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Psychosomatic Medicine 68:531-537 (2006)
© 2006 American Psychosomatic Society

ORIGINAL ARTICLES

Psychosocial, Hemostatic, and Inflammatory Correlates of Delayed Poststress Blood Pressure Recovery

Andrew Steptoe, DPhil and Michael Marmot, PhD, FRCP

From the Department of Epidemiology and Public Health, University College London, London, UK.

Address correspondence and reprint requests to Andrew Steptoe, Department of Epidemiology and Public Health, University College London, 1-19 Torrington Place, London WC1E 6BT, UK. E-mail: a.steptoe{at}ucl.ac.uk


   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 METHODS
 RESULTS
 DISCUSSION
 NOTES
 REFERENCES
 
Objective: Delayed poststress cardiovascular recovery has been associated with cardiovascular disease risk. This study assessed relationships between systolic blood pressure (BP) recovery, psychosocial risk factors, and delayed recovery of inflammatory and hemostatic variables.

Method: Data were analyzed from 228 middle-aged men and women from the Whitehall Psychobiology study who performed color/word and mirror-tracing tasks. Systolic BP recovery was assessed as the difference between baseline and levels recorded 40 to 45 minutes poststress. Associations were analyzed with socioeconomic markers (grade of employment, education, income), psychosocial factors (social isolation, hostility, mental health, financial strain), and recovery of heart rate, heart rate variability, von Willebrand factor, factor VIII clotting activity, plasma fibrinogen, and plasma viscosity.

Results: Systolic BP was on average 6.19 ± 9.6 mm Hg higher on recovery than baseline. Delayed BP recovery was associated with lower grade of employment, lower education and lower income independently of age, gender, and systolic BP stress reactivity. Delayed BP recovery was related to social isolation and poor mental health independently of age, gender, socioeconomic position, and task reactivity. Delayed systolic BP recovery was also associated with delayed recovery in diastolic BP, heart rate, factor VIII, and plasma viscosity but not delayed heart rate variability recovery, independently of age, gender, body mass, and task reactivity.

Conclusion: Socioeconomic and psychosocial risk factors for cardiovascular disease are related to delays in poststress recovery. Delayed systolic BP recovery may be a marker for prolonged responses in hemostatic variables that have a direct influence on cardiovascular disease pathogenesis.

Key Words: cardiovascular disease • mental stress • recovery • socioeconomic status • blood pressure • hemostatic responses

Abbreviations: BMI = body mass index; BP = blood pressure; SES = socioeconomic status; vWF = von Willebrand factor; CHD = coronary heart disease; SF36 = Short Form 36; C.I. = confidence interval.


   INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
METHODS
 RESULTS
 DISCUSSION
 NOTES
 REFERENCES
 
Biological stress responses have two dimensions that are potentially relevant to health outcomes: response magnitude (reactivity) and duration. There is growing interest in individual differences in poststress recovery or prolonged biological activation after stressors are terminated (1,2). McEwen (3) has argued that delayed recovery is one manifestation of chronic allostatic load and the failure of biological regulatory processes that results from sustained or repeated challenges to the system over extended periods. Less effective poststress recovery may be linked with perseverative cognitions and ruminative thoughts about task performance (4).

Evidence for the clinical relevance of variations in recovery after psychological stress is sparse. Most interest has focused on cardiovascular diseases such as hypertension and coronary heart disease (CHD). A number of investigations have reported that a positive family history of hypertension is associated with delayed poststress blood pressure (BP) and heart rate recovery (5,6). Patients with untreated hypertension have a greater area under the curve (combining reactivity and recovery) in response to color/word and cold pressor tasks than individuals with high-normal blood pressure BP (7). Strike et al. (8) found that patients with coronary artery disease showed more prolonged elevations than controls in peripheral vascular resistance after color/word and mirror tracing tasks, with higher levels up 120 minutes poststress.

Delayed cardiovascular recovery after physical exercise appears to have prognostic significance, although the literature is not consistent (9). Delayed BP recovery after treadmill exercise was found to predict future hypertension in the Framingham offspring study (10), while delayed heart rate recovery predicts mortality (11). Similarly, delayed systolic BP recovery after bicycle ergometry has been associated with future stroke (12) and myocardial infarction (13).

