Psychosomatic Medicine
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
This Article
Right arrow Abstract Freely available
Right arrow Figures Only
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Matthews, S. C.
Right arrow Articles by Dimsdale, J. E.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Matthews, S. C.
Right arrow Articles by Dimsdale, J. E.
Related Collections
Right arrow Depression
Right arrow Blood Pressure
Right arrow Other Cardiovascular Medicine
Psychosomatic Medicine 67:509-513 (2005)
© 2005 American Psychosomatic Society

ORIGINAL ARTICLES

Depressive Symptoms Are Associated With Increased Systemic Vascular Resistance to Stress

Scott C. Matthews, MD, Richard A. Nelesen, PhD and Joel E. Dimsdale, MD

From the University of California, San Diego, Department of Psychiatry, San Diego, California.

Address correspondence and reprint requests to Scott C. Matthews, MD, San Diego VA Health Services, 3350 La Jolla Village Drive, Mail Code 116A, La Jolla, CA 92161. E-mail: scmatthews{at}ucsd.edu


   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 METHODS
 RESULTS
 DISCUSSION
 NOTES
 REFERENCES
 
Objective: The deleterious effects of major depressive disorder on cardiovascular (CV) functioning are well known. However, the etiologic mechanisms underlying this association are incompletely understood. In the current study, subjects with varying degrees of depressive symptoms performed a stress task while CV reactivity was measured. We hypothesized that high levels of depressive symptoms would be associated with altered CV reactivity.

Methods: Ninety-one healthy volunteer subjects performed reactivity testing while measures of impedance cardiography and autonomic nervous system function were obtained. Subjects completed the Center for Epidemiological Studies Depression Scale (CES-D) and were categorized into either the high depressive (i.e., CES-D ≥16) or low depressive (i.e., CES-D <16) symptoms group.

Results: Task performance was associated with increases in systemic vascular resistance (SVR) (p = .001), mean arterial pressure (p = .001), and heart rate (p = .005), and decreases in cardiac output (p = .001), heather index (p = .001), and stroke volume (p = .05). After controlling for screening mean arterial pressure, an interaction effect of stress by mood group on SVR (p = .01) was observed; subjects with high amounts of depressive symptoms manifested significantly greater SVR at baseline and in response to a stressor task than did subjects with low amounts of depressive symptoms.

Conclusions: These results suggest a mechanism that may partially explain the increased CV morbidity associated with depressive symptoms. In future studies, it may be useful to examine if treatment of depressive symptoms alters CV reactivity.

Key Words: depressive symptoms • systemic vascular resistance • reactivity • mirror star tracing task

Abbreviations: ANS = autonomic nervous system; CESD = Center for Epidemiological Studies Depression Scale; CO = cardiac output; CV = cardiovascular; DSM-IV = Diagnostic and Statistical Manual, Fourth edition; HI = Heather index; HR = heart rate; HRV = heart rate variability; HRVhf= high-frequency HRV; MAP = mean arterial pressure; MDD = major depressive disorder; MI = myocardial infarction; PNS = parasympathetic nervous system; POMS = Profile of Mood States; MSTT = mirror star tracing task; SNS = sympathetic nervous system; SV = stroke volume; SVR = systemic vascular resistance.


   INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
METHODS
 RESULTS
 DISCUSSION
 NOTES
 REFERENCES
 
Depressivesymptoms are associated with major psychiatric and medical illnesses, and with exposure to stressful life events. The adverse impact of these depressive symptoms on all-cause mortality has been repeatedly described (1–5), although discrepant reports exist (6–13). Numerous studies have also focused on the impact of depressive symptoms, specifically on cardiovascular (CV) mortality. Whereas the majority of this literature indicates that depressive symptoms are associated with increased CV mortality (14–18), there are negative studies as well (8,19,20). Two recent metaanalyses address this issue. In their analysis of 22 published studies, van Melle et al. report that postmyocardial infarction (MI) depression is associated with a 2- to 2.5-fold increased risk of mortality or an adverse cardiac event within 2 years of the MI (21). Similarly, Barth et al. indicate that depressive symptoms (as well as clinical depression) have an unfavorable impact on mortality in patients with coronary heart disease (22). It is conceivable that depressive symptoms are associated with increased CV mortality in a dose-dependent fashion, with the greatest risk being associated with major depressive disorder (MDD). In one study of 896 post-MI patients, level of depression at admission was significantly related to cardiac mortality at 5-year follow up (23). However, the mechanism that underlies the association between depressive symptoms and CV mortality is incompletely understood.

