Psychophysiological factors in ventricular arrhythmias and sudden cardiac death

Journal ojPsychosomam Printed in Great Britain.

Research,

Vol. 33, No. 5, pp. 621-631.

1989. 0

0022-3999/89 s3.00 + .oo 1989 Pergamon Press plc

PSYCHOPHYSIOLOGICAL FACTORS IN VENTRICULAR ARRHYTHMIAS AND SUDDEN CARDIAC DEATH DANIEL C. HATTON, EUGENE R. GILDEN,* MARY ELLEN EDWARDS, JOEL CuTmR,t JACK KRON~ and JOHN H. MCANULTY~ (Received 25 October

1988; accepted in revised form

12 May 1989)

Abstract-Plasma catecholamine levels were measured preceding programmed electrophysiological studies of patients who had survived a ventricular tachyarrhythmia episode. Psychological assessments of desire for control, locus of control and behavior pattern were obtained. Psychophysiological variables were analysed with respect to the severity of arrhythmias induced by the electrophysiological procedure. Analysis of data from 17 subjects showed desire for control was significantly higher in those with induced sustained arrhythmias than in those in which nonsustained arrhythmias were induced. No relationship was found between behavior pattern and arrhythmia severity or plasma catecholamine levels. There was a significant interaction between desire for control and behavior pattern with respect to epinephrine level. The findings indicate that psychological factors such as desire for control may be associated with potentially lethal arrhythmias and implicated in sudden cardiac death.

INTRODUCTION DEATH resulting from a lethal cardiac rhythm, often termed sudden cardiac death, is the leading cause of mortality among middle-aged American men [ 11. While many such deaths are in fact sudden they should not be thought of as unexpected or unexplainable. Most fatalities resulting from disturbances in heart rhythms occur in individuals who have previously been identified as manifesting traditional risk factors for coronary artery disease [2]. Although some details of the population at risk for sudden cardiac death are known [3], the factors that precipitate the lethal event have not been identified. Lown [4] suggests that in an electrically unstable heart, alterations in neural outflow to the heart initiated by psychological factors, can be considered a transient risk factor for lethal arrhythmias. The experimental studies of dogs by Lown, Verrier and their colleagues [5-81 have demonstrated that the threshold for ventricular arrhythmia can be significantly affected by behavioral factors. Case history approaches suggest that psychological factors are important in the occurrence of serious arrhythmias in humans. Greene, Goldstein and Moss, [9] suggested that the combination of depressed and aroused psychological states may produce neurally mediated responses conducive to sudden death. Likewise, Myers and Dewer [lo] concluded that physical activity and acute psychological stress that

*Department of Medical Psychology, Linfield, College McMinnville, Oregon 97128. tDepartment of Medicine, Division of Cardiology, Oregon Health Sciences University, Portland, Oregon 97201. Ph.D., Department of Medical Psychology, Address correspondence to Daniel C. Hatton, L-470, Oregon Health Sciences University, 3181 SW. Sam Jackson Park Road, Portland, Oregon 97201 3098. 621

622

DANIEL C. HATTON ef al.

