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AEON(~'I, ~T. S., MD, KAPLA~N, M..A., MD, and JACOB, D., MD~ -Long Beach Veters~us A~ministration Hos.pital, and California College of MediCine, IYvine "Tobacco: A precipitating factor in angina pectoris.." (A~uals of Internal ~dicine 69/S: 529-536, September 1968) "Ten m~le smokers ~-at least 20 cigarettes daily for at least i~ • years_~ with c~assical angina pectoris due to coronary artery disease were ekercised in an upright position with a fixed exercise load on a bicycle ergometer.u~til they develbped ~e first m~ifes~tion of angina pectoris. each performed this ~xercise four t~es in a n~n-smoking s~t~ and ~es after smoking a cigarette of high nicotine content for fiv~ . ~nutes. All subjects developed angina sooner if they smoked before exer- ~islng.... .~. . • . ~"Patients with co~ona~'heartlisease increase~the myocardial mand for oxygen when the~'exerc~e~' The present.study indicates tha~ this Inerease..i.s even greater when the exercise is preceda~by smoki~g"--.because .-smoking increases the oxygen consumption of the heart. "After smbking and exercising p~tients with coronary disease c~uot meet the increased demands for m~ocardial oxygen, and therefore ~y develop angina sooner." V I T104682238

SMOKING AND THE HEART Cigarette smoking and heart disease: an update ~/"Wilbert S. Aronow, M~D. It is not enough for physicians to strongly urge patients to stop smoking-they should support restrictions against smoking in public places. It would be a step in the right "direction if doctors' waiting rooms, hospitals, and clinical laboratories protected nonsmokers with coronary heart disease from the harmful effects of cigarette smoke. I will review what is known about the relation of cigarette smoking to heart disease, em- phasizing the mechanisms by which smoking harms the heart. In light of current evidence, it appears that even stronger warn- ings and more stringent guide- lines are warranted for people who smoke. • The .evidence In 1975, the cardiovascular group at the World Conference on Smoking and Health agreed that the burden of evidence, experi- mental and epidemiologic, pointed to a causal relation be- tween smoki.ng and cardiovascu- lar diseases, including coronary heart disease, peripheral vascu- lar disease, and cerebrovascular disease. Research has shown that to- bacco smoke contains more than 4000 different components, but nicotine and carbon monoxide appear to be the most injurious. Carbon monoxide and nicotine cause harmful effects to the car- diovascular system, and these ef- fects may be especiaily harmful for patients with cardiovascular disease. It has recently become appar- ent that these noxious agents exert deleterious effects in many different ways and that even nonsmokers who are exposed to cigarette smoke may suffer un- toward effects. Furthermore, since there is.no known safe level of either nicotine or carbon monoxide for the cardiovascular system, it appears that cigarette smoke poses a substantial health hazard for both smokers and nonsmokers who have cardio- vascular disease. Risks of smoking Numerous studie~ have shown that cigarette smoking contrib- utes to coronary heart disease in the following ways: • It increases the incidence of myocardial infarction. • It increases mortality from coronary heart disease. • It increases the incidence of" sudden death, from coronary heart disease. Heavy smokers have a higher incidence of myocardial infarc- tion and mortality from coronary heart d{sease than do light smok- ers. It is also known that people who sto.p smoking have a lower incidence of myocardial infarc- tion and death from coronary heart disease than do. those who continue to smoke. Moreover, autopsy studies have shown a re- lation between cigarette smoking and coronary atherosclerosis. Coronary risk factors Of course, coronary heart dis- ease is caused by the interaction of many factors. Risk factors other than smoking, including hypertension, hypercholesterol- emia, hypertriglyceridemia, dia- betes mellitus, marked obesity, and sedentary lifestyle, further increase the risk of coronary heart disease. All things consid- ered, the greater the tobacco consumption, the greater the number of coronary risk factors. Moreover, the greater the degree of abnormality of these risk fac- tors: the greater the likelihood that coronary heart disease will develop. (continued) T104682239

