approaches to altering the type a behavior pattern

8
CARL E. THORESEN, Ph.D. MICHAEL J. TELCH, M.A. JEAN R. EAGLESTON, M.A. Approaches to altering the Type A behavior pattern Dr. Thoresen is prOfessor of education and psychology, Stanford University; Mr. Teich is a predoctoral fellow, Stanford Heart Disease Prevention Program; and Ms. Eagleston is a research assistant, Stanford Boys Town Centerfor Youth Development. Reprint requests to Dr. Thoresen, School of Education, Stanford University, Stanford, CA 94305. ABSTRACT: The Type A behavior pattern, a risk factor for coro- nary heart disease, is described in terms of the expanded cogni- tive social learning model that takes into account the interdepen- dent influences of behavioral, environmental, cognitive, and physiologic components. Six studies aimed at altering the behav- ior pattern are discussed in light of this conceptual framework. Among the issues involved in designing and conducting treat- ment programs are the targets of behavior (e.g., impatience or hostility) for change; the type of client populations to treat (e.g., teenagers, post-coronary patients); and treatment techniques (e.g., relaxation procedures, cognitive restructuring, mass media programs). For at least three decades, cardio- vascular and cerebrovascular dis- eases have been the most signifi- cant cause of death and disability in the United States and other western cultures. About 600,000 Americans die every year from coronary heart disease (CHD) with about 35% of these deaths (over 200,000) occur- ring prematurely in persons under 65 years of age. 1 Medical research has made us realize that the vascular diseases and other chronic disorders, espe- cially those involving the heart, are complex multidimensional prob- lems not caused directly by any single factor, such as excessive di- etary intake of cholesterol or ciga- rette smoking. Some investigators are beginning to realize the magni- tude of the problem, specifically, the intimate relationship of heart disease and contemporary lifestyle, especially daily habit patterns, and a few are starting to understand the imperative for a broad inclusive framework in conceptualizing the many factors contributing to CHD.2 Even when elaborate mul- tivariate statistical analyses are performed, less than one half of the variance associated with CHD is accounted for by risk factors such as hypertension, cigarette smoking, body weight, family history, physi- cal activity, and serum cholesterol level. The association of CHD with combinations of cigarette smoking, hypertension, elevated serum cho- lesterol, excessive dietary fats, and other factors leads to the question of what causes these behaviors and patterns. Obviously, other factors play a role in the development of CHD, because (I) not all persons with a high rate of risk factors de- velop CHD, and (2) many persons suffering myocardial infarction, stroke, or angina are known to have relatively low levels, if any, of these risk factors. 472 PSYCHOSOMATICS

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Page 1: Approaches to altering the Type A behavior pattern

CARL E. THORESEN, Ph.D.

MICHAEL J. TELCH, M.A.

JEAN R. EAGLESTON, M.A.

Approaches to alteringthe Type A behavior pattern

Dr. Thoresen is prOfessor of education and psychology, Stanford University; Mr.Teich is a predoctoral fellow, Stanford Heart Disease Prevention Program; and Ms.Eagleston is a research assistant, Stanford Boys Town Centerfor Youth Development.Reprint requests to Dr. Thoresen, School ofEducation, Stanford University, Stanford,CA 94305.

ABSTRACT: The Type A behavior pattern, a risk factor for coro­nary heart disease, is described in terms of the expanded cogni­tive social learning model that takes into account the interdepen­dent influences of behavioral, environmental, cognitive, andphysiologic components. Six studies aimed at altering the behav­ior pattern are discussed in light of this conceptual framework.Among the issues involved in designing and conducting treat­ment programs are the targets of behavior (e.g., impatience orhostility) for change; the type of client populations to treat (e.g.,teenagers, post-coronary patients); and treatment techniques(e.g., relaxation procedures, cognitive restructuring, mass mediaprograms).

For at least three decades, cardio­vascular and cerebrovascular dis­eases have been the most signifi­cant cause ofdeath and disability inthe United States and other westerncultures. About 600,000 Americansdie every year from coronary heartdisease (CHD) with about 35% ofthese deaths (over 200,000) occur­ring prematurely in persons under65 years of age.1

Medical research has made usrealize that the vascular diseasesand other chronic disorders, espe­cially those involving the heart, arecomplex multidimensional prob­lems not caused directly by anysingle factor, such as excessive di­etary intake of cholesterol or ciga­rette smoking. Some investigatorsare beginning to realize the magni­tude of the problem, specifically,

the intimate relationship of heartdisease and contemporary lifestyle,especially daily habit patterns, anda few are starting to understand theimperative for a broad inclusiveframework in conceptualizing themany factors contributing toCHD.2 Even when elaborate mul­tivariate statistical analyses areperformed, less than one halfof thevariance associated with CHD isaccounted for by risk factors suchas hypertension, cigarette smoking,body weight, family history, physi­cal activity, and serum cholesterollevel.

The association of CHD withcombinations of cigarette smoking,hypertension, elevated serum cho­lesterol, excessive dietary fats, andother factors leads to the questionof what causes these behaviors andpatterns. Obviously, other factorsplay a role in the development ofCHD, because (I) not all personswith a high rate of risk factors de­velop CHD, and (2) many personssuffering myocardial infarction,stroke, or angina are known to haverelatively low levels, if any, of theserisk factors.

