Psychosomatic Medicine Tips for Better Browsing
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
This Article
Right arrow Abstract Freely available
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
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Virtanen, R.
Right arrow Articles by Airaksinen, J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Virtanen, R.
Right arrow Articles by Airaksinen, J.
Related Collections
Right arrow Parasympathetic Nervous System
Right arrow Sympathetic Nervous System
Right arrow Blood Pressure
Right arrow Health Psychology
Right arrow Personality
Psychosomatic Medicine 65:751-756 (2003)
© 2003 American Psychosomatic Society

ORIGINAL ARTICLES

Anxiety and Hostility Are Associated With Reduced Baroreflex Sensitivity and Increased Beat-to-Beat Blood Pressure Variability

Raine Virtanen, MD, Antti Jula, MD, Jouko K. Salminen, MD, Liisa-Maria Voipio-Pulkki, MD, Hans Helenius, MSc, Tom Kuusela, PhD and Juhani Airaksinen, MD

From the Department of Medicine (R.V., L.-M.V.-P., J.A.), Turku University Central Hospital; Research Department of the Social Insurance Institution (A.J., J.K.S.); and the Departments of Biostatistics (H.H.) and Applied Physics (T.K.), University of Turku, Turku; and the Department of Medicine (L.-M.V.-P.), Helsinki University Central Hospital, Helsinki, Finland.

Address reprint requests to: Raine Virtanen, MD, Department of Medicine, Turku University Central Hospital, Kiinamyllynkatu 4-8, FIN-20520 Turku, Finland. Email: raine.virtanen{at}fimnet.fi


   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 METHODS
 RESULTS
 DISCUSSION
 CONCLUSION
 ACKNOWLEDGMENTS
 REFERENCES
 
OBJECTIVE: The purpose of this study was to determine whether psychological factors are associated with heart rate variability (HRV), blood pressure variability (BPV), and baroreflex sensitivity (BRS) among healthy middle-aged men and women.

METHODS: A population-based sample of 71 men and 79 women (35–64 years of age) was studied. Five-minute supine recordings of ECG and beat-to-beat photoplethysmographic finger systolic arterial pressure and diastolic arterial pressure were obtained during paced breathing. Power spectra were computed using a fast Fourier transform for low-frequency (0.04–0.15 Hz) and high-frequency (0.15–0.40 Hz) powers. BRS was calculated by cross-spectral analysis of R-R interval and systolic arterial pressure variabilities. Psychological factors were evaluated by three self-report questionnaires: the Brief Symptom Inventory, the shortened version of the Spielberger State-Trait Anger Expression Inventory, and the Toronto Alexithymia Scale.

RESULTS: Psychological factors were not related to HRV. Anxiety was associated with decreased BRS (p = 0.001) and higher low-frequency (p = 0.002) power of systolic arterial pressure variability. These associations were independent of age, gender, other psychological factors, heart rate, and systolic and diastolic blood pressures. Hostility was an independent correlate of increased low-frequency power of diastolic arterial pressure (p = 0.001) and increased high-frequency power of systolic arterial pressure (p = 0.033) variability.

CONCLUSIONS: Anxiety and hostility are related to reduced BRS and increased low-frequency power of BPV. Reduced BRS reflects decreased parasympathetic outflow to the heart and may increase BPV through an increased sympathetic predominance.

Key Words: heart rate variability, • blood pressure variability, • baroreflex sensitivity, • Brief Symptom Inventory, • Spielberger State-Trait Anger Expression Inventory, • Toronto Alexithymia Scale.

Abbreviations: BPV = blood pressure variability;; BRS = baroreflex sensitivity;; BSI-37 = shortened 37-item version of the Brief Symptom Inventory;; HRV = heart rate variability;; STAXI = Spielberger State-Trait Anger Expression Inventory;; TAS-26 = Toronto Alexithymia Scale.


   INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
METHODS
 RESULTS
 DISCUSSION
 CONCLUSION
 ACKNOWLEDGMENTS
 REFERENCES
 
Power spectral analysis of HRV has been used to assess whether sympathetic and parasympathetic modulation of the heart rate is associated with cardiovascular morbidity, psychological distress, and psychiatric disorders. While the high-frequency power of HRV is an indicator of parasympathetic cardiac modulation, the low-frequency power of HRV reflects both sympathetic and parasympathetic modulation (1). In the general population, low HRV is associated with increased risk of death from several causes (2–4) and with increased risk of cardiac events (5, 6).

Previous studies of associations between psychological factors and HRV have been carried out predominantly with selected groups of subjects suffering from psychiatric disorders (7–11) or with apparently healthy volunteers (12–16). Although reduced HRV based on 24-hour recording of the heart rate is associated with depression in patients with coronary artery disease (17, 18), short-term HRV measured at supine rest does not differentiate depressive patients from their healthy controls (9, 19, 20). No data exist of the relationship between HRV and depression in the general population. In apparently healthy volunteers, anxiety has been associated with decreased total, low-frequency, and high-frequency powers of HRV (12, 13). Hostility has been linked to decreased high-frequency power of HRV (15). Some data suggest that alexithymic individuals have sympathetic overactivity (16). To the best of our knowledge, no population-based study exists on the effects of anxiety, hostility, or alexithymia on the power spectral components of HRV.

Suppressed anger and hostility (21, 22), alexithymia (23, 24), anxiety (22, 25, 26), and depression (26) have been associated with hypertension. Negative affects composed of anxiety, anger, or sadness increase blood pressure temporarily (27) and may thereby also increase 24-hour BPV. Increased daytime systolic BPV in turn is associated with increased cardiovascular mortality (28). To date, no prognostic data are available from the short-term BPV. The power spectrum of beat-to-beat BPV is composed basically of the same spectral components as that of HRV. Changes in the low-frequency power of BPV have been suggested to reflect changes of central sympathetic nervous control (29, 30). However, the high-frequency power of BPV is determined largely by mechanical effects of respiration on intrathoracic pressure and cardiac filling (30). Thus, exploring the beat-to-beat BPV could give additional information from autonomic nervous function because association of psychological factor with an increased low-frequency power of BPV might indicate increased sympathetic modulation. Concurrently with this assumption, anxiety has been related to increased low-frequency power of systolic BPV (13).

BRS reflects vagal modulation of heart rate by the arterial baroreceptors. A low BRS predicts increased cardiovascular mortality (31). Only a paucity of data are available concerning the effects of psychological factors on BRS. Previous studies suggest that BRS correlates inversely with higher levels of anxiety (10, 14, 32) .

The impact of psychological factors on BPV and BRS is largely obscure. There is also insufficient data concerning the relation of psychological factors to HRV in healthy subjects representing the general population. Therefore, we wanted to study whether psychological factors, namely, somatization, depression, anxiety, hostility, phobicity, anger expression, and alexithymia, are associated with HRV, BRS, and beat-to-beat BPV in healthy middle-aged subjects of the general population. We expected that these factors would be associated with reduced HRV, increased beat-to-beat BPV, and diminished BRS.


   METHODS
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
RESULTS
 DISCUSSION
 CONCLUSION
 ACKNOWLEDGMENTS
 REFERENCES
 
Subjects
An age- and gender-stratified random sample consisting of 45 subjects of each gender and each 10-year age group (35–44, 45–54, and 55–64 years) was drawn from the national population register of inhabitants residing in the vicinity of Turku in southwestern Finland. Medical history, clinical examination, routine biochemical tests, exercise ECG, and echocardiographic examination were used to exclude subjects with any disease known to influence the autonomic nervous system. Therefore, we excluded subjects with diabetes mellitus, coronary artery disease, congestive heart failure, previous cerebrovascular events, claudication, hemodynamically significant valvular disease, significant anemia (hemoglobin <110 g/l for men and <100 g/l for women), chronic alcoholism, antihypertensive medication, anti-ischemic agents, or other confounding medication (ß-blocker eye drops, teophyllamine, ß2-sympathomimetics, antidepressants, neuroleptics and previous or prevailing antineoplastic medication). From 269 subjects, 72 were excluded because of these criteria. Power spectra could not be computed reliably in 47 of the remaining subjects because of ventricular or atrial arrhythmias or technical artifacts. The final analyses included data from 150 subjects (79 women and 71 men). The study was conducted following the Second Declaration of Helsinki and was approved by the ethical committee of the Social Insurance Institution of Finland. All subjects gave their informed written consent.