_4,.0830, New Z~.e~n~ Medicat Jom'n~.'Smoking and Co~on~.cy Heart. D~. New Zealand Medical Iournal sudd~ d~ ~ c~, ~I k ~ ~. I~ o~ ~techo~e ~ele~ ~d ~boxyhemoMo~ . ~e posm~d. Un~ some o~er ~sk factors, smo~ng ~ ~n~o~able, ~d ~sul~ of ~on of smok~g ~ mo~ ~m~m ~ ~e ~o~ of die~, blood pr~s~e ~ent, ~d ~pid4owe~s ~. Not o~y ~e ~idud or phy~c~, but ~o ~e comm~i~ ~ ~ke p~ ~ smo~8 con~ol: leg~a~on ~ h~ w~gs on packe~ ~e ex~pl~ of ~6smo~8 T!04682240

l~ew Zealand l~dlcal Journal 7~/~81: ..369-70~ ~une 19~ ~ A/~~ Smoking and Coronary Heart Disease " Few u~ould debate that coronary heart disease is one of the most important health problems of our , time. This has been underlined by an authoritative : report by a committee of the National FIeart Founda- tion of New Zealandt as well as by a committee of the Royal Society of .N'ew Zealand." It is now time that the.emphasis was shifted from stating the facts towards doing something about them. It is not sufficient to suggest that we build more coronary care units, or join the mobile CCU band- wagon; nor s~qll the increasing use of coronary, angio- graphy as a means of more precise diagnosis and prognosis, or the proliferation of coronaw revascu- larisation surgical centres be any real answer to . coronat3' artery disease. These deal with the estab- lished disorder and overlook the fundamental fact that the largest proportion of those who die from corona~, heart disease are well and truly dead and buried before such treatments or procedures can be contemplated. This ~point has again been highlighted by a report of the Edinburgh Community Study,a a project in which an attempt was made to document • all suspected acute coronary heart attacks in patients ° under 70 )'ears living in Edinburgh during the course : of one year. A third of the patients died and in half of these, death occurred within one hour, with 75 • percent o~'curring outsi:.!e hospital, and in the _.:^.:'. ....a .......... ,.,_ reach the pati • . before, death. If there is to be any solution to these depressing sta.tistlcs, it will come from the approach of primal- prevention, namely, the early identification of risk factors and the institution of appropriate methods to control them. And this brings us to cigarette smoking. , The facts are these. Cigarette smoking'plays a / contributory rather than a prima~ role in the causa- tion of coronary heart disease m contrast to its causal relation to lung cancer and chronic obstructive bronchopulmonary disease. The association is ~tron~er in males than females, in younger subjects than okfer. and in those who smoke more heavily. The duration of the smoking habit see~ris less significant in contrast to lung cancer, and cessation 6f smoking is accom- panied by a decreased risk of death from coronary heart disease. Pipe and cigar smok~:rs have a mucl~ lower risk of coronary disease. The association between smoking and corona~" heart disease is strongest for myocardial infarction and sudden death while the evidence against angina is conflicting. Cigarette smoking appears to exert its effect indepen. dentl.v of other risk factors such as a raised se,'um cholesterol, high blood pre.