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ST. LUKE'S HEv;L?H SC1Ep;!'gS LIBRAPY trcti~e: T~ n;l: ;el t y G ct_:!ed by copylight lLlv (i)tle 17 U!S. Code). lnrrrnauun)r/ Journal'o(Cardrolug%: 3? /~1y91 )'_17-L5,, 24- c : 19`)1 Llkesicr Science Publuhers B:V. All rights reserved 0167-5273/9li/S03.50 .aDO VIS 01h'S'73H 100=36Z CAR'DIO 01349 Indoor passive smoking: its effect on cardiac performance A. Leone, L. M'ori, F. Bertanelli, P. Fabiano and M. Filippelli Dfnsiun of AJrdicine. Crtt Hospital Ponrrrmoli. Lunigiana. Imis (Recei.rd .4 December 199U: revision accepted'_U Muy 1991/', Leone A. 41ori L. Bertanelli F. Fabianu. P: Filippelli M. Indoor passive smoking: its eflfact on cardhac performance. Int J Cardiol 199'1:33:'_-i7-'_5'_. We studied 19 nonsmoker male volunteers. 9 hcalths ('mean age 30.4 = 8.51, and 10 w-iih preciuus m}ocardiai infarction (mean age 43.8 =5.3), who underwent exercise stress testing twice: in a smuke-frec environment an& in a smoking environment (carbon monoxide concentration 30-35 ppm). We measure& peak exercise power. time to reco.er} of pre-exercise heart rate, expired concentration of carbon monoxide and plasma carbon monoxide. Obtained data were compared by using t-test. P < 0:0: was statistically significant. Mean data observed in healthy people were as follo..s. Peak exercise power 220 = 30 watts in a smoking environment versus 220 = 30 in a smoke-free environment (P> 0.05). Time to recosery of pre-excrcise heart rate 19 -_ 4 minutes in a smoking environment versus 8.5 _4 in a smoke-free environment ( P < 0:0C): Expired concentration of carbon monoxide before exercise :-3 = 2.01 ppm versus 8.5 = 1.6 (P< 0.01) after exercise in a smoking environment, and 2.3 = 2 ppm before exercise varsus 2.1 = 1.9 after exercise in a smoke-free en\ironment ( P> 0.0: ). Plasma carbun munu\id'e before exercise 1.4 = 0.:17c versus1.7 _ 0.,3 after exercise in, a smoking en%irnnment ( P> 0.04), and 1.2 = 0:arc before exercise versus 1.2 = 0A in a smoke-free environment ('P > 0.115 )'. Corresponding measurements in survivors of infarctiun were as fulluws: peak exercise puwcr 80 = 25 watts versut, 120 -_ 20 ( P< 0.01), time to recovery of pre-cxercise heart rate :I = 2.5 mi'nutes \ersus 1_'.3 - 2.0 (~P 0.01), expired' carbon monoxide 0.6 = 0._' ppm %ersus 5'= 1.2 (1P' < 0.01) in a smoking ent irtln- mc,tt andl 1.2 - 0.8 versus 1.3 _ 0.6 ( P> 0.05) in a smoke-free cn.ironment. plasma carbon monoxide 1.?' = O:f61c .ersus 23 ± 0.4 ( P< 0.01) in a smoking en.irunment and 1.2 y 0.1 versus 1.2 = 03 ( P > 0:05) in a smoke-free environment. Cardiac response to the exercise is significantly wursened by passi\c smukec especially in those subjects with pre.•ious myocardial infarction. Key'wttrd's; Passive smoking: Infarcted people , Introduction [ li-.3J. A strongly incriminating relatiunship bc- twern cigarcttc smoking an& mvucardiai inf'urc- Stnoking interferes negatii.•ely with cardiitc per- fion, has been shown by numerous studie. formance and is responsible for uarcliuc pnthulug}• but a quantitative assessment of the alteratiunN caused', aruteli~ hy passi\c smoking on cardia~ performance in hcalthy peopll and those ..ith rnmp.rndrner r.- IDr'. \ur.•/nl Lomr. \t.D.. \~I:1i Phm tn~ prC\'It1tlSmYt9carljlall lnl:lrcLrln h;lN nol, \,:t' h,.c.1Y ~-..;'1II")'l .I,Icllltlr-a \l.Ilr.111PI: ll.ll{. Cltah6hclj.