Altered hemodynamic and autonomic nervous system (ANS) functioning have been associated with depressive symptoms, and such alterations may partially explain depression’s relationship to increased CV morbidity. MDD has been associated with ANS dysfunction as reflected by: 1) decreased overall heart rate variability (HRV); 2) decreased high-frequency HRV (HRVhf), which specifically reflects parasympathetic nervous system (PNS) activity; and 3) increased low-frequency HRV, which provides an estimate of sympathetic nervous system (SNS) tone (15,24–26). Related studies have linked these physiological changes with poor clinical outcomes. Low overall HRV, which reflects either increased sympathetic activation and/or decreased PNS tone, is a strong and independent predictor of post-MI mortality (27,28).

Subclinical depressive symptoms in the absence of psychiatric illness are common, and the "normal range" of these symptoms in the general population is wide. Prior research supports the notion that subclinical mood symptoms are associated with altered CV reactivity both at rest and in response to stress. In one study that examined resting impedance measures underlying blood pressure in healthy volunteer subjects without psychiatric illness, the fatigue–inertia and tension–anxiety subscales of the Profile of Mood States (POMS) (29) were negatively correlated with stroke volume (SV). The study also found that the POMS fatigue–inertia subscale was negatively associated with cardiac output (CO), and the POMS fatigue–inertia subscale was positively correlated with systemic vascular resistance (SVR) (30). Depressive symptoms have also been associated with altered hemodynamic responses to stress. In another study of 60 healthy women with varying levels of subclinical depressive symptoms, performance of a speech task was associated with increased plasma norepinephrine, CO, heart rate (HR), systolic and diastolic blood pressure, and a shorter preejection period, suggesting that subclinical depressive symptoms are associated with increased SNS activity in women performing a speech task (31).

In the current study, two groups of subjects were examined: 1) a group with a high level of depressive symptoms, i.e., Center for Epidemiological Studies Depression Scale (CES-D) (32) of ≥16, and 2) a group with a low level of depressive symptoms, i.e., CES-D <16. The mirror star tracing task (MSTT), which has been shown to induce robust changes in CV reactivity (33–36), was administered while various measures of ANS and hemodynamic functioning were recorded.

We hypothesized that high levels of depressive symptoms would be associated with increased SNS (both alpha and beta adrenergic) output and decreased PNS tone in response to stress. Support for these hypotheses would add to an existing body of literature suggesting a relationship between subclinical depression and altered CV reactivity, and may speak to a putative mechanism that may partially mediate the relationship between subclinical depressive symptoms and CV morbidity.


   METHODS
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
RESULTS
 DISCUSSION
 NOTES
 REFERENCES
 
Subjects
Ninety-one subjects signed informed consent and completed this study that was approved by the University of California San Diego Human Research Protection Program. Individuals were coded as Euro-American or black on the basis of self-report. During the initial screening visit, subjects had a history and physical examination, and completed the CES-D, a 20-item self-report instrument that is a valid and reliable measure for assessing level of depressive symptoms. Based on the commonly used cutoff score of 16, subjects were placed into either the high depressive (i.e., CES-D ≥16) or low depressive (i.e., CES-D <16) symptoms group. Subjects were excluded if they had MDD or another Axis I psychiatric diagnosis, according to the Diagnostic and Statistical Manual, Fourth edition (DSM-IV).

To decrease the amount of medical comorbidities, all subjects were between 18 and 50 years old and between 85% to 150% of ideal body weight. Women who were taking oral contraceptives or hormonal replacement therapy, menopausal women, and those who were pregnant were excluded. However, restrictions regarding the timing of the menstrual cycle were not imposed. Hypertensive subjects who were currently receiving antihypertensive medication completed a careful tapering program followed by a 3-week drug washout. Any patient whose blood pressure was >180/110 mm Hg while off treatment left the protocol and returned to active treatment.

