INTERNKI'IONAL JOURNAL O1" BEIIAVIORAI, MEDICINE, 1( 1 ), 55-75 Copyright ~-) 1994~ I,awrence Erlbaum Associales~ Inc.

Psychophysiological Effects of Cardiac Rehabilitation in

Post-Myocardial Infarction Patients

C)rjan Sundin, Arne 0hman, Gunilla Burell, Thomas Palm, and Gunnar Strdm

Psychophysit~logical reactivity and cardiovascular functioning were assessed in 40 patients with coronary heart disease before and after taking part in either a Type A modification training program or a control condition. Treated patients showed an overall attenuated heart rate (HR) response and prolonged diastolic time to mental stress performance, during recovery and rest periods, as com- pared to control patients. No other measure, including impedance-cardiogra- phy-der ived measures, differentiated the two groups. The treatment group sho,.ved reduction from before to after treatment in 24-hr minimum HR level and decreased frequencies o f premature ventricular contractions, whereas the control group showed an opposite trend, Results from an exercise lest suggested the same direction f<~r resting I:[R. and double-pr~duc'~ levels. The two groups did not differ in maximal systolic and diastolic blood pressure or in maximal double-product levels, despite a differential development, in favor of the treal- meal group, in maximal work capacity,

Key words: Type A behavior, coronary heart disease (CIID), myocardial infarc- tion (MI), behavioral intervention, preventricular contractions, heart rate (HR)

()rjan Snndin, Dcparlme~t o[ Clinical Psychology and Department cff Clinical Physiology, IJppsala University. Uppsala. Sweden; Arne 6hrnan and Thomas Palm, Department of Clinical P,';ychology, Uppsala University, UppsaIa, Sweden; Gunilla Ilurell, Departments of Cardiovascu- lar Surgery, Uppsala University I[ospital, Uppsala, and Ume~ University Hospital~ Ume~, Sweden; Gunnar Strdm, Department of Clinical Physiology, Uppsala Universily, Uppsala, Sweden.

This research was supported by Sweden Tercentenary Foandalion Grants 83/108:1-4 and 88/229:1[ -2) to Arne ~hman.

Currespondenee concerning Ibis article Should be addressed to Orlon Sundin. Department of Clinical Neuroscience, Yd, Section of Psychiatry and Psychology, Karolinska Hospital, ST 171 76 Stockholm. Sweden.

56 SUNDIN, OIlMAN, BURELL, PAl.M, S'L'I~.O.M

Although seldom incorporated into clinical practice, behavioral/psychologi- cal interventions appear quite successful in reducing coronary heart disease (CHD) recurrence and mortality rates (Buretl ctal., this issue; Frasure-Smith & Prince, 1989; Friedman et al., 1986; Patel ct al., 1985). Interventions utilizing stress-reduction techniques have been shown to improve patients' risk status by affecting factors such as coronary artery occlusion (Ornish el at., 1990), frequency of angina (Ornish et al., 1983), blood pressure (BP) levels (Pate/el at., 1985), blood lipid levels (Ornish cl al., 1983; Palel ctal., 1985), and severe arrhythmias (Gruen, 1975).

Several studies (Burell el al., this issue; Frasure-Smith & Prince, 1989; Mendes de Leon, Powell, & B. H. Kaplan, 1991; Oldenburg, Perkins, & Andrews, 1985; Suinn, I975) have also reported improvements in psycho- logical well-being among patients participating in stress-reduction pro- grams. Studies on the effect of stress-management programs on hypertensive and healthy men have reported similar results (Roskies et al., 1986; Steptoe, Patti, Marmot, & Hunt, 1987). Because emotional problems and psycholog- ical distress provide significant predictors of mortality among post-myocar- dial infarction (MI) patients (i.e., Mumford, Schlesinger, & Glass, 1982; Wiklut]d, ] 984), such results add further weight to behavioral interventions as a tool in cardiac rehabilitation.