Few longitudinal studies of delayed recovery after psychological stress have been carried out. Borghi et al. (14) tested 44 young borderline hypertensives with a mental arithmetic task and followed them up 5 years later. Findings were complicated by the fact that individuals with high lymphocyte sodium were put on low sodium diets. An association between delayed BP recovery and future hypertension was observed, but this was no longer significant after intracellular sodium and BP stress reactions were entered into the regression model. Stewart and France (15) reported a positive association between systolic BP during recovery from cold pressor, ischemic pain, and physical exercise but not mental arithmetic tasks and resting BP 3 years later. Treiber et al. (16) found no relationship between recovery BP aggregated across orthostatic and behavioral stressors and resting BP 4 years later in a large sample of normotensive youths.

These studies of recovery after psychological stress have been conducted on samples of children and young adults. We have recently investigated poststress recovery in healthy middle-aged men and women (17). Participants were reassessed 3 years after stress testing involving color/word and mirror tracing tasks. Resting systolic BP on follow-up was predicted by impaired poststress systolic BP recovery independently of baseline BP, BP levels during stress, age, gender, socioeconomic status (SES), body mass index (BMI), and smoking. The odds of an increase in systolic BP ≥5 mm Hg were 3.50 for individuals with poor poststress recovery, independent of covariates. In a separate analysis, we found that increases in waist circumference and waist/hip ratio in men were also predicted by poor systolic BP recovery independently of baseline adiposity and other covariates (18). These data suggest that disturbances in prompt BP recovery may become more relevant to cardiovascular disease risk with advancing age.

The processes through which delayed BP recovery promotes disease are poorly understood. One possibility is that delayed recovery is associated with psychosocial risk factors for cardiovascular disease so may be either a marker or mediator of psychosocial effects. CHD risk is inversely related to SES, and we have found that impaired poststress recovery of BP and heart rate variability is more common in lower SES groups as defined by occupational grade (19). Relationships between impaired recovery and hostility (20,21) and John Henryism in black men (22) have also been described. The first purpose of the present analyses was to explore the psychosocial correlates of poor poststress systolic BP recovery in our middle-aged sample. We assessed relationships with other markers of SES, namely, education and income, so as to determine whether the link between recovery and SES generalizes beyond occupational grade. Additionally, associations with social isolation, hostility, mental health, and financial strain were analyzed.

Another possibility is that impaired poststress BP recovery is a marker of prolonged responses in other biological variables implicated in cardiovascular pathology. Stress stimulates inflammatory, hemostatic, and rheologic responses relevant to atherogenesis, including increases in fibrinogen, von Willebrand factor (vWF), factor VIII clotting activity, and plasma viscosity (23). In other analyses from this data set, some of these variables showed incomplete recovery 45 minutes poststress (24,25). It is possible that individuals whose systolic BP recovery is delayed after behavioral stress show prolongation of hemostatic responses, indicative of an extended procoagulatory and proinflammatory state. We therefore hypothesized that delayed systolic BP recovery would be associated with poor recovery in these biochemical measures. We also assessed whether delayed systolic BP recovery was associated with the recovery profile of other cardiovascular parameters, namely, diastolic BP, heart rate, and heart rate variability. It was hypothesized that diastolic BP and heart rate recovery would be positively related to systolic BP recovery because these measures share common autonomic regulatory processes. By contrast, the dominant influence on heart rate variability is parasympathetic rather than sympathoadrenal (26), so we reasoned that the association with systolic BP recovery would be weak. In all analyses, we also tested whether associations with BP recovery were independent of BP reactivity because the latter is well established as an indicator of future CHD risk (27,28).


   METHODS
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
RESULTS
 DISCUSSION
 NOTES
 REFERENCES
 
Participants
Participants in this study were 125 men and 103 women drawn from the Whitehall II epidemiological cohort. The Whitehall II cohort consists of 10,308 London-based civil servants, recruited in 1985 to 1988 to investigate demographic, psychosocial, and biological risk factors for CHD (29). Volunteers for this study were recruited on the following criteria: aged 45 to 59 years, based in the London area, not planning to retire for at least 3 years, white European origin, no history of CHD, and no previous diagnosis or treatment for hypertension. Participants were drawn equally from higher (administrative and professional), intermediate (senior executive officers), and lower (executive officers, clerical, office support) employment grades. The study was approved by the UCL/UCLH Committee on the Ethics of Human Research.