Reactivity Testing
Reactivity testing was performed within approximately 2 weeks of the screening visit. Subjects were tested in a sound-attenuated room at 8:30 am while seated in a comfortable reclining chair. On arrival to the laboratory, subjects rested quietly for 30 minutes. After this acclimatization phase, subjects rested quietly for an additional 3 minutes (resting baseline) and then performed the MSTT. The MSTT has been used extensively in psychophysiological experiments to probe CV reactivity and has been shown to induce changes in blood pressure (BP) and SVR (33–36). In this task, subjects trace the outline of a star using its mirror image for 3 minutes.

During resting baseline and during performance of the MSTT, electrocardiography (ECG; model 78352C; Hewlett Packard; Andover, MA), impedance cardiography (Minnesota Impedance Cardiograph 304B; Surcom, Minneapolis, MN), and BP (Colin Pilot, Houston, TX) were monitored continuously to obtain dependent measures of ANS and hemodynamic functioning. To record the impedance cardiography measures, impedance cardiographic tape was applied in a standard tetrapolar configuration. A BP cuff and ECG electrodes in a modified lead I or lead II configuration that maximized the R wave were then applied. The ECG, BP, and impedance waveform signals were recorded and relayed to an analog-to-digital converter (DT2801; Data Translation; Marlboro, MA), sampling at 1 kHz per channel and stored in a computer for subsequent review, artifact rejection, and calculation. These data were collected in 3-minute epochs. The review and calculation of HRV were performed using a program developed at the University of Miami, Behavioral Medicine Research Center (37,38). This program calculated the variables of LF power and HF power from spectral analyses. Stroke volume (SV), SVR, and Heather index (HI) were calculated using standard formulas from BP, ECG, and impedance cardiography data (39). Details of the instrumentation and calculation (40) of the physiological variables have been previously described in detail. SVR and HI provide sensitive and reliable measures of alpha and beta SNS activity, respectively (39). Parasympathetic activation is reflected in HRVhf (41).

Analyses
The dependent variables were HR, HRVhf, HI, SV, MAP, CO, and SVR. To examine main effects of stress and interaction effects of stress by depression on these dependent variables, a two (task, i.e., baseline versus stress) by two (mood group, i.e., high/low depression) repeated-measures analysis of variance (SPSS for Windows 9.0; SPSS, Chicago, IL (42)) was performed. Then, to control for the potential confounding variables of gender and ethnicity, data were analyzed using a two (task, i.e., baseline versus stress) by two (gender, i.e., male versus female) by two (ethnicity, i.e., Euro-American versus black) by two (mood group, i.e., high/low depression) repeated-measures analysis of variance.

A post-hoc analysis of simple effects was then performed. Independent-samples t tests were performed to compare SVR during the baseline condition between the high and low depressive symptoms groups, and to compare SVR during performance of the MSTT between the high and low depressive symptoms groups. Paired t tests were performed to compare SVR during baseline with SVR during performance of the MSTT within the high and low depressive symptoms groups.


   RESULTS
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
 RESULTS
DISCUSSION
 NOTES
 REFERENCES
 
The sociodemographic characteristics and values for relevant physiological measures during screening of study participants are outlined in Table 1. At initial assessment, the high and low depressive symptoms groups were not significantly different in age, gender, ethnicity, screening MAP, or body mass index (Table 1).


View this table:
[in this window]
[in a new window]
  		TABLE 1. Sociodemographic and Baseline Physiological Variables for Depressed and Nondepressed Subjects

 

The repeated-measures analysis revealed a main effect of stress on several variables of interest. Task performance was associated with significant increases in SVR (p = .001), MAP (p = .001), and HR (p = .005), and significant decreases in SV (p = .05), CO (p = .001), and HI (p = .001). More interestingly, an interaction effect of stress by mood was observed on SVR (F[1,88] = 7.43, p < .01). Subjects with high depressive symptoms responded to stress with a particularly pronounced increase in SVR (Fig. 1). This interaction remained significant after controlling for ethnicity, gender, and screening MAP (F[1,82[rsqb = 7.87, p < .01). The analysis of simple effects revealed significant increases in SVR from baseline to task within the high depressive symptoms (p < .0001) and within the low depressive symptoms (p < .0001) groups. Independent-samples t tests revealed significant differences in SVR between the high and low depressive symptoms groups both during baseline (p < .05) and during performance of the MSTT (p < .005). There were no significant interactions of ethnicity by stress or gender by stress on SVR. No significant interactions of stress by mood group on HR, HRVhf, HI, MAP, CO, or SV were observed (Table 2).