cause catecholamine release are significant factors in sudden death. In a review of sudden death accounts, Engel [l 1] concluded that an important underlying factor was sudden unexpected loss of control of the environment. Lown and DeSilva [12] reported that I 1 of 19 patients suffering from potentially lethal arrhythmias showed an increase in the frequency of premature ventricular contractions during an interview focused on stressful areas of their lives. In a similar investigation, Reich, DeSilva, Lown and Murowski [13] found that slightly more than 20% of survivors of life threatening arrhythmias studied were classified by the investigators as having experienced some sort of psychological trigger for the event. The authors note that a factor in many of these ‘psychological trigger’ cases is anger associated with a fear of loss of control. In his review of the literature Binik [14] concludes that controllability is a potent variable in the pathogenesis of sudden death. Thus the case study literature supports the hypothesis that psychological stressors, particularly those related to loss of environmental control, are related to sudden cardiac death and that catecholamines may play a mediating role in this relationship. The premise is rendered even more compelling by the fact that investigators from a diversity of theoretical and methodological backgrounds have identified psychological factors as important in sudden cardiac death. Because of the importance of coronary heart disease in sudden cardiac death, another suggested risk factor in the development of potentially lethal arrhythmias is the type A or coronary prone behavior pattern [15. 161. The findings concerning the exact nature of the relationship between behavior pattern and cardiovascular disease are somewhat inconsistent [17, 211. However. two studies in which cardiac arrhythmias were investigated in relationship to behavior pattern revealed an increased prevalence of ectopic beats among those exhibiting the Type A pattern than in the Type B group [22, 231. Despite the controversy surrounding the relationship between behavior pattern and coronary heart disease, the outcome of these two studies suggests that analysis of behavior pattern may be a fertile area in which to explore the relationship between behavior and sudden cardiac death. To address the important lack of data connecting physiological and psychological variables with regard to sudden cardiac death, this study was designed to investigate psychophysiological parameters in a population known to be at great risk of sudden death; sudden death ‘survivors’. The study was carried out in conjunction with clinical diagnostic Programmed Electrical Stimulation (PES).

METHOD

Survivors of ventricular tachycardia or ventricular fibrtllation (those at high risk for recurrence) who were admitted to the hospital to undergo clinicalPES studies were recruited to participate in a study of psychophysiological aspects of cardiac arrhythmias, Patients on beta-blockers were excluded from the study. Antiarrhythmic drugs were stopped for 4 half-lives prior to evaluation. Subjects had to be over I8 years of age, have English language skills and the physical and cognitive capacity to consent and participate. From those who agreed to participate, informed consent was obtained prior to electrophysiological evaluation. The study protocol included the col!ection of psychosocial, chemical and physiologic data in addition to the clinically planned and indicated PES. .411 protocols were approved by the Oregon Health Sciences University, institutional Review Board. Committee on Human Research.

Psychophysiological

factors

in arrhythmias

623

Procedures Psychosocird evaluation. During hospitalization, patients completed three paper and pencil measures. The Jenkins Activity Survey for Health Prediction (JAS) [24] was used to assess the Type A behavior pattern. While the Structured Interview technique [25] for assessing behavior pattern is regarded as the preferred assessment tool [26], the Structured Interview is designed to be and is reported by interviewees to be very stressful. Given the fragile nature of the subject group, the JAS was considered a more appropriate measure. Two measures of control were used. The Burger and Cooper [27] Desirability of Control scale was used to determine the degrse of subjects’ desired control over their environments. In addition to the desirability of control scale, the Multidimensional Health Locus of Control scale (MDHLC) developed by Wallston, Wallston and Devellis [28] was given to the subjects. This instrument consists of three separate scales. The Internal Health Locus of Control (IHLC), measures the degree to which patients believe that their health is a function of their own behavior. The Chance Health Locus of Control (CHLC), measures the extent to which an individual believes that health is a matter of fate, luck or chance. The Powerful others Health Locus of Control scale (PHLC), measures the belief that a person’s health is determined by the actions of ‘powerful others’ such as family members, friends, and health care professionals. Chemicd eduation. Immediately prior to the PES procedure a 10 ml blood sample for catecholamine assay was obtained. Blood samples were injected into iced, heparinized glass tubes and centrifuged at 4°C within 15 min of collection. After being centrifuged, plasma was frozen at -80°C until assayed for catecholamine content. Catecholamines were extracted on alumina and assayed using high performance liquid chromatography with electro-chemical detection (Bioanalytic Systems 400) [29]. The detection limit with this system is less than 1Opgjml for norepinephrine and epinephrine with a test-retest reliability greater than 90%. Physiologic eanlua~ion. After the blood samples were drawn, patients underwent programmed electrical stimulation of the heart. This clinical procedure consists of direct electrical stimulation of the ventricle in an attempt to induce ventricular arrhythmias. If an arrhythmia can be induced, a patient is likely to have a clinical recurrence if left untreated. Serial attempts to induce the rhythm while antiarrhythmic drugs are given can identify agents which prevent inducibility. If sent home on these drugs, the chance of recurrence of the rhythm is lowered significantly [30]. Ventricular programmed electrical stimulation was delivered through a hexapolar subclavian pacing catheter positioned at the apex of the right ventricle. A digital stimulator delivered rectangular pulses of 2 msec duration and twice diastolic threshold. The stimulation protocol has previously been presented in detail [31l33]. Briefly, the ventricle was paced for six beats at a rate of 100 beats per minute. A seventh pacing extrastimulus was delivered starting at 400 msec after the sixth paced beat, and brought closer by 10 msec intervals until refractoriness occurred or a sustained arrhythmia was induced. If a sustained ventricular arrhythmia was not produced this process was repeated using paced beats at a rate of 150 beats per minute. The process was repeated with two extrastimuliat the two heart rates with the first extrastimulus fixed at 30 msec longer than the ventricular refractory period, and the second scanning diastole in 10 msec intervals as described above. This was followed by introduction of a third and then a fourth extrastimulus until a sustained rhythm was induced. Any stimulus type producing a ventricular tachyarrhythmia (not requiring cardioversion) was repeated and induction of the arrhythmia confirmed before proceeding with the protocol. If stimulation from the right ventricular apex was not successful in producing a sustained ventricular tachyarrhythmia, the stimulation sequence was repeated from the right ventricular outflow tract. An eight point rhythm scoring system [34] was used to quantify the results of testing. Rhythm scores ranged from 1 (no ventricular arrhythmias induced) to 8 (ventricular tachycardia at a rate greater than 300 beats per minute or ventricular fibrillation induced). Heart rate, rhythm, and blood pressure were recorded immediately before each programmed stimulation procedure. Following completion of PES, patirnts were moved from the cardiac catheterization laboratory to the cardiac care unit (CCU) of the hospital. Within 24 hours of being moved to the CCU, after recovery from the PES procedure, subjects were presented with the psychological measures and asked to complete them.