Measures
The primary measure of SES was occupational status or grade of employment. The British civil service is divided into 12 grades, and these were grouped into 3 categories in the present study (30). Additionally, we recorded educational attainment, and the sample was divided into three groups: basic education, high school or equivalent, and college and above. Annual personal income was assessed in 8 categories that were later collapsed into three: <£20,000 ($35,000), £20,000–£34,999 ($35,000–$61,000), and ≥£35,000 ($61,000). Social isolation was measured with questions concerning contact with family, friends, and relatives, derived from the Close Persons Questionnaire (31). This measure has previously been found to predict psychiatric morbidity and health status in the Whitehall II Study (32,33). Respondents were given points on the social isolation measure if they lived alone, if they had no relatives outside their household, never visited or were never visited by relatives or friends, or had no relatives or friends whom they saw at least once a month. Scores could range from 0 (no social isolation) to 3 (maximum isolation). Scores on the measure were skewed, so participants were categorized into isolated (1–3) or not isolated (0). Hostility was assessed with a 22-item version of the Cook-Medley hostility scale adapted from the full scale for the Whitehall study (29). Scores could range from a minimum of 0 to maximum of 22, and the Cronbach {alpha} for the scale in this sample was 0.83. Mental health was assessed with the 5-item general mental health scale from the Short Form 36 (SF36) Health Survey, a widely used and well-validated measure (34,35). Scores were scaled so that 0 = worst possible health and 100 = best possible health, and the Cronbach {alpha} was 0.81. Financial strain was measured with an adaptation of the Pearlin et al. (36) economic strain measure, which assesses difficulty paying one's bills, being able to replace items such as furniture or a car when needed, and being able to provide for one's family in terms of food, clothing, and medical care. Eight items were presented, with response options ranging from 1 = no difficulty to 3 = very great difficulty, and responses were summed (Cronbach {alpha} = 0.86).

Procedure
Participants were tested in the morning or afternoon in a light- and temperature-controlled laboratory. They were instructed not to have drunk tea, coffee, or caffeinated beverages or to have smoked for at least 2 hours before the study and not to have consumed alcohol or to have exercised on the evening before or the day of testing. BP and heart rate were monitored continuously from the fingers of the nondominant arm using a Portapres-2 (37,38) while the electrocardiogram was measured for the assessment of heart rate variability, as detailed previously (19). After instrumentation and the insertion of a venous cannula for the periodic collection of blood samples, the participant rested for 30 minutes. A baseline blood sample was drawn, and BP and heart rate were recorded for a 5-minute period. A rating of subjective stress was also taken on a 7-point scale where 1 = low and 7 = very high. Two behavioral tasks were then administered in random order; these were a computerized version of the color-word interference task and mirror tracing (19,24). Each lasted for 5 minutes, during which BP and heart rate were recorded continuously. After each task, the participant rated task stress, difficulty, and task involvement on 7-point scales. There was no monitored intertask interval. A second blood sample (stress measure) was drawn immediately after the task period and a third after 45 minutes' quiet rest (recovery measure). During the poststress period, participants read or watched nature videos. A final subjective stress measure was obtained after the final blood sample.

Assays
Venous blood samples were collected in citrated (0.109 mol/L; 9:1 v:v) and K2-EDTA (1.5 mg/ml) tubes and were centrifuged at room temperature, and the supernatant plasma was snap frozen at –70°C within 1 hour. Plasma viscosity was measured in the K2-EDTA samples in a semiautomated capillary viscometer (Coulter) at 37°C. Factor VIII activity (one-stage assay) and vWF antigen (ELISA, DAKO) were assayed in citrated plasma (39). Clottable fibrinogen was measured by an automated Clauss assay in a MDA-180 coagulometer (Organon Teknika, Cambridge, UK) using the manufacturer's reagents and the International Fibrinogen Standard (40). Factor VIII and plasma viscosity data were skewed, so were log transformed before analysis.

