Temporal stability of the hemodynamics of cardiovascular reactivity

Temporal stability of the hemodynamics of cardiovascular reactivity

International Elsevier PSYCHO Journal of Psychophysiology, 95 10 (1990) 95-98 00306 Short Communications Temporal stability of the hemodynamic...

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International Elsevier

PSYCHO

Journal

of Psychophysiology,

95

10 (1990) 95-98

00306

Short Communications

Temporal stability of the hemodynamics of cardiovascular reactivity Andrew

Sherwood,

Department

of Psychiatry

J. Rick Turner,

Kathleen

(Accepted

Key words: Cardiovascular

C. Light and James A. Blumenthal

Uniuersity of North Carolina, Chapel Hill, NC (U.S.A.) and Department Duke Uniuersrty Medical Center, Durham, NC (U.S.A.)

reactivity;

Temporal

stability;

8 March

Hemodynamic

of Psychiatry,

1990)

response;

Psychosocial

stress; Impedance

cardiography

Cardiovascular responses to a competitive reaction-time task were monitored in 13 male subjects tested twice, 3 months apart. The temporal stability of blood pressure responses was in line with previous reports. However, in this study impedance cardiography permitted the investigation of the hemodynamic adjustments underlying the observed blood pressure responses. Analyses revealed that cardiac output and total peripheral resistance responses displayed temporal stability, indicating that subjects’ blood pressure responses on the two occasions were the result of similar hemodynamic responses. These data thus extend the literature by demonstrating that the hemodynamic response pattern itself represents a stable individual difference variable.

Although studies of individual differences in psychophysiological responses to stress have long been of interest to investigators of psychosomatic disorders, they have recently received renewed attention (e.g. see Krantz and Manuck, 1984; Manuck et al., 1986; Turner, 1989). If stress responses are to be implicated in the disease process, certain fundamental characteristics require careful consideration. One such characteristic is the temporal stability of these responses, The pathological potential of exaggerated stress-induced cardiovascular responses depends in part on those responses reflecting a stable and reproducible tendency of certain individuals. In other words, the potential long-term predictive significance of high and low cardiovascular stress responses is

Correspondence: A. Sherwood, CB #7175, Building A, University of North Carolina, 27599 U.S.A. 0167-8760/90/$03.50

Medical Chapel

Research Hill, NC

0 1990 Elsevier Science Publishers

substantially enhanced if they are shown to display consistency across both time and different stressors. The present report focuses on the first of these two requirements. Reports by several investigators have documented temporal stability of blood pressure and heart rate reactions to behavioral challenges (e.g., Carroll et al., 1984; Light, 1981; Turner et al., 1986; Allen et al., 1987). Manuck and colleagues (Manuck and Schaefer, 1978; Manuck and Garland, 1980) employed a concept formation task to investigate stability of responses over both a oneweek and a thirteen-month time period. Impressive stability was observed for heart rate (HR) and systolic blood pressure @BP), but not for diastolic blood pressure (DBP) (Y ‘sdO= 0.69, 0.68 and 0.46 respectively for the one-week interval; r ‘s,, = 0.81, 0.63, 0.24 respectively for the thirteen-month interval). Similarly, Allen et al. (1987) reported SBP and HR response stability, but not DBP response stability, over a 30-month test-retest interval for a

B.V. (Biomedical

Division)

96

shock-avoidance reaction-time task. Turner et al. (1986) found marked temporal consistency of heart rate reactivity to a video game task over a mean interval of 20.4 months (r3K = 0.74). Although there is ample evidence that cardiovascular reactivity, in terms of blood pressure or heart rate response, is a relatively stable characteristic over time, there is a lack of data regarding the underlying hemodynamics of blood pressure responses during stress. Since blood pressure is the product of cardiac output and total peripheral resistance, blood pressure responses during stress can be the result of changes in cardiac output, changes in total peripheral resistance, or a combination of changes in both. Recent evidence suggests that the underlying hemodynamics of blood pressure responses during stress may be especially relevant to the etiology of hypertension (Anderson et al. 1988; Light and Sherwood, 1989). It is therefore important to determine whether similar blood pressure responses observed on two occasions of testing are the result of similar hemodynamic adjustments. The preceding heart rate data provide some suggestion of hemodynamic stability, since heart rate is a key determinant of cardiac output. The present report provides direct evidence with regard to hemodynamic stability over time, although, owing to the small sample size, it should be regarded as preliminary. The report is based upon data collected in a study reported by Sherwood et al. (1989) which investigated the effects of aerobic exercise training on cardiovascular reactivity among a group of healthy adults. In that study, 13 control subjects (males, aged 33-56 years; mean = 41.8; S.D. = 5.8) underwent a strength training program designed to provide subjects with experimenter attention and similar weekly time commitments as the aerobic intervention, but to produce no change in cardiovascular function. Stress reactivity in these subjects was tested before and after the 3-month training interval. The task employed was a 5-min competitive reaction-time task, preceded by a 15min rest period. During the task, subjects competed for a ‘winner-take-all’ $20 bonus. The task involved presentation of 5-letter words at intervals ranging

from 8 to 38 (mean = 18) s. Each subject was required to depress a button as quickly as possible if a target letter, individually designated during pre-task instruction, appeared in the word. With time penalties imposed for incorrect responses, the winner was the competitor with the lowest total reaction-time score at the end of the task. Arterial blood pressure was measured non-invasively using the auscultatory method, and impedance cardiography (see Sherwood et al., 1989) was utilized to permit non-invasive monitoring of cardiac performance. Processing of the impedance cardiogram was accomplished using a computer-based system described in detail by Sherwood et al., 1986). This system was used to derive cardiac output (CO). HR, stroke volume (SV) and pre-ejection period (PEP). Total peripheral resistance (TPR) of the systemic vasculature was derived on the basis of concurrently recorded blood pressure and cardiac output measurements. Reactivity scores for each measure were calculated on each occasion of testing by subtracting values during the last 5 min of the pre-task rest period from those seen during the first 2 min of the reaction-time task. Pearson correlation coefficients were then calculated between the reactivity scores obtained for each variable. The results of these analyses are presented in Table I. Inspection of Table I reveals that the test-retest correlations for HR. SBP and DBP are very much consistent with previous studies (e.g. Manuck and Garland, 1980; Allen et al., 1987). Furthermore, correlation coefficients for CO, SV,

TABLE

I

Test-retest Peanon correlations In = 13) of cardiovascular trwty to the competitive reactron-trme task Cardiovascular Measure

Correlation Coefficient

SBP

0.671 *

DBP

0.305

HR

0.909

CO

0.814

* *

sv

0.868

* *

PEP

0.820

* *

TPR

0.679

*

* PcO.02;

**

P
* *

reac-

97

PEP and TPR also indicate significant and substantial consistency of response over the 3-month test-retest interval. Allen et al. (1987) provided speculative interpretation for the observed lack of DBP response stability to their shock-avoidance reaction-time task. They suggested that DBP responses may be less stable because of their dependence upon vascular tone. In particular, they argued that during exposure to a stressor, circulating catecholamines may exert both vasoconstrictive and vasodilatory effects, with overall changes in vascular tone representing a potentially unstable individual difference variable. The present results of a significant positive test-retest correlation for TPR response, but non-significant correlation for DBP, suggest that individual differences in vascular responses are relatively stable, and do not account for the lack of DBP response stability. It is striking that of the 7 hemodynamic response parameters examined in the present study, only DBP response failed to exhibit stability. As was the case for Allen et al. (1987) our interpretation of this perplexing phenomenon can only be speculative. We suggest that an interplay of 3 aspects of the DBP response may collectively account for the absence of its temporal stability, First, DBP response is determined by the complex interaction of changes in vascular and myocardial activity, and therefore will demonstrate a level of stability limited by that for both of these factors combined. Second, the magnitude of changes in DBP during typical active coping tasks tend to be less pronounced than those for either SBP or HR. Therefore, restricted range effects may partially contribute to the reports of non-significant DBP test-retest correlations. In this regard, it is of interest that over a similar 30-month interval, Allen et al. (1987) observed significant test-retest consistency associated with the large magnitude DBP responses to a cold pressor task (Kendall’s 7= 0.269, P -C0.05, n = 25) but non-significant results associated with the marginal DBP responses to the reaction-time task (Kendall’s r = 0.083, P = ns., n = 25). Finally, DBP is generally acknowledged to be a more difficult parameter to determine accurately than either SBP or HR and it is likely that measurement error may play a

significant role in the apparent lack of temporal stability for DBP. Studies that have examined inter-task stability of hemodynamic response patterns have found that individuals do tend to exhibit such stability (Dembroski and MacDougall, 1983; Sherwood et al., 1989). The results of the present study provide preliminary evidence of the temporal stability of the hemodynamic adjustments underlying blood pressure responses during psychosocial stress. It is therefore tentatively concluded that the hemodynamic patterns underlying blood pressure responses are stable individual difference characteristics. This study was supported by National Institutes of Health Grants HL30675, HL18976, HL01096, and AG04238, and by a grant from the John D. and Catherine T. MacArthur Foundation Research Network on the Determinants and Consequences of Health-Promoting and HealthDamaging Behavior. Allen, M.T., Sherwood, A., Obrist, P.A., Crowell, M.D. and Grange, L.A. (1987) Stability of cardiovascular reactivity to laboratory stressors: A 2: year follow-up. J. Psychmom. Res., 31: 639-645. Anderson, N.B., Lane, J.D., Muranaka, H., Williams Jr., R.B. and Houseworth, S.A. (1988) Racial differences in cardiovascular reactivity to mental arithmetic. Inl. J. Psychophysid, 6: 161-164. Carroll, D., Turner, J.R., Lee, H.J. and Stephenson, J. (1984) Temporal consistency of individual differences in cardiac response to a video game. Biol. Psychol., 19: 81-93. Dembroski, T.M. and MacDougall, J.M. (1983). Behavioral and psychophysiological perspectives on coronary-prone behavior. In T.M. Dembroski, T.H. Schmidt and G. Blumchen (Eds.) Biobehouioral Bases of Coronary Heart Disease Karger, Base]. Krantz, D.S. and Manuck, S.B. (1984) Acute psychophysiologic reactivity and risk of cardiovascular disease: a review and methodological critique. Psycho/ Bull., 96: 435-464. Light, K.C. (1981) Cardiovascular responses to effortful active coping: implications for the role of stress in hypertension development. Psychophysiology, 18: 216-225. Light, K.C. and Sherwood, A. (1989) Race, borderline hypertension and hemodynamic responses to behavioral stress before and after beta-adrenergic blockade. Health Psychoi., 8: 577-595. Manuck, S.B. and Garland, F.N. (1980) Stability of individual differences in cardiovascular reactivity: a thirteen-month follow-up. Physiol. Behau., 24: 621-624. Manuck, S.B., Kaplan, J.R. and Matthews, K.A. (1986) Behav-

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ioral antecedents of coronary artery disease and atherosclerosis. Arteriosclerosis, 6: 2-14. Manuck, S.B. and Schaefer, D.C. (1978) Stability of individual differences in cardiovascular reactivity. Physiol. Behau.. 21: 675-678.

Sherwood, A., Allen, M.T., Fahrenberg, J., Kelsey. R.M., Lovallo, W.R. and van Doomen, L.J.P. (1989) Committee report: methodological guidelines for impedance cardiography. Psychophysiology, in press. Sherwood, A., Allen, M.T., Obrist, P.A. gnd Langer, A.W. (1986) Evaluation of beta-adrenergic influences on cardiovascular and metabolic adjustments to physical and psychological stress. Psychophysiology, 23: 89-104. Sherwood, A., Dolan, C.A. and Light. K.C. (1989) Hemody-

namics of blood pressure responses during active and passive coping. Psychophysiology, in press. Sherwood, A., Light, K.C. and Blumenthal, J.A. (1989) Effects of aerobic exercise training on hemodynamic responses during psychosocial stress in normotensive and borderline hypertensive Type A men: a preliminary report. Psychosom. Med., 51: 1233136. Turner, J.R. (1989) Individual differences in heart rate response during behavioral challenge. Psychophysdogy, 26: 497-505.

Turner, J.R., Carroll, D.. Sims, J., Hewitt, J.K. and Kelly, K.A. (1986) Temporal and inter-task consistency of heart rate reactivity during active psychological challenge: a twin study. Physiol. Behau., 38: 641-644.