472 PSYCHOSOMATICS

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TIle Type A behavior pattern

Building on the psychosocial or"personality" perspective of earlierinvestigators,3.4 Friedman and Ro­senman, in the late I950s, started toobserve the behavior and charac­teristics of their patients with coro­nary conditions. They identified aconstellation of observable behav­iors, which became known as theType A behavior pattern.s

With remarkable consistencythey noted a ubiquitous hurried­ness, impatience, sense of "time ur­gency," a pervasive pattern ofcom­petitive striving, and frequentlyand readily aroused angry and hos­tile feelings and behavior. The keytheme they noted was struggle-in­cessant efforts to overcome real orimagined obstacles imposed bytime, events, and especially otherpeople. They defined the Type Abehavior pattern as:

an action-emotion complex that isexhibited by those individualswho are engaged in a chronic andIncessant struggle to achieve moreand more in less and less time(thus giving rise to a sense of timeurgency or "hurry sickness") andwho also usually (but not always)exhibit a free-floating but well-ra­tionalized hostility.6

In a series oflaboratory and fieldstudies, results began to confirm arelationship between the observ­able pattern of behaviors and anumber of physiologic indicatorsassociated with CHD.7 Two majorprospective studies, the WesternCollaborative Group Study and theFramingham Study, have sinceconvincingly shown that personsmanifesting the Type A pattern areat sign~cantly greater risk for allforms of cardiovascular disease.8•9

Other investigators have providedcollaborative evidence in a variety

JUNE 1981 • VOL 22 • NO 6

of ways that shows a significantrelationship exists between theType A pattern and physiologicfactors, especially elevated levels ofserum cholesterol, epinephrine,norepinephrine, and triglycerides;increased blood coagulation time;and postprandial sludging oferythrocytes. 'o A meeting convenedby the National Heart, Lung, andBlood Institute of medical and be­havioral scientists recently con­cluded that evidence of a substan­tial predictive relationship betweenthe Type A behavior pattern andCHD was clearcui."

Cognitive socialleaming model

When we tum to the few publishedstudies of treating Type A behav­ior, almost all suffer from seriousmethodologic and conceptual limi­tations. The absence of an ade­quate conceptual framework to en­compass major components andthemes of the Type A pattern hasbeen a major obstacle in develop­ing effective treatment studies.How one conceptualizes the TypeA pattern strongly influences howone attempts to alter it. For exam­ple, a narrow conceptualization ofType A behavior as the chronicstimulation ofphysiologic variableshas led to the development of in­tervention strategies aimed pri­marily at reducing physiologicarousal. For example, while variousforms of relaxation training mayhelp reduce physiologic arousal,they may have little impact onother features of the behavior pat­tern, such as beliefs fostering hos­tile behavior or social behavior en­couraging excessive commitments.What is needed is a conceptualframework broad enough to cap­ture the complexity of the Type Apattern, yet flexible enough to bereadily altered by research data.

We have found that an expandedcognitive social learning modelprovides a useful framework fordesigning, implementing, and eval­uating treatment. This frameworkrecognizes the interdependent andreciprocal influences of behavioral,environmental, cognitive, andphysiologic factors.'2,I) The modeldenies that anyone of these factorsis sole influence and instead offers aperspective much like the biopsy­chosocial framework proposed byEngeJ.l4

One advantage of the cognitivesocial learning model is that it pro­vides ways of studying relation­ships among components of theframework, thus facilitating the de­velopment of treatment strategies.For instance, hostility is a Type Acharacteristic that has been shownto be related to CHD.'s Accordingto a cognitive social learningmodel, an adequate conceptualiza­tion of the role of hostility in theType A pattern must consider (I)cognitivefactors (e.g., the belief thatone must beat the other person be­fore getting beaten); (2) behavioralfactors (e.g., angry verbal out­bursts); (3) physiologic factors (e.g.,increases in heart rate during anangry outburst); and (4) environ­mental factors (e.g., media depict­ing hostility as a "normal" reactionto stress).

Of the above four factors, cogni­tive processes such as basic beliefs,attributions, and expectancies havereceived the least amount of atten­tion from researchers. We suspect,however, that it is the person's per­cept~onsofhimselfor herself, work,family, community, and God thatcreate his or her reality, the foun­dation on which the other threefactors are based. In advancingcognition factors as the core, weseek to direct attention to an area

473

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Type A behavior

that well deserves rigorous inquiry.But is an expanded cognitive so­

cial learning model the best or theonly valid way of thinking aboutthe Type A behavior pattern?Probably not. However, at thispoint it does appear quite useful,especially in planning for treat­ment. Undoubtedly, the model willbe altered on the basis of empiricalfindings and clinical experiences inthe way that the early theoreticaland treatment orthodoxy withinbehavior therapy has been ex­panded dramatically in the pastdecade. 13. 16 Using our expandedcognitive social learning model as aguide, let us now examine the fewmajor efforts to modify the Type Apattern.