RESULTS

Complete data were available for 17 subjects. The subjects ranged in age from 27 to 74 years with an average age of 55.6 years. Two subjects were women. Four subjects had a history of ventricular fibrillation, and the remaining 13 had experienced clinical ventricular tachycardia episodes.

DANIEL C. HATTON ef al.

624 TABLE I.-SUMMARY

OF MEAM ANL, STANDARD ERRORS OF THE MEAN (SEM)

Mean 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11.

Internal control (IHLC) Other people control (PHLC) Chance control (CHLC) JAS Type A/B (A/B) JAS speed and impatience (Speed) JAS job involvement (Job) JAS hard driving (Hard) Desire for control (DC) Arrhythmia response (Arrhy) Epinephrine (E) Norepinephrine (NE)

SEM

N

28.94

0.90

23.41 18.24 211.35 162.06 161.67 119.31 103.29 4.35 251.64 363.00

1.76 1.56 20.76 17.31 13.15 1.23 4.20 0.20 52.81 42.44

17 17 17 17 17 17 17 17 17 17 17

Cardiologists scored the responses to PES as a normal part of the clinical protocol. Table I shows the means and standard errors of the psychophysiological variables assessed. To explore the possibility that the severity of induced arrhythmia, as indexed by the clinical scale, is related to psychophysiological variables, intercorrelations of the measures assessed were examined. The intercorrelation matrix of psychological variables and arrhythmia response is presented in Table II. Since many correlation coefficients were computed some would be expected to be statistically significant based on chance alone. The intercorrelation matrix is presented only to provide a description and summary of the data. As expected. Table II shows that a number of significant intercorrelations were found among the psychological variables assessed. The desire for control was related to JAS assessed Type A behavior pattern scale scores (r = 0.685, p < 0.01) and the speed and job involvement subscales of the JAS (r = 0.712, p < 0.01; Y = 0.527, p < 0.05). The correlation with the hard-driving, competitive JAS subscale was not significant. Type A scores were related in a positive fashion to other subscales of the JAS. Those with high Type A scores tended to discount the importance of chance with regard to their health (Y = -0.509, p < 0.05). The severity of induced arrhythmia response showed a significant positive relationship with the desirability of control (I = 0.555, p < 0.05). Interestingly, the desire for control was negatively related to pre PES systolic blood pressure (r = -0.746, p < 0.01). Other than the expected correlation between systolic and diastolic blood pressure, no other correlations were found among the physiological parameters measured. Because the arrhythmia scale responses developed for clinical use were not normally distributed, additional analyses were performed in which the original eight point arrhythmia response scale was divided into two groups; those in whom a sustained ventricular arrhythmia was induced with PES and those in whom nonsustained arrhythmias were induced. There were 5 subjects in the nonsustained group and 12 in the sustained arrhythmia group. Those with sustained arrhythmias scored significantly higher (f value -2.58, df = 15, p < 0.05) on the desire for control scale than did those with nonsustained arrhythmia response (see Fig. 1). Mean catecholamine differences between the sustained (E = 3 18.7 NE = 371.8) and