STRESS AND THE PROGRESSION AND RECURRENCE OF CHD

Data suggest that stressors influence development, progression, and recur- rence of CHD partly through the conventional risk factors (for reviews, see Johnston, 1989). However, stressors may also directly affecl disease-relatcd factors. J. R. Kaplan et al. (1983) reported development of atheroma in the coronary arteries of cynomolgus macaque monkeys as a resul! of an interac- tion between individual characteristics (e.g., level of dominance) and social stress. Subsequent studies with beta-blocking agents showed that this effect was of sympathetic origin (J. R. Kaplan, Manuck, Adams, Weingand, & Clarkson, 1987). Laboratory stressors such as electric shock--which stimu- late sympathetic activity--appear to reduce the threshold for serious arrhyth- mias in dogs with experimentally induced ischemia (see Verricr, 1987, for a review), thus suggesting an additional possible (electrophysiological) route connecting stress with CHD. Consequently, sympathico-adrenal hyperreac- tivity has been suggested as a common physiological pathway through which psychosocial factors may promote or precipitate CHD (Krantz, Contrada, Hill, & Friedler, 3988; Krantz & Manuck, 1984; Williams, 1985; Wright, Contrada, & Glass, 1985).

Recent studies on CI4D patients provide partial support for such a notion, because experimentally induced mental stress has been shown to restrict cc~ronary btood flow in patients with angina pectoris (Rozanski el al., 1988).

e v a ~ Y 57

Furthermore, cardiovascular reactivity (e.g., BP reactivity), coinciding with those events, has been suggested as a potential contributor to athcrosclerotic plaque rupture in patients with mental-stress-induced transient ischemia (Bairey, Krantz, & Rozanski, 1990). Tavazzi, Zotti, and Rondanelli (1986) reported that laboratory stresso~s could ~ower the threshold for lethal ar- rhythmias in patients with coronary artery disease. Manuek, Olsson, Hjemdahl, and Rehnqvist (1992) found that patients later experiencing a recurrent event showed increased BP reactivity to mental stress, compared to patients not suffering a recurrent event. Wielgosz et al. (1988) reported an inability to unwind after stress as a strong predictor of coronary events. Changes in sympathetic tonus have also been suggested as a potential factor in recurrent episodes and sudden cardiac death due to the association of these events to early morning hours and BP elevations (Cruiekshank & Smith, 1989). Perhaps reflecting this latter proposal, Perski and co-workers re- ported that higher 24-hr minimum heart rate (HR) (Perski et al., in press) and 24-hr average HR. (Perski, Hamsten, Lindvall, & Theorell, 1988) correlated with progression of atherosclerosis in coronary patients.

INDIVIDUAL CHARACTERISTICS, CARDIOVASCULAR REACTIVITY, AND CHD

Studies examining the interaction among individual cttaracteristics, stress, physiological reactivity, and CHD (as proposed by, e.g., J. R. Kaplan et al., 1987; J. R. Kaplan et al., 1983; Thoresen & Ohman, 1987) have also gener- ated suggestive results. Typically, the individual characteristic studied in such cases has been Type A behavior (e.g., Rosenman, 1991)~a risk factor for coronary events at least among middle-aged men not at elevated risk due to other risk factors (Matthews & Haynes, 1986; Miller, Turner, Tindaic, Posavac, & Dugoni, 1991). Corse, Manuek, Cantwell, Giordanni, and Mat- thews (1982) reported larger diastolic BP (DBP) response among post-Ml patients, as compared to healthy controls, during a complicated cognitive task. However, individuals with Type A behavior showed pressor responses larger than those showed by individuals not exhibiting this behavior, irre- spective of coronary status. Krantz et at. (1981) reported that coronary patients with Type A behavior displayed larger systolic BP (SBP) and HR responses to stress than did coronary patients without Type A behavior. Using impedance cardiography, Sundin, 0hman, Palm, and Strfm (1993) found that post-M! patients exhibited overall elevated pressor responsivity to both mental and physical challenges. The higher reactivity during mental stress was attributed to changes in cardiac output, whereas the higher pressor response during cold pressor appeared to be afterload dependent. Sundin et al. (1993) also showed that Type As, irrespective of coronary status, dis- played higher pressor response to both mental and physical tasks. These results suggest that a beta-adrenergie-<lriven hyperreactivity and a disease-

associated impaired left ventricular function in CHD patients may combine with heightened vascular reactivity to enhance risk of further coronary events in patients exhibiting Type A behavior.