Selected treatment studiesSuinn'7 conducted some of the ear­liest published attempts at alteringthe Type A pattern. The brieftreatment program (five hours)used for postmyocardial infarctionpatients consisted of: (I) training inprogressive muscle relaxation; (2)identifying varying levels of muscletension that accompany stress; (3)practicing relaxation as a copingresponse to stressful imagery; and(4) using imagery to practice be­havior incompatible with the TypeA pattern. Compared with a controlgroup, the patients reported morelifestyle changes and greater im­provements in their subjective andphysiologic reactions to stress. Un­fortunately, these results are diffi­cult to interpret since Type A be­havior was not objectively assessed,potential nonspecific treatment ef­fects were not controlled, and astatistical analysis of the findingswas not reported.

More recently Suinn andBlooml8 tested a slightly modifiedversion of the earlier program with

474

a sample of healthy Type A per­sons. Unlike the earlier study, sub­jects were not asked to rehearsebehavior incompatible with theType A pattern. The investigatorsused the Jenkins Activity Survey, aself-report measure of Type A be­havior that consists of "job in­volvement," "speed impatience,"and "hard driving" scales. After thetreatment program, subjects in thetreatment group reported lowerscores on the "hard driving" scale,compared with those of controlsubjects. Contrary to earlier find-

The duration ofthe benefitsoftreatment seems a farmore meaningful index tlumthe results obtainedimmediately after treatment.

ings, no significant differences werefound on physiologic measures.

lenni and Wollersheiml9 com­pared Suinn's program with a cog­nitive treatment approach consist­ing of the reevaluation and reap­praisal of tension-related thoughtsconcerning time-pressure, hostility,and competitiveness. The cognitivetreatment was significantly moreeffective in reducing scores, on theBortner Rating Scale, for subjectsclassified as "high" Type A personsthan for other subjects. No dif­ferences in blood pressure or serumcholesterol were found between theexperimental and control subjects.A major problem in this study wasthe use of a paper and pencil mea­sure (the Bortner Scale) which hasnot been validated; unlike theStructured Interview (the methodused in the Western CollaborativeGroup Study), the Jenkins ActivitySurvey, and the Framingham TypeA Scale, the Bortner Scale has not

been demonstrated to predict coro­nary heart disease.

Roskies and associatesl° com­pared the relative effectiveness ofbehavioral group therapy and psy­chodynamic group therapy in al­tering the Type A behavior patternin 25 healthy men in one ofthe veryfew well designed studies of thistype to date. Behavioral grouptherapy consisted of training ingeneral relaxation skills and dailyself-monitoring of tension levels. Inpsychodynamic group therapy, an­alytic interpretation was focused onincreasing the subjects' awarenessof their current Type A behavior;the pattern was presented to thesubjects as a reenactment of ·anoutdated family script. After 14weeks of treatment, no differencesbetween the two groups werefound. However, significant im­provements over 14 weeks in serumcholesterol, systolic blood pressure,self-reported health, family andemployment satisfaction, and senseof time pressure were found forboth treatments. No differenceswere found on measures of stateand trait anxiety, diastolic bloodpressure, or serum triglycerides.Data from seven men, who werelater treated in a special behaviortherapy group but excluded fromthe original data analysis becausethey had CHD, were later analyzedand compared with the original twogroups.21 Post-treatment resultsafter six months resembled earlierfindings, with some exceptions.Unlike the initial results, diastolicblood pressure levels for theseseven subjects were significantlyreduced, and their perceptions ofwork responsibility were lowered.Further, after six months signifi­cant differences in serum choles­terollevels were found between thethree treatment groups (psycho-

PSYCHOSOMATICS

Page 4: Approaches to altering the Type A behavior pattern

dynamic therapy, 240 mg; behaviortherapy, 220 mg; special behaviortherapy, 187 mg). At the six-monthfollow-up observation, treatmenteffects were maintained less suc­cessfully in the psychodynamicgroup than in the behavioral group.The delayed effects of treatmentsuggest that outcome may dependon the combined inftuence of thetype of treatment, time, and theperson's clinical status. The dura­tion of the benefits of treatmentseems a far more meaningful indexthan the results obtained immedi­ately after treatment.

The only other noteworthy treat­ment study reported to date as-

sessed the relative effectiveness ofbehavior therapy, supportive grouptherapy, and "minimal treatment"for healthy male executivesPThose receiving "minimal treat­ment" completed assessment mea­sures, met for one therapy session,and were urged to reduce Type Abehavior. Behavior therapy con­sisted of stress management train­ing coupled with self-control tech­niques designed to reduce the fre­quency and intensity of individu­ally specified Type A behaviors.Supportive group therapy was in­tended to help subjects becomeaware of their Type A behaviors,identify Type A behavior in their

daily living, and change this be­havior. However, specific behav­ioral techniques were not offered.Both treatment approaches hadmore favorable effects on severalaspects of the Type A pattern thandid "minimal treatment." Signifi­cant reductions in stress, accordingto self-ratings and physiologic indi­ces, were found, although reliefwasless marked in the group receivingsupportive therapy.

