi, Sweden, Canaddan war veterans, British doctors (Doll-Hi1L)i, and Japan. All showed aniincreased risk of coronary disease in smokers, he said.

C 6. He also referred to MRFIT as showing a lower mortality in the men who stopped smoking. The data are "compelling" about the benefits of smoking ces- sation in regard to heart disease as well as lung cancer and pul- monary ailments. 8. "E'lectrophysiologic (EP) effects of cigarette smoking in man" -- R'OBERT PETERS, Baltimore. This poster presentationidescribed a study on 16 male smokers, 9 of whom were taking beta blockers for heart disease. Cardiac catheterization was performed on the subjects and blood samples were taken for measurement of nicotine, carboxyhemoglobin and~ catecholamine levels at baseline and 2'0 minutes after two cig- arettes were smoked. There was a significant increase in all the subjects in con- centrations of the three parameters cited above. However, there was no significant correlationibetween pharmacological and1EP data. Two subjiects in each group (those taking beta blockers and those not) had increased ventricular irregularities after smoking, buit no sus- tained~rapid heart beat. The conclusions: Smoking has catecholamine-like effects on parts of the conduction system that may occur even in the presence of beta blockade. Smoking had a minimal and transient affect on arrhythmia. 9. At the conclusion of the Surgeon General's press conference in Washington on November 27, the AHA held its own press conference in Anaheim. Present were about 10 reporters and: AN'TONIO GOTTO, Jr., Dallas, AHA president (he took office at the meeting); THOMAS RYAN, Boston, AH'A president-elect designate; WILLIAM KANNEL, Boston; and'JOHN HOLBROOK, Salt Lake City, chairman of the AHA Subcommittee on Smoking. They said what one would expect them to say in suchicircum- stances, including a statement that tobacco farmers could switch to other crops and~make a living. It was quite dull,, in fact. The AHA statement of "reactions" to the SG's report was what one expected. It noted that Kannel and Holbrook had contribbuted to the report. These quotes from the statement may be of interest: 03734629 "By even a conservative interpretation of the data in the Surgeon General's report, up to 170,000 Americans will die pre- maturely each year of heart and blood vessel complications directly related to smoking. This number is even greater than, the 129',0000 premature deaths fromiluing cancer and other respiratory diseases in 1982 which were related to smoking. Viewed over the 1!ong term, the cost in human lives from conitinuied smoking,is staggering: As many as 10% of all Americans now alive may die prematurely of heart disease related to their smoking behavior. Based on our current population, this means 24 million premature deaths due to smok-

,, 7. ing,.... Th~e American Heart Association accepts the challenge in- herenit inithese find'ings. It pledges to contimue unrelenting ef- forts to make"'the American public more aware of both the grievous dangers of smoking,and the health benefits that can quickly come from its cessation." 10. "Family history of sudden, unexpectedideath identifies relatives at high risk of coronary artery disease (CAD)" -- THOMAS PEARSON, Baltimore. While it has been recognized for years that CAD aggregates in families, it"s possible that all relatives of coronary patients may not be at the same risk. Certain subgroups may be at exceptionally high risk. Also, it's n~ot known by wha:t mechanism heart disease occurs in certain families. One theory is that certain inherited risk factors (e.g., elevated blood'cholesterol, hypertension or diabetes), or certain learned risk factors (e.g., smoking)i also aggregate in families. Relatives are more likely to have these risk factors and,eventually get CAD. Another theory is that some of the risk is mediated by these risk factors, but that additional mech- anisms may act to cause heart disease to occur in certain families. Detailed family histories, including whether close relatives died suddenly or unexpectedly, were obtained from1577 white men whoo underwent coronary angiography. It wa.s seen that men with CAD had significantly more frequent family histories than men without disease (5,4% vs. 309 positive histories ). Other risk factors, including smoking, were analyzed, but the association persisted even after adjustment... Only in men under 50 years of age did diseasedimenihave more frequent family histories of disease than did disease-free men. Family history was not associated with disease in men 50 years or older. A history of CAD in a relative under 60 years was associated with disease in these young mien, but coronary disease in relatives over 60 did noit predict disease. The question most strongly, identifying diseases vs. non- diseased mien concerned a history of sudden, unexpected death in one or more relatives. Significantly more diseased thaninon-diseased men had both a positive family history and a history of a relative dying suddenly of'coronary disease. If a subject had a positive family history, but no history of suddent death in the family, there was no difference between diseased and non-diseased men. 11. "Clustering of healith-related habits within spouse pairs" -- JACK HOLLIS, Portland', OP. Q3734s30 A study was donie to determine the degree tolwhiich a variety of health-related habits and riisk factors were shaired within couples. The study populationiconsisted of 2'01 couples, nearly all of them married, from a subset of households participating in a family heart study community dietary intervention program.

C 8. Members of spouse pairs were found to be similar in terms of a number of dietary patterns. The strongest associations were for be- haviors invol~'inig smoking, alcohol, caffeine and marijuana. (Men with smoking wives were 2.6 times more likely to smoke than men with nonsmoking wives.) On the other hand, reported leisure tiime activities and Type A personality measurements were glenerally dissimilar within couples. "Thiese findings add to a growing body of evidence suggesting that the most appropriate targets for health behavior change ef- forts may not be high risk individuals, but rather the entire fam- ily unit." 12. A mail survey of physicians in four Midwestern towns,, reported~by RICHARD GRIMM, Minneapolis, disclosed these attituded' aboult.heart disease prevention: risk factors cited, in order of decreasing importance, were blood pressure, heredity and smoking; weight, stress and diet were seen as less important; physicians felt they were most effective with blood pressure and much less so withidiet, exercise and smoking; direct advice was considered as having a mod'erate to large effect impact onihelpling patients to stop smoking. MISCELLANEOUS ITEMS: ROBERT CASE of New York said the Type A concept may have been overstated. He studied a large number of patients two weeks after their heart attacks and checkedithem again three years later. His conclusions: Type A behavior didn't cause greater initial heart damage or result in a worse health history later. New AHA officers: President, ANTONIO GOTTO, Jr., Bobland Vivian Smith Professor and chairman, department of medicine, at Baylor College of Medicine, Houston. Chairman of the Board, J. FRAN'KLIN1SMITH, Johnstown, PA, former president of the Pennsylvania Electric Co. Board chairman-elect is RIC'HAR'D A. BOEHNING, a lawyer in Lafayette, IN. President-elect is THOMAS'J. RYAN', professor of mediicine at Boston University School of Medicine. -END- .r .~ w SN3A315 C ~ C~~IgI~ w