241 The purpose of this study was to investiEate, quantitatively. the effects of' passive smoking oncardiac performance of healthy people and'thosc winhiprcvious myocardial infarctionL Materials and Methods 19 nonsmoker male volunteers (Table 1'J, 9 healthr aged from 17 years to 4431years (mean, age with 1 standard deviation 30.5 ± 8.5 years), and 10 with previous myocardial infarction aged, from 43 years to59 ycars (mcan, age with ± standard deviation, 518 ± 5.3 years) were studied. The healthy people had no history of any illnesses at all.. Their resting 12-lead electrocardiogram wati normal. The suhjccts, who survivec1' a first acute mvocarclial infarction; had had an.anterior infarc- ticm in 5 cases and an inferior infarction in 5 cases. All suhjcct,. gave their: informed cun.c:n1 to he inclucJed! in this,stud\. The studietli population undL•r..cnt exercise stress testing on a bicycle ergomcterl tW ice: the first time, the subject perf'urmed the exercise in sixtn cubic metrrs enclosed space not polluteti' h% cigarette smoking. On the second occa,ioni the amhicnt: atmrrsphcrc was polluted by 3t)-35 ppm carbon monoxide concentration we reached hs the combustion of 15 to 2U1ciiarcttcs within half an hour hy utiing a,witchmer machine connected to a Procr;tmmahlc In1ru-rLd SpectnophutomctCr at Variable Pathwav (Wilks Mhd. ttiO'). This device allinticd u; to mcanurc carbon monoxide comccn- rm1sLL I tration and maintain it at the desired le%el during exercise stress testing. Each studied subject was test and control ofl himself. During and: after exercise, electrocardio- graphic Ieads V2-V6 were displayed continuouslti on a monitor scope, and once every . minute a 12-lead electrocardiogram was recorded'. Sjstolie blood pressure was also~ recorded~ with a sph,,g- momanometer during the last. minute of the excr- cise, In each studied subject we assessed the peak exercise power, time to recovery of pre-exerci,c heart rate and~ carbon.monuYidc concentration of'f both expired air and plasma before and af2ar exercise. Statistical methods Standard statistical methods were usco. All data were compare& by using the r-te,t !''< u.u5 was taken to denote statistical siLnificancc. The data arc presented as means - SD. Results The result, t)1 this studr are summarized tmi the Tables 2-5. Peak exercise prt%ccr (Table 2) of healthy people ranged from I4U~ to 260 u ttts (mean '_2(l - 3(1) in a .mt>hc-Crcr emironmupnt.. and! frumi 1'SO to '_bl) «att. lmcan; 22f/1-_ ?O4 in a, smoking environment. The rorrespcondin_ fiLurr. in survivttrs o( infarctitm wurr 8(1 tu I-40 %kattN (mean 120 - ,f)) in a smo{,u-ticr cminonrncnt. and~(i(1 to 1211 watts (mean \tl='-5) in a,mokrne, environment. a statisticalk tiicnlticant Liltfcrcncc (P<(I.t111. Time to rccoverv of prc-cxerci.e heart rate (Table 3) for he;tlth~ people was -i'i to I`s" minutc.. I tcatthy pcort)c Numhrr 9 Mran agc (years) 30:5=K.5 Sex (mrlc) 9 TADLL ? CIwruclcr .iics uf thr .tudird n ipuLwun. Nirpreviuuti medical history Survivors of infarctiun Number t) t'cak exereise tx>`aer (satta, mean -_ SD, in the .tud rd r>•+nu- lauom. Mean age (years) . 53,K± 5.3 Subtrcts, Smoking Jmnle-trce r-tc.t Sex (male) ttl' cnvtrnnmrnt rn% tronmn nl infarction anterior inferior tt) 55 S Ilu:ttthy penr,tc Sunisor. .11 ml:irctiomi __n-_ tn ti11-.~ __n-_ 1_11-_I1 J. u,ol

:49. "I A{iLE 3 Time to reco.en oflpre-rzerctse heart rate (mmutesl, mean- SD: in the stuJteJ pupuiauun. Subjects Smoking ' enN ir(lnmenl Smoke-free environment I-rest Hs;ilth% people 19_-a 8L(i_.i P<0.011 Survivurs of infarction, 21- ::5 1'_:3/) -? P < 0.011 (mean 8.50 ±.3) in a smoke-free environment. and H toi_'5 minutes (mean 19'y 4) in a smoking environmenti with a statisticalh• significant differ- ence PP < Uj01). The corresponding parameterss in survivors of intarcniun ranged Erom, 10 to 15 minutes (mein 11, _10), im a smoke-free ern i- ronmtnn. and from IS to 2,; minutes (mean 21 = 2.50) in the envirunmant polluted by cigarette Smctke., a Ytclristic:tll> >i_ntticant dilt'urcncc (P < t).111 ). The rcsultN cunccrnin-g, the ctmccntration of cxpircJ' uancon munu.\idc are di,pla}u7J' in Table 4. In hraltfi% ~oluntecr, thcrc vas ntl dittercncc in the values priclr tu J\crciNr betweLn the smok- in_ and smoi.r-trcc umirunmrnts (2..'+ =_'.01 ver- ,tiuN _. 3- 2'.0': ppm ). In the smuke-t'ree em inrn~ l - ment. thrre .vus nu sl_nificant chan=e aftcr exer- cisc (2.11= 1.9! /'> (LII5). svhurcati in thr :mc)kin_ environment there %%a:, a,i_niticant increa,e lto T.\131.L J' 8'.5 ± 1.6. P < 0.01) after exercise. In survivors of' myocardial infarction. the concentration prior to exercise was significantly lower in the smoking environment than in the smoke-free environment (0.6 ± 0.2 versus- 1.2 ± 0:8, P < 0:05). In the smoke-free environment, there was no significant change in the concentration after exercise ('13 ± 06, P> 0.05), whereas in the smoking environ- ment there was a significant increase (to 5.2.± 1.2,, P < 0!01)~after exercise. Although the two groups had different age distributions, there was no sig- nificant difference inithe measurements betw•een thc survivors and the healthy voluntcers. except for the concentration of' espired carbon monoxide after, exercise in the smoking environment (healthy 5.5 -- 11.6 versus survisors 1.2. P < Ua01 ). The results uf, cconcentration of csrbon monox- ide in the planmu arc cJiSpla%ud in Table 5. lin~ hcalth~ %wlunteer, there v.as no dilltcrr%e in thr, result~ prior to exercise between the :mokinz antj' smukc-trcr em irunmentv ( 1.-t =0.: \er,us 1._ = 0.a''r' )~ In, neither the timokin_ environmc.rn~ nor thc smoke-free environment \&as there a signifi- cant change after exercise (1.7 = U:4. P > U!O5and 1..'_ U.-i'. P>(1.05. re,pecu\ely): In ,ur,i.or, of intarction there was no dilterence in the pre- exercise concentration het>,.rvn ttie smoking anS smokr-trec rn\ irtmmentn (1.2 _ 1):ln rersu% l.' = I:-qitrcil .':irh,m nwn,na,fe lTrpml: mc.in = 11), in the tuJi.J n thul.iti„n. Sul•trrt• 1moF,mi tmtnmment licatthy pooplc Sunn+v, nltNUrcuoni nlea hc;tlth\ ,,wrn nor. rPR'-CXCrct.C Pu.lrv\l'rUtSl Ir I C..t _.. __.tll 1,"- Ln P~ 11.111 U:n-11.: 5'-l._ l':IL111 P> 0:1)i' P<(EII I TABLE ~ Pta.ma r:tr(wm mom+siJe ma:tn + 5D: in the studieJ txtpulau m. Suhlcets Smoking omvtutnment Ptr-etrrcue Pna-exercise /.test t1L•althy petiplc ILJ -_ Il::. I.;'-_ 11.4 P> 0,05 5utvi.ott, of inl:trcuwm II' - Il:Ifr, _:3,+ 11.4 P< O.INII 1moL,'c ttuu rnriranmrnt, Prc-rWri ur Ro.t•rwrrt.a r-te.t L:-tl.ti 1.z_0.6 P> U~Ufi P>(1;05 P > u:u5 P > 0.05, Smoke-free environment Pre-exercise Post-exercise r-sesl 1..'= ILa 1 LZ -_ 04 P> I1:0I; 1.:'- 0;1 lL'_ -(1:3, P> I1;1)5 ' r•tr.tho:dthM unrn,irn P ilif~' f:IIJ)~ P>(1.04Z P> 0 I14Z

250 0.1). In the smoke-free environment,, there was no significant change in the plasma concentration after exercise (1.2 ± 03, P> 0.05), whereas in the smoking environrnent there was a significant in- crease (to: 2.3 ± 0.4, P< 0.01) after exercise. AI1 though the two groups ha& different age distribu. tions, there was no significant difference in the plasma carbon monoxide measurements between the survivors and the healthy volunteers, except for the post-exercise plasma carbon monoxide in the smoking environment (healthy 1.7 ± 0.4 ver- sus survivors 2.3 ± 0.4,, P < 0.05 )! Discussion. For many people, exposure to environmental tobacco smoke is a potcntiall hazard' of daily life. We planned this study since of many air pollu- tants, the components of cigarette smoke have an vrigin both indoors and outdoors [7], and can cause serious effects on the cardiovascular system [8]l Cigarette smoking can lead to catccholaminc release which enhances platelet adhesiveness. Cigarette smoking and', nicotine may also increase myocardial electrical instability: heart rate and systolic blood pressure exacerbating the athero- scicrotic process. Carbon monoxide increases the blood's carboxyhcmoglobin lcvel'because its affin- ity for hemoglobin is much greater than that of oxygen, diminishes oxygen transport capacity and damages directly myocardial mitochondria and; endothclium [9]: Cardiac effects are the result of the degree of exposure to~smoking and usually do~not become apparent for days after exposure 110). The acute response of the heart to passive smoking has not yet been carefully evaluated. Our data seem to show two different types of response, the one for the healthy subject and' the other for the subject with previous myocardial infarction. However,, some characteristics were similar. A significant reduction of peak exercise power (33.4% in this study) has been seen im people with previous myocardiali infarction who have un- dergone exercise stress testing ima a smoking cnvi- ronment compared to their response inia;smukc- free environment ( P< 0.01'1). Healthy people did not have impaired' peak exercise power. in a smoking environment„ time to recovery of pre-exercise heart rate was prolonged in both groups. In our opinion that may be the conse- quence of decrease& environmentali oxygen avail- ability. It is known indeed that the environmenn is fundamental' for human, homeostasis, and de- creased environmental oxygen is potentially ' harmful for life. Three main observations on expired carbon monoxide and plasma carbon~ monoxide can be made from this study. Firstly, pre-exercise an& post-exercise measvrements were similar or not statistically different (P> 0.05) for all pcople in a, smoke-free environment. Secondly, in a smoking environment, post-exercise plasma carbon monox- ide of survivors of infarction was statisticall.~ higher (P <0.05) than that of healthy people. Thirdly, in the smoking environment post~ex- ercise expired carbon monoxide was significantl% lower (P <0.01) in survivors of infarction if com- parc& to hoalthy controls. Although there is a siEnificant, difference between the survivors and healthy controls as regards their post-cxercise expired carbon monoxide and plasmal carbon monoxide, this may not necessarily ba due whollk or even partiallyy to the previous myocardial in- farction, as the two groups had different age distributions. Since the values of cxpircd carbon monoxide and plasma carbon monoxide prior to exercise were similar (P> 0.U5)' in both groups. we believe the previous myocardial infarction combined with exercise stress testing in the smok- ing environment is a responsible factor of the aforesaid occurrence. Survivors of infarction of- ten have cardiac failure, even if sometimes silent. as a probable consequence of impaire&hacmod~- namics. Such pathology may affect the blood gas exchange as well as the ventilation/perfusion ratio. However, this hypothesis should be further investigated. Acute exposure to passive smoke impairs the cardiac performance of both survivors of infarc- tion and hcalthy voluntccrs. Survivors, who often have hacmodynamic impairment, should avoid in- door %paees polluted by cigarette smoke. The f'ucn that passive smoking also claarlj aff'cct.s the car-

diac measurements made in the healthy volun- teers has implications for public health and legis- lation. References 1 Doyle JT, Dawber TR. Kannel WB. Kinch SH. Kahn HA. The relationship of cigarette smoking to coronary heant disease. 1 Am fuled~Assoc 1964;190:886-890:, 2 Hammond'EC, Garfinkel L. Coronary heart disease, stroke and aortic aneurysm. Arch Environ Health 1969;19:167- 18'-. 3 Reid'DD. Hamilton PJS. McCartney P, Rose G. Jarret H. Keen H. Smoking and other risk factors in coronary heart disease in British ciNil sarvants. Lancet 1976:ii:979-9l+4: 4 Leone A. Tagliagambe A. Long-term prognosis of in- farctrd smokers: is it affected by smoking ceasauon': In: Aoki M, Hisamichi S, Tommaga~ S. eds. Smoking and health 1987, Amsterdam. Elsevter/North,Hulland. 1988: 723-726:. 5 Kaufman DW;,Helmrich SP„RosemberY L. Miettinen OS, Shapiro S. Nicotine and earbon monoxide content of cigarette smoke and the risk of myocardial infarction in young men. New Engl J1 Mcd 1983,308:409-413. 6 Leone A, Lopez M. Oral eontraception„ovariao disorders and tobacco in myocardial infarction of woman, PatholoY- ica 1986;78i237-242. 7 Bell JNB. Comparative eriteria for indoor and'ambient air quality-biology considerations. l'n:,Perry R, Kirk PW, eds. Indoor and ambient air quality. London: Selper Lad, 1988:13-23. 8' Leone A. Passive smoking in infarcted patients: role of indoor exposure. In: Perry R. Kirk PW. eds:. I'ndoor and ambient air quality. London: Selper Ltd. 1'988.211-21a1 9' Astrup P. The arterial wall in atherogenesis. ln: Cavallero. ed! Atherogenesis: Padua: Piccin Medieal' Book. 1965;77- 93. 1(li Moeschlin S: Poisoning. Diagnosis an& treatment. New York: Grune Stratton- 1965'25-233.