Data Reduction and Analysis
BP and heart rate were averaged into baseline, color-word task, mirror-tracing task, and recovery trials, and the two task trials were aggregated. Heart rate variability was measured in terms of the average root mean square of successive differences (RMSSD) of R-R intervals for each trial. Equipment faults led to substantial loss of data for heart rate variability, so these analyses are based on 151 participants. Complete blood data were available for the following numbers: vWF 214, factor VIII and fibrinogen 215, and plasma viscosity 207. Responses during task and recovery periods in BP, heart rate, heart rate variability, vWF, factor VIII, fibrinogen, plasma viscosity, and subjective stress were analyzed with repeated-measures analysis of variance and post hoc comparisons made with Tukey's least significant difference (LSD) test.

Systolic BP recovery was scored as the difference between levels during the 40 to 45 minutes posttask trial and baseline so that more positive scores indicate poorer recovery (sustained BP above baseline). Associations between the systolic BP recovery index and SES were analyzed with linear regression on systolic BP recovery scores, with the SES measure, age, gender, and systolic BP task reactivity (task-baseline change) as independent variables. Results are presented as standardized regressions (ß), and unstandardized regression coefficients (B) with 95% confidence intervals (C.I.). Relationships with psychosocial factors were analyzed with regression on systolic BP recovery. Two models were tested for each variable. In model 1, the psychosocial variable was entered into the regression, along with age, gender, and systolic BP reactivity. In model 2, grade of employment was added as an additional covariate.

The relationship between systolic BP recovery and recovery in other biological variables (diastolic BP, heart rate, heart rate variability, vWF, factor VIII, fibrinogen, and plasma viscosity) was assessed by computing recovery change scores for measures (recovery – baseline). A series of linear regressions was carried out with these recovery scores as dependent variables. BMI was included as an additional factor in these analyses, in the light of its association with inflammatory and hemostatic variables (41). In model 1, age, gender, BMI, systolic BP recovery index, and the baseline of the biological measure being analyzed were included as independent variables. Model 2 added systolic BP reactivity and task reactivity in the biological measure being analyzed so as to assess whether associations were independent of reactivity effects. The variance (r2) accounted for by the full models is presented, along with regression coefficients for systolic BP recovery.


   RESULTS
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
 RESULTS
DISCUSSION
 NOTES
 REFERENCES
 
The participants are described in Table 1. Average age was 52.3 years, and there was a slight preponderance of men. The proportion of current smokers was low (8%). Nearly half the participants were categorized as socially isolated, whereas ratings of hostility and financial strain were low on average. Ratings on the SF36 mental health scale were well below the optimum score of 100, indicating moderately impaired functioning.


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  		TABLE 1. Participants in the Study

 

Repeated-measures analysis of variance confirmed main effects of trial for systolic and diastolic BP and heart rate (F(2,450) = 382.9, 403.7, and 321.0, respectively, p < .001), heart rate variability (F(2,300) = 48.3, p < .001), vWF (F(2,426) = 6.48, p = .002), factor VIII and fibrinogen (F(2,428) = 15.7 and 22.0, respectively, p < .001), plasma viscosity (F(2,412) = 53.2, p < .001), and subjective stress (F(2,450) = 595.2, p < .001). As can be seen in Table 2, behavioral tasks induced increases in BP, heart rate, VWF, factor VIII, fibrinogen, plasma viscosity and subjective stress, and reductions in heart rate variability. Participants rated the tasks difficult (mean, 5.62 ± 1.1) and involving (mean, 5.72 ± 1.1) on average. By the time of the 45 minutes posttask sample, there was complete recovery in heart rate, heart rate variability, vWF, factor VIII, and subjective stress; indeed, heart rate had fallen below baseline and heart rate variability was greater than baseline in the recovery trial. Recovery was incomplete on average for systolic and diastolic BP, plasma fibrinogen, and plasma viscosity. A direct comparison of recovery change from baseline in the four hemostatic variables confirmed that the difference between completeness of recovery was significant for plasma viscosity versus vWF and factor VIII, and for fibrinogen versus Factor VIII (all p < .001).