~sure and physical inac- tivity, but when combined with one or more of these factors the risk increases considerably. There are some conflicting studies including the Seven Countries Stud.v,* a prospective investigation of coronary heart disea:e in I2_.000 men a~ed -t0-59 years in ]:inland. Crecce. haly. Japan. Ncthe,-lands. ~;ugo- slavia and the USA. Only in the American men was there the usual association between smoking and coronary disease; the Japanese and Finns were the heaviest smokers but their coronary incidence was not related to their smoking habits. However, the absolute numbers of coro.nary episodes in these populations was relatively small and a more recent report~ after 10 years of observation, suggests that in the case of the Finnish men a relationship has been established. Other ,,a'iters. inclndin,g Seltzer.0 suggest that there may be a coustitutional and genetic predisposition both to smokln2 and to eoronaD- heart disease, for there is certainly evidence that smokers differ from non-smokers in various aspects of personality and behaviour. Twin studies are often cited in support of the constitutional theeW but most of these involve numbers which are too small for valid conclusions. The judgment of the US Surgeon-General in 1971~ is a fair expression of the present position: "Data from numerous prospective and retrospective studies confirm the judg'ment that cigarette smoking• is a significant risk factor contributing to the develop- ment of coronary heart disease including fatal coronary heart disease and its most severe expression, sudden and unexplained death." Similar conclusions were expressed in the second report from "the Royal College of Ph)'siclans.s , That a relationship exists is therefore no longer in serious doubt, but there is certainly no agreement on the mechanism by whi[h smoking increases the risk of coronary disease. On the other hand, there are pathological studies which suggest that coronaD' atherosclerosis is enhanced by cigarette smoking and is related to the amount smoked.~ Furthermore, the considerably higher mortality from no~f-s.vphil~tic aortic aneurysm in smokers may also point to a possible influence of smoking on the atherosclerotic process. On the other hand, the epidemiologlcal data is more in keeping with the theory that the effect of smoking is acute in its action and possibly rever- sible. It" is suggested that cl.earette smoking hy con- tributing to the release of catecholamines, causes increased myocardial wall tension, contraction velocity and heart rate, and thereby increases the work of the heart and the myocardial demand for oxygen and other nutrients. Another theory is that carboxyhae- moglobin, for~ned fi'om the inhaled carbon monoxide diminishes the availability of oxygen to the myo- card~um and may also contribute to the development of atherosclerosis.. By a mecha,dsm of this sort in a person with impaired coronary circulation, smoking ma.v " trigger" myocardial ox.vgen deficits and lead to serious cardiac arrhythmlas. As yet these hypotheses have not been reasonably substantiated. Cigarette smokin,~ may not 1)e the most i~np • of the coronary risk factors but tt is something which. is amenable to correction. Furthermore. the rewards in terms of reduced coronary risk may well he achieved more quickly as a result of stopphlg smoking than by other measures such as diet. blood pressure treatment, lipid-lowering drugs and so on. For the T104682241

I~.~orts at hlgher ~sk ~uch as those ~,-i~h hypertension or a m~d ~e~ ~ol~terol~ ~e tr~tment of ~mok- ~ dependence is ~ fundamental pa~ o~ manage- m~t; indeed, the family d~mr ha~ a duty to ~eek out such high risk patients and to treat them. The ~on who actually has corona~" dise~e is usually ~ willing to renounce smoking and this should be pa~ of the them~utic pro~amme, although as yet • e evidence that long-te~ pro~msis is improved by ~ me~ure alone ~ not conclu~ve. It is naive to th~k that the t~a~ent of cigarette dependence is ~imple and there is no magic fo~ula. However, there m mine evidence ~at fi~ advice from a family d~tor is as effective as more ela~rate method~ such ~ hypnosis and the use of