EuropeanHeartJournal(2001)22,1082–1101 doi:10.1053/euhj.2000.2534,availableonlineathttp://www.idealibrary.comon Review Article Social and psychosocial influences on sudden cardiac death, ventricular arrhythmia and cardiac autonomic function H. Hemingway1,2, M. Malik3 and M. Marmot1 1International Centre for Health and Society, Department of Epidemiology and Public Health, University College London Medical School, London, U.K.; 2Department of Research and Development, Kensington & Chelsea and Westminster Health Authority, London, U.K.; 3Department of Cardiological Sciences, St George’s Hospital Medical School, London, U.K. Introduction another possibility, that aspects of the psychosocial environment related to social position may be in- Theimportanceofabetterunderstandingofarrhythmic volved[9]. risk lies, in public health terms, in the prevention of Recently reviewed evidence from prospective epi- sudden cardiac death. Approximately 50% of all demiological studies[10], supported by non-human pri- coronary deaths are sudden, occurring within 1h of mate data[11], suggests that psychosocial factors—such the onset of symptoms[1]. Most cases of sudden car- as anxiety, depression, hostility/Type A behaviour, diac death have coronary artery disease present at social supports and work characteristics—may play a autopsy[2,3],althoughinapproximately50%thiswillnot direct causal role in coronary heart disease. These have been clinically apparent prior to death[4]. Sudden studiesmostlyrelateasinglequestionnairemeasurement cardiacdeathismostoftenduetoventricularfibrillation of a psychosocial factor to incident coronary events andcardiacautonomicfunctionmayplayanimportant many years later. Such measurements may reflect role in setting the arrhythmic threshold[5,6]. Figure 1 chronic exposure to an adverse psychosocial environ- illustratesthissimplemodelofarrhythmicriskandgives ment which is relatively stable over time. The risk the structure for this review. observed in these studies tends to be distributed in a Sudden cardiac death is not, however, distributed dose–response fashion and is not confined to the ex- equallyinsociety.Inonestudyof1608casesofsudden tremesofthedistribution.Sincesuddencardiacdeathis cardiac death, the age-adjusted rates of sudden cardiac acommonmodeofcoronarydeath,suchassessmentsof death were higher among those with less education, an effect which was stronger than for people dying of non-suddencardiacdeath[1].Educationallevelandother markers of social position, such as occupation and Coronary income, consistently show inverse associations with the artery incidence of cardiovascular disease[7]. Social status may disease influence coronary risk via the behavioural risk factors ofsmoking,exerciseanddiet.However,thefindingthat Cardiac Ventricular Sudden social position gradients in heart disease are observed autonomic arrhythmia cardiac amongnon-smokersandareindependentoftheclassical function death riskfactorsofcholesterolandbloodpressure[8]suggests (Tables 1, 6 (Table 5) (Tables 1–4) and 7) Revisionsubmitted7November2000,andaccepted8November Social and psychosocial factors 2000. Figure 1 Possible pathways by which social and psycho- Correspondence: Harry Hemingway, International Centre for social factors may influence sudden cardiac death, Health and Society, Department of Epidemiology and Public Health, University College London Medical School, 1–19 ventricular arrhythmia and cardiac autonomic function. TorringtonPlace,LondonWC1E6BT,U.K. (Tables where evidence is reviewed.) 