View larger version (11K):
[in this window]
[in a new window]
  		Figure 1. Interaction of depressive symptoms and stress on systemic vascular resistance. The interaction of stress (base versus task) and mood (high depressive symptoms versus low depressive symptoms) on systemic vascular resistance was significant at p < 0.01.

 

View this table:
[in this window]
[in a new window]
  		TABLE 2. Interaction Effect of Mirror Star Task Performance by Level of Depression on Several Physiological Variables of Interest

 


   DISCUSSION
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
 RESULTS
 DISCUSSION
NOTES
 REFERENCES
 
In the current study, a high level of depressive symptoms was related significantly to increased SVR. Specifically, an interaction effect of depression level (high/low) by stress (task/baseline) on SVR was observed such that a high level of depression was associated with significantly greater SVR at rest and, particularly so, during performance of the MSTT. Prior studies have shown that gender (34,43) and race (44–48) can contribute significantly to physiological reactivity and SVR in particular. However, in the current study, no significant interactions of gender by depression or ethnicity by depression on SVR were observed, indicating that these factors were not confounding the relationship between depression and SVR.

These results are consistent with a study by Yu et al., which reported that SVR at rest was positively correlated with scores on the POMS fatigue–inertia subscale (30). Our study provides complementary evidence that extensive depressive symptoms, as revealed by the CES-D, are associated with increased SVR at rest. Reservations have been raised about the validity of using baseline measures of CO and therefore SVR (49). The current study extends our previously noted observations of baseline differences to differences observed when subjects are stressed, an area in which impedance cardiography measures are on firmer ground. In this context, we found that depressive symptoms are associated with greater SVR during stress.

Interestingly, we observed no significant interactions of stress by mood group on MAP, CO, HR, HRVhf, HI, or SV. Additionally, when the high and low depressive symptom groups were analyzed together, MSTT performance was associated with decreased HI, a sensitive measure of beta-adrenergic tone. Additional research using multiple tasks in a large sample of patients with various degrees of depressive symptoms is needed to fully explain this finding. Perhaps MDD is associated with central ANS changes that result in dysfunction across a broad range of CV measures, whereas the presence of subsyndromal symptoms affects peripheral ANS changes reflected in increased SVR. Also of note is the fact that the MSTT has been previously shown to affect primarily SVR through increased alpha-adrenergic tone (36,50), and additional research using multiple different tasks is needed to understand the role that specific tasks may play in selective activation of the alpha adrenergic nervous system.

The current study suggests a mechanism whereby subclinical levels of depression may have deleterious CV effects. Prior research has described a dose-response relationship between depressive symptom severity and CV events. In one cohort study of generally healthy outpatients, an increase in depressive symptoms over time was significantly associated with MI, stroke, and death (51). In a related study, increased depressive symptoms were associated with an increased risk of subsequent cardiac mortality. In that study, cardiac patients with a CES-D score of ≥16 relative to cardiac patients with a CES-D score of <16 had a relative risk of subsequent cardiac mortality of 1.6, and noncardiac patients with a CES-D score of ≥16 relative to noncardiac patients with a CES-D score of <16 had a relative risk of subsequent cardiac mortality of 1.5 (52).

Although the underlying mechanism that explains the relationship between depressive symptoms and CV morbidity remains incompletely understood, some of the same physiological alterations that have been proposed to contribute to CV morbidity in MDD have also been described in patients with subclinical levels of depression. For example, altered platelet function has been demonstrated in patients with subclinical depressive symptoms (53). Although the current study suggests that depressive symptoms are associated with alterations in CV reactivity, further research is needed to replicate this finding and to understand whether altered CV reactivity is associated with adverse CV outcomes in patients with subclinical depressive symptoms.