smoking cessation clinics. Perhaps if docto~ were to give a little more time to di~ssing the question and to ~e follow-up of the pafien~ results would be 6etter. The control of smoking is not entirely an indi- ~dua[ or indeed a medical problem. The community ~ a whole is invoN-cd, for s~iety has condoned the habit over many yea~, and has accepted the image of the smoker as one to be admired for manliness or ~auty, sexual attractiveness, poise and relaxation. We have given the .young no chance and it is the older generation who must share the blue for every new adolescent who takes up smoking. Le~slation by Government will not eliminote smoking but if those r~nsible for the health of this counhT do not make •eir own posilion utterly dear, they cannot expect the young to be impressed. ~us, the Government m~t cease to be concerned with the 56 million ~d l~nd its full weight to some of the measures which enlightened administrators are adopting in o~her parts of the world. Health warnings on packels, publication o~ tar m~d nicotine contents on cigarette packages, restriction of advertising and promotion, "ant'm'noking advertisements on television, all will play some part in the gradual breakdo~snn of the social acceptance of the smoking habit. Even certain taxa- tion measures might discourage cigarette smoking in the same way as happened with gin in the 19tb. century. Corona_,7 disease is ~. problem in New Zealand and cigarette smoking is a part of it. The time has arrived for acdo.n. I. National Heart Foundation of New Zealand (197[). Coronary Heart Disease. A ,Veto Zealand Report. Dunedin: John Mclndoe Ltd. 2. Royal S.ociety of New Zealand. (1971). Corona~ Heart Duease. Wellington: Dav:d Jones Ltd. 3. A~strong, A., Duncan, B., Oliver, M. F., Julian, D. G., Don~d, K. W., Fulton, M., Lutz, W., Morfison, L, (1972). Natural history of acute coron~ h~t at~ek~: a eo~nunity study, gr. Hcarl 3~, 67-80. 4. Key~, A. (1970). Corona~ he~t di~s~ in seven wire. Circul~gio~, ~1, Suppl., 1. 5. Pun~r~ S.,.P~6r~I~, K. (1970). Oigarette smoking and ~e ask ot death lrom eorona~ heart dise~e in east and west Finland. Scan. ]. Clin. ~b. 25, Suppl., 113, 38. 6. Sel~er, G. C. (1070). The effect of cigarette smoking on corona~ hea~ disease. Wlmre do we stand now~ Arch. ~nMron. Ht~lth, 20~ 41fl-4~3. ' 7. US Public Health Sen-ice (1971). Tile HtaltA qucn¢t~ oI Smoking.. A Report of the Surgeon- General, Washington, US Department of Health, Education and Well, e, Publication No. (HSM) 8. Ro)'al College of Physlclans'(1971). SmoMng and Now. London: Pitman Medical and Scientific Pub- lishing ~o.~ Ltd. 9. Auerbach, O., Hammond, E, C, Garfinkel, E. Smoking in relation to atherosderosls of the ¢orona~ arteries. N. Engl. ]. M~d., 273. 775-779. Repor Medical Research Council Report on Marijuana* Infroducflon At its mee.tir;g in April 1970 the Medical Research Council's attentmn was drawn t,> d.e need the requirements in New Zealand f,~r research on heahh asp~ts (,f marijnana u~ge. Ald.:,:;gh this committee as up was deslg~ated as an ad E,:.c cq,:~mi~teu on marijuana re~rch, the um of all cannabis preparations sidereal. In compliance whh d:e Narcotics Act (19651 the term ~nnabls is therefore used d:r~.ughout. An ad committee ~us set up to examh:e this field and make recommendations to oumcil, the membership o[ the com- bi~hemis~- division, DSIR), Pro~essor F. N. Fas6er (department ,)f pharmacology, U::~ershy V. ltodge (sciemific ~cretarF. Medical Research Council), *The furl report of this e,,:n::,ittee is available to interested research worke:s from: The Liaison Officer. .~,fedlrn[ Research Counc;[ .f New Zealand, Sclmol of Medicine. University .