0195-668X/01/221082+20$35.00/0 (cid:1)2001TheEuropeanSocietyofCardiology Review 1083 psychosocial factors may predict sudden cardiac death Method simplybecausetheypredictatherothromboticdiseaseof coronary arteries. Identification of relevant articles in English language Acutepsychosocialstressors—definedaseventspro- peer-reviewed journals was carried out using PubMed ducing demands likely to tax or exceed an individual’s from 1970–1999 (www.ncbi.nlm.nih.gov/PubMed). As adaptive responses over minutes, hours and days— well as using MESH headings (psychosocial, social, may,inaddition,representmoreproximate‘triggers’of sudden death, ANS and arrhythmia) articles were also suddencardiacevents.Suchacutepsychosocialstressors identified by searching on any author who had contrib- may trigger ischaemia or infarction[12] in the setting of uted one relevant article and by using the artificial coronary disease. Whilst laboratory-based measures of intelligence ‘Related Articles’ function in PubMed. The acute psychological stress have been extensively studied bibliographies of all retrieved articles were hand the challenge lies in determining the effects of real life searched for further relevant articles. Each study was acute stressors. categorized as positive if one or more measure of social Determining the causality of putative psychosocial position or psychosocial factors showed a significant factors in arrhythmic risk may yield important insights (P<0·05) association with sudden cardiac death, ven- into the pathogenesis of arrhythmic risk itself, mech- tricular arrhythmia or cardiac autonomic function. A anisms by which psychosocial factors might cause positive study is denoted by a + in the last column of coronary heart disease (in which electrophysiological Tables 1–7. In the absence of any previous systematic pathwaysareoneofanumberunderconsideration)and, review in this area, a relaxed definition of a positive ultimately, strategies for prevention of sudden cardiac study was deliberately chosen, and no study was death. As numerous reviews demonstrate, the clinical excluded on the grounds of methodological quality. and biological plausibility for social and psychosocial factors being associated with arrhythmic risk is not at issue.Thequestionliesinthequalityandconsistencyof the totality of evidence that psychosocial factors play a Animal studies causal role. Given the possibility that both chronic and acute psychosocial stressors affect arrhythmic risk, the Animal studies, unlike human studies, offer the import- evidence for a causal association has to be considered ant advantages of direct study of arrhythmia precipi- across a range of study designs. In prospective studies tation;manipulationofpsychosocialstressorswhichare of psychosocial factors and sudden cardiac death, observable, and not relying on language based self- distinguishing acute from chronic effects may not be reports which have a potential for bias. However, in possible. animals and humans ventricular fibrillation and sudden Pharmacologicalinterventionmayplausiblyinfluence death remain rare events and most animal models have theassociationsinFig.1.Howevertherearefewstudies thereforeconcentratedonproxies,suchasthethreshold examiningtheextenttowhichsocialpositionorpsycho- for repetitive ventricular activity. 