I.000

0.360 0.202 - 0.098 0.208 0.106 -0.118 0.141 0.143 0.204 -0.548*

**p < 0.01.

*p < 0.05.

1 2 3 4 5 6 7 8 9 10 11

1

IHLC

1.000 0.148 0.006 0.362 -0.337 0.064 -0.017 0.032 0.275 0.274

2

PHLC

1.000 -0.509* -0.316 -0.382 -0.098 -0.415 0.056 -0.283 -0.078

CHLC

3

1.000 0.755** 0.449 0.673* 0.685** 0.246 0.205 0.304

4 A/B

1.000 0.368 0.503* 0.712** 0.464 0.385 0.194

5 Speed

0.115 0.527’ 0.319 -0.261 -0.458

1.000

6 Job

1.000 0.398 0.025 -0.078 0.303

7 Hard

1.000 0.555; 0.269 -0.056

8 DC

TABLE II.-INTERCORRELATIONS BETWEENMEASURES FOR THE 17 SUBJECTS

1.ooo 0.359 -0.141

9 Arrhy

1.000 0.223

10 E

1.000

11 NE

626

DANIEL C. HATTON

E[ (11.

nonsustained (E = 122.8 NE =: 336.4) groups were in the expected direction but did not reach statistical significance. Catecholamine levels were higher than normal values reported by others [35, 361. Mean norepinephrine level prior to the programmed stimulation procedure was 363.0 pg/ml and epinephrine level averaged 257.6 pg/ml. Since the programmed stimulation procedure itself is extremely stressful and anxiety provoking these higher than normal findings were not unexpected. For a control group consisting of seven volunteers from the staff, average catecholamine levels were in agreement with those reported for the normal population. Mean norepinephrine value for these seven individuals was 281 pgiml and the average epinephrine level in these controls was 36 pg:‘ml. In order to examine interactions among the psychological and physiological factors, behavior pattern and desire for control groups were formed. The Type A behavior pattern was found in seven subjects. The remaining 10 were Type Bs. To form the desire for control groups, the median on the Desirability of Control scale was used to divide subjects into high desire for control and low desire for control. There were nine subjects in the low desire for control group and eight in the high desire for control group. Figure 2 shows that both epinephrine and norepinephrine levels were higher in Type B than Type A subjects but this did not reach statistical significance. Finally, interactions between behavior pattern, desire for control, and physiological responses were explored. Figure 3 demonstrates that although desire for control and behavior pattern show no independent relationship to epinephrine level, their interaction is significant (F = 4.73, df = 1, p < 0.05). The interaction was not significant for norepinephrine. DISCUSSION

The outcome of this study supports the premise that psychological factors are important in susceptibility to cardiac arrhythmias. Specifically, our data suggest that individuals high in the desire for control are more likely to experience sustained

125 z L 100 +c 1 0 0 75 b -t ? .z n

50

r

t

25 0i

-

Ventrjcular

Arrhythmia

Response

FIG. 1.--Mean desire for control score for those with nonsustained arrhythmias and sustained arrhythmias (ventricular tachycardia or ventricular fibrillation) induced by programmed electrophysiological studies. The sustained groups scored significantly higher on the desire for control scale (*[I < 0.05).