~f Auckland, Private Bag. Auckrand. "Profes~or'R. W. Medllcott (department of psychological medicine, University of Otago) and Dr D. F. Nelson (chemistry div,slon, DSIR, Auckland). The committee reviewed the information on cannabis available from both overseas and local sources, and in the light of this 1,as made the various rec/,mmcndatinas which are summarlsed below. Altlmugh there is now an increasing vokmm of relevant lherature un experience xvhh cannabis in ofl~er countries, the c,,m:oittee wa~ able to find very little factual inf.rma- d,,n ,,n the sltuati,m in New Zealand. Prc~irainary surveys Lave been carried m~t am, mS ~tudc,~ts it~ sc~ra~ urha~ areas and ~thers arc either planned or h~ pr,,grcss. H-wryer. ~uch rcsnhs as are avaihblc can only be regarded as tenta-" five and do not ncccssarily zcprcsent dm p~cmre as a whole. The o,mmiltee recommended that pri,,rity shmdd be g~veu to research which will provide valid inh,rmati,n on ~he nature and extent of ~nuahls usage in New Zealand and wt:icl~ will offer possible s,'utlons to the s~cial pr,,hlcu, s wt:ict~ thi¢ pn~. Spccialiscd research in t,ther fields is also required because of the growing cannabis problem in New T104682242

ATLA A CONSTITUTION D 200 558 k I HEALTH: HeartStrainiCan Br ng on,Au inu Angina pecteris is featured by severe pain in the mid-chest re- gion-~ightness, burning, fullness or ~i sense of pressure there. It may also radiate to neck, shoul- der and arms. Indeed, it resembles the feel- ing of a heart attack in many cases, Yet an electro-cardiogram may show no sign of abnormality. Or agaia the angina may be accompanied by known heart dls- orders, It can, with the same parent, symptoms, come from a variety of causes. The simplest to understand is! a narrowing of the arteries which ~ serve the heart muscle. H the muscle is not getting enough, cir- culation to mee¢ the labor de- - mended of it, the result is. pain. It resembles an acute muscular spasm or cramping anywhere else. • . Too much heart strain can briag on an attack. This may mean only an amount of activity which exceeds the ability of the heart to fulfill its functions with adequate ease. For one person this may mean walldng up a flight of stairs or strolling s e v e r a 1. blocks, Likewies, since digesting food draws blood to that area, a heavy meal can start an attack. other physic~l conditions may play a role..Hyperthyroidism, anenda and disorders of the ..aorta i are known to cause or contribute, l Angina .is relatively.. ¢ o m m o n among people with! diaries. And in some cases nO':l~hysical reason for the attacks can be found at all, This, as you may well imag- ine, 'is the subject of 'some in- tense research. . : ,... la some instances t~ stems from a weakness of ~e heart it: self, and yotrjust.have to accept this unhappy fact," i l~ft., ~hough: femporary; that the pmn ce~/ses'ahd the heart catch~~ .~ to ade~ate .~er. ~e eff~t of.~e tablet, however, is bH~. Fo~n~el~ ~ere is no. par~cu 1~ ]~t. ~ the n~r w~ch d~ ~ ~ ~ely.' Nei~e~ • e~. lose. ~elr But if'you have ~he problem, you can still be a great deal more corrffort~ble with it. : • Irt some instmaces permanent correction or lessening of the se- verity" may be possible. The most effective relief is bY placing a nRroglyceMn tablet un- der the tongue. It gives sufficient l with ordy a few a day. O~hers requir6 a •considerable number for: , comfort. : On occasion it is better to use longer-lasting nitrite tablets in- , stead of, the nitroglycerin. With either . medication, however', a , great.d'e~of; ,~.e success depends, upor/', the. patient, himself., He, , usually., ld~rn~ qmckly to recog- nize how much. e~ertibn he"can stand without suffering an '--how. much- he. can eat, h~ f~ and'how fast be d~ w~k. ~g from ~fice ~ park~g lot t~ much, ~en tak~g a ni~o pill bertrand ~ . ~i~ ~ • ja~t wRhout ~. ~am~g. ~ .only h~ way ~d th~ miring ' do~ to re~ ~f~ a f~ ~nut~. c~ wa~ ~f the pain. ~e h~ must have i~ r~i~ f~m stra~ If the "bI~ cholesterol is ~gh, r~u~ of i.t by diet ~d m~i- cation ~met~es r~uces ~en ~a, ~eractive thy, ~d or di~tes ~ at ~e root ~: trouble, it must' ~ con~, ,;~itt~g ~g is wlse, ~.. bac~ ag~a~ an~na. '., .