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  		TABLE 2. Psychobiological Responses During Mental Stress Testing, Means ± SD

 

Systolic BP was on average 6.19 ± 9.6 mm Hg higher in the recovery than baseline trials, with individual differences ranging from 33.7 mm Hg higher to 27.0 mm Hg lower during recovery. This variation is illustrated in Figure 1, where participants have been divided into tertiles of the systolic BP recovery index (recovery minus baseline). It can be seen that systolic BP was comparable in the baseline and task trials in the three tertiles and differed only during recovery. Nevertheless, the systolic BP recovery index correlated positively with systolic BP stress reactivity (r = 0.23, p < .001), indicating that more reactive individuals showed more delayed poststress recovery.


Figure 14
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  		Figure 1. Mean systolic BP in mm Hg during baseline, task, and recovery trials in participants with the greatest (solid line, triangle), intermediate (dashed line, circles), and poorest (dotted line, squares) poststress recovery. Error bars are standard error of the mean.

 

Systolic BP Recovery and SES
Linear regression on the systolic BP recovery index confirmed the association with grade of employment we have previously reported (B = 3.03; C.I., 1.15 to 4.54; p < .001, after adjustment for age, gender, and systolic BP task reactivity). Systolic BP recovery was more effective among participants from higher grades of employment. Similar results emerged when SES was defined by educational attainment (B = –2.01; C.I., –3.46 to –0.56; p = .007) and income (B = –3.14; C.I., –4.85 to –1.43; p < .001). Recovery was delayed in individuals with lower education and lower income. These models accounted for 8.8% to 11.6% of the variance in the systolic BP recovery index.

Psychosocial Factors and Systolic BP Recovery
Relationships between psychosocial factors and BP recovery were also analyzed using linear regression. The results indicated that delayed systolic BP recovery was associated with social isolation (p = .030, r2 = 0.077), poor mental health (p = .015, r2 = 0.078), and greater financial strain (p = .007, r2 = 0.085), independent of age, gender, and systolic BP reactivity (Table 3). The association with hostility was positive but not significant (p = .22). When grade of employment was added to the model, the association with financial strain was no longer significant (p = .18). This suggests that the relationship between delayed systolic BP recovery and financial strain was secondary to the influence of SES, which is itself a strong predictor of financial strain. However, the associations between social isolation and impaired mental health and delayed BP recovery remained significant (Table 3), and both models accounted for 13.4% of the variance. By way of illustration, systolic BP was on average 7.31 mm Hg above baseline in the recovery trial in socially isolated participants, compared with 4.81 mm Hg in those who were not isolated (values adjusted for age, gender, systolic BP reactivity and grade of employment). People with mental health ratings in the lowest tertile averaged 7.21 mm Hg above baseline in the recovery trial, compared with 5.14 mm Hg for those in the highest tertile.


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  		TABLE 3. Regressions of Psychosocial Factors on Systolic BP Recovery

 

Associations With Recovery of Other Biological Variables
The relationship between systolic BP recovery and recovery of the other biological variables recorded during stress testing is summarized in Table 4. The systolic BP recovery index was strongly associated with diastolic BP recovery (p < .001, r2 = 0.156), and this remained true after adjusting not only for baseline diastolic BP but also for systolic and diastolic BP stress reactivity (p < .001, r2 = 0.398). Thus, individuals who showed effective systolic BP recovery were also more likely to have low diastolic BP during the recovery period. The association with heart rate recovery was also significant after taking systolic BP and heart rate stress reactivity into account (p = .028, r2 = 0.370). By contrast, there was no significant association between systolic BP and heart rate variability recovery.