There are a number of next steps suggested by this study. First, a research diagnostic interview was not administered. Although subjects were excluded if they had a MDD or other DSM-IV Axis I psychiatric illness, a standardized diagnostic measure was not used, and we cannot definitively rule out the presence of MDD. Second, only 24 subjects had high levels of depression. In future research, it would be useful to study a larger group of subjects that includes both a subgroup of subjects with MDD as well as a subgroup of subjects with a broad range of subsyndromal depressive symptoms. Additionally, because there is ample research showing the values obtained from a single reactivity paradigm administered at a single time have limited reproducibility, future studies might also profitably compare the hemodynamic and autonomic effects of depressive symptoms in terms of responses elicited by multiple stressors on several occasions (54). What is needed to interpret and understand the biologic significance of the current findings is a study in three groups of subjects (i.e., MDD, subclinical depressive symptoms, and healthy volunteers) that implements multiple tasks (i.e., one task such as the MSTT that probes alpha adrenergic functioning, as well as a second task that perturbs the beta adrenergic system) on several occasions. Although the current data do not support general statements about the effects of depressive symptoms on cardiovascular reactivity, and the specific biologic significance of the observed depression by stress interaction on SVR remains uncertain, our study does provide a useful groundwork for follow-up studies that may examine how the presence, and potentially treatment, of depressive symptoms affects CV reactivity.


   NOTES
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
 RESULTS
 DISCUSSION
 NOTES
REFERENCES
 
Received for publication September 7, 2004; revision received January 20, 2005.

This work was supported by grants HL36005, HL44915, RR00827, and 5T32MH18399 from the National Institutes of Health.