Clinical Psych~a~;~~ ~e~ Tcrk~ ,...A , IBB! Coronary-Prone .Behavior Linked to Angina Pectoris infernational Medi¢¢~l Ne~t'x Service MILWAUKEE m Coronary-prone be- haviors .~re found to be related to angina pectods but not to coronary occlusion as measured by artedography in 2,215 employed men patients, say ~D.F. _Iran-~ns~D'_Y°ung _and associates at me Med~cat L;ollege0t Wisconsin and the Veterans Administration Medical Cant~r, Wood, Wis. A questionnaire given to the subjects 24 hours before they under,vent c~rdiac catheterization measured competitive- ness, being ha~d driving, having a fiery temper, meeting deadlines and quotas. being ambitious, dissatisfaction, immo- bilization, perfectionism, impulsive- ness, anomie, and isolation. Nearly all of the behavioral items were more common in the patients with angina than in the patients without angina, the investigators say (J. Psychosbm. Res. 24:31 t-18, 1980). In cont~tst, nonbehaviora[ factors such as serum cholesterol, serum tri- giycerides; and history of sm.gking were related to coronary occlusion bat not to angina. T104682244

Cardiac Munchausen Syndrome - "re ~ "EDrrom: We +epo.rt t~ case consldm-ed a tother sopl~sficated "cardiac" example of Munchausen syndrome. A 28-year-old white man was transferred to the New York Hospital (New York, New York) because of chest paim His histo~ included rheumatic fever, at ag~ 3 and 6, and the later development o£ orthopnea, nocturnal dyspnea, pedal edema, and |nability to keep up. Mu]tiple episodes of palpita- tion and syncope during his tecas led to -~ clinical diagnosis miu-al stenosh, and quinidine was given. At age 17 he developed angina l~cctod,~. From 1963 to 1970, while a premedical student at Yale University, his nitroglycerin requirement increased. In March 1972, he again developed symptoms of congestive heart failure, while in Germany. An ¢chocardiogram at the Nymphca- b~rg Hospital in Munich showed a "floppy posterior leaflet~" and g coronary arteriogram show~l a "blockage of the l~ft anterior descending artery, right ma~n coronary artery spa~n and cardiomegnly." Recatheterizadon in .lone 1973 confirmed the fmdlng~. Surgew w~ deferred and warfarin sodium (Coumadlr~®*) therapy begun. In October 1973, whim sdll in Germany, he suffered "an acute myocardial infarction" com- plicated by ventriculur tachycardia. He was depolarized."many" tim~, and a temporary pacemaker y~as imerted. $uhsequendy, be wa~ well until 10 days before admimion, when he ~ mltted el~where with ~evere chest pain. ~.r~al .elccu-ocardio- grax~ showed T-wave changes in leads I, II, aVL, and V2 to VS. Cardiac ~nzymes wer~ elevated, but narcotic injecdom had been given for relief of l~aln. He reported that a grand- f~ther bad Marian's r/ndrome and that hi~omot~er and a • bad mitr~ valve dipole. His parents were separated and their whereabouts unknown. His wife had d~¢d recently ~n an auto accident in England. The patent had worked in a pet shop whets he studied in ra~ ~he "myocardial" effects of po~.~ium- d~pleted diets. He had ~ee= a volunmer amhula.qce driver. He reported allergy to perdci]lia, pentazocine (Talwin®t) mot- * ]~atdo Lal~tat~ri©s, Inc., Garden City, Ne~ York. 1' W~t~'op L~orat~de$, New ¥or~ New Yor~ Comment~ submitted/or publication must be typed double- ~paced, ~nd text length must not exceed 500 words. Com- plete references must be ]urniM, ed, as specified in "Infor- mation ]or Authors" {page 1-6). ~pecific permisMon to publish $hould be appended as a postscript. Publication depends on availability of space: we give preference to comment on recent content and to new information, Let- ters for this section should be concise--the Editor reserves the right to shorten them and make changes that accord with o'ur atyle. phln~, halopcridol and chlorpromaz/ne. ~Phys[ca~ examination showed a chronicalIy ~l appear[he young man, with a high arched palate and, negative wrht thumb sign. An early systolic ejecdon murmur was prt~.