Commendably, this study em­ployed several psychometric, phys­iologic, and self-report measures,thus providing a comprehensiveevaluation of treatment effects. Thegroup receiving "minimal treat-

, Table-Stud" on Tre8tment of Type A Behavior

I T ,a.-_ ..... ..rest uaed to ...... treatment' ..IIIIIy .... WRIInI ............ EIIIr........ ...... .......... ....,... &IIl .....I.1

Suinn et aP1 X X S BN-20·Treatment: 2 wi< (5 hr)

Suinn & Blooml8 X S,P P E,BN-14Treatment: 3 wk (6 hr)

Jenni & Wollersheim'9 X X P S,P P,E,BN-42Treatment: 6 wi< (9 hr)

Roskies et al2021 X X S,P S,P,E S,P,E,BN-33Treatment: 20 wi< (14 hr)

Levenkronl2 X X X S,P S,P S,P,E,B SN-38Treatment: 8 wi< (12 hr)

Recurrent Coronary X X X X S,P S,P,E S,E,B S,PPrevention Progra~32'

N -1,035·Treatment: 5 yr (est 120 hr)·Sub/8C1S were postcoronary patients.'Measures: S - SeIf·report; P - Standardized psycho8ome1ric instrument; E- External observers: 8 - BiochemICal assay

JUNE 1981 • VOL 22 • NO 6 475

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Type A behavior

ment" allowed evaluation of thepossible effects on subjects of vol­unteering for treatment and com­pleting various assessment mea­sures. The identification of individ­ualized Type A behavior was amost interesting aspect ofthe study.The value of personalized treat­ment goals well deserves furtherstudy.

A growing body of research sug­gests that the Type A behavior pat­tern is multidimensional with cog­nitive, behavioral, physiologic, andenvironmental components in­teracting in a complex system. Theintervention studies just describedpaid little or no attention to thebehavioral, cognitive, and environ­mental components as targets forintervention. As the Table illus­trates, in these studies interventionfocused primarily on the physio­logic aspect of the Type A pattern(i.e., reducing the physiologicarousal caused by stressful situa­tions). While not denying the im­portance of teaching Type A per­sons to cope with stress, more at­tention might be given to helpingthem modify the conditions that setthe stage for behavior characteristicof the Type A pattern.

Further, five of these six studiesfailed to evaluate all four targetareas-cognitive, behavioral, physi­ologic, environmental. The en­vironmental component in particu­lar was largely ignored. Anotherissue involves the method ofassess­ment. Only the most recent studieshave assessed treatment by usingmultiple measures within a giventarget area. We feel the complexityof the Type A behavior patterndemands a variety of assessmentstrategies, i.e., self-report question­naires, standardized psychometricinstruments, external observation,and biochemical assays.

476

Recurrent coronaryprevention program

In contrast to the treatment studiesalready discussed, the RecurrentCoronary Prevention Program(RCPP), a five-year trial currentlyunderway, is seeking to demon­strate reduced morbidity and mor­tality by altering the Type A pat­tern in more than 1,000 post-in­farction men and women in the SanFrancisco Bay Areap·24 The majortreatment program, based on anexpanded cognitive social learningmodel, is offered in small groups of

Research suggests that theType A behavior pattem ismultidimensional withcognitive, behaviora~physiologic, andenvironmental componentsinteracting in a complexsystem.

eight to ten participating persons.Treatment in the cognitive area

includes self-instructional training,evaluation of basic beliefs, activelistening, and mental relaxation. Inthe behavioral part of the program,participants learn to alter certainspeech patterns (e.g., interrupting),psychomotor actions (e.g., em­phatic gesturing), and other physi­cal activities (e.g., hurried walking).In the environmental area, specificfeatures Of the work and home set­tings are scrutinized. For example,spouses of participants are en­couraged to change social behaviorthat may elicit unnecessary stress.The basics of social problem-solv­ing are presented to help partici­pants alter stressful environmentalfactors, such as a place of workwhere a supervisor engenders ex­cessive stress. In the physiologic

aspect of treatment, participantsare informed about biochemicalprocesses in stress reactions, such asthe role of norepinephrine in thecardiovascular system in responseto events perceived as threateningor challenging. They learn thatanger, irritation, aggravation, andimpatience are associated with in­creased production of the catechol­amines and of serum cholesterol.The comparison treatment in thestudy is provided in cardiologist­led small groups focused on diet,medication, and physiology.

Based on various measures (e.g.,self-report, biochemical assay) oftreatment of the targets discussed,results to date are encouraging. Therecurrence rates of infarctions forthe behavior change treatment andthe cardiologist-led group treat­ment are below the rates for controlsubjects, post-infarction patientsreceiving routine medical care, aswell as for nonsmoking subjects re­ceiving placebos in the NationalCoronary Drug Project (a cohorthighly similar to that in the currentRCPP).2S However, not all treatedsubjects are showing clearcutchanges in stress-related behavior,although some have dramaticallyreduced their commitments andmodified their sense of time ur­gency and hurriedness. A few havealtered their angry behavior andtheir related feelings of hostility.Most, however, are still working onunderstanding their hostile feelingsand are trying to change them. Ef­forts in this direction seem crucial;angiographic studies of pre-coro­nary subjects suggest that chronichostility may be the major patho­genic facet of the Type A pattern.15

DiscussionAmong the issues involved in de­signing and conducting treatment

(continued)

PSYCHOSOMATICS

Page 6: Approaches to altering the Type A behavior pattern

onedose••• onenight's sleepDO more••• no less

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One 3().mg capsule. h.s.-/l.",ulud/lll dosalle.One 15.mgcapsule. h.s. -T<~umm~I/"~" iniliuldusage[orelderlyordebililaledpaliems.INDICATIONS AND USAGE: Restorile (temaze·pam) is indicated for the relief of insomnia associatedwith complaints ofdifficulty in falling asleep. frequentnocturnal awakeninl\S' and/or early morning awaken·ings. Since insomnia 15 often transient and intermiuent.the prolonged administration ofRestoril isgeneraDy notnecessaryor recommended. ReslOriI has been employedfor sleep maintenance for up to 35 consecutive nights ofdrugadministration in sleep laboratory studies.