Procedures
Evaluation of Psychological Factors
For the evaluation of psychological factors, three self-report questionnaires were used: a shortened 37-item version (BSI-37) of the original 53-item Brief Symptom Inventory (33), the shortened version of the Spielberger State-Trait Anger Expression Inventory (STAXI) (34), and the Toronto Alexithymia Scale (TAS-26) (35). The BSI-37, validated in a Finnish population study, does not cover psychotic symptoms (36). The total score of the BSI-37 divided by the number of items, known as general severity index, was used as an indicator of psychological distress. Symptom dimensions for somatization, depression, anxiety, hostility, and phobicity were derived from the BSI-37. The total score of the TAS-26 was used as an indicator of alexithymia. The TAS-26 consists of four factors, which describe difficulty in identifying and distinguishing between feelings and bodily sensations (Factor 1), difficulty in describing feelings (Factor 2), reduced daydreaming (Factor 3), and externally oriented thinking (Factor 4). The STAXI consists of 31 items, which reflect the intensity of feelings of anger (state anger), the disposition to experience anger (trait anger), behaviorally expressed anger (anger-out), suppressed anger (anger-in), and self-control of anger behavior (anger control).

Cardiovascular Measurements
Blood pressure and heart rate were estimated by a trained nurse and averaged over 4 duplicate measures (24). Blood pressure was recorded in seated posture with a mercury sphygmomanometer, always between 8 and 10 AM according to the guidelines of the American Society of Hypertension (37). ECG and beat-to-beat blood pressure recordings for the assessment of HRV, BPV, and BRS were carried out between 8:30 AM and 12 noon in an isolated examination room at a stable temperature between 20°C and 22°C. The subjects were requested to avoid coffee, tea, cola drinks, and smoking for 12 hours and alcoholic beverages for 24 hours before investigations. A light breakfast was allowed not later than 2 hours before these investigations.

ECG was recorded after 10-minute supine rest for 5 minutes while subjects were resting in a supine position and breathing with a controlled frequency of 15 per minute (0.25 Hz). R-R intervals were measured from the precordial leads V1–V6 of a standard 12-lead ECG. Simultaneous beat-to-beat blood pressure recording was obtained by the photoplethysmographic technique (Finapres 2300, Ohmeda, Eaglewood, CO, USA) from the middle phalanx of the left middle finger held at the heart level. The automatic servo-adjustment option of the device was disabled during the recording. The method has been found to provide an accurate estimate of BPV (38, 39). Beat-to-beat ECG and blood pressure signals were digitized and fed into a personal computer. Subjects with time series showing unstationarity, artifacts, or arrhythmias, even a single precocious beat, making it impossible to obtain a minimum of 4-minute continuous recording, were discarded from the analyses. The time series were detrended, linearly interpolated, resampled at 5 Hz, and subjected to a Partzen window. The power density spectra of HRV, systolic arterial pressure, and diastolic arterial pressure variabilities were then computed over low-frequency (0.04–0.15 Hz) and high-frequency (0.15–0.4 Hz) bands using a fast Fourier transform algorithm and triangular smoothing.

BRS was calculated by cross-spectral analysis (40, 41) between the R-R interval and systolic arterial pressure variabilities in the low-frequency band, provided that the coefficient of coherence was >0.50 and that the phase between variabilities was negative. Data of seven subjects did not meet the coherence and phase criteria but were used to calculate the power spectra of HRV, systolic arterial pressure, and diastolic arterial pressure variabilities. Spectral analyses were performed with CPRS 2.41 software (CardioPulmonary Research Software, Absolute Aliens Ay, Turku, Finland).

Statistical Analyses
Before statistical analyses, the skewed distributions of the measures of HRV, BPV, and BRS were transformed logarithmically. The summary statistics are given as mean (SD). Interrelations between psychological factors and univariate associations between psychological factors and measures of HRV, BPV, and BRS were studied with Pearson’s correlation coefficients. Multivariate associations of psychological factors with the measures of HRV, BPV, and BRS were evaluated with a single linear regression analysis for each dependent variable. In this analysis, age and gender were forced to control their effects, and psychological factors were tested in a stepwise manner. Finally, heart rate and systolic and diastolic blood pressures were forced in the model to evaluate whether the possible associations of psychological factors with dependent variable result from their associations with heart rate or blood pressures. Statistical analyses were performed with SPSS 10.0 software (SPSS Inc., Chicago, IL). p values <0.05 were considered as statistically significant.


   RESULTS
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
 RESULTS
DISCUSSION
 CONCLUSION
 ACKNOWLEDGMENTS
 REFERENCES
 
The demographic characteristics, psychological measures, and measures of HRV, BPV, and BRS of the study subjects are presented in Tables 1 and 2Go. Psychological measures were interrelated. Particularly, symptom dimensions of the BSI-37 were related to each other (correlation coefficients, r, ranging from 0.41 to 0.68). Anxiety and hostility scores of the BSI-37 correlated with anger-out (r = 0.24 and r = 0.41, respectively), state anger (r = 0.45 and r = 0.29), and trait anger (r = 0.37 and r = 0.49) scores of the STAXI. The total score of the TAS-26 correlated with the score of anxiety of the BSI-37 (r = 0.32).


View this table:
[in this window]
[in a new window]
  		TABLE 1. Characteristics and psychological measures of the study subjects
 

View this table:
[in this window]
[in a new window]
  		TABLE 2. Frequency domain measures of HRV, BPV, and BRS
 
Psychological Correlates of HRV
Increased behaviorally expressed anger (anger-out) correlated with increased low-frequency power of HRV (r = 0.18, p = 0.032). None of the psychological factors predicted HRV according to the multivariate regression analyses.

Psychological Correlates of BPV
Higher scores of somatization, depression, anxiety, hostility, phobicity, the general severity index of the BSI-37, and state anger of the STAXI were associated with higher low-frequency power of BPV (range of Pearson’s r from 0.16 to 0.31). According to the multivariate regression analyses, increased anxiety was associated with increased low-frequency power of systolic arterial pressure variability (p = 0.001, model R2 = 0.11) and increased hostility with increased low-frequency power of diastolic arterial pressure variability (p < 0.001, model R2 = 0.09), independently from age, gender, and other psychological factors. Associations between anxiety and the low-frequency power of systolic arterial pressure variability and between hostility and the low-frequency power of diastolic arterial pressure variability remained essentially unchanged after heart rate and systolic and diastolic blood pressures were added to the model (Table 3).


View this table:
[in this window]
[in a new window]
  		TABLE 3. Final multivariate regression models of LF powers of BPV and BRS
 
A higher score of somatization (r = 0.23) and a lower score of anger-in (r = -0.16) were associated with increased high-frequency power of systolic arterial pressure variability. According to the multivariate analysis, reduced anger-in (p = 0.020) and increased hostility (p = 0.033) were associated with increased high-frequency power of systolic arterial pressure variability independently from age, gender, other psychological factors, heart rate, and systolic and diastolic blood pressures. None of the psychological variables was associated with the high-frequency power of diastolic arterial pressure variability.

Psychological Correlates of BRS
Higher scores of somatization, depression, anxiety, hostility, phobicity, and the general severity index of the BSI-37 were associated with reduced BRS (range of Pearson’s r from -0.19 to -0.29). According to the multivariate regression analysis, higher age (p < 0.001), higher anxiety (p < 0.001), and a lower total score of the TAS-26 (p = 0.050) were associated with reduced BRS independently from age, gender, and other psychological factors (model R2 = 0.25). The association between a higher score of anxiety and lower BRS remained unchanged, but the association between the total score of the TAS-26 and BRS disappeared after heart rate and systolic and diastolic blood pressures were added to the model (Table 3).


   DISCUSSION
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
 RESULTS
 DISCUSSION
CONCLUSION
 ACKNOWLEDGMENTS
 REFERENCES
 
Our study demonstrates that, in the middle-aged men and women of the general population, psychological factors are associated with increased BPV and reduced BRS independently of age, gender, blood pressure, and heart rate. The psychological measures correlate strongly with each other. Among them, increased anxiety and hostility seem to be the strongest determinants of increased low-frequency power of BPV and reduced BRS.

Psychological Factors and HRV
The relations of psychological factors to HRV have usually been examined in small case-control studies with patients suffering from various psychiatric disorders (8–11, 19) or in apparently healthy volunteers (12–15). Results from these studies suggest that panic disorder or increased anxiety (8, 11–14, 19) and increased hostility (15) are associated with decreased HRV, especially when measured in upright posture. Results concerning depression are inconsistent (17–19). Although reduced HRV based on 24-hour heart rate recording has been linked to depression in patients with coronary artery disease (17, 18), short-term HRV has not been found to differentiate patients with major depression from their healthy controls (19). Our findings suggest that the low-frequency and high-frequency powers of short-term HRV under supine resting conditions do not reflect symptoms of anxiety, hostility, and depression of middle-aged healthy men and women.

Several factors may explain our negative findings in regard to the association between psychological factors and HRV. We used population-based setup and excluded subjects using antidepressants and neuroleptics known to influence on the autonomic nervous system. Thus, patients with major depression and panic disorder were not included. A population-based setup and exclusion of medicated patients with psychiatric disorders may decrease variability in the psychological measures and thereby dampen the possible associations between HRV, anxiety, hostility, and depression. We measured HRV from short-term recordings acquired under controlled laboratory conditions while subjects were resting in a supine position. However, the effects of psychological symptoms, such as hostility, on HRV may only be revealed in recordings that are sufficiently long to produce transactions between individuals and their environments (15). Posture may also modify results during short-term recordings, as persons with panic disorder or anxiety have been found to have altered HRV only in the standing position and not at supine rest (8, 9, 11, 19).

Psychological Factors and Increased BPV
Anxiety, hostility, and depression have been proposed to be associated with diminished autonomic control of the heart, which may disinhibit pathogenic BPV and thereby increase the risk of coronary artery disease (42). However, the literature of the relations of BPV and psychological factors is limited. Higher anxiety symptom scores were related with increased low-frequency power of BPV in 117 apparently healthy adults recruited from an outpatient clinic (13). In a small study with 25 unmedicated subjects, behaviorally expressed anger was associated with increased low-frequency power of systolic BPV (43). Adolescents with high systolic BPV have been found to be characterized by type A behavior and also by high levels of hostility (44).

We found that a higher score of state anger and higher symptom scores of depression, somatization, anxiety, hostility, and phobicity were related to increased low-frequency power of BPV. Anxiety and hostility were the strongest determinants of increased low-frequency powers of systolic arterial pressure and diastolic arterial pressure variabilities, and they explained BPV over age, gender, heart rate, and blood pressure. Our multivariate models explained only a small fraction of the variation in the low-frequency power of BPV. Thus, the vast majority of the short-term spontaneous variation in the low-frequency power of BPV is explained by other factors not examined in this study. Our findings of increased low-frequency power of BPV in association with increased anxiety and hostility suggest a link between psychological distress and increased sympathetic modulation. Psychological factors were not associated with the high-frequency power of diastolic arterial pressure variability, and the associations between the high-frequency power of systolic arterial pressure and anger-in or hostility were only weak. This finding is logical because the high-frequency power of BPV reflects principally rhythmic changes of intrathoracic pressure owing to respiratory mechanics (30).

Numerous population-based studies suggest a relationship between anxiety and depression and the development of coronary artery disease (45). Some prospective studies relate increased hostility to increased coronary artery disease incidence (46–50), whereas negative findings have also been reported (51, 52). Large-scale prospective studies are needed to explore whether increased low-frequency power of BPV explains increased coronary artery disease risk in association with anxiety and hostility.

Psychological Factors and Reduced BRS
We found that depression, increased anxiety, hostility, phobicity, and the general severity index of the BSI-37 were related with decreased BRS but not with HRV. Anxiety was the strongest psychological determinant of decreased BRS, independently from age, gender, the other psychological factors, heart rate, and blood pressures. Our finding of decreased BRS in association with increased psychological distress is consistent with recent studies. Watkins et al. found that decreased BRS was associated with higher levels of anxiety in healthy volunteers (14) and in subjects with depression (10) or acute myocardial infarction (32). Furthermore, anxiety was not associated with the high-frequency power of HRV (10) or was only modestly associated with reduced respiratory sinus arrhythmia (14). Thus, our study and the previous studies (10, 14) suggest that BRS reflects more sensitively than HRV effects of psychological factors on autonomic nervous function, when the short-term measurements are made at supine rest.

Causality
Because of the cross-sectional nature of our study, we cannot draw definitive conclusions concerning the causality between psychological factors, BPV, and BRS. Previous studies have shown that parasympathetic blockade with atropine increases BPV (53). According to experimental animal studies, removal of baroreceptor control by lesions of the nucleus tractus solitarius increases blood pressure as well as blood pressure reactivity to behavioral, emotional, and environmental stimuli (54–56). Thus, decreased baroreceptor control of the heart in association with increased anxiety and hostility may reflect decreased vagal flow to the heart, which in turn may result to increased BPV through increased sympathovagal balance. Alternatively, these psychological stressors may primarily increase BPV, which in turn may lead to increased baroreceptor loading and decreased BRS. Further studies are needed to explore the mechanisms by which psychological factors are associated with decreased BRS and increased BPV.

Limitations
Effects of psychological factors on autonomic activity may depend on age (15). Thus, our findings may be limited to subjects in an age group of 35 to 64 years. A short-term recording in supine rest may lead to an underestimation of the relations between psychological factors and HRV. The confounding effects of antidepressants and neuroleptics on autonomic nervous function were controlled by excluding subjects using such medications. This procedure decreases variability in depression scores among the study subjects and may thus dampen the association between depression, HRV, BPV, and BRS.


   CONCLUSION
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
 RESULTS
 DISCUSSION
 CONCLUSION
ACKNOWLEDGMENTS
 REFERENCES
 
Psychological factors, particularly increased hostility and anxiety, are related to reduced BRS and increased low-frequency power of BPV. Our findings suggest that decreased parasympathetic outflow to the heart and increased sympathetic predominance may at least partly explain increased cardiovascular morbidity and mortality in association with increased anxiety and hostility. However, further studies are needed to test this hypothesis and to explore the exact mechanisms by which psychological factors are associated with decreased BRS and increased BPV.


   ACKNOWLEDGMENTS
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
 RESULTS
 DISCUSSION
 CONCLUSION
 ACKNOWLEDGMENTS
REFERENCES
 
Supported in part by grants from the Research Foundation of Orion Corporation and from Turku University Foundation.

Received for publication June 21, 2002.


   REFERENCES
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
 RESULTS
 DISCUSSION
 CONCLUSION
 ACKNOWLEDGMENTS
 REFERENCES
 