PURPOSE OF THE PRESENT STUDY

If cardiovascular responsiveness provides a crucial link mediating the rela- tion between Type A behavior and CHD outcomes, it could be predicted that a treatment program successfully resulting in reduced Type A behavior would also result in dampened cardiovascular reactivity. Accordingly, the purpose of the present study was to examine the effects of a behavior modification program, based on the Recurrent Coronary Prevention Project (RCPP; Powell & Thoresen, 1987), on cardiovascular reactivity and cardiac functioning as measured in the stress laboratory, during 24-br Holler record- ings, and during an exercise test.

METHOD

Subjects

Forty patients selected from a primary sample of 161 patients from the Section of Cardiology, Department of Internal Medicine, University Hospi- tal of Uppsala, were enrolled in the study. All patients had a diagnosed MI based on clinical signs, blood enzyme changes, and electrocardiographic (ECG) changes specific for MI. The patients were nonsmokers, and the majority was rated as belonging to New York Heart Association (NYHA) Class 1 or 2, According to a predetermined criterion score on the Videotaped Structured Interview (VSI; to be discussed), they had to exhibit marked Type A behavior. After applying these criteria, 52 patients were enrolled to partic- ipate in the study. Three patients refused further participation after initial assessments.

The remaining 49 were randomly assigned either to a Type A treatment condition (25 patients) or to a eardiologic counseling control condition (24 patients). Two patients randomized to the treatment group died early in treatment (1 after the first treatment session, 1 after three sessions). Three patients in the treatment group changed from beta-blockers to no medication, and 3 patients in the control group changed from no medication to beta- blockers during the treatment year. One patient in the controJ group refused to participate in assessments after the treatment year. Thus, 9 patients were excluded, and, in the statistical analysis of the data, 40 patients remained, 20 in each group.

Routine medication was similar in the two groups. No attempt was made to interlere with routine medical chcckups. Therefore, the two groups did not differ in amount of professional medical care and clinical monitoring. Table I presents descriptive variables at study entry.

CV REACI:WI tY 5 g

TABLE 1 Baseline Sociodemographlc and Medical Characteristics by Group

Characteristic

Group

Experimental Control

M SD M SD

Age (years) 5 ; 7 7 : 6 ~ 5;9 BSA before treatment t ,~2 ~ ! t~3 {~ BSA after treatment i ' 3 0;i2 ~'3~ Smoking (percentage past

smokers) Self-reported family history

(percentage with hypertension or ischemic heart disease) 5

Current medication (percentage on beta-blocker) ~ 6

Number of previous Mls ........ | , I7 Minor anginal symptom

(percentage after MI) 3 6i~ NYHA class In)

1 7 2 i2 3a 1

Married (percentage) ~ ~0

Treatment

The treatment patients received thi r ty- t i re 90-rain sessions spaced over a 1-year period, During the first 6 months, they met once a week; thereafter, they met once every 2 weeks, Six sessions with a cardiologist were included. The cardiologic counsel ing control patients received six 90-rain sessions with the same cardiologist during the 1-year period. The purpose of the counsel ing group was to control for the effect of information about medica- tion and traditional risk factors and risk indicators, Thus, this group was given more health care attention than patients in standard care. However , Type A was not an issue, Because this group met less frequently than patients in the treatment groups, one can assume that social tics between group members did not develop to the same degree. Each group consisted o f 6 to 8 participants.

The treatment format is described in Burell el al. (this issue) and followed closely the model used in RCPP. Treatment goals were (a) to decrease t ime-urgent and aggressive behaviors, muscle tension, and hostile attitudes and (b) to increase social skills and the ability to unwind, Educat ion about Type A behavior (e.g., through systematic self-observat ion and study of audiotaped and videotaped material), behavioral change (e.g., rote-playing,

60 SUNDIN, OIIMAN, BURELL, PALM, STROM

behavior drills, modeling), relaxation practices, and cognitive restructuring (e.g., review of thought patterns, evaluation of basic attitudes, and applica- tion of cognitive techniques) were tools of treatment. Each session covered brief relaxation, review of driIIs, discussion of and conclusions from daily experiences, introduction of new ideas and material, and a new homework assignment.