~.:. Ther~ was no diastolic murmur, flick, opening snap, or gallop. There wax the scar of a previous cutdown site in the right ant.-. cubital fossa. An electrocardiogram sh6wed non-specific ST-T s~gment abnormalities in lead aV.L A portable chest film showed no cardiomegaly. Several inconsistencies were apparent. These was no cardiomegalz. The patient could not remember the name of the physician who pr~cribed nitroglycerin over a year period. Inqnixy faile~i to support that he had been at Yale. The Deborah Hospital in Trenton, New Jersey had no 1971 "medical records of him. The Nymphenburg d/tal does not.do cardiac catheterizations, and the alleged cardiologist was not on the sta~. The patent's sister was not at the address supplied. For inapparent ~¢asons, the patient manufactured this complicated history. We believe, however, that he may have had cardiac disease (floppy rnitra.1, valve) because of h/s ready willingness to undergo echocardiography. He possibly had had earlier cardiac studies, which explaim the cutdown scar..Unfortunately a technical failure oc- curred during echocatdiography, and, bef0r¢ ~he study could be completed, the patient signed out of the hospit~l ~gter being confronted with 'the inconsistencies of his medical history. When the case was presented at medical grand rounds, a visiting house officer recalled seeing the patient under sim~ar citcumstanc~ at another hospital New York City. Department of Medicine • The New York Hospital-CornelI Medical Center New York, New York 10021 . C~tTa/'..~ ~ £',~.- ,~t~.,,.,,.,,.,,~.....= Z..- L~.: ;, ....... COMMENTS AND CORRKCTION Carbon Monoxide and Angina Pectoris TO T~ ~DITOR: I wish to point out that many individuals /n the alr pollution control field fed publication is synono- mous with authenticity. I've reviewed the literature and am appalled at the poor quality experiments used to sub- stantiate low episode criteria levels, justifying harsh abate- ment proceedings. I believe Doctor Aronow's studies (Ann Intern Med ~.~ Oc(obertP74 • Annals of Internal M~ldieln~ • Volume ,~1 * Nutnber4 77:669.676, i972) in carbon monoxide are grossly de- fecdve. His sampling is too small, or he would not ha>'e had 30% ST-segment depression in his first series of .10 subjects, with none in his second series of I0. .--'-'~ That all the patients had previous transmural infarctio.', and half of them had angiograms showing lesions of 50"- narrowing or greater does not prove that they had ,an: underprofused myocardium at the time of carbma mon- oxide exposure. Most patients with transmural infarcts make complete recovery. The most cridcal defect of the studies is that the end point, angina, was purely subjective. The bias of the o~- server is obvious. According to the Long Beach pr,':: Telegram, Doctor Aronow stated that 50,% of his paticnu with angina will be relieved by a placebo. It would have been far more beneficial to have had sizable group of patients with angiograph-proved artcr:- osclerorie lesions of 75% or greater, who had ST-scan:ca,' depression of 2 mm or more after maximum stress One could use a more accurate unit oi measurement T104682245

as the systolic time interval times the mean arterial preao ~e to estimate the work load of tho heart. Pulse rate times systolic pressure is not a scientific unit. Two of the three patients in the first group of ten, who had ST-se.~nent depression, were smokers. The study should be performed on nonsmokers. No e.Ran was made to overcome the Hawthorne the test subject's producing what is expected. Those in the fast study knew that they were being exposed to CO, which the observers felt would be deft/mental to heart trouble. In the first study, subjects rode the freeway with purified air fi'om a Bird Mark 8 Respirator" with a slight end- expiratory pressure. Although th~ Pc: and Pco~ were not ¢ha~ged, there is no evidence that there was not improved oxygenation by this end pressure. The arterial sampling was conducted after the patient got back #am the ride so that