12/12 of the identified social factors influence aspects of drug prescribing, studies (Table 1) were positive and all examined acute compliance or pharmacological action. psychosocial stressors. Taken as a whole, these studies Previousreviewsofthisareahavenotbeensystematic provide important evidence for a model of sudden in the identification of literature for review, the method cardiacdeathcausationinwhichcentralandautonomic ofdescribingindividualstudyresultsorinthemethodof (sympathetic and parasympathetic) nervous system summarizing findings from diverse types of study. For influences on ventricular arrhythmias are mediated these reasons, gaps in current understanding are not by environmental, presumed psychosocial, stressors. clearlydefinedandnon-contributorystudiescontinueto Studiesinpigswithcoronaryocclusioninanunfamiliar bepublished.Itwastheobjectiveofthisreviewtherefore laboratory setting found that latency to ventricular to determine the strength and consistency of evidence fibrillationwaslengthenedbyadaptation,beta-blockade forassociationsbetweensocialandpsychosocialfactors or blockade of frontal cortical brain stem path- and sudden cardiac death, ventricular arrhythmia and ways[13,14]. A study of male rats faced with aggressive cardiacautonomicfunction.Thestructureofthisreview lactating female rats found that 12/12 rats developed (outlined in Fig. 1) is based on each of the measured ventriculartachycardia,precededbyperiodsoflowR-R outcomes:suddencardiacdeath,ventriculararrhythmia variability (using telemetrically recorded ECGs). and cardiac autonomic function. There is an important role for further animal work, Itisimportanttorecognizethatthisreviewislimited particularly when observations are made in the natural topublishedstudies;sincepublicationismorelikelyfor environment, for example using telemetrically recorded positivethannegativefindingsthereisapotentialbiasof ECGs, and social factors which are real life (such as overstatingtheimportanceoftheobservedassociations. dominance) or long term can be studied. For example, The potential influence of pharmacological intervention Eisermann[15] studied rabbits in a semi-natural environ- on the association between social position or psycho- ment and found that a measure of social position socialfactorsandarrhythmicrisk,seldomthesubjectof (dominance) was associated with radiotelemetric heart primary research, was considered outside the scope of raterecordingsover1500days;subordinaterabbitshad this review. chronically elevated heart rate not explained by limited EurHeartJ,Vol.22,issue13,July2001 1084 H. Hemingway et al. ntal mary me m + + + + + + + + + + + + ri Su e p rdiacautonomicfunctioninex Results loweredinslingdogs loweredbeforecoronaryocclusionintheslinggroup7/8dogsplacedinslingdevelopedVPBorVT;noneincagegroupcardiomyopathyconsistentwithreflexcatecholaminereleaseVFdelayedorpreventedbyadaptationorbetablockade avoidancemonkeysshowedmoremyofibrillardegenerationand3diedsuddenlyafterbradycardiaassociatedwithcirculatingcatecholaminesventriculararrhythmiasoccurredin7/7restrainedguineapigs;coupletsandVTin3;noarrhythmiainunrestrainedguineapigsreduceriskofVFbyfrontalblockadeoffrontalcorticalbrainstempathways vagalblockadewithatropinereducedthresholdinsling;propranololpreventedthedecrease;bilateralstellectomyffaordedonlypartialprotectionVTin12/12malerats,precededbyperiodsoflowR-Rvariability;moremarkedthancontrols(exposedonlytonovelenvironment)socialstressorassociatedwithmoresympatheticchangesandVPBthanthenon-socialstressorhighersympathetictone,lowparasympatheticantagonismandmoreVPBinwildtyperats a c ulararrhythmiaand Outcome thresholdforrepetitiveventricularresponse thresholdforrepetitiveventricularresponsesVPB,VT ventriculararrhythmiascardiomyopathylatencytoVF autopsyfindingssuddendeath thresholdforrepetitiveventricularresponseVPB,VT