Psychophysiological

0 [z1

factors

621

Epinephrine Norepinephrine

TYPE A (4

in arrhythmias

TYPO B

Behavior

Pattern

FIG. 2.-Mean plasma catecholamine levels (epinephrine and norepinephrine) for those classified with the Type A behavior pattern and the Type B behavior pattern. Although higher levels were found in those with the Type B behavior pattern no significant differences were found with respect to behavior pattern.

ventricular arrhythmias following direct cardiac stimulation than are individuals lower in the desire for control. In addition, desire for control interacts with the coronary prone-behavior pattern in relation to epinephrine response in this particular cardiac catheterization environment. These findings suggest that arousal of the sympathetic nervous system, perhaps caused by an exaggerated need for environmental control, may make both behavior pattern and desire for control risk factors for sudden cardiac death. Reich [37] notes that victims of sudden cardiac death are a medically heterogeneous group. Thus it is important to develop profiles of patients who appear to be prone to the development of arrhythmias. Clearly, based on this study as well as the case history approaches of other investigators [l&12] the desire for control appears to be a potential risk factor in such susceptibility. Eliot and Buell [14] note that among the effects of excessive catecholamine release is an increased susceptibility to arrhythmia generation. Verrier and Lown [38] found that emotional stress can cause disordered cardiac rhythms. This study suggests

a

01

~

Low

?gh

r)esire

for Coritrcl

FIG. 3.-The interaction of behavior pattern and desire for control on plasma epinephrine levels. Group Ns: low control-Type A, 3; low control-Type B, 6; high control-Type A, 4; high control-Type 8, 4; Analysis of variance shows a significant interaction but no significant main effects.

628

DANIEL C. HATTON et al.

that one factor in creating the emotional stress is a desire for control over the environment. The Type A behavior pattern was also found to be related to psychological and physiological measures used in this study. The discovery that the desire for and not the perception of control is related to the Type A pattern supports Dembroski, MacDougall and Musante’s [39] suggestion that anly a desire for control, not a belief that one has control is related to behavior pattern. A puzzling finding was the fact that Type Bs manifested higher catecholamine levels than did the Type As. Others have reported that significantly higher catecholamine levels are found in those with the Type A behavior pattern [4&42]. However, most of these studies used the structured interview to assess behavior pattern and used younger adult subjects. Age may be an important variable to consider, since the relationship between behavior pattern and cardiovascular disease has been found to decline with age [20]. It may be that the JAS measure is tapping other components of behavior pattern associated with differences in catecholamine response in this relatively older subject group. As Matthews et al. [26] have pointed out, both methods measure drive, energy level, and competitiveness, but the correlation between them averages only 0.50 suggesting that they tap different components of behavior pattern as well. Not all studies of Type A/B differences in physiological response have found Type As more responsive. For example, Gilden and Cole [43] demonstrated that under different attention conditions Type Bs actually show greater cardiac responses than Type As. Thus it is probably inaccurate to view physiological hyperresponsivity as an inevitable concomitant of coronary prone behavior. Personality and environmental demands both appear to exert important influences on physiological responses. Investigations by Glass have shown that those with Type A behavior patterns respond differently to situations threatening environmental control, reacting more strongly with either attempts to reassert control or giving up, helplessness [41,44]. Glass’s work is consistent with the results from this study, suggesting that the coronary prone behavior pattern is related to a lack of flexibility in physiological responses, that results in excessive, all or none responses to environmental demands. A recent report of cardiovascular reactivity and behavior pattern under betaadrenergic stimulation and blockade [45] also did not find greater reactivity in Type A subjects leading the authors to suggest that the relationship between Type A and reactivity may be far more complex than it had originally appeared to be. Most other investigations of plasma catecholamines and behavior patterns have been conducted under laboratory conditions. The PES testing situation is very different, an environment which is alien and perhaps frightening to many patients. Thus it is not unreasonable to speculate that faced with this uncontrollable situation, Type A patients are more apt to give up and are thus less aroused autonomically in the catheterization environment. This may explain Ragland and Brand’s [46] recent report that Type As live longer after first myocardial infarction than Bs perhaps Type As respond to their first cardiac event by giving up, becoming less vigilant in their attempts to control their environment. In a recent report, Abbott Peters and Vogel [47] noted that while overall Type A ratings show stability over time, there was a consistent decrease in the Hard Driving and Competitive

Psychophysiological

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component of the JAS during the year following a major coronary event despite the lack of behavioral intervention. One other finding which was somewhat unexpected in this study was the lack of relationship between norepinephrine and the other variables measured. There is a substantial amount of evidence of the differential activation and release of norepinephrine and epinephrine. Epinephrine levels are much more sensitive to psychological stress than are norepinephrine levels. Turton, Deegan and Coulshed [48] observed a four-fold increase in plasma epinephrine in anticipation of cardiac catheterization but only a two-fold increase in norepinephrine. Dimsdale and Moss [49] demonstrated that public speaking causes a greater release of epinephrine than norepinephrine whereas exercise has the opposite effect. The outcomes of these two studies are commensurate with a number of psychophysiological studies that have demonstrated a dissociation between the release of norepinephrine and epinephrine [50]. The sensitivity of epinephrine to psychological stress suggests that the high levels of epinephrine observed in the present study may have been due to the anxiety provoked by the procedure. In a psychologically stressful situation, desire for control interacts with behavior pattern to produce extreme epinephrine responses. High control Type As may give up (or use denial), while high control Type Bs may panic. These findings suggest that the trend in physiological reactivity research toward exploring more broadly defined psychological features, such as desire for control, and moving away from Type A behavior [51] may indeed be more fruitful. This study supports the notion that the occurrence of lethal cardiac arrhythmias is at least in part related to psychological variables. The data indicate that pathological and potentially lethal arrhythmias are most easily generated in those individuals who are high in the desire for control and who manifest high levels of epinephrine in their blood. While the Type A behavior pattern was not found to be related to PES outcome, it was found to interact with a high desire for control in its relation to epinephrine responses. Further research is clearly needed to more precisely establish the relationship between control preferences and the development, treatment, and prevention of potentially lethal cardiac rhythms. Acknowledgements-This work was supported by the National Heart Lung and Blood 5T32 HL07332 and a grant from the American Heart Association, Oregon affiliate.

Institute

grant

REFERENCES 1. 2. 3. 4. 5. 6. 7.

KULLEK L, PERPERJ, CCK~PERM. Demographic characteristics and trends in ASHD mortality: Sudden death and myocardial infarction. Circularion 1975; 51/52 III: 27-33. HINKLE LE. Short-term risk factors for sudden death. In Sudden Coronary Death (Edited by GREENBERG HM, DWYER EM), vol 382. New York: New York Academy of Sciences, 1982. PITT B. Sudden cardiac death: role of left ventricular dysfunction. In Sudden Coronary Death (Edited by GREENBERG HM, DWYER EM), vol 382. New York: New York Academy of Sciences, 1982. LOWN B. Sudden cardiac death: Biobehavioral perspective. Circulation 1987; 76 (Supp I): I-186-1-196. LOWN B, VERRIER RL, CORBALAN R. Psychologic stress and threshold for repetitive ventricular response. Science 1973; 182: 834836. _ LOWN B, VERRIER RL, RA~INOWITZ SH. Neural and nsvchologic mechanisms and the oroblem of sudden cardiac death. Am J Cardiol 1977; 39: 89(r961: LOWN B, DESILVA RA, REICH B, MURAWSKI BJ. Psychophysiologic factors in sudden cardiac death. Am J Psvchiutry 1980; 137: 1325.

DANIEL C. HATTON et ul.

630

8. VEKR~ERRL. LOWN B. Behavioral 9. 10. Il. 12. 13. 14. 15. 16. 17.

18. 19. 20.

21. 22. 23. 24. 25. 26.

27. 28. 29.

30.

31. 32. 33. 34.