The cardiologie counseling group sessions were focused on risk factors other than Type A behavior. Education about the disease; discussion of individual medication; life habits; complications or problems related to symptoms; depression; anxiety; and ways to alleviate unhealthy habits of living constituted the content. Both patient groups were therefore encour- aged to alter and improve their dietary and exercise routines. However, no participant in either group was simultaneously a member in any exercise or dietary program.

Apparatus and Recording Methods

VSI. The Swedish version of the VSI was evaluated by 42 indicators scored on 7-point rating scales. Three dominating factors, Self-Reported Type A Behavior, Speech Characteristics, and Hostility, were formed through item analysis. The interviews were conducted and scored by a trained interviewer and rater blind to group distributions. Intcrrater agree- ment, measured as intractass correlation, was .77 between the Swedish rater and an experienced interviewer from the Meyer Friedman Institute. Alpha coefficients for total VSI score as well as for subseales derived from .psycho- metric analyses based on 282 interviews were close lo .80 (see Ohman, Burell, Ramund, & Fleischmann, 1992, for a more detailed description of the Swedish version of the VSI).

Psychophysiological laboratory. SBP and DBP were measured using a Bosch semi-automated BP instrument and were read digitally to the nearest

2 mm Hg- -onee during each experimental period, except for the rest period during which two consecutive measurements were made and their average va lue was used. Mean arterial pressure (MAP) was conventionally calcu- lated as DBP plus one third of pulse pressure.

Stroke volume (SV), HR, pre-ejection period (PEP), and left vcntricular ejection time (LVET) were measured using a Minnesota Impedance Cardio- graph (Model 304A) and four aluminized Mylar tape electrodes, applied as described by Kubicek, Patterson and Witsoe (1970). In order to ensure that the tape electrodes were equally spaced during pretreatment and posttreat- men/ testirtg, the distances b e t w e e n the two inner tapes wcre measured at

three different locations on the torso and the back, respeelively. A strain gauge respiration belt was used to monitor respiration so thai impedance waveforms could be measured at the end of the respiration phase. SV was

calculated according to the standard equation (Kubieek et al., 1970), and only those dZ/dt waveforms that occurred during the expiration phase were used. HR was also scored during the expiration phase, by measuring the time intervals between QRS complexes. To measure the end of LVET, a Siemens Elema Emt 25C phonocardiographic microphone (permitting recordings of heart sounds) was placed on the sternum, approximately 5 cm above the xiphoid-sternal joint. PEP was measured from the foot of the ECG R-wave to the onset of LVET, as defined by the dZ/dt B-point. Cardiac output (CO) was determined by multiplying the mean HR value for each period by the value of mean SV. Totalsperipheral resistance (TPR) was calculated and expressed in dyne.see.cm" using the formula TPR = MAP (mm Hg) x 79.92 / CO (1/min) (Guyton, 1981). Rate pressure product (i.e., double product IDP]) was expressed as (HR x SBP) x 0.001 and was used as a measure of demand for coronary flow. Diastolic filling time (DT) was calculated by subtracting the total eleetromechanical systole from the ECG R-R interval and was used as a measure of opportunity for coronary flow (Larsen, Sehneiderman, & DeCarto-Pasin, 1986).

All physiological data were recorded using a Mingograph 81 jet ink writer (Siemens Elema, Solna, Sweden) run at 50 mm/see. All impedance data were edited for artifacts before data reduction. Individuals scoring the psycho- physiological data were blind to group allocations.

Exercise test. SBP and DBP were obtained by standard cuff sphygmo- manometry. HR was obtained from standard ECG measurements. Individuals collecting and scoring exercise data were blind to group distributions.

Holter recording. Two-channel Holter ECG measurements were taken during 24 hr. Each minute, average HR, minimum HR, and maximum HR were computed. Premature atrial contractions (PACs) and premature ventric- ular contractions (PVCs) were measured during 24-hr recordings and were analyzed according to conventional standards. Individuals collecting and analyzing data from the Holter recordings were blind to group distributions.

Procedure

Psychophysiologicallaboratory. All experiments were performed from 9 to 11 a.m. with the patient in a semi-reclining position. After the various electrodes and transducers had been attached, initial instructions were given, and the patient was told to relax during a 15-min rest period. Each task were preceded by a short formal instruction followed by a 1-min rest and/or anticipation period. A 5-min recovery period followed cacti task. Counterbalancing was not done mainly due to the nature of the two arithme- tic tasks (to be discussed).

62 SUNDIN, OHMAN, I]UREI.I., PALM, STROM

During the first two tasks, Visually Presented Arithmetic 1 (VPI) and 2 (VP2), each patient was told to either add or subtract the result from two different calculations, presented on the same slide, depending on whether the results from the first calculation were higher (subtract) or lower (add) than the second calculation. During the first condition (VP1) the patient advanced the slide tray by pressing a button and hence could control the pacing of the task (see Bohlin et al., 1986, for a detailed description of this task). The second condition (VP2) was similar to VP1 except that the pace was exter- nally controlled by the experimenter. The performance rate matched the mean of the first 2 rain of the sell-paced condition. This allowed comparison between controllable and uncontrollable situations with work pace kept constant (Bohlin et al., 1986). During the third and fourth tasks, Auditory Presented Arithmetic (AP1 and AP2), each patient was instructed to subtract serial 7s from a four-digit number during a 2-rain period. The difference between the third task (AP1) and the fourth task (AP2) was that the patient, during AP2, was mildly harassed. During isometric exercise, each patient performed the handgrip for 2 min at one third of his previously determined maximum voluntary contraction. During the l.-min cold pressor test, each patient lowered his left hand (up to the wrist) into a bucket containing water iced to approximately 3 ~

Exercise test. An exercise test was generally performed at least 2 days apart from the psychophysiological laboratory test. After an initial 10-min rest period, each patient was asked to stand up. Subsequently, he followed a ramp-type bicycle workload procedure, with successively increasing steps of 10 to 20 W/min, until his submaximum capacity was reached. Thus, patients also rated their perceived effort and exertion according to the Borg CR-10 Scale (Borg, 1982). The test was interrupted when the patient reached the highest level on either effort or exertion. A 10-min recovery period com- pleted the exercise test.

Holler recording. After a 10-min relaxation period, a Holler HR tape recorder was attached, and patients went about their normal activities during lhe following 24 hr. However, patients were asked to monitor and rate taxing physical and psychological activities once an hour during daytime and once between 12 p.m. and 5 a.m. The Holter recording was generally completed on the morning before the psychophysiological laboratory stress test.

Data Reduction and Analyses

Psychophysiological laboratory data. The mean of the last 2 min of the 15-min rest period preceding the test formed the baseline value. In general, data were collected twice during each task, after 30 sec and afler 90 sec, respectively. However, because the cold pressor test lasted only 1 rain,

there was only one data period for this task. Mean values were computed for each task. The mean value of Minutes 4 and 5 following the test formed the recovery value. Because previous studies from our laboratory (Sundin & 0hman, 1992; Sundin et al., 1993) have shown a high comparabili ty between the nonmanipulated version of the two different mental arithmetic tasks (VP1 and API ) and the manipulated version (VP2 and AP2), peak values from each task were collapsed to form one VP task and one AP task. Thus, in the analyses of the psyehophysiological data, there are baseline values, four stress test values, and a recovery value.

Exercise test data. Recordings of HR, SBP, and DBP were done con- currently during the workload test as well as during rest, postural change, maximal work, and recovery. However, the [ast 2 rain of the rest period were collapsed to form a mean rest value. During postural change and maximal work, there was only one data period. The last minute of the subsequent rest period was used as recovery value.

Holter recording data. HR, PAC, and PVC data were sampled and analyzed for artifacts using a Marquette Holier recording apparatus. Average 24-hr HR was computed. Minimum HR and maximum HR were averaged over 4 beats (Perski el al., in press). Total numbers of PACs and PVCs were computed.

Statistical treatment of data from the psychophysiological laboratory ex- periments and the exercise test was accomplished using multivariate analysis of variance (MANOVA) and repeated analysis of covariance (ANCOVA) on mean levels from each occasion and task. Pretreatment values on each variable served as covariates. ANCOVA was used in order to reduce bias caused by any pretreatment differences. Data from Holier recordings were analyzed using analysis of variance (ANOVA) and ANCOVA on mean levels from each occasion. Missing data on some measures resulted in lower num- bers of patients in some analyses.

RESULTS

According to ANOVAs, the two groups did not differ in age, body-surface area (BSA), smoking, medication, number of previous Mls, anginal symp- toms, NYHA classification, or marital status. Table 1 presents descriptive variables at study entry.

Treatment Effect on Type A Behavior and Recurrences

As documented in Burell et at. (lhis issue), the intervention program had significant effects on various aspects of Type A behavior. Table 2 shows treatment effects on mean Type A scores from the VSI and on mean values

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68 SUNDIN, OItMAN, I]UREI.L, PALM, STROM

For HR rest values, there was a significant effect of group, F(1, 35) = 5.25, p < .02, with the experimental group showing posttreatment rest values lower than those of the control group. DP showed an equivalent significant effect of group for rest values before exercise test, F ( I , 38) = 8.65, p < .005. For DBP, there was a marginally significant effect of group for recovery values, F(1, 36) = 3.61, p = .06. The experimental group tended to recover faster than the control group. There was a similar tendency for SBP, F(1, 36) = 2.61, p < .1I. No measure showed group effects during maximal work despite the significantly higher maximum work capacity displayed by the experimental group as compared to the control group, F(1, 34) = 5.7, p = .02 (see Figure 2).

Holter Recording Data

ANOVA revealed no pretreatment group differences on any measure. Distri- butions for measures of ectopic rhythms, PACs, and PVCs were negatively skewed, with a few individuals showing highly deviant values. To rectify the distributions, the values were log-transformed before analyses. As for the exercise test, ANCOVA was performed for each measure with pretreatment level serving as covariate.

Ratings of taxing physical and psychological events were generally very low-- typical ly with a mean below 1.5 on a 4-point rating scale ranging from no strain to maximal strain. No group differences appeared. The ANCOVA on PVCs showed a significant effect of group, F( I , 30) = 7 .17,p < .02, with the experimental group showing fewer posttrealment PVCs than the control group (see left graph of Figure 3). Analysis of HR frequency per hour showed that the experimental group displayed lower minimum HR, F(I , 33) = 3.87, p < .05, and a tendency to lower 24-hr average values than those displayed by the experimental group, F(1, 33) = 3.3, p < .08.

DISCUSSION

The results of this investigation show that a psychological treatment pro- gram resulting in reduced Type A behavior has some beneficial effects on cardiovascular functioning and responsiveness in CHD patients. Reactivity data from the psychophysiological laboratory, however, were somewhat disappointing, as we could not demonstrate substantial group differences as a function of treatment on cardiovascular reactivity. In 1his respect, these results add to recent doubts concerning the predictive power of cardiovascu- lar reactivity during the rehabilitation process (Julius, 1989; Rosenman, 1991; Roskies et al., 1986). However, as displayed in Figure 1, the two groups appeared to show a differential development across conditions in HR and DT. Whereas the treatment patients showed an attenuated HR response and prolonged DT, the control patients showed the opposite development. Although this differences appeared 1o be most clear-cut during rest, the

CV REACTIVITY 69

statistical testing demonstrated an overall effect for HR and a more specific DT effect pertaining to mental task performance periods and rest and recov- ery periods.

The result from the exercise test showed that, in comparison to control patients, treatment patients had Lcnerally lower resting HR levels and lower resting DP levels (indicating lower cardiac oxygen consumption). In addi- tion, there were trends toward lower SBP and DBP recovery levels. How- ever, the groups did not differ in HR and BP during maximal workload. Nevcrthclcss, treated patients showed an increase in maximal tolerated workload from prctreatment to posttreatment, increased work capacity in the absence of group differences in concomitant pressor or HR elevations sug- gests more efficient cardiovascular functioning in the treatment group.

Holter recording revealed a significant difference between treatment and control patients in total 24-hr PVCs after treatment. Interestingly, the treat- meat group showed a reduction in PVCs from pretreatment Io posttreatment, whereas the control group showed an increase. Reduced minimum HR and marginal group difference in mean 24-hr HR level in the same direction further strengthen the observations from the psychophysiological laboratory and the exercise test.

The relative similarity of our results to results from studies examining effects of exercise in cardiac patients (Rovario, Holmes, & Holmsten, 1984) might suggest Ihat difference in the magnitude of exercise could explain our data, particularly when it is realized that exercise may result in decreased Type A behavior (Blumenthal c ta l . , 1982). However, there is no indication in our study that the amount of exercise differed in favor of the experimental group. Furthermore, no patients in our groups even came close to the quite strenuous levels of exercise used in the exercise programs. As evident from Table 1, the BSA values of the two groups were remarkably similar and stable from before to after treatment, which implies that the two groups maintained their weights across occasions (i.e., no weight reduction as a result of exercise occurred). However, the "cross-over effects" of the two treatment modes are thought-provoking with regard to the reduced Type A behavior after exercise training (Blumenthal et al., 1982) and the increased work capacity after Type A behavior modifieation. Thus, one may speculate about potential eommonalit ies between intervention programs focusing on exercise and Type A modification.

Other investigators have suggested that physiological effects of Type A behavior may be secondary to lack of social support (Orth-Gom6r & Unden, 1990). The same grou F (Unden, Orth-Gom~r, & Elofsson, 1991) reported a correlation between low social support and elevated 24-hr mean HR levels. Thus, if the Type A modification program resulted in improved social sup- port in the experimental group, the lower HR observed in the treated patients could be accounted for. However, as reported elsewhere (Burell ct al., this issue), using the same measure of social support, we found no difference between experimental and control groups. Similarly, results from RCPP

70 SUNDIN, OHMAN, BUREI.|~ PALM, STRI~M

(Powell & Thoresen, 1987) suggested that Type A behavior modification treatment was only marginally associated with improvement in social sup- port (albeit defined by a different scale). Thus, social support is less likely as an explanatory candidate for the efficacy of Type A modification training with regard to lowered HR and PVCs.

Because the treatment effects on physiological measures that we observed (i.e., reduced resting HR and number of PVCs) are similar to elf eels obtained by beta-blocking medication, it is important to stress that the proportion of patients on beta-blockers was similar in the two groups and that patients who had their medication regime changed during the treatment year were ex- cluded from the analyses. Thus, the observed results appear to be effects of differential treatment.

The present results suggest that a treatment program focusing on Type A behavior has beneficial effects on cardiovascular functioning, number of PVCs, and HR. However, several aspects of the present design make definile conclusions difficult. First, belonging to a group and getting feedback and advice from its members (i.e., social support) may have played an important role, not only for the inducement of therapeutic change, but also for adher- ence to medical regime. Because this last factor was not direclly measured, we cannot firmly state that adherence to medication was the same in both groups. However, the two groups did not display differences in either tonic or phasic BP levels as would have been expected from differential intake of beta-blockers.

Second, given the large number of measures in this study in comparison with lhe relatively small sample size, there is an increased likelihood of obtaining chance findings. However, the similarity in the directions ol the findings (e.g., with regard to HR levels) from exercise testing, Holter record- ing, and laboratory stress testing provides some assurance that the results reflect real changes (e.g., in resting HR).

Third, the results are restricted to middle-aged male palienls who had comparably high Type A behavior scores and moderate-size Mls and who were judged as belonging to NYHA Classes 1 and 2.

Overall, the results imply that Type A modification did not alter cardio- vascular reactivity per se, but rather only some indicators of cardiovascular function, primarily during resting conditions. Why the treatment patients did not obtain decreased reactivity per se is only open to speculation. It is possible that changing a manifest stress-induced physiological response pattern requires a more applied relaxation treatment approach than the one we used. To obtain effects of treatment on stress reactivity, it is possible that the patients should have been actively encouraged to practice whatever coping skills they had acquired during treatment in the stress test. The difference in HR and DT provides at least some evidence of reductions in reactivity. On the whole, however, the results imply that, once under stress, treated patients showed cardiovascular reactivity as large as that of the control patients.

{,v 7!

An alternative route is to suggest that the treatment program may have induced the patients to reduce the number of stress- inducing events they encountered by anticipating and avoiding them. If so, the resulting lower physiological basal levels might be the gain of a generally more relaxed life style. In a retrospective study comparing several risk factors, Wielgosz el al. (1988) reported that inadequate relaxation and an inability to unwind had the strongest independent association with an acute MI. One may further specu- late whether the common component between exercise and Type A modifica- tion previously discussed could be related to opportunilies and skills in relaxation. Interestingly, Braekett and Powell (1988) reported an association between sudden death and levels of Type A behavior. Their results suggested that the risk of sudden death in posl-Ml patients could be strongly reduced by reductions in Type A behavior. Brackett and Powell also suggested that the reported association would best be explained as a sympathetically medi- ated effect on the myocardium.

The physiological interpretation of our findings remains somewhat spec- ulative. Prolonged DT in treatment patients, in the absence of group differ- ence in DP, impIies an equal demand but unequal opportunities for coronary flow (Larsen et al., 1986). Together with lower HR levels, lower minimum HR, and reduced number of PVCs, these cardiac data suggest that treatment patients may have developed a reduced risk of coronary complications be- cause brief deficiencies in coronary blood flow may result in arrhythmias and pump failure. This interpretation, then, is consistent with findings dem- onstrating sympathetic influence on cardiac arrhythmias (Tavazzi et al., 1986; Verrier, 1987).

Differential development in the numbers of PVCs in the two groups may be of clinical importance due to the association between PVCs and sudden death (Lown, 1979; Rich, Saini, Kleiger, de Velde, & Fridlund, 1988). Lowered HR levels after treatment in the treatment patients may also be clinically important. An association has been shown between low HR and prevention or delay in development of arteriosclerotic plaques in coronary arteries of primates (Beere, Glagov, & Zarins, 1984) and humans (Perski et al., 1988). Reduced minimum HR displayed by the treatment group also appears to be of significance, because Perski et al. (in press) reported that higher minimum HR correlated with progression of athcrosclerosis in coro- nary patients. From this perspective, the results from the exercise test also invite speculations about a decreased rate of progression of the disease as a result of reduced Type A behavior. This is consistent with several previous studies reporting therapeutically induced reductions in stress-related behav- ior in coronary patients. Thus, Friedman et al. (1986) reported reductions of angina for the RCPP behavioral treatment group. Furthermore, Ornish et al. (1990) reported actual reversal of coronary atherosclerosis in patients re- ceiving a combination of stress-management training and traditional risk- factor reduction. Nevertheless, the actual physiological mechanism through which stress or Type A reduction influences coronary-relevant endpoinls

72 StJNDIN, OHMAN, BUREI.L, PALM, STR()M

remains unclear. Lower HR values imply lower sympathetic tone, but the only measure, besides HR, that distinguished the two groups was DT. These measures, however, in combination with the reduced PVC t'requeneies and lowered minimum HR, could suggest parasympathetic involvement mani- fested in enhanced vagal activity in the treatment patients. AIIhough this remains a tentative speculation, vagai influence has been proposed as exert- ing a pronounced indirect influence on venlricular contractility by antago- nizing the beta-adrencrgic inotropic response (see Levy, Martin, & Stuesse, 1981). However, because we did not measure vagal activity directly, this proposal remains a hypothesis to be seriously considered in future studies.

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