VF thresholdforrepetitiveventricularresponse telemetricECGforHRV(timedomain)andVPB,VT ditto ditto c encardiacdeath,ventri Relievingfactor cageinsoundattenuatedroom ditto adaptationtolaboratorypropranolol avoidancemonkeycouldmakealeverresponsecage unrestrained adaptationtolaboratorycryoblockadeoffrontalcorticalbrainstempathwayscentralpropranololcageatropinebeta-blockadestellectomy ation. associationswithsudd Acutepsychosocialfactor Pavloviansling:tensiononleashandsoundofswitchprecedingelectricalshockditto psychological(restraintstress)unfamiliar(laboratory)vsfamiliarsurroundings:electricalshock:yokedmonkeyhadnocontrolPavloviansling restraintstress unfamiliarlaboratoryelectricalshock Pavloviansling 12males(intruders),aggressivelactatingfemalerats(residents) socialstressor(defeat)non-socialstressor(restraint)defeat dia;VF=ventricularfibrill ychosocialfactors: Experimentalsetting conscious conscious;coronaryocclusion conscious conscious;coronaryocclusion 11pairs(1avoidance1yoked) conscious coronaryocclusion coronaryocclusion =ventriculartachycar s T p V ositionand Animal dog dog pig pig squirrelmonkey dog guineapig pig dog rat(Wistarmale) rat(wildtype) rat(Wistarandwildtype) maturebeat; p e r Table1Socialanimalstudies Author,year [54]Lown1973 [55]Corbalan1974 [56]Johansson1974 [13]Skinner1975 [57]Corley1977 [58]Liang1979 [59]Natelson1979 [14]Skinner1981 [60]Verrier1982 [61]Sgoifo1994 [62]Sgoifo1997 [63]Sgoifo1998 VPB=ventricularp EurHeartJ,Vol.22,issue13,July2001 Review 1085 y d r e a u m n m + + + + + + + + + nti u o S C Results acuteangeroranxietysuperimposedonabackgroundofdepressionSCDincreaseinmagnitudeoflifechangesinprior6monthsSCDhadmoreintensestress30minpriortoonsetofsymptomsandhadlowersocialclasslessmarried,moreeducationalincongruitywithspouses,fewerchildren:12/64(vs0)haddefinitepsychiatrichistory30hadlongstandingstress,leadingtodeathwithin2–24hfromsymptomonset,withdefiniteAMI;23patientshadacutestress,deathoccurredlessthan2hfromsymptomonsetanduncommonlyhadAMI15/497hadnoevidenceofinternalinjuryinwhom10hadmyofibrillardegeneration(vs0/15ofcomparisongroup)SCDcaseshadmorepsychiatrichistory,smoking,deathofsignificantotherwithinlast6monthsandlesseducationcomparedwithcontrolsSCDpeakonSaturday:inmendecreasingtrendthroughtoFridayregardlessofbaselinediseasecaseseriesofunexplainednocturnaldeathsnotedamongrefugees trospectivestudies Psychosocialfactor(A=acute,C=chronic) A,C A,C:42lifechangequestionsA,Csocialposition(socialclass) C A,C:longstandingstressincludingtroublesatwork,familyacutestress(emotional+physical) A:inferred A,C:28recentlifeevents,socialposition(education) A:inferred C:inferred,refugeesfromS.E.Asia e r ddencardiacdeathin Comparisongroup none 279AMIsurvivors 100AMIsurvivors 64liveage-relatedneighbourhoodcontrols none ffi15roadtracaccidentdeaths 80liveage-,race-,sex-matchedcontrols none none u s h ms) s:associationswit eaths SCDtiming(froonsetofsymptom ns <1h <24h <24h <24h murdervictims <24h <24h unexplainednocturnaldeaths r d facto rdiac Age 55·6 56 ns 55·6 31–83 1–82 25–64 ns 19–51 al ca oci den psy sychos Sud %auto ns ns 100 23 100 100 52·5 ns 100 p d sitionan Number%women) 5(0) 26(18) 00(0) 4(100) 18(20) 5(40) 0(100) 054(33) 8(0) o ( 2 1 1 6 1 1 8 1 1 p Table2Social Author,year [64]Greene1972 [65]Rahe1973 [66]Myers1975 [67]Talbott1977 [68]Rissanen1978 [22]Cebelin1980 [23,69]Talbott1981 [28]Beard1982 [70]Kirschner1986 EurHeartJ,Vol.22,issue13,July2001 1086 H. Hemingway et al. y r a m m + + + + + + u S Results