35. 36.

stress and cardiac arrhythmias. Ann Rev Physiol 1984; 46: 155Sl76. GREE~X WA, GOLDSTEIX S,Moss AJ. Psychosocial aspects of sudden death. Arch Int Med 1972; 129: 725-731. MYERS A, DEWAR HA. Circumstances attending 100 sudden deaths from coronary artery disease with corner’s necropsies. Bril H J 1975; 37: 1133-l 143. ENC~ELGL. Sudden and rapid death during psychological stress, folklore or folk wisdom? .4nnals Itl/ Med 1971; 74: 771 -782. LOWN B, DESILVA RA. Roles of psychologic stress and autonomic nervous system changes in provocation of ventricular premature complexes. Am J Cardiol 1978; 41: 979%988. REICH P, DESILVA RA, Lowe B, M~JROWSKI BJ. Acute psychological disturbances preceding life-threatening ventricular arrhythmias. JAMA 1981; 246: 233-237. BINIK YM. Psychosocial predictors of sudden death: A review and critique. Sot Sci Mud 1985: 20: 667480. ELIOT RS, BUELL JC. Role of emotions and stress in the genesis of sudden death. J Am Coil Curdiol 1985; 5: 95B-98B. THE REVIEW PANEL ON CORONARY-PRONE BEHAVIORANI) CORONARY HEART DISEASE.Coronary-prone behavior and coronary heart disease: A critical review. Circulation 1981; 63: 1199-1215. KRANT DS, L~JNDBERCU, FRANKENHAEUSERM. Stress and Type A behavior interactions between environmental and biological factors. In Hundhook ofpsvchology and health. Vol. J S/ress. (Edited by BAUM A, SINGER J). Hillsdale NJ: Lawrence Erlbaum Associates, 1987. HAYNES SG, MATTHEWS KA. Review and methodological critique of recent studies on Type A behavior and cardiovascular &ease. Ann Beh Med 1988; 10: 47-59. KRANTZ DS, CONTRADA RJ, HILL DR, FRIEDLER E. Environmental stress and biobehavioral antecedents of coronary heart disease. J Consulf C/in Psycho1 1988; 56: 333-341. WILLIAMS RB, BAREFOOTJC, HANEY TL, HARRELL FE. BLUMENTHALJA, PRYOK DB, PETERSON B. Type A behavior and angiographically documented coronary atherosclerosis in a sample of 2289 patients. Psychosom Med 1988; 50: 139%152. HECKER MHL, CHESNEY MA, BLACK GW, FKAUXCHI N. Coronary-prone behaviors in the Western Collaborative Study. Psvchosom Med 1988; 50: 153-164. JENNINGS JR, FOLLANSBEEWP. Type A and ectopy in patients with coronary artery disease and controls. J psychosom Res 1984: 28: 449-454. VAN EGEREN LF. ABELSONJL. SNIDEKMANLD. interpersonal and electrocardiographic responses of Type As and Type Bs in competitive socioeconomic games. J pswhosom Rex 1983; 27: 53%59. JENKINS CD, ZYZANSKI SJ, ROSFNMAN RH. Jenkins Acticitv Sun~ey. New York: The Psychological Corporation, 1979. JENKINS CD, ROSENMAN RH, FRIEDMAN M. Replicability of rating the coronary-prone behavior pattern. Brit J Pru> Sot Med 1968; 22: 16-22. MATTHEWS KA, KRANTZ DS, DEMBROSKITM, MACDOUGALL TM. Unique and common variance in Structured Interview and Jenkins Activity Survey assessments of the Type A behavior pattern. J Person Sot Ps.vch 1982; 42: 303.~ 313. BURGER JM, CARPER HM. Desirability of control. Morir Emot 1979; 3: 381&393. WAI.LSTON KA, WALLSTON BS. DEVELLIS R. Development of the health locus of control (MDHLC) scales. Heal Ed Mon 1978; 6: 161~170. GOLDSTEIN DS. FUERS~EIN G. Izzo JL. Korl~ 1J. KEISER HR. Validitv and reliabilitv of liauid chromatography with electrochemical detection for measuring plasma levels of norepinephrine and epinephrine in man. Lift, Sci 1981; 28: 467~~471. WILBER DJ, GARAN H, FIXKELSTEIN D, KELI.Y E, NEWELI. J, MCGOVERN B, RUSKIN JW. Out of hospital cardiac arrest: Use of electrophysiologic testing in the prediction of long term outcome. New Engl J Med 1988; 318: 19-24. KKON J, LI CK, MURPHY E, et aI. Sudden death prediction by programmed electrical stimulation following myocardial infarction. Wesr J Med 1986; 145: 639444. KKON J, LI CK. MURPHY E, ef ~1. Prognostic Value of Programmed Electrical Stimulation in patients with a recent episode of unstable angina. Am Hearf J 1986; 112 (1): l-8. LI CK, MCANULTY JH, KRON J. MIJRPHY E. Value of triple and quadruple extrastimulus technique in induction of clinical ventricular tachycardia and fibrillation. e/in Ris 1983; 31: 12A. _ KUDENCHUK PJ. KKON J. WALANCE CC. et ul. Renroducibilitv of arrhythmia induction with intracardiac electrophysiologic testing: Patients with clinical sustained ventricular tachyarrhythmias. J Am Coil Curdiol 1986; 7: 819%!QS. DIMSDALE JE. Generalizing from laboratory studies to field studies of human stress physiology. Psychworn Med 1984; 46 (5): 463469. TAG(;ART P, CARUTHERSM, SOMERVILLEW. Electrocardiogram, plasma catecholamines and lipids and their modification by oxprenolol when speaking before an audience. Luncer 1973; 2: 341-346.