DOI:10.1097/01.psy.0000160467.78373.d8


   REFERENCES
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
 RESULTS
 DISCUSSION
 NOTES
 REFERENCES
 

  1. Anda R, Williamson D, Jones D, Macera C, Eaker E, Glassman A, Marks J. Depressed affect, hopelessness, and the risk of ischemic heart disease in a cohort of US adults. Epidemiology 1993;4:285–94.[Medline]
  2. Black SA, Markides KS. Depressive symptoms and mortality in older Mexican Americans. Ann Epidemiol 1999;9:45–52.[CrossRef][Medline]
  3. Everson SA, Roberts RE, Goldberg DE, Kaplan GA. Depressive symptoms and increased risk of stroke mortality over a 29-year period. Arch Intern Med 1998;158:1133–8.[Abstract/Free Full Text]
  4. Schulz R, Beach SR, Ives DG, Martire LM, Ariyo AA, Kop WJ. Association between depression and mortality in older adults: the Cardiovascular Health Study. Arch Intern Med 2000;160:1761–8.[Abstract/Free Full Text]
  5. Whooley MA, Browner WS. Association between depressive symptoms and mortality in older women. Study of Osteoporotic Fractures Research Group. Arch Intern Med 1998;158:2129–35.[Abstract/Free Full Text]
  6. Anstey KJ, Luszcz MA. Mortality risk varies according to gender and change in depressive status in very old adults. Psychosom Med 2002;64:880–8.[Abstract/Free Full Text]
  7. Blazer DG, Hybels CF, Pieper CF. The association of depression and mortality in elderly persons: a case for multiple, independent pathways. J Gerontol A Biol Sci Med Sci 2001;56:M505–9.[Abstract/Free Full Text]
  8. Coryell W, Turvey C, Leon A, Maser JD, Solomon D, Endicott J, Mueller T, Keller M. Persistence of depressive symptoms and cardiovascular death among patients with affective disorder. Psychosom Med 1999;61:755–61.
  9. Everson-Rose SA, House JS, Mero RP. Depressive symptoms and mortality risk in a national sample: confounding effects of health status. Psychosom Med 2004;66:823–30.[Abstract/Free Full Text]
  10. Fredman L, Magaziner J, Hebel JR, Hawkes W, Zimmerman SI. Depressive symptoms and 6-year mortality among elderly community-dwelling women. Epidemiology 1999;10:54–9.[CrossRef][Medline]
  11. Roberts RE, Kaplan GA, Camacho TC. Psychological distress and mortality: evidence from the Alameda County Study. Soc Sci Med 1990;31:527–36.
  12. Schoevers RA, Geerlings MI, Beekman AT, Penninx BW, Deeg DJ, Jonker C, Van Tilburg W. Association of depression and gender with mortality in old age. Results from the Amsterdam Study of the Elderly (AMSTEL). Br J Psychiatry 2000;177:336–42.[Abstract/Free Full Text]
  13. Zheng D, Macera CA, Croft JB, Giles WH, Davis D, Scott WK. Major depression and all-cause mortality among white adults in the United States. Ann Epidemiol 1997;7:213–8.[CrossRef][Medline]
  14. Blumenthal JA, Lett HS, Babyak MA, White W, Smith PK, Mark DB, Jones R, Mathew JP, Newman MF; NORG Investigators. Depression as a risk factor for mortality after coronary artery bypass surgery. Lancet 2003;362:604–9.[CrossRef][Medline]
  15. Carney RM, Rich MW, teVelde A, Saini J, Clark K, Freedland KE. The relationship between heart rate, heart rate variability and depression in patients with coronary artery disease. J Psychosom Res 1988;32:159–64.[CrossRef][Medline]
  16. Frasure-Smith N, Lesperance F, Talajic M. Depression and 18-month prognosis after myocardial infarction. Circulation 1995;91:999–1005.[Abstract/Free Full Text]
  17. Schulz R, Drayer RA, Rollman BL. Depression as a risk factor for non-suicide mortality in the elderly. Biol Psychiatry 2002;52:205–25.[CrossRef][Medline]
  18. Wulsin LR, Vaillant GE, Wells VE. A systematic review of the mortality of depression. Psychosom Med 1999;61:6–17.[Abstract/Free Full Text]
  19. Lane D, Carroll D, Ring C, Beevers DG, Lip GY. Mortality and quality of life 12 months after myocardial infarction: effects of depression and anxiety. Psychosom Med 2001;63:221–30.[Abstract/Free Full Text]
  20. Mendes de Leon CF, Krumholz HM, Seeman TS, Vaccarino V, Williams CS, Kasl SV, Berkman LF. Depression and risk of coronary heart disease in elderly men and women: New Haven EPESE, 1982–1991. Established Populations for the Epidemiologic Studies of the Elderly. Arch Intern Med 1998;158:2341–8.[Abstract/Free Full Text]
  21. van Melle JP, de Jonge P, Spijkerman TA, Tijssen JG, Ormel J, van Veldhuisen DJ, van den Brink RH, van den Berg MP. Prognostic association of depression following myocardial infarction with mortality and cardiovascular events: a meta-analysis. Psychosom Med 2004;66:814–22.[Abstract/Free Full Text]
  22. Barth J, Schumacher M, Herrmann-Lingen C. Depression as a risk factor for mortality in patients with coronary heart disease: a meta-analysis. Psychosom Med 2004;66:802–13.[Abstract/Free Full Text]
  23. Lesperance F, Frasure-Smith N, Talajic M, Bourassa MG. Five-year risk of cardiac mortality in relation to initial severity and one-year changes in depression symptoms after myocardial infarction. Circulation 2002;105:1049–53.[Abstract/Free Full Text]
  24. Carney RM, Blumenthal JA, Stein PK, Watkins L, Catellier D, Berkman LF, Czajkowski SM, O’Connor C, Stone PH, Freedland KE. Depression, heart rate variability, and acute myocardial infarction. Circulation 2001;104:2024–8.[Abstract/Free Full Text]
  25. Guinjoan SM, Bernabo JL, Cardinali DP. Cardiovascular tests of autonomic function and sympathetic skin responses in patients with major depression. J Neurol Neurosurg Psychiatry 1995;59:299–302.[Abstract/Free Full Text]
  26. Rechlin T, Weis M, Spitzer A, Kaschka WP. Are affective disorders associated with alterations of heart rate variability? J Affect Disord 1994;32:271–5.[CrossRef][Medline]