  1. Task Force of the European Society of Cardiology and the North American Society of Pacing and Electrophysiology. Heart rate variability: standards of measurement, physiological interpretation, and clinical use. Eur Heart J 1996; 17: 354–81.[Free Full Text]
  2. Tsuji H, Venditti FJ, Manders ES, Evans JC, Larson MG, Feldman CL, Levy D. Reduced heart rate variability and mortality risk in an elderly cohort: the Framingham Heart Study. Circulation 1994; 90: 878–83.[Abstract/Free Full Text]
  3. Dekker JM, Schouten EG, Klootwijk P, Pool J, Swenne CA, Kromhout D. Heart rate variability from short electrocardiographic recordings predicts mortality from all causes in middle-aged and elderly men: the Zutphen study. Am J Epidemiol 1997; 145: 899–908.[Abstract/Free Full Text]
  4. Dekker JM, Crow RS, Folsom AR, Hannan PJ, Liao D, Swenne CA, Schouten EG. Low heart rate variability in a 2-minute rhythm strip predicts risk of coronary heart disease and mortality from several causes: the ARIC study. Atherosclerosis Risk In Communities. Circulation 2000; 102: 1239–44.[Abstract/Free Full Text]
  5. Tsuji H, Larson MG, Venditti FJ, Manders ES, Evans JC, Feldman CL, Levy D. Impact of reduced heart rate variability on risk for cardiac events: the Framingham Heart Study. Circulation 1996; 94: 2850–5.[Abstract/Free Full Text]
  6. Liao D, Cai J, Rosamond WD, Barnes RW, Hutchinson RG, Whitsel EA, Rautaharju P, Heiss G. Cardiac autonomic function and incident coronary heart disease: a population-based case-cohort study. Atherosclerosis Risk in Communities Study. Am J Epidemiol 1997; 145: 696–706.[Abstract/Free Full Text]
  7. Asmundson GJ, Stein MB. Vagal attenuation in panic disorder: an assessment of parasympathetic nervous system function and subjective reactivity to respiratory manipulations. Psychosom Med 1994; 56: 187–93.[Abstract/Free Full Text]
  8. Middleton HC, Ashby M, Robbins TW. Reduced plasma noradrenaline and abnormal heart rate variability in resting panic disorder patients. Biol Psychiatry 1994; 36: 847–9.[CrossRef][Medline]
  9. Tulen JHM, Bruijn JA, de Man KJ, van der Velden E, Pepplinkhizen L, Man in ’t Veld AJ. Anxiety and autonomic regulation in major depressive disorder: an exploratory study. J Affect Disord 1996; 40: 61–71.[CrossRef][Medline]
  10. Watkins LL, Grossman P, Krishnan R, Blumenthal JA. Anxiety reduces baroreflex cardiac control in older adults with major depression. Psychosom Med 1999; 61: 334–40.[Abstract/Free Full Text]
  11. Yeragani VK, Pohl R, Berger R, Balon R, Ramesh C, Glitz D, Srinivasan K, Weinberg P. Decreased heart rate variability in panic disorder patients: a study of power-spectral analysis of heart rate. Psychiatry Res 1993; 46: 89–103.[CrossRef][Medline]
  12. Kawachi I, Sparrow D, Vokonas PS, Weiss ST. Decreased heart rate variability in men with phobic anxiety (data form the normative aging study). Am J Cardiol 1995; 75: 882–5.[CrossRef][Medline]
  13. Piccirillo G, Elvira S, Bucca C, Viola E, Cacciafesta M, Marigliano V. Abnormal passive head-up tilt test in subjects with symptoms of anxiety power spectral analysis study of heart rate and blood pressure. Int J Cardiol 1997; 60: 121–31.[CrossRef][Medline]
  14. Watkins LL, Grossman P, Krishnan R, Sherwood A. Anxiety and vagal control of heart rate. Psychosom Med 1998; 60: 498–502.[Abstract/Free Full Text]
  15. Sloan RP, Shapiro PA, Bigger JT, Bagiella E, Steinman RC, Gorman JM. Cardiac autonomic control and hostility in healthy subjects. Am J Cardiol 1994; 74: 298–300.[CrossRef][Medline]
  16. Fukunishi I, Sei H, Morita Y, Rahe RH. Sympathetic activity in alexithymics with mother’s low care. J Psychosom Res 1999; 46: 579–89.[CrossRef][Medline]