The possibility that the insomnia may be related to acondition for which there is more specific treatment.should beconsidered.CONTRAINDlCATIONS: Restoril is contraindicatedin pregnanl women. Benzodiazepines may cause fetaldamage when administered during pregnancy. AnincreaSed risk of congenital malformalions associatedwith lhe use of diazepam and chlordiazepoxide duringthe first trimester of pregnancy has been suggested inseveral studies. Also. ingestion of lherapeutic doses ofbenzodiazepine hypnotics during the last weeks ofpregnancy has resulted in neonatal CNS depression.Consider a possibility of pregnancy when institutinglherapy or whether patient mtends to become pregnanl.PRECAUTIONS: In elderly and debilitated palients. itis recommended that initial dosage be limited 10 15 mg.The usual precautions are indicated for severer)'depressed patients or those in whom there is any evi­dence of latent depression; it should be recognized thatsuicidal tendencies may be present and protective mea·sures may be necessary.

If Restoril is to be combined with other drugs havingknown h)'pnotic properties or CNs-depressant effects.due consideration should be given 10 potential additiveeffects.

Restoril is a controlled substance in Schedule IV.Caution must be exercised in addiction·prone individu­alsorthose who might increase dosage.Informalion for PalienlS: Patients receiving Restorilshould be cautioned about possible combiried effectswith alcohol and other CNS depressants. Patientsshould becautioned nOllOoperate machinery or drive amotor vehicle. They should be advised of the possibilityofdisturbed nocturnal sleep for the first or second nightaflerdisconlinuing lhe drug.Laboralorv Tests: The usual precautions should beobserved in patients with impaired renal or hepaticfunction. Abnormal ~ver functIOn tests as weD as blooddyscrasias have been reponed with benzodiazepines.~regnancy: Pregnancy Category X. See Contraindica­tlOns.Pediatric Use: Safely and effectiveness in children belowtheageofl8years have not been established.ADVERSE REACTIONS: The most commonadverse reactions were drowsiness. dizziness and leth·argy. Other side effects include confusion. euphoriaan-d relaxed feeling. Less commonly reponed wereweakness. anorexia and diarrhea. Rarely reponedwere tremor. ataxia. lack of concentration. ross ofequilibrium. falling and palpitations. And rarelyreponed were hallucinations. horizontal nystagmusand paradoxical reactions. including excilement. stim·ulation and hyperactivity.DOSAGE AND ADMINISTRATION: Adults: 30 mgusual dosage before reiiring; 15 mg may suffice in some.Elder~I' anif debilitated: 15 mg recommended initiallyuntil individual response is determined.SUPPUED: ReslOril (Iemazepam) capsUles-IS mll.maroon and pink. imprinted "RESTORIL 15 mg ;30 m~. maroon and blue. imprinted "RESTORIL30 mg'. Packages of 100. 500 and ControlPake pack­ages of 25 capsules (continuous reverse-numbered rollofsealed blisters).Before prescribing. set' package insert for full productmfonnallOn.

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Type A behavior

programs to alter the Type A be­havior pattern are the targets ofbehavior change, the kinds of per­sons who make appropriate clients,and choices of treatment methods.• Treatment targets. Many possiblefeatures of the Type A patternmight be the targets for change:readily observable behavior, suchas speech interruptions or emphaticgesturing; psychomotor activities,such as rapid eating or walking;composite behavior including hos­tility or a sense of urgency; specificbiochemical markers, including ex­cessive physiologic reactivity; andbasic beliefs or fears, especiallythose concerned with oneself, ca­reer, and family. A major issue iswhether 10 attempt to change se­lected specific behaviors or theglobal lifestyle. Another issue con­cerns the magnitude of change.Should treatment focus on reduc­ing the severity of the Type A pat­tern or on changing the patternsubstantially enough to approxi­mate the behavioral characteristicsof a Type B pattern?

At present we simply do notknow which features of the behav­ior pattern are pathogenic. Not allcharacteristics of the Type A be­havior pattern necessarily repre­sent a predilection to coronaryevents or even to disease, in gen­eral. However, in a study ofmatched pairs of men in the West­ern Collaborative Group Study,"competitive drive" and "impa­tience" differentiated those whodeveloped CHD'from those whodid not.26 Angiographic studies andpreliminary findings from theRCPP coupled with clinical experi­ence suggest that excessive angerand hostility may be the crucialpathogenic aspects of Type A be­havior. However, until empiricalfindings further substantiate this

478

view, it seems prudent to help per­sons alter the Type A pattern in amore general way.• Client selection. Three levels ofintervention with the Type A pat­tern have been suggested by Ros­kies: (I) primary prevention seekingto prevent the development of thebehavior pattern among young ad­olescents as well as adults enteringhigh-risk life situations (e.g.,women re-entering the work force);(2) secondary prevention for personswho are obviously Type A andtherefore are at increased risk for

Perlulps a combination ofcommunity-based mediaprograms andface-to-facegroup sessions would proveeffective.