menwithwiveswhohadmorethan12yearseducationvslesseducationhadoddsratio0·80(95CI0·5–1·3)forprimarycardiacarrest41suddendeathsinJanuary1991vs22inJanuary1990observedvsexpectedcasesofSCDamongthosenotworkingPwas56vs30(<0·0001).Noffdierencesinobserved/expectedinnon-manualormanualoccupationsage-adjustedratesofSCDbydecreasingeducationalcategorieswere88·9,95·2,129·2per100000(16,26,54%ofSCD);vs99·4,111·2and123·8fornon-suddencardiacdeath24casesofSCDondayofearthquakevsdailymeanof4·6priortoearthquakehigherrateofSCDduringthreatofwarbutnotsignificant;noassociationwithdegreeofthreatffindierentgeographicalregions Psychosocialfactor(A=acute,C=chronic) C:socialposition(wife’slevelofeducation) A:inferred,threatofwar C:socialposition(occupation) C:socialposition(education) A:inferred,Northridgeearthquake A:inferred,threatofwar d. Comparisongroup 133malecontrolschosenbyrandomdigitdialling January1990(notundermissilethreat)expectednumbersbasedonallCHDdeathsinmenaged30–69 1585non-suddenCHDdeathsand1053CHDdeathsunknowntiming meandailyrateofSCDpriortoearthquake 213casesinfivecontrolperiods ardiacdeath;ns=notstatefactorwasinferred. cal Suddencardiacdeaths %autopsyAgeSCDtiming(fromonsetofsymptoms) ns25–75fatalandnon-fatalprimarycardiacarrest nsnsns 7230–69<1h ns25–>85<1h 10038–92<1h ns76·3ns CHD=coronaryheartdisease;SCD=suddenxtofkininterviews,exceptwherepsychosoci Table2Continued Author,yearNumber(%women) [71]Strogatz1988133(0) [25]41(ns)Meisel1991 [72]Sexton1993155(0) [1]1608(43)Escobedo1996 [24]24(24)Leor1996 [26]68(44)Weisenberg1996 AMI=acutemyocardialinfarction;Sourceofpsychosocialdatawasne EurHeartJ,Vol.22,issue13,July2001 Review 1087 y r a mm + + + (cid:2) + + u S % ulations Results excessofSCDonMondays;onlyinthosewithoutpreviousCHDffRR=5·0fortheeectofeducationffnosignificanteectofpsychosocialstressloweducationwasandpsychosocialfactorswerenotassociatedbluecollarprotective phobicanxietyassociatedwithSCD(RR=6·08(95CI2·35–15·73)notnon-fatalMIRR=5·73(95%CI1·26–26·1) p po of y n h g o udiesinhealt SCDtimin <24h ns directobservatisuddenlossofconsciousness1–24h<1h<1h <1h t s e tiv ber c m spe nu ro D: p C 52 7 5 3186 6 n S 1 2 6 191 2 i rdiacdeath up(years) =notstated. a w s c o n dden Foll 29 6·5 20 18 2 32 ction; ctors:associationswithsu Psychosocialfactor(A=acute,C=chronic) A:inferredfromdayofweek C:socialposition(cid:1)(education7years)andcontinuouspsychosocial(cid:2)stress1yearC:socialposition(education),TypeA,TypeB,hostilityC:socialposition(occupation)C:anxiety(Crown–Crisp) C:anxiety(CornellMedicalIndex) disease;MI=myocardialinfar fa art psychosocial Ageatentry 25–34(69%) 25–59 54–62 46–68 42–77 21–80 =coronaryhe D positionand Totalsample(%women) 3983(0) 2455(0) 301(0) 7591(0) 33999(0) 2280(0) acdeath;CH Table3Social Author,year [27]Rabkin1980 [123]Salonen1982 [73]Hinkle1988 [19]Kagan1989 [20]Kawachi1994 [21]Kawachi1994 SCD=suddencardi EurHeartJ,Vol.22,issue13,July2001 1088 H. Hemingway et al. y r a mm + + (cid:2) + + + ns Su o heartdiseasepatientpopulati Results SisyphuspatternandTypeAmorefrequentamongcasesthancontrolsandpredictedSCDamongthosewithcomplexVPBloweducationhad33%mortalityvs9%inbettereducated;notpresentamongthosewithoutcomplexVPBnoneofthefourfactorsexplainedthelargesocialffposition(education)dierencesinSCDratesisolationandstresscombinedtopredictSCDinboththosewithandwithoutVPB Loweducation,TypeAandotherpsychosocialfactorspredictedSCDbutnotnon-suddencardiacdeathdepression,TypeB onary ming arrest sincor SCDti ns <1h <1h <1h <1h cardiac e di r stu CD:mbe e Su 3 s s 8 3 s v n 2 n n 6 2 n ti c e p osp wurs) thsuddencardiacdeathinpr PsychosocialfactorFollo(A=acute,C=chronic)(yea C:Sisyphuspattern,10TypeA,depression