Psychophysiological 37. 38. 39. 40. 41. 42. 43. 44. 45. 46. 47. 48. 49. 50.

51.

factors

in arrhythmias

631

REICH P. Psychological predisposition of life-threatening arrhythmias. Ann Rer Med 1985; 36: 397405. VERRIERRL, LOWN B. Experimental studies of psychophysiological factors in sudden cardiac death. Acta Med &and 1982; 660 (suppl): 57. DEMBROSKITM, MACDOUGALL JM, MUSANTE L. Desirability of control versus locus of control: Relationship to paralinguistics in the Type A interview. Health Psychol 1984; 3: 15-26. FRIEDMAN M, BYERS SO, DIAMANT J, ROSENMANRH. Plasma catecholamine response or coronaryprone (Type A) to a specific challenge. Metubolistn 1975; 4: 205-210. GLASS DC, CARVER CS. Helplessness and the coronary-prone behavior pattern. In Human Helplessness (Edited by GARBER J, SELIGMAN J). New York: Academic Press, 1980. W:L.LIAMS RB, LANE JD, KUHN CM, MELOSH W, WHITE AD, SCHANBERGSM. Type A behavior and elevated physiological and neuroendocrine responses to cognitive tasks. Science 1982; 218: 483485. GILDEN ER, COLE DA. Allocation of attention, Type A behavior and cardiac response in a dual task setting. Psychophysiology 1983; 20: (abstract): 443. GLASS DC Behavior patterns, stress and coronary disease. New Jersey: Erlbaum, 1977. KRANTZ DS, C~NTRADA RJ, LARICCIA PJ, et al. Effects of beta-adrenergic stimulation and blockade on cardiovascular reactivity, affect, and type A behavior. Psychosom Med 1987; 49: 146158. RAGLAND DR. BRAND RJ. Type A and mortality from coronary heart disease. New Engl J Med 1988; 318: 65-69. ABBOTT AV, PETERSRK, VOGEL ME. Temporal stability and overlap of behavioral and questionnaire assessments of type A behavior in coronary patients. Psychosom Med 1988; 50: 123-138. TURTON MB, DEEGAN T, COULSHED N. Plasma catecholamine levels and cardiac rhythm before and after cardiac catheterisation. Brit H J 1977; 39: 1307-1311. DIM~DALEJE, Moss J. Short-term catecholamine response to psychological stress. Psychosom Med 1980; 42: 493-497. DIMSDALEJE. Measuring human sympathoadrenomedullary responses to stressors. In Handbook of Psychology and Healthy. Vol. 5 Stress. (Edited by BAUM A, SINGER J). Hillsdale NJ: Lawrence Erlbaum & Associates, 1987. DIMSDALEJE. A perspective on type A behavior and coronary disease. IVew Engl J Med 1988; 318: llc-112.