  27. Bigger JT Jr, Fleiss JL, Steinman RC, Rolnitzky LM, Kleiger RE, Rottman JN. Frequency domain measures of heart period variability and mortality after myocardial infarction. Circulation 1992;85:164–71.[Abstract/Free Full Text]
  28. Kleiger RE, Miller JP, Bigger JT Jr, Moss AJ. Decreased heart rate variability and its association with increased mortality after acute myocardial infarction. Am J Cardiol 1987;59:256–62.[CrossRef][Medline]
  29. McNair D, Lorr M, Droppleman L. Profile of Mood States: Manual. San Diego, CA: Educational and Industrial Testing Service; 1981.
  30. Yu BH, Nelesen R, Ziegler MG, Dimsdale JE. Mood states and impedance cardiography-derived hemodynamics. Ann Behav Med 2001;23:21–5.[CrossRef][Medline]
  31. Light KC, Kothandapani RV, Allen MT. Enhanced cardiovascular and catecholamine responses in women with depressive symptoms. Int J Psychophysiol 1998;28:157–66.[CrossRef][Medline]
  32. Radloff LS. The CES-D scale: a self-report depression scale for research in the general population. Appl Psychol Meas 1997;3:385–401.
  33. Bardwell WA, Ziegler MG, Dimsdale JE. Influence of cholesterol and fasting insulin levels on blood pressure reactivity. Psychosom Med 2000;62:569–75.[Abstract/Free Full Text]
  34. Gillin JL, Mills PJ, Nelesen RA, Dillon E, Ziegler MG, Dimsdale JE. Race and sex differences in cardiovascular recovery from acute stress. Int J Psychophysiol 1996;23:83–90.[CrossRef][Medline]
  35. Hurwitz BE, Nelesen RA, Saab PG, Nagel JH, Spitzer SB, Gellman MD, McCabe PM, Phillips DJ, Schneiderman N. Differential patterns of dynamic cardiovascular regulation as a function of task. Biol Psychol 1993;36:75–95.[CrossRef][Medline]
  36. Saab PG, Matthews KA, Stoney CM, McDonald RH. Premenopausal and postmenopausal women differ in their cardiovascular and neuroendocrine responses to behavioral stressors. Psychophysiology 1989;26:270–80.[Medline]
  37. Han K, Nagel JH, Hurwitz BE, et al. Decomposition of heart rate variability by adaptive filtering for estimation of cardiac vagal tone. In: Nagel JH, Smith WM, eds. Bioelectric Phenomena, Electrocardiography, Electromagnetic Interactions, Neuromuscular Systems. New York: IEEE Publishing Services; 1991:660–1.
  38. Nagel JH, Han K, Hurwitz BE, et al. Assessment and diagnostic applications of heart rate variability. Biomed Eng Appl Basis Commun 1993;5:147–58.
  39. Kubicek WG, Kottke J, Ramos MU, Patterson RP, Witsoe DA, Labree JW, Remole W, Layman TE, Schoening H, Garamela JT. The Minnesota impedance cardiograph—theory and applications. Biomed Eng 1974;9:410–6.[Medline]
  40. Nelesen RA, Yu H, Ziegler MG, Mills PJ, Clausen JL, Dimsdale JE. Continuous positive airway pressure normalizes cardiac autonomic and hemodynamic responses to a laboratory stressor in apneic patients. Chest 2001;119:1092–101.[Abstract/Free Full Text]
  41. Porges SW, Bohrer RE. Analyses of periodic processes in psychophysiological research. In: Cacioppo JT, Tassinary LG, eds. Principles of Psychophysiology: Physical, Social and Inferential Elements. New York: Cambridge University Press; 1990:708–53.
  42. Norusis MJ. SPSS Base System User’s Guide. Chicago: SPSS Inc; 1990.
  43. Light KC, Turner JR, Hinderliter AL, Sherwood A. Race and gender comparisons: I. Hemodynamic responses to a series of stressors. Health Psychol 1993;12:354–65.[CrossRef][Medline]
  44. Anderson NB. Racial differences in stress-induced cardiovascular reactivity and hypertension: current status and substantive issues. Psychol Bull 1989;105:89–105.[CrossRef][Medline]
  45. Calhoun DA, Mutinga ML, Collins AS, Wyss JM, Oparil S. Normotensive blacks have heightened sympathetic response to cold pressor test. Hypertension 1993;22:801–5.[Abstract/Free Full Text]
  46. Fang CY, Myers HF. The effects of racial stressors and hostility on cardiovascular reactivity in African American and Caucasian men. Health Psychol 2001;20:64–70.[CrossRef][Medline]
  47. Finney ML, Stoney CM, Engebretson TO. Hostility and anger expression in African American and European American men is associated with cardiovascular and lipid reactivity. Psychophysiology 2002;39:340–9.[CrossRef][Medline]
  48. Thomas KS, Nelesen RA, Dimsdale JE. Relationships between hostility, anger expression, and blood pressure dipping in an ethnically diverse sample. Psychosom Med 2004;66:298–304.[Abstract/Free Full Text]
  49. Sherwood A, Allen MT, Fahrenberg J, Kelsey RM, Lovallo WR, van Doornen LJ. Methodological guidelines for impedance cardiography. Psychophysiology 1990;27:1–23.[Medline]
  50. Llabre MM, Saab PG, Hurwitz BE, Schneiderman N, Frame CA, Spitzer S, Phillips D. The stability of cardiovascular parameters under different behavioral challenges: one-year follow-up. Int J Psychophysiol 1993;14:241–8.[CrossRef][Medline]
  51. Wassertheil-Smoller S, Applegate WB, Berge K, Chang CJ, Davis BR, Grimm R Jr, Kostis J, Pressel S, Schron E. Change in depression as a precursor of cardiovascular events. SHEP Cooperative Research Group (Systoloc Hypertension in the elderly). Arch Intern Med 1996;156:553–61.[Abstract/Free Full Text]
  52. Penninx BW, Beekman AT, Honig A, Deeg DJ, Schoevers RA, van Eijk JT, van Tilburg W. Depression and cardiac mortality: results from a community-based longitudinal study. Arch Gen Psychiatry 2001;58:221–7.[Abstract/Free Full Text]
  53. Berk M, Kirchmann NH, Butkow N. Lithium blocks 45Ca2+ uptake into platelets in bipolar affective disorder and controls. Clin Neuropharmacol 1996;19:48–51.[Medline]
  54. Kamarck TW, Jennings JR, Pogue-Geile M, Manuck SB. A multidimensional measurement model for cardiovascular reactivity: stability and cross-validation in two adult samples. Health Psychol 1994;13:471–8.[CrossRef][Medline]