there was time for readjustment. ST-,.egment depression has dubious medical merit, as it wa~ on the Holier system, which was not calibrated. S6me ¢ardlologisLs accept 1.5 mm ST depress/on, but few accept I mm as suggestive of an/schemi¢ response. I urge the editorial board to be more ~'itical of by analyzing the methods used in the study. This stud~ is quoted, as ~, basis for ~t.ablish/~ the ambient air qualities on a federal basis. I do not believe that it is of lul~Ident scientific reliability to wan'ant such a status. bel/eve the edi.torial board has to assume some o£ the zesl~asib/lity for this having occurred. 3400 West Lom/ta Blvd. Torrance., Cali/omia 90505 In re~pon~e: [Tiu'ee paragrapl~s restating findings and concluslonx in References 1-3 were dropped to shorten thi$ letter o/ r~ ~o~e.] ~ pafien~ who p~p~ed ~ ~e two ~di~ (I, 2) ~d ~c ~0n~ ~na p~ods ca~ed by docu- m~ coro~ ~ ~e. S~ of ~ 10 pad~u who ~dp~ in ~ ~ay study ~d ~o~£p~c evi- ~n 50% ~ow~g of ~e lumen of at I~t one major v~ before ~ s~dy. ~¢ ~r ~o~ pafien~ had a d~eated ~sm~ my~ ~ at 1 ~ old. Two of ~ f0~ ~tie~ ~ve ~d coronw ~o~phy performed dnce the f~ay study, aod bo~ pafi¢~ ~d angiograp~c evidence of sig~fi~t coron~ ~W d~e. ~ 10 patien~ who pa~cipated do~]e-bfind study~d ~o~p~c evince Of ~¢ many ~conceptions ~ted in Dr. L~coe's lett~, "~t 50~ of the padcn~ ~ angina wiR be refiev~ by a placebo" ~ one o[ the more gla~g. Dr. Aronow pob~shed ~0 foflowing s~tcment: "I shoed ~ to emphas~¢ ~¢ p~nt ~t a mediation giver wi~ en- • usi~m may improve an~nal symptoms in at lc~t p~ cent of patients" (4). This statemcn~ is in no way relevant to the conclmio~ of the ~udi~ (i-3), t~ of w~ were double-bl~d (2, ~), showing the adve~¢ o£ breathing CO in concentrations present in heavy atmo- spheric pollmion on exercise-induced angina. The end point chosen to evaluate a~.gina pectoris must include pain. Bias-was eliminated by performing double- blind studies (2, 3). The product o[ heart rate tim~s systolic blood pressure at the onset of angina pectoris is a useful index (5). The unit of measurement systolic t/me interval times the mean arterial pressure has not appeared ia the literature and is not clearly definable. None of the patients smoked for at least 8 hours before the per~.ormance of the free,ray study or during the study (1). T~.e integrity o£ the investigators precluded any at- tempt ~ in~uenee the sub~ec~s into a "specific" pattern response. During the freeway study, the patients breathed com- pressed nix from a tank through a mask, using a Bird Mark 8 Respirator, with pressure settings and flow rates redui~ed and a built.in expiratory leak, so that signilicant posltiv.¢ pressure was not applied. There was no positive end-expiratory pressure. The arterial blood gas measure- meuts at th~ time of exercise testing did not show any alterations in ventilatory effects. Two doubl~-blind studies (2, 3) have aLso con/L,'med the adverse effect of breathing ~0 ppm o~ carbon monoxide versus compre~ed, put/fled air on exercise-induced angina. Tl~ most generally accepted criterion for ischernic ST segment depression is ST segment depression equal to or greater .than 1 mm below the r~ting level, with the ST se~men~ extending hor/zontally for at least 0.08 second, or with downward sloping of the ST segment WR,~ S. A~o~row, ~., F.~,.¢j,. C~ardigvascalar Div/slon University of California /xvine, California" I. A~o,~ow WS, Hxams CN, Isa~2. MW, et ah ~e~ of fray t~v~ ~ an~ ~o~ A~ Intern M~ ~:~9~76, 1972 Z ~oa~ W~ I~ ~: ~on mono~ effect on ~d~ ~a ~ ~ I~ Med 79:392-39~, 19~3 e~ ~ lnt~ M~ ~9:ag~0, 197~ 2~:~19520, 197~ ~37-~, 197a ele~ra~hy, ~ono~o~phy, a~x~rdi~a~y, and s~t~ ~ inte~a~ in Non~v~ire Medwds ~ e~t~ by Zous~lc~z S. Spr~gfitld, ~o~, Ch~les C ~r. In pr~ for I974 The typescripts of references 1-3 were reviewed before publication by consultants with e.rpert competence in the relevant disciplh~es and not by members o/the Editorial Board.--The Editor ~nm~nt~ and ~orr~ctlon 5~,~ T104682246