CHD, and (3) tertiaryprevention forpatients who have had an infarct orwho suffer from angina.l7 At thelevel of secondary prevention, spe­cific groups at particularly high riskcould be identified. For example,the Framingham data suggest thatemployed Type A women withthree or more children are at sub­stantial risk for CHD.28 Suchwomen as well as other Type Apersons who have a number ofother risk factors, such as hyper­tension and smoking, may be ap­propriate candidates for interven­tion. It is clear that it is not wise towait until a heavy smoker has had amyocardial infarction or has devel­oped emphysema before suggest­ing ways to stop smoking. Simi­larly, reserving treatment for onlypost-myocardial infarction patientsindeed might well be offering toolittle too late to too few.

Primary prevention with theType A pattern is an intriguing

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Page 7: Approaches to altering the Type A behavior pattern

".

proposition. Should we developeducational programs to stem atleast the extreme versions of theType A pattern rather than wait forchronic disease to develop? Someevidence shows that the behaviorpattern is clearly present in youngchildren and early adolescents,29.3oand a substantial number ofstudieshave demonstrated various fea­tures of the pattern in college stu­dents.31 Currently at Stanford weare initiating a series of studies toassess the behavior pattern in chil­dren and adolescents with an eye toplanning primary prevention (andintervention) studies at a later time.-Treatment methods. Interventionhas ranged from an exclusive focuson altering physiologic responses tostressful situations, using progres­sive muscle relaxation (sometimescoupled with teaching awareness ofbehavior via self-monitoring), to aninclusive focus on altering all facetsof the pattern via a groupladmin­istered program using multipletechniques. Which treatment mo­dalities are most effective? That willdepend on the targets selected fortreatment, and there are not yetsufficient data to provide a defini­tive answer. Our experience sug­gests that treatment should bedirected at physiologic, environ-

......NCES1. Havlik RJ, Feinleib M: Proceedings of the

Conference on the Decline in Coronary HeartDiseue Mortality. Bethesda, Md, NationalHeart, Lung, and Blood Institute. Oct 24-25,1978.

2. Farquhar JW: The American Way of Life NeactNot Be Hazardous to Your Health. Stanford.CaHt, The Portable Stanford, 1978.

3. Dunbar HF: Psychosomatic Diagnosis. NewYork. Paul B. H~ber, 1943.

4. Osler W: Lectures on Angina Pectoris andAllied States. New York, Appleton. t892.

5. Friedman M, Rosenman, RH: Type A Behav­ior 8IId Your Heart. Greenwich, Conn, Faw­cett. 1974.

6. Friedman M: Type A behavior pattern: Some

JUNE 1981 • VOL 22 • NO 6

mental, behavioral, and cogmtlveaspects of the Type A pattern. Amulti-component treatment ap­proach, such as the one used in theRCPP, introduces clients to a vari­ety of skills and strategies (e.g.,physical and mental relaxationskills, communication skills, mod­eling, daily drills, and cognitiverestructuring techniques such asself-instructional training). Self­managed behavioral changes,whereby the participants them­selves learn how to apply skills to avariety of situations, are high­lighted. In keeping with the ex­panded cognitive social learningmodel discussed earlier, treatmentaddresses the environmental com­ponent by trying to engage thespouse, other family members, andthe client's co-workers in the treat­ment program. A major effort ismade to provide social supportthrough the treatment group and tosecure the support of significantpersons in the client's life.

To date all intervention has beenface-to-face in format. Our experi­ence suggests that this is crucial foradults with well-established TypeA patterns, especially post-coro­nary patients. The Stanford HeartDisease Prevention Program hasbeen relying primarily on a media-

of its pathophysiological components. BullNY Acad Mad 53:593-604. 1977.

7. Friedman M: Pathogenesis of Coronary Ar­tery Disease. New York, McGraw-Hili, 1969.

8. Rosenman RH, Brand RJ, Jenkins CD, et al:Coronary heart disease in the Western Col­laborative Group Study. Final follow-up expe­rience of 8 1/2 years. JAMA 233:872-877.1975.

9. Haynes SG, Feinleib M, Kannel WB: Therelationship of psychosocial factors to coro­nary heart disease in the Framingham Studypt III, Eight-year incidence of coronary heartdisease. Am J Epidemiol 111: 37-58, 1980.

10. Dembroski TM, Weiss SM. Shields. JL. et al:Coronary-Prone Behavior. New York,Springer-Verlag. 1978.

based format (e.g., radio and TVannouncements, newspaper arti­cles, brochures) to reduce heart dis­ease risk factors in all residents of acommunity.32 It remains to be seenif substantial reductions in theType A pattern can be effected withsuch a mass-media strategy. ·Cer­tainly such innovative approachesdeserve thoughtful consideration.Perhaps a combination of commu­nity-based media programs andface-to-face group sessions wouldprove effective.

Another intriguing possibility isoffering treatment in the work en­vironment. We suspect that inter­vention programs built into theworking day would not only be wellreceived by participants but wouldhave a significant influence onType A behavior. Work- andschool-based programs appearespecially promising ways of im­plementing preventive efforts. 0

Preparation ofthis article was supportedin part by National Institute of MentalHealth grant no. 27551, Stanford BoysTown Center for Youth Development,and the Luke Hancock Foundation. Thecooperation and encouragement ofMeyer Friedman, M.D., and Ray Ro­senman, M.D., are gratefully acknowl­edged.