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  		TABLE 4. Systolic BP Recovery and Recovery of Other Biological Responses

 

Two of the hemostatic and rheologic variables (factor VIII and plasma viscosity) showed robust associations with the systolic BP recovery index. Factor VIII (p = .033) and plasma viscosity (p = .041) were more elevated 45 minutes poststress in individuals who showed delayed BP recovery. These associations remained significant when factor VIII and plasma viscosity stress responses were entered into the regression models, together with systolic BP stress reactivity. Consequently, the associations with the recovery were not secondary to reactivity effects, even though in both cases task reactivity was positively associated with delayed recovery (B = 0.50; C.I., 0.362 to 0.64; and B = 0.43; C.I., 0.342 to 0.60, respectively; p < .001). In the case of vWF, there was a significant association with the systolic BP recovery index (p = .033) that was no longer significant after BP and vWF stress reactivity had been taken into account (p = .21). The recovery of vWF was strongly associated with the magnitude of vWF stress reactions (B = 0.53; C.I. 0.41 to 0.65; p < .001), suggesting that the association between vWF recovery and systolic BP recovery was secondary to reactivity effects. The association between systolic BP recovery and fibrinogen recovery was not significant. The variance accounted for by the full models was 30.4% (vWF recovery), 24.8% (factor VIII recovery), 24.0% (fibrinogen recovery), and 27.% (plasma viscosity recovery).

There were no significant associations between systolic BP recovery and subjective stress ratings either during tasks or recovery, or with ratings of difficulty and involvement in the tasks.


   DISCUSSION
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
 RESULTS
 DISCUSSION
NOTES
 REFERENCES
 
The purpose of these analyses was to learn more about the characteristics of delayed poststress BP recovery, assessing both the psychosocial factors associated with recovery and the relationship between BP recovery and response profiles in other biological variables. The study involved secondary analysis of previously published data (19,24,25) and was therefore constrained by the measures available in this data set. In particular, we were limited to a single measure of systolic BP recovery, namely, the difference between values 40 to 45 minutes poststress and baseline. The assessment of cardiovascular recovery has become increasingly sophisticated, and measures of time to recovery, area under the curve, and latent growth curve modeling have all been applied (2,20). Our method of assessment was a simple arithmetic difference at a fixed point poststress, so we do not have information about the time course of the recovery curve.

A striking feature of the analysis is that both systolic and diastolic BP were elevated above baseline 40 to 45 minutes poststress. This contrasts with many recovery studies that have assessed changes over the first 5 to 10 minutes after stress. Rather few investigations have measured recovery at this longer interval, though von Känel et al. (42) observed complete BP recovery on average 45 minutes poststress in a similarly aged sample of apparently healthy men. The explanation for the continued elevation in BP in the present study is not clear but may relate to the specific protocols used or the BP measurement procedures. The likely significance of delayed recovery levels is reinforced by the observation that they are associated with progression over 3 years in clinic BP levels (17) and with waist circumference (18). Our study unfortunately included no measures of perseverative cognition, so we do not know whether participants' thoughts over the recovery period helped to sustain elevated BP (4,43). However, self-rated stress had returned to baseline by the time of the BP recovery sample, and there was no association between BP recovery and task appraisals. Consequently, any effect of cognitive rumination on systolic BP recovery was not manifest in affective differences as captured by our measures. The absence of correlations between subjective experience and systolic BP recovery may reflect a lack of conscious awareness of persistent biological activation.

We previously observed that delayed BP recovery was more common among lower-SES individuals as defined by grade of employment (19). Occupational grade might be criticized as indexing only one element of SES, and it could also be argued that grade of employment within a large stable organization such as the British Civil Service might not relate to other markers of social position. However, the same association between delayed BP recovery and SES was obtained with classifications on the basis of education and income, indicating that effects are generalizable.

We tested whether delayed BP recovery was related to psychosocial risk factors for cardiovascular disease. Social isolation, financial strain, poor mental health, and hostility have all been related to future CHD in prospective epidemiologic observational studies (44,45). These factors are also associated with lower SES (29,46), so we tested relationships with systolic BP recovery both with and without grade of employment in the regression model. The results indicate that delayed BP recovery was significantly related to social isolation, poor mental health, and financial strain, independently of age and gender (Table 3). The association with financial strain did not survive additional statistical adjustment for grade of employment, suggesting that the effect was probably secondary to its correlation with SES. But the links between delayed recovery, social isolation, and poor mental health were independent of SES, indicating that psychosocial characteristics may be directly related to recovery. We did not confirm the relationships described previously between disturbed BP recovery and hostility (20,21). Llabre et al. (20) used the same measure of hostility but assessed recovery only over 6 minutes poststress. Anderson et al. (21) had a different measure of hostility, and this may account for the difference in results. It is also possible that the challenges in this study did not elicit the hostile traits necessary for heightened cardiovascular activation.

We were particularly concerned in these analyses to discover whether the associations with recovery were independent of reactivity effects. When recovery is assessed at a single point poststress, it is possible that more reactive people might show delayed recovery, even though their rate of recovery (as a function of time) is unaffected. In this sample, reactivity and recovery were moderately positively correlated, indicating that a confound might be present. Nevertheless, the association between recovery and psychosocial factors was independent of reactivity effects.

We hypothesized that one reason why delayed BP recovery might predict future cardiovascular pathology is that it is associated with delayed recovery of inflammatory, hemostatic, and rheologic factors. Fibrinogen, vWF, factor VIII, and plasma viscosity have all been related prospectively to increased risk of future CHD, independently of standard risk factors (47–49). Poststress recovery of vWF and factor VIII was complete on average by the time the 45-minute blood sample was drawn. This is consistent with von Känel et al.'s (42) study in which recovery of vWF was also complete by 45 minutes poststress. A reduction in the plasma fibrinogen below baseline was described by these authors, but we could not replicate this finding.

The analysis of associations between recovery patterns in different biological variables indicated that delayed BP recovery was correlated with delayed poststress recovery of vWF, factor VIII clotting activity, and plasma viscosity (Table 4). The association with fibrinogen recovery was not significant, even though fibrinogen is a major determent of plasma viscosity. Interestingly, the relationships with factor VIII and plasma viscosity remained significant after controlling both for BP stress reactivity and reactivity in factor VIII and plasma viscosity respectively. Slow BP recovery appears to be associated with delayed return to baseline levels in procoagulatory hemostatic and rheostatic measures but not with the inflammatory marker (fibrinogen). These broader patterns of biological adaptation may account for the potentially pathogenic effects of delayed BP recovery.

As expected, systolic BP recovery was strongly associated with individual differences in diastolic BP recovery. Similar autonomic processes govern stress responses in systolic and diastolic BP, so comparable changes during recovery were anticipated. By contrast, systolic BP recovery was not related to recovery of heart rate variability and only inconsistently with heart rate recovery (Table 4). It is possible that heart rate variability is a marker of distinctive parasympathetic processes that are independent of the mechanisms governing systolic BP recovery. Heart rate variability is also related to psychosocial risk factors for CHD differently from systolic BP (50). However, the finding may also be a result of the timing of recovery measures. Both heart rate and heart rate variability had returned to baseline by the time of the recovery sample, and individual differences in recovery might be more striking at an earlier stage after stress.

The limitations of this study should be recognized. Data were collected from healthy white middle-aged men and women, and results may not generalize to other groups. Poststress recovery was assessed at a single point, and the recovery curve could not be modeled. A crucial issue is that recovery was assessed after behavioral tasks but not physical activity or another challenge. We do not therefore know whether these associations are limited to recovery from psychological stress or would also be present after other physiological perturbations. The answer to this question would shed light on whether disturbances in recovery are neocortical in origin or emerge through differences in nonspecific physiological regulatory processes. Nonetheless, these findings are consistent with the notion that delayed poststress BP recovery is associated with psychosocial risk factors for cardiovascular disease and with hemostatic processes that contribute to CHD pathology.

This research was supported by the British Heart Foundation and the Medical Research Council, UK. These analyses were stimulated by discussions with the MacArthur Network on SES and Health. We are grateful to Sabine Kunz-Ebrecht, Pamela J. Feldman, Natalie Owen, Bev Murray, and Gonneke Willemsen for their involvement in data collection and to Gordon Lowe and Ann Rumley for carrying out the hemostatic analyses.


   NOTES
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
 RESULTS
 DISCUSSION
 NOTES
REFERENCES
 

Received for publication November 3, 2005; revision received February 15, 2006.

DOI:10.1097/01.psy.0000227751.82103.65


   REFERENCES
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
 RESULTS
 DISCUSSION
 NOTES
 REFERENCES
 

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