This article has been cited by other articles:


Home page
 Qual Health ResHome page
E. C. Ward, L. O. Clark, and S. Heidrich
African American Women's Beliefs, Coping Behaviors, and Barriers to Seeking Mental Health Services
Qual Health Res, November 1, 2009; 19(11): 1589 - 1601.
[Abstract] [PDF]

Home page
 J. Appl. Physiol.Home page
G. Deley, R. D. Lipman, J. P. Kannam, C. Bartolini, and J. A. Taylor
Stress responses and baroreflex function in coronary disease
J Appl Physiol, February 1, 2009; 106(2): 576 - 581.
[Abstract] [Full Text] [PDF]

Home page
 Arch Gen PsychiatryHome page
A. H. Glassman, J. T. Bigger, M. Gaffney, and L. T. Van Zyl
Heart Rate Variability in Acute Coronary Syndrome Patients With Major Depression: Influence of Sertraline and Mood Improvement
Arch Gen Psychiatry, September 1, 2007; 64(9): 1025 - 1031.
[Abstract] [Full Text] [PDF]

Home page
 Psychosom. Med.Home page
L. M. Christian and C. M. Stoney
Social Support Versus Social Evaluation: Unique Effects on Vascular and Myocardial Response Patterns
Psychosom Med, November 1, 2006; 68(6): 914 - 921.
[Abstract] [Full Text] [PDF]

This Article
Right arrow Abstract Freely available
Right arrow Figures Only
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Matthews, S. C.
Right arrow Articles by Dimsdale, J. E.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Matthews, S. C.
Right arrow Articles by Dimsdale, J. E.
Related Collections
Right arrow Depression
Right arrow Blood Pressure
Right arrow Other Cardiovascular Medicine

HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS