Cardiac Arrhythmias, Snoring, and Sleep Apnea

Cardiac Arrhythmias, Snoring, and Sleep Apnea Vi ctor Hoffst ein , M.D ., Ph.D. ; and Su san Mat eika , B.S c. We investigated the frequeney of eardiac arrhythmias in patients suspected of having sleep apnea, and related them to the severity of apnea , snoring, and nocturnal hypoxemia. We pro speetively studied 458 patients who had nocturnal polysomnography which included objective measurement of snoring (quantified by the number of snor es per hour of sleep [snoring index (SI)]and maximum nocturnal sound intensity [(dBmax)], as well as examination of the electrocardiogram (modified lead 2). We found 58 percent prevalence of arrhythmias in patients with sleep apnea (apnea jhypopnea inde x=AHI > 10), vs 42 percent in nonapneic controls (x 2 = 16.7, p
uration <90 percent had arrhythmia s vs 40 percent of patients with mean nocturnal oxygen saturation >90 percent (x 2 =7.4, p=0.006), and 70 percent of patients with AHI 2:40 had arrhythmias vs 42 percent with AHI .:510 (x 2 =9.2, p=0.002). We conclude that patients with sleep apnea as a group have higher prevalence of cardiac arrhythmias than non apneic patients and that snoring alone, without concomitant sleep apnea, is not associated with increased frequency of cardiac arrhythmias. (Chest 1994; 106:466-71)

S everal stud ies show a linkage, and perhaps a causal association, between slee p apnea a nd heart di sease .l" There is e vidence that patients with sleep apnea have higher mortality from cardiovascular causes than nonapneic individuals. One possibility that might expla in this association may be increa sed prevalence of cardiac arrhythmias in apneic patients. Although there are several investigations dealing with th e mech anisms of alt ered cardiac rhythm in pati ents with recurren t episodes of upper airway obstru ction and hyp oxem ia at night,5,7-9 th ere is only one large scale clinical study dealing with description of ca rd iac arrhythmias in patients with obstructive sleep apnea .l" Ne it he r th at st udy nor som e of the other ones, II involving consid erably smaller number of patients, however, had a control group composed of nonapneic individuals. Furthermore , association between snoring alone , without apneas, and ca rd iac arrhythmias has not been examined , despite epidemiologic evidenc e id entifying snoring as a risk factor for coro nary artery and cerebrovascular di sease .I 2, 13

The purpose of the present in vestigation wa s to compare th e fr equency of cardiac arrhy th m ias in patients with and without slee p apnea and to exam ine separat ely th e relationships between the arrhythmias and the sev erity of apnea , hypoxemia, and snori ng.

*From the Departm ent of Medi cine, St. Michael 's Hospital , Toronto, Ont ar io, Canada . Man uscrip t receiv ed August 30, 1993; revision accepte d Decem ber 9. Reprin t requests: Dr. Hoffstein , St. M ichael's Hospital , 30 Bond Street , Toront o, Ontario, Canada M5B n VR 466

AHI=apnea jhypopnea index;COMB=combined atrial and ventricular arrhythm ias; dB=decibel; dBmax=maximum nocturnal sound intensity; Lo02S= lowest nocturnal oxygen saturation; Mn02S=mean nocturnal oxygen saturation; NSR=normal sinus rh ythm; OSA=obstructive sleep ap nea; SI=snoring index; SUPRA=supraventrieular arrhythmia; TST85%=percent of sleep time spent at oxygen saturation lower th an 85 percent; VE:."JT=ventricular arrhythmia

M ETHODS

Patients We studied 458 consecutive and unselect ed pati ent s ref erred to th e sleep clinic at St. Micha el' s Hospital for evaluation of possible slee p apnea. Snor ing was the ch ief complaint in the vast majorit y of patients, although daytime sleepiness and tir edness wer e also common.

Polysomnographi c Measurem ents In all 458 pati ents, we carried out nocturnal polysomn ogr aphy, whic h included me asur em ents of EEG , subme nta l, and ant erior tibi al EMG, oro nasal flow using th ermistor s, chest wall and abdomi na l excur sions using inductan ce pleth ysomography, oxygen satur ation using finger oximete r, and single-lead electrocardiogr am using mod ified pr ecordial lead elect rode. Snorin g was measur ed in 388 pati ents using a microphone-sound m eter system as described befor e. 14 In short, it was done by placing the mi crophon e abov e the nasion (on the foreh ead ), conn ecting the m icroph one to th e sound met er (mode l SL120 , Pacer Industries; Chippew a Falls, Wis) calibrated betw een 40 and 100 decib els (d B) and displa ying sound intensity alon g with other poly somnograp hic var iabl es on th e strip ch art recorder . W ith this setup norm al br eathing regi ster s at less than 50 dB; spikes in sound inten sity high er th an 50 dB are counted as snores. Cardiac Arrhythmias. Snoring. and Sleep Apnea (Hoffstein and Mateika)

All polysomnograms wer e scored in th e usual mann er . Apn eas and hypopn eas were ide ntified as eithe r complete or incomplet e (greater than 50 percent ) episodes of cessation of br eath ing lasting longer th an 10 s. Th e number of such ep isodes per hour of sleep is term ed a pnea/ hy popnea ind ex (AI-II). Sim ilarly, snores were counted and th e num ber of snores per hour of sleep is ter med snoring index (SI); maximum nocturnal sound int ensity (d Bmax) was also record ed . Three indices of nocturnal oxyge nation were used : lowest nocturnal oxygen satura tion (Lo0 2S), mean nocturnal oxyge n satura tion (Mn0 2S), and pe rcen t of sleep tim e spent at oxyge n satura tion lower than 85 percent (TST85%). Th e latter measurement was availabl e in 350 pati ent s. Ca rd iac rat e and rh ythm were assessed by exam ining the modified lead 2 electroca rd iogra m. Lowest, high est, and mean heart rat es we re recorded . Arrh ythmias we re classified acco rdi ng to th eir or igin, as is usuall y done during sta nda rd polysomn ogra ph y. Supra ventricular arrhy thm ias wer e di vided into sinus and atrial. Th e form er included sinu s brad ycardia (rate less th an 40/min), sinus tach ycardia (ra te > 120/min), sinus arrhythmia (irre gu lar rh ythm with rat e between 60 and iOO/min), and sinus arrest (pause lasting longer than 2 s). The latter included wander ing pacemaker , prem ature contrac tions, paroxysma l tachyca rd ia, flutt er , and fibrillati on. Jun ctional rh ythm , atrioventri cul ar blocks, and bundle brunch blocks were identified and recorded separa tely. Ventricular arrhythmias incl uded pr ematur e contractions, tach ycardia, flutt er , and fibrillation .

Statistical Analysis Th e goa l of sta tistica l analysis was to det ermine whether th er e is any relat ionship betw een th e typ e of arrhy thm ia and th e seve rity of a pnea , nocturnal hypoxemi a, and snoring. This was acco mplished as follows. First, we groupe d all pati ent s int o the following "arrhy thmia groups": (I ) normal sinus rh ythm (NSR), (2) suprave ntric ular arrh ythmia (SUPRA), which included sinus and atrial arrhythmias , (3) ventricular arr hy thmia (VE NT) , which included pr emature ventricular contractions, atrioventricular block, and junctional beats, and (4) combined atrial and vent ricul ar arrhythmias (C OMB). We then used Kruskall-Wallis statistics to com pare ap nea (Al II), snoring (SI, dBmax), and oxygenation (Lo0 2S, Mn02S and TST 85%) amo ng the different arrhy thm ia groups. Second , we exami ned the same pr oblem from a differ ent viewpoint , based on the hypothesis that pati ent s with severe apnea, hypoxemia, and snor ing ar e mor e likely to have cardiac ar rhythmias than pati ents without apn ea , hypoxemia, or snoring. To test this hypothesis we select ed subgroups of pati en ts "at the opposite ends of th e spectrum" as far as th e severity of th eir

Table i-Anthropometric and Sleep Data Variab le"

No.

Mean ± 5D

Range

Age Wt B\1l 51 dBmax Lo0 2 Mn02 T 5T 85 % HR mean HR lowest HR highest

458 458 458 388 388 458 458 350 458 458 458

48± 13 89± 22 31 ±7 384 ±353 89 ±10 81± 12 92 ±3 9 ± 15 68 ± 10 57 ± 11 85± 14

14-78 44-182 17-65 0-184 35-110 10-95 72-98 0-88 42-114 18-95 51-200

*Wt =w eight (kg), BMI= body mass index (kg/ m 2), HR=nocturn al heart rate.

nocturnal events is concerne d . To exam ine the effect of snori ng, we com pared nonapneic nond esaturating light snor ers (AH I :510, SI <100, Mn02S>90%) with nonapn eic nondesaturating heav y snore rs (AH I :510, Mn02S > 90%, SI >400). To exa m ine the effect of nocturnal hypoxemia, we com pa red nonapneic nonsnoring pati ent s without nocturnal oxyge n desaturati on (AHI :510, SI <100, Mn02S > 90%) with nonapneic nonsnoring pati ents who desaturat e at night (AH I :510, SI <100, Mn02S < 90%). To exam ine the effect of apnea we com pa red nonapneic nondesatur at ing nonsnorers (AH I :510, Mn02S > 90%, SI <100) with apneic nond esaturatin g nonsnorers (AH I 2:40, Mn02S >90%, SI < i OO). Chi-sq uare statistics with Bonf erroni corre ctions wer e used to compare th e frequ en cy of arr hy thm ias within each group. 15 All sta tistica l ana lysis was done using SAS soft wa re (T he SAS Institute ; Gar y, NC) version 6.04. R ESULTS

Tabl e 1 summarizes the cha racte ristics of the patient population examined in this study. Th er e wer e 336 men and 122 women . Most pa tien ts (244/458) did not have obstructive sleep apnea (OSA) (AHI <10),121/458 (26 percent) had AHI between 10 and 30, 41/458 (9 percent) had AHI betw een 30 and 50,

Ta b le 2-List of Medications Use d by All Patients

No. Calcium channel blockers Beta blockers Diuretics ACE-inhibitors Digoxin Antiarrhythm ics Antihype rtensives Theophyllines Beta-agonists Tricyclic antide pressants Total

AHI :5 10

IO
30
AHI>50

244 [5 12

121 4 9 8 2 3 2 I 1 2 3 40

41 5 2 6 2 4 1 1 2 2 3 34

52 3 3 7 4 2 0 6 2 3 2 38

II

9 6 2 2 3 16 II

102

CHEST I 106 I 2 I AUGU ST, 1994

467

Table

3-Cardiac Rhythm During Sleep

AI-II:::;10

1\'0_ I\'SR SUP RA VENT CO MB* AT R+ AVB AT R+ J UN AT R+PVC AVB+S IN PVC +SIN AT R+AVB+SII\' AT R+ PVC+SIN AT R+AVB+SIN + PVC

244 141 (58 %) 54 (22%) 28 (11%) 2 1 (9%) 0 0 11 0 9 0 1 0

IO
30 < AH I:::;50

121 (46%) (27%) (16%) (11 %) 0 0 4 0 8 0 1 0

20 9 6 6

41 (49%) (22%) (15 %) (15%) 0 I 2 0 2 0 1 0

AH I>50 13 15 10 14

52 (25 %) (29%) (19%) (27%) I 0 5 1 4 1 0 2

*T his incl ud es com bina tion of th e followi ng arrhythmias: AT R =atria l, AVB=atriov en lricular block , J UN =juncti on al rh ythm , PVC=prem ature ventricula r con tractions, SIN = sinus a rrhy thmi a.

and 52/458 patients (11 percent) had AHI > 50. There wer e 82 pati ents with histor y of cardiac disease (hy pe rtension, 51; previous myocardial infarction , 6; angina pectoris, 5; congesti ve heart fail ure , 4; coronary arter y disease , 13; arrhythmia, 3, and 10 patients with chronic obstructive lun g di sease. Th e gener al categories of medications used by th e pati ents ar e listed in Table 2. We note that the majorit y of patients on medications di~ not hav e sleep apnea. Overall, there was no significant difference (by X2 statistics) between th e proportion of apneic patients taking medications as compar ed with nonapneic pati ent s. Of the 458 pati ents, 228 had various cond uction abnormaliti es, and of th ose 125 had slee p apnea (ie, AHI > 10). Thi s result s in 58 percent (125/ 214) prevalenc e of arrhythmias am ong patient s with OSA, which was significantly higher than 42 percent (103/ 214) pr eval ence of arrhy thmias among patients without OSA (x 2 = 12.0, p
the arrhythmia categories as defined above. There was a significant diff er enc e in all of th ese variables exce pt SI and dBmax between th e groups, with Kurskall-Wallis X2 ran gin g from 17 to 26, p
APNEA AND SNORING •

AHI

~ 51

D dBma x

100 )(

J5'" "'0

s:-e

75

50

25

a NOCTURNAL OXYGENATION •

MnOzsal

~ LoOzsat

D T5T85%

100 ~

tl

~ "IiUl

75

50

N

o

25

o

NSR

SUPRA

VENT

COMB

CARDIAC RHYTHM F IGURE 1. Apnea, snoring, a nd noctu rnal h y poxemia in patients g ro uped accord ing to th e ir a rr h y th mia.

Cardiac Arrhythmias, Snoring , and Sleep Ap nea (Hoffstein and Mateika)

Tabl e 4-Subgroups of Patients Used to Examine the Effec t of Apne a, Noc turnal Hypoxemia , and Sno ring on Preval en ce of Arrh yt hmias % With Arr hythmia

No.

AHI

51

Mean 0 25

101 47

4 ±2 5 ±3

36 ± 27 644±246

94 ±2 93 ± 2

38 39

Mn025~ 90

11

Mn025~ 90

233

5 ±2 4± 3

409 ± 588 221 ±249

88 ± 2 94 ±2

82* 40

238 33

4± 3 59±14

229 ± 273 549 ± 235

94±2 93±2

42 70*

Effect of snoring 51 ~ IOO

5 1~400

Effect of noctu rnal hypoxemi a

Effect of apnea A HI ~lO AH I~40

"Significan tly (p < O.Ol) higher than in the control group.

feet of sno ring we sele cted non apneic , nondesaturating light and heavy snorer s, based on th e snoring index of less than 100 or greater than 400. W e found no significan t d iffer en ce in th e prevalen ce of arrhy thmi as bet ween th ese two gr oups (x 2 = 0 .001, p=0.971 ). To exa mi ne the effec t of noc turnal hypoxemia, we sho uld ideall y com pare non apneic nonsnoring nonhyp oxem ic group with nonapneic nonsnoring hyp oxemic gro up. Not un expectedly, however , th er e wer e no hypoxemi c nonapneic nonsnorer s-most hypoxem ic pati ents either sno re or have slee p apnea . Therefore , since snoring d id not affect th e prevalen ce of arr hy thmias an ywa y, we examined th e effec t of hy poxe m ia on th e frequen cy of ca rd iac arr hy thmias by com pa ring non apneic nonhypoxem ic group with nonapneic hypoxemic group witho ut any restriction on sno ring . That is wh y the sno ring index is relativel y high in both gro ups (Ta ble 4), altho ugh th e d ifference was not statistically sign ificant by the W ilcoxon Rank Sum Test (p = 0.1787). H ypoxemia was defined based on mean nocturnal oxygen saturation lower th an 90 per cent. The prevalen ce of supraventricular and ventricul ar arrhythmias was significantly higher in hyp oxemic pati ents (X2 = 7.4, p=0.006). The select ion of subgrou ps to exa mine th e effec t of apnea on th e prevalen ce of a rrhy thmias follow ed th e same genera l guide lines as was used for hypoxemia. We com pa red nonhypoxemic non apneic patients (mea n noc turn al oxygen saturation >90 %, AH I <10) with nonhypoxemic significan tly apneic (AH I > 40) pati en ts, without any restr icti ons on sno ring . The prevalence of arr hy thmias, particularl y th e supraventricu lar and com bine d ones, was sign ifica ntly high er (x 2 = 9.2 , p = 0.002) in the apneic grou p. D ISCUSSION

This study shows th at (I ) pat ients with obstru ctive slee p apnea ha ve high er pr evalen ce of arr hy thm ia th an no napne ic patients, (2) pa tie nts wit hout arrh ythmias, as a gro up , have less seve re apnea and nocturnal hy poxemi a th an pati ents with arrhyth-

mi as, and (3) preval ence of arrhy thmi as is indepen dent of snoring, but it is linked to slee p apnea and nocturnal hypoxemia. The study design has certain limitati ons which could conceivably influence som e of our conclusions. On e of th e drawbacks is the use of only a single lead (mod ified lead 2) ECG. This wo uld under estimate th e pr evalen ce of abnormal axis, ST seg ment, T -wave, and QR S abnormalities, but it is not likely to affec t th e det ecti on of cond uction abno rma lities or ca lculation of heart ra te-which was th e primary purpose of our study . Neverth eless, th e abs en ce of a full 12lead ECG pr evented us from more d et ail ed classification of atriove ntr icular block and gra ding of premature ventricular contrac tions, as was d one in previous in vestlgatlons.U'J! Anothe r drawback is th at we did not exami ne normal iie, nonsnoring , non apneic) controls taken fr om th e healthy population . Although we identified suc h subg roup among our 458 pati ents, they all came fr om sleep clinic population. It is possible that a patient found to be a non apneic nonsnorer when slee ping in th e laboratory on th e night of the sleep study is a habitual snore r and has a pneas when slee ping at home . This, ho wever , is unlikely given th e published results regarding th e reproducibility of a pnea and snoring. On th e othe r hand , our study has severa l unique features not present in pr evious in vestigations: (1) it incl udes a lar ge group of subjects, all studied prospectively, (2) th er e we re man y no na pne ic patients who co uld serve as controls, and (3) we measur ed sno ring and related it to arrhy thm ias wi thout th e confo unding effec t of a pnea a nd hypoxemia. Only one large scale study, which could be com par ed wit h th e pr esent one , was performed in th e past.l'' The authors exa m ine d 400 patients wit h OSA for ca rd iac arrhythmias during slee p. They found th at 48 percent of pati ents had cardiac arrhythmia recorded during th e slee p study night. Ther e we re at least 75 patients (20 per cent) who had ventricular CHEST / 106/ 2 / AUGUST. 1994

469

arrhythmias. No control group was stud ied , althoug h th er e we re 50 pati ents who serve d as th eir own control s an d who improved afte r tr eatm ent with tracheoto my . Ther e is evide nce suggesting th at disturbances of ca rdiac rhythm , particul arl y ven tricular ectopy , in OSA pa tien ts may not be relat ed to slee p at all , being also pr esent during wa kef ulness. Mille r ' ! reviewed th e results of 24 h Holter monitoring in 23 pat ients with OSA and fo un d 78 per cent pr evalen ce of a rr hy thmias d uring slee p. Since man y patients also had ca rd iac arrhy thm ias during wakefulness, howeve r, th e author concl ude d th at the pr evalen ce of serio us arrhythmias during slee p is low. Although he did find a significantly high er pre valence of sinus a rrhy thmias during slee p com pared with wakefulness, he was unable to show that for ventricular arrh yth mias. Our result s show a significa ntly higher pr eval en ce of ca rd iac arr hy thmias, whe the r suprave ntricular or ventricular, am ong pati ents wit h OSA. Unlike othe r autho rs,lO,ll we found that atrioventricula r block , sinu s pau ses, and jun ctional rh yth m we re un common amo ng our pati ents , seen in only 2 to 3 per cent of th ose with OSA, vs 8 to 11 per cent found by othe rs.lO,ll Although we found a sta tistica lly significant increase in th e prevalence of ca rdiac a rrhy thm ias a mong pati ent s with OSA, it is im porta nt to note that non ap ne ic pati ents in our study also had a high pr evalen ce of th ese arrhy thmias (42 per cent), similar to an observa tion by F lemo ns et al. I 6 On e possibilit y is that it reflects our pa rti cular pati ent population , all of whom wer e ref erred becau se of slee p d isturbance and many of whom wer e on medi cati ons. Another possibility, however, is that it sim ply reflects th e fa ct th at nocturnal arrhythmias a re com mon in th e gen eral population , occurring in abo ut 50 percent of healthy people. l7- l9 We believe that statisticall y significant increase in a rrhy thm ias amo ng patients with OSA found in th e cur ren t study reflects th eir underl ying disea se. The dat a presented in Table 4 sup ports th is hypothesis; fur the rmo re, whe n we exa mined our pati ents with most serious arrhythmias-bigemin y, trigeminy, quad rige mi ny , sinus pau ses, asystole-we found that as a group th ey ha d most seve re a pnea (AH I> 40) and hyp oxemia (more than 19 pe rce nt of total slee p time spent at oxyg en satura tion lower tha n 85 per cent). Our result s pr ovide indirect evidence , but not a conclusive pr oof , that th er e is an ind ependent relationship between ca rd iac a rr hythmias, apnea , and nocturnal hypoxemia . We cons ide r our evide nce ind irect beca use it is based on sta tistica l ana lysis of subg roups mat ch ed for apnea an d mean oxygen saturati on , rat her than on direct com pa rison of the fr e470

quen cy of arr hy thm ias in th e same gro up of a pnei c hypoxemic subjects bef or e and afte r elim ination of a pnea a nd hyp oxemia. Ther e is othe r ev ide nce suggesting th at apnea and hypoxemia ma y ha ve independent, per haps an add itive , adv erse effect on cardiac funct ion. Fo r exam ple, nonap neic pat ients with nocturnal hyp oxemia d ue to chronic obstructive lun g disease ha ve mo re ven tricular ec to pics during sleep.2o,21 Altho ugh not d irect ly dealing with a rrh ythmias, th er e is ev ide nce th at hypoxemia alone does not explain incr eases in blood pressur e seen in slee p apnea ,22 sugges ting that a pnea may have an add itional, independent effec t of th e regulation of nocturnal sym pathe tic ac tivity. La stly, increased sym pa the tic activity, due to hypo xemia , and increased vag al act ivit y, due to repetitive episodes of upper ai rway obstruction , may both ha ve arrhythmogenic effect on th e m yocardium .P It appears that com bina tio n of apnea and oxygen desaturation provide sufficie nt str ess on th e heart to pr edi spose th ese pati ents toward de velopment of ventricular arrhythmia s. Meas urements of sno ring in our lar ge group of pati ent s permit us to com ment on th e possible associa tion bet ween sno ring and arrhyth mias. This issue is cur ren tly of inter est becau se of several stud ies indi cating th at snoring alone , witho ut a pneas , may be a risk factor for coronar y a rte ry and ce re brov asc ular disease. l2,13 We found no d iffer en ce in th e prevalen ce of arrhy thm ias bet ween nonsnorer s and hea vy sno re rs. These obse rva tions imply that ca ution mu st be exe rcise d in interpreting result s of epidemiologic surveys comparing ca rd iac func tion in snore rs and nons norers; in th e abs ence of slee p stud ies, significa nt diff er en ces between the two gro ups may be from "conta m ina tion" of th e sno ring gro up by individuals with slee p apne a and hypoxemia . W e conclude that cardiac arr hy thm ias are more com mo n in patients with slee p a pnea than in nonapneics, that snoring alon e, without slee p apnea or hyp oxemia , do es not significantly aff ect cardiac rh ythm , and that presen ce of a pnea and nocturnal hyp oxemia is associat ed with incr eased pr e val en ce of ca rd iac ar rhy thm ias. R EFERENCES

Shepa rd JW , Jr. Hypertension, cardiac arr hythmias, m yocar dial infar ction, and strok e in relation to obstructive sleep apn ea . Clin Ch est 1992; 13:437-58 2 Parish JM, Shepa rd JW , Jr. Car d iovascular effects of sleep disorders. Chest 1990; 97:1220-26 3 Koskenvuo M. Ca rdiovascular stress and sleep. Ann Clin Res 1987; 19:110-13 4 Koehler U, Dubl er H, Glaremin T, Junk erm an H, Lubber s C, Ploch T , et al. Noct urna l myocard ial ischem ia and card iac arrhythm ia in pati ents with sleep a pnea with and without coronary artery di sease. Klin Wochenschr 1991; 69:474-82

Moo

Cardiac Arrhythmias, Snoring. and Sleep Apnea (Hoffstein and Mateika)

5 Stoohs R, Guilleminault C. Cardiovascular changes associated with obstructive sleep apnea. J Appl Physiol 1992; 72:583-89 6 Fletcher EC, Schaaf JW, Miller J, Fletcher JG. Long-term cardiopulmonary sequ elae in pati ents with sleep apnea and chronic lung disease. Am Rev Respir Dis 1987; 135:525-33 7 Scharf SM, Graver LM, Balaban K. Cardiovascular effects of periodic occlusions of the upper airway in dogs. Am Rev Respir Dis 1992; 146:321-29 8 Guillemin ault C, Connolly S, Win kle R, Melvin K. Cyclical variation of the heart rate in sleep apnea syndrome. Lance t 1984; 1:126-31 9 Andreas S, Hajak G, von Breska B, Ruther E, Kreuzer H. Cha nges in heart rate during obstructive sleep apnea. Eur Respir J 1992; 5:853-57 10 Guillem inault C, Connolly SJ, Winkle RA. Cardi ac arrhythmia and conduction disturb ances during sleep in 400 pati en ts with sleep apnea synd rome. Am J Card iol 1983; 52:490-94 II Miller WP. Cardiac arrhythmia and conduction disturbances in the sleep apnea syndrome. Am J Med 1982; 73:317-21 12 Kosken vuo M, Kapr io J, Partin en M, Langinvainio I-l, Sarn a S, Heikkila K. Snoring as a risk factor for hypertens ion and angina pectoris. Lanc et 1985; 1:893-95 13 Koskenvuo M, Kaprio J, Telakivi T, Partinen M, Heikkila K, Sarna S. Snoring as a risk factor for ischemic heart disease and stroke in men . Br Med J 1987; 294:16-9 14 Hoffstein V, Mateika S, Metes A. Effect of nasal dilation on snoring and apneas during different stages of sleep. Sleep 1993; 16:360-65

15 Altman DG. Practical statistics for med ical research. London : Chapman & Hall, 1991; 259-61 16 Flemon s WW , McDonald M, Remm ers JE, Gillis A. Card iac dysrhythmias and sleep apnea [abstract). Am Rev Respir Dis 1992; 145:A443 17 Sobotka PA, Mayer JI-I, Bauernf eind RA, Kanakis C, Jr., Rosen KM. Arrh ythmi as docum ent ed by 24-hour continuous ambulatory monitoring in young women withou t apparent heart disease. Am Heart J 1981; 101:753-59 18 Brodsky M, Wu D, Denes P, Kanak is C, Rosen KM. Arr hythmias documented by 24-hour continuous electrocardiographic monitorin g in 50 male medical stude nts without apparent heart-disease. Am J Cardiol 1977; 39:390-95 19 Viitasalo M, Halonen L, Partin en M, Iivanain en M, Kala R, Eisalo A. Sleep and cardiac rhythm in healthy men. Ann Med 1991; 23:135-39 20 Douglas NJ. Nocturnal hypoxem ia in patients with chronic obstru ctive pulmonary disease. Clin Chest Med 1992; 13:523-32 21 Flick MR, Block AJ. Nocturnal vs diurnal card iac arrhythmias in pati ents with chronic obstructive pulmonary disease. Chest 1979; 75:8-II 22 Ringler J, Basner RC, Shannon R, Schw artzstein R, Mann ing H, Weinb erger SE, et al. Hypoxem ia alone does not explain blood pressure elevati ons after obstructive apn eas. J Appl Physiol 1990; 69:2143-48 23 Verrier RL, Kirby DA. Sleep and cardiac arrhythm ias. Ann NY Acad Sci 1988; 533:238-51

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