  17. Krittayaphong R, Cascio WE, Light KC, Sheffield D, Golden RN, Finkel JB, Glekas G, Koch GC, Sheps DS. Heart rate variability in patients with coronary artery disease: differences in patients with higher and lower depression scores. Psychosom Med 1997; 59: 231–5.[Abstract/Free Full Text]
  18. Carney RM, Saunders RD, Freedland KE, Stein P, Rich MW, Jaffe AS. Association of depression with reduced heart rate variability in coronary artery disease. Am J Cardiol 1995; 76: 562–4.[CrossRef][Medline]
  19. Yeragani VK, Pohl R, Balon R, Ramesh C, Glitz D, Jung I, Sherwood P. Heart rate variability in patients with major depression. Psychiatr Res 1991; 37: 35–46.[CrossRef][Medline]
  20. Lehofer M, Moser M, Hoehn-Saric R, McLeod D, Liebmann P, Drnovsek B, Egner S, Hildebrandt G, Zapotoczky HG. Major depression and cardiac autonomic control. Biol Psychiatry 1997; 42: 914–9.[CrossRef][Medline]
  21. Kahn HA, Medalie JH, Neufeld HN, Riss E, Goldbourt U. The incidence of hypertension and associated factors: the Israel Ischemic Heart Disease Study. Am Heart J 1972; 84: 171–82.[CrossRef][Medline]
  22. Perini C, Müller FB, Bühler FR. Suppressed aggression accelerates early development of essential hypertension. J Hypertens 1991; 9: 499–503.[CrossRef][Medline]
  23. Todarello O, Taylor GJ, Parker JDA, Fanelli M. Alexithymia in essential hypertension and psychiatric outpatients: a comparative study. J Psychosom Res 1995; 39: 987–94.[CrossRef][Medline]
  24. Jula A, Salminen JK, Saarijärvi S. Alexithymia: a facet of essential hypertension. Hypertension 1999; 33: 1057–61.[Abstract/Free Full Text]
  25. Markovitz JH, Matthews KA, Kannel WB, Cobb JL, D’Agostino RB. Psychological predictors of hypertension in the Framingham Study: is there tension in hypertension? JAMA 1993; 270: 2439–43.[Abstract]
  26. Jonas BS, Franks P, Ingram DD. Are symptoms of anxiety and depression risk factors for hypertension? Longitudinal evidence from the National Health and Nutrition Examination Survey I Epidemiologic Follow-up Study. Arch Fam Med 1997; 6: 43–9.[Abstract]
  27. Brown DE, James GD, Nordloh L. Comparison of factors affecting daily variation of blood pressure in Filipino-American and Caucasian nurses in Hawaii. Am J Phys Anthropol 1998; 106: 373–83.[CrossRef][Medline]
  28. Kikuya M, Hozawa A, Ohokubo T, Tsuji I, Michimata M, Matsubara M, Ota M, Nagai K, Araki T, Satoh H, Ito S, Hisamichi S, Imai Y. Prognostic significance of blood pressure and heart rate variabilities: the Ohasama study. Hypertension 2000; 36: 901–6.[Abstract/Free Full Text]
  29. Schächinger H, Weinbacher M, Kiss A, Ritz R, Langewitz W. Cardiovascular indices of peripheral and central sympathetic activation. Psychosom Med 2001; 63: 788–96.[Abstract/Free Full Text]
  30. Zhang R, Iwasaki K, Zuckerman JH, Behbehani K, Crandall CG, Levine BD. Mechanism of blood pressure and R-R variability: insights from ganglion blockade in humans. J Physiol 2002; 543: 337–48.[Abstract/Free Full Text]
  31. La Rovere MT, Bigger JT, Marcus FI, Andrea M, Schwartz PJ. Baroreflex sensitivity and heart-rate variability in prediction of total cardiac mortality after myocardial infarction: ATRAMI investigators. Lancet 1998; 351: 478–84.[CrossRef][Medline]
  32. Watkins LL, Blumenthal JA, Carney RM. Association of anxiety with reduced baroreflex cardiac control in patients after acute myocardial infarction. Am Heart J 2002; 143: 460–6.[CrossRef][Medline]
  33. Derogatis LR, Melisaratos N. The brief symptom inventory: an introductory report. Psychol Med 1983; 13: 