11. Coronary-prone behavior and coronary heartdisease: A critical review. Report of theCoronary-Prone Behavior Review Panel,Bethesda, Md, National Heart, Lung, andBlOOd Institute, National Institutes of Health,December, 1978.

12. Bandura A: Social Learning Theory. Engle­wOOd Cliffs. NJ, Prentice-Hall, 1977.

13. Thoresen CE, Coates TJ (eds): The BehaviorTherapis/. Monterey. Calif, BrOOks/Cole,1980.

14. Engel GL: The need for a new medical mOdel:A challenge for biomedicine. Science196:129-196,1977.

15. Williams RB, Haney TL, Lee KL, et al: Type Abehavior, hostility, and coronary atheroscle­rosis. Psychosom Med 42:539-549, 1980.

(continued)

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Page 8: Approaches to altering the Type A behavior pattern

L1MBITROLtt TABLETS Tranquilizer-AntldeprHlClnt'1'1111 pIIlCrlblng. pllOll conl,,1t complltl procl"et InfOrmotlon.a nmmary of wIllcll fOllows:IndlcDflonl: Relief of moderofe to severe depression ossociOled with mOderOleto severe anxiety.ContrDlndlcDflonl: Known hypersensitivity to benzodiozepines or tricyclicantidepressonts Do not use with monoomine oxidase (MAO) inhibitors orwithin 14 days following discontinuOlion 01 MAO inhibifors since hyperpyreticcrises, severe convulsions ancl deOlhs hove occurred with concomitant use;then initiofe cautiously, gradually increasing dosage until optimal response isochieved. ContraindicOled during ocute recovery phose following myocardialinfarctionwarnlngl: Use with great core in pOlients with history of urinary retention orangle-closure glaucoma. severe constipotion may occur m potients takingtricyclic anlldepressants and antiChOlinergic-type drugs. Closely supervisecardiovascular pOlienls. (Arrhythmias, sinus tochycardia and pralongOlion ofconduction time reported with use of tricyclic antidepressants, especially highdoses Myocardial infarction and stroke reported With use at this closs 01drugs.) Caution potlents about possible combined effects with alcohol andother CNS depressants and against hOzardous occupot.ions requiring completemental alertness (eg, operofing mochinery, drlvmg)

UN,_ In "'-Inflne,: UN of minor trDlHI"lIlzlrs during ttll fIrsttrlmutlr 1II00Id almost always be avoldld blctJu.. of IncllCllldrllk of conglnltal malformatlonl 01 1",ll1ICIln IIVtrol ltudlu.Conlldlr passlblllty of p....nancy wIlln nltltuttng tIllropy; adYl..pottlnts to dllCu.. tIllropy If tillY Intend ta or do bleoml p....nant.

Since phySical and psyChOlogical dependence to chlordiazepoxide hove beenreported rarely, use caution in administering Limbitrolto addiction-proneindividuals or thOse who might increase dosage; withdrlM'Ol symptomsfollowing discontinuOlion of either component alone hove been reported(nausea, headoche and malaise for amitriptyline; symploms [includingconvulsions1Similar to lhose of barbiturOle withdrQIMJI for chlordiazepoxide)Prlcaullonl: Use with caution in potients with a hislOry at seizures, inhyperthyroid potlents or Ihase on thyroid medicOlion, ancl in potients wilhimpoired renal or hepotic function Because of the possibility of suicide indepressed patients, do nOI permit easy occess to large quantities in lhesepotients. Periodic liver function tests and blood counts are recommendedduring prolonged treofment Amitriptyline component may block oction ofguanethidine or Similar antihypertensives Concomitant use with otherpsychOtropic drugs hOs not been evaluOled: sedOlive effects may be additiveDiscontinue several days betore surgery Limit concomitant administrOlian atECT to essential treatment see Womings for precautions about pregnancyLimbitrol should not be token during the nursing period Not recommendedin children under 12 In the elderly ancl debililOled, limit 10 smallest effectivedosage to preclude ataxia, oversedation, confusion or antiChOlinergic effectsAdwfH R_tlonl: Most frequently reported are thOse associOled with eithercomponent alone: drowsiness, dry mouth, constipotion, blurred vision,dizziness and blooting. less frequently occurring reactions include vividdreams, impotence, tremor, confUSion ancl nasal congestion Many depressivesymptoms including anorexia, fOligue, weakness, resllessness and lethargyhove been reported as side effects ot both Limbitrol ancl amitriptylineGranulocytopenia, jaundice ancl hepotic dysfunction hove been observedrarelyThe following list includes adverse reoctions not reported with Limbitrol butrequiring considerOlion because Ihey have been reported wilh one or bothcomponents or closely related drugsCardiovascular Hypotension, hypertension, tOChycordio, polpitOlions, myo­cordiol inforction, orrhythmios, heort block, strokePSyChiatriC. EuphOrlo, opprehension, poor concentrOlion, delusions, hOlluci­nOlions, hypomonio ond increosed or decreased libidoN8urologiC. IncoordinOlion, OIoxia, numbness, tingling and poresthesios o."heextremities, extrapyromidol symptoms, syncope, changes in EEG poffernsAnficnolinBrgic Disturbance at occammOdation, poralytic ileus, urinaryretention, dilOlOlion of urinory troclAI/Brgic.· Skin rosh, urticaria, photosensitizOlion, edema of foce ancl tongue,pruritus.Hematologic. Bone morrow depression including ogronulocytosis,easinophilia, purpuro, thrombocytopenio.Gostroint8stina" Nouseo, epigostric distress, vomiting, onorexia, stomOlitis,psculiar toste, diarrhea, block tongue.Endocrine: Testicular swelling and gyn8j:omastio in the mole, breastenlargement, galactorrhea and minor menstrual irregularities in the femaleand elevotion and lowering at blood sugar levels.Other: Headache, weight gain or loss, increosed perspiration, urinaryfrequency. mydriasis, Jaundice, alopecio, poratid swelling.ChInloIagI: ImmediOlely hospitalize potienl suspected at having token onoverdose. Treatment is symptomOlic and supportive. IV odministrOlion of I to3 mg physostigmine solicylate has been reported to reverse the symptoms 01amitriptyline poisoning. see complete product informOlion for manitestOlionand treatmentDosagl: Individualize according to symptom severity and potient responseReduce to smallest effective dosage when sotisfactory response is obtained.larger portion 01 doily dose may be token 01 bedtime Single h. s dose maysuffice for some potients. lower dosoges are recommended for the elderly.Limbitrol 10-25, initiol dosage oIlhree 10 four tablets doily in divided doses,increased to six tablets or decreased to two tablefs doily os required. Limbitrol5-12.5, initial dosage of three to tour toblets doily in divided doses, forpotients whO do not tolerOle higher doses.How Suppllld: White, film-cooted toblets, each containing 10 mg chlor­diazepoxide and 25 mg amitriptyline (as the hydrachloride soli) and blue,film-cooted tablels, each containing 5 mg chlordiazepoxide and 12.5 mgamitriptyline (as the hydrachloride sall)-bOllles of 100 and 500; Tel-E-Dose"packages 01100, availoble in trays ot 4 reverse-numbered boxes 01 25,and in boxes containing 10 strips 0110; Prescripfion Poks 0150.