C:socialposition3(education),lifestress,socialisolation,TypeA,depression C:wifeassessedmood,3·5communication,anxiety/worry,striving C:socialposition3(education),lifestress,socialisolation,TypeA,depressionC:socialposition4·5(education)TypeA(videotapedinterview) C:anxiety,depression,nsTypeA,B,socialsupportanddesirability cardiacdeath;ns=notstated. wi en tors:associations Patientgroup MIsurvivorsand67healthyage,sex,typeofjobmatchedcontrolsMIsurvivors MIsurvivors MIsurvivors MIsurvivors:mean42months (cid:2)10VPBperhour(cid:2)or5non-sustainedVT6–60dayspostMI urebeat;SCD=sudd fac y mat ychosocial Ageatentr 25–80 30–69 35–74 30–69 53 ns ntricularpre ps ve positionand Totalsample(%women) 67(21) 1739(0) 1684(0) 2062(0) 1012(8) 331(ns) arction;VPB= Table4Social Author,year [74]Bruhn1974 [75]Weinblatt1978 [76]Ruberman1983 [77]Ruberman1984 [30]Brackett1988 [78,79]Ahern1990 MI=myocardialinf EurHeartJ,Vol.22,issue13,July2001 Review 1089 y d r e a u val mm + + + + + + + (cid:2) ntin r u o e S C t n tricularfibrillationandQTi Results VPB>6perminuteoccurredin6/23subjects,butin0/8whentreatedwithoxprenololvs6ship’spilotswithoutaberrantbeatsweremoreneurotic;aberrantbeatsoccurredmainlyattimesofmanoeuvringshipsinhazardousconditionsprolongedQTintervalwasmorefrequentandmoresevereamongdepressedthancontrolsshorterinphysicalratherthanemotionalstressdepressionmorecommonthanamongcontrols shortenedinmostwhorespondedwithangertothestressfulsituation;lengthenedin2whoreactedwithdespondencyQTinterval59–67mslongerthanatsameheartrateduringstableconditions notrelatedtoemploymentgrade n e v ulartachycardia, Ventriculararrhythmia:type(npatients) VPB,catecholamines (cid:2)VPB1(n=8)onambulatoryECG QTinterval QTinterval VPB>30perhourandnoMI QTinterval QTinterval,cyclelengthbeforeandfirst30safteremergencycallVPBonrestingECG c aturebeats,ventri Psychosocialfactor(A=acute,C=chronic) A:publicspeaking C:Eysenckneuroticism C:depression C:personalityinventories:72scales A:inactivity,neutraldiscussion,stressfuldiscussion,reassurance A:awakeningfromemergencycalls C:socialposition(civilserviceemploymentgrade) m e withventricularpr Design reallifestressor reallifestressor controls(healthy752,substanceuse44)emotionalandphysicalstress34age-andsex-matchedgeneralmedicalorsurgicalcontrolslaboratorystressor reallifestressor cross-sectional ctors:associations Patientgroup healthy(17hospitaldoctors) ship’spilots depressedanddrugfree 38arrhythmia,30with>30VPBperhourandnoMI healthyphysicians populationbased,civilservants a f social Age 21–58 39–63 ns 19–69 26–74 29–52 40–69 o h c nandpsy Totalsample%women) 23(91) 14(0) 21depressed 102(37) 17 30(30) 17000(0) o ( ti si able5Socialpo uthor,year ealthypopulations[80]Taggart1973 [81]Cook1982 [82]Rainey1982 [83]Hijzen1985 [84]Katz1985 [85]Huang1989 [32]Toivonen1997 [33]Hemingway1999 T A H EurHeartJ,Vol.22,issue13,July2001 1090 H. Hemingway et al. y d r e a u mm + + + + + + + + + + + ntin u o S C Results VFprecipitatedbyrecallofemotionalstressreducedasaresultofthewardround11/19showedanincreaseinVPBactivity amongthosewithcomplexVPBloweducationhad33%mortalityvs9%inbettereducated;notpresentamongthosewithoutcomplexVPBVPB>4perminuteweresignificantlymorecommonduringstress depressioninhealthymenwasassociatedwithprognosticallysevereventriculararrhythmiagradeofVPB(couplets,salvosofVT)associatedwithtimingofthegame 25patientswereexperiencingacuteemotionaldisturbancesduring24hprecedingarrhythmia4/12TypeAand0/6non-TypeAonlycompetitivebehaviourassociated TypeAwasassociatedwithhigherprevalenceofectopy Ventriculararrhythmia:type(npatients) VF(2) ventriculararrhythmiaVPB VPBon3hECG VPBmeasuredforeachof62min VPBon24hECG VPB,VTon24hECG VTsymptomaticcardiacarrest VTorVF ventriculararrhythmia VPB Psychosocialfactor(A=acute,C=chronic) A:recallofintenseemotionA:pulsepalpationonwardroundA:mentalarithmetic,readingtask,emotionalrecallC:socialposition(education)lowsocialsupport A:twoindependentratingseachminuteofdegreeofstressthepatientshowedemotionsprofileindexdepressionTypeAffCelticplay-os interviewedbycardiologistandpsychiatristfortriggersTypeA TypeA,depression,anxiety,competitivebehaviourTypeAandperformancetasks r r r o o ff o Design clinicalstressor clinicalstressor laboratorystress crosssectional laboratorystress(62minfilmedpsychiatricinterview)crosssectional reallifestressor(watchingabasketballplayoonTV)retrospective clinicalstressor clinicalstressor laboratorystress T I V Patientgroup patientwithVF patientsinCCU ventriculararrhythmia MIsurvivors MI 50CHD50highrisk50healthyavidCelticsbasketballfan,2monthspostM 62cardiacarrestsurvivors55symptomatic coronaryarterybypassgraftcoronaryarterybypassgraft 11CHD11healthyvolunteers 9 9 8 Age 39 59 0–6 38 58 54 7–7 8–6 54 57 3 1 3 n) Totalsample%wome 1(0) 225(42) 19(10) 1739(0) 1(0) 150(0) 1(ns) 117 26(0) 104(0) 22(0) ( d Table5Continue Author,year Patientpopulations[86]Lown1976 [87]Lynch1977 [88]Lown1978 [75]Weinblatt1978 [89]Donlon1979 [90]Orth-Gomer1980 [91]Graboys1981 [34]Reich1981 [92]Krantz1982 [93]Freeman1984 [94]Jennings1984 EurHeartJ,Vol.22,issue13,July2001 Review 1091 y r a m + + (cid:2) + + (cid:2) + + m u S Results 7patientsdevelopedVTduringstress;VFprovokedin2patientswithextrastimuliduringstress5/6hadmarkedpsychologicalstress;VTrelatedtosympatheticactivityandimprovedbybeta-blockerduring38monthfollow-upneitherrelatedtoarrhythmiaffiseverityortreatmentecacy distressshoweddirectrelationtoVPBonfollowupindependentofcardiacriskandprescriptionofbeta-blockersassociatedwithdesireforcontrol ffnoeects commonestprecipitantwasemotionalstress 5/21depressedvs3/82non-depressed Ventriculararrhythmia:type(npatients) meanventricularrefractoryperiod,unsustainedVT,VF VT programmedelectricalstimulationofarrhythmia VPBover1yearfollow-up(n=59)bytranstelephonicECG VTsustainedorVF VPBon24hECGatbaselineand3,6,12monthfollow-up syncopeandventriculararrhythmiaVTon24hECG notstated. = Psychosocialfactor(A=acute,C=chronic) mentalarithmeticstressor psychologicalstress depressionandcognitiveimpairment depression,SCL-90sumofninescales desireforcontrol,locusofcontrolandbehaviourpatterndepression,anxiety,anger,TypeA acuteemotionalstress depressiononstandardizedinterview arprematurebeat;ns ul c sor p m m ntri Design laboratorystres prospective,38monthfollow-u prospective prospective,12follow-up directcardiacstimulationatcatheterizationprospective,12follow-up retrospective cross-sectional rction;VPB=ve a Patientgroup MImean37d ventriculartachyarrhythmiawithoutstructuraldisease programmedelectricalstimulationforventricular(66),supraventricular(12)arrhythmiasorsyncope(10)MIsurvivors electrophysiologicalstudiesforVF(4)orVT(13)MIsurvivors6–60d(cid:2)10VPBperhror(cid:2)5runsofunsustainedVTLongQTsyndrome CAD nit;MI=myocardialinf u Age 51 22–60 52·2 54·5 27–74 59 21atfirstcontact60 arycare n o Totalsample%women) 19(0) 6(100) 88(39) 125(26) 17(12) 277(17) 328probands(69)103(82) CCV=cor ( n; o able5Continued uthor,year [95]Tavazzi1986 [35]Brodksy1987 [36]Kennedy1987 [96]Follick1988 [97]Hatton1989 [31]Follick1990 [98]Moss1991 [99]Carney1993 F=ventricularfibrillati T A V EurHeartJ,Vol.22,issue13,July2001
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