~ROCHE ROCHE PRODUCTS INC~ ManOli, Puerto Rico 00701

Type A behavior

16. Krumboltz JD, Thoresen CE (eds): Counsel­ing M8thods. New York, HolI, Rineharl &Winston, 1976.

17. Suinn RM: The cardiac slress managementprogram for Type A patients. Cardiac Reha­bilitation 5:13-15,1975.

18. Suinn RM, Bloom LJ: Anxiety managementtraining for Panern A behavior. J BenavioralMedicine 1:25-35, 1978.

19. Jenni MA. Wollersheim JP: Cognitive therapy,stress management training, and the Type Abehavior pallern. Cognitive Therapy and Re­search 3:61-73,1979.

20. Roskies E, Spevack M, Surkis A, et al:Changing the coronary-prone (Type A) be­havior pallern in a nonclinical population. JBenavMed 1:201-216, 197B.

21. Roskies E, Kearney H. Spevack M, et al:Generalizability and durability of treatmenteffects in an intervention program for coro­nary-prone (Type A) managers. J Behav Mad2:195-207, 1979.

22. Levenkron JC: Modifying the Type A coro­nary-prone behavior panern: A comparisonof three intervention approaches. SI. Louis,Washington University, 1979, Unpublisheddoctoral disserlalion.

23. Friedman M: Type A behavior: A progressreporl. The Sciences 20: 10-11, 28, February1980.

24. Friedman M, Thoresen CE, Gill JJ: Type Abehavior: lis possible role, detection, andlateralization in patients with ischemic hearldisease, in Hurst JW (ed): Hearl Update V.New York: McGraw-Hili, 1981, pp 88-99.

25. The Coronary Drug Project: Clofibrate andniacin in coronary heart disease. JAMA231:360-381,1975.

26. Mallhews KA, Glass DC, Rosenman RH, el al:Competitive drive, Pattern A, and coronaryhearl disease: A furlher analysis of some datafrom the Western Collaborative Group Study.J Chronic Dis 30:489-498, 1977.

27. Roskies E: Considerations in developing atreatment program for the coronary-prone(Type A) behavior pallern, in Davidson P(ed):Behavioral Medicine: Changing Health LiteStyles. New York, Brunner/Mazel, 1979, pp299-333.

28. Haynes 50, Feinleib M: Women, work, andcoronary hearl disease: Prospective findingsfrom the Framingham Hearl Study. Am JPublic Health 70:133-141, 1980.

29. Manhews KA, AngUlo J: Measurement of theType A behavior panern in children: Assess­ment of children's competitiveness, impa­tience-anger, and aggression. Child Dev51 :466-475, 1980.

30. Siegel JM, Leitch CJ: Type A behavior inadolescence: The Tacoma Study. Read be­fore the 20th Conference in CardiovascularDisease Epidemiology, San Diego, Calif,March 1980.

31. Dembroski TM, MacDougall JM, Herd JA, etal: The Type A coronary-prone behavior-pat­tern: A review. National Hearl, Lung, andBlood Institute, 1980.

32. Maccoby N, Farquhar JW, Wood PW, et al:Reducing the risk of cardiovascular disease:Effects of a community-based campaign onknowledge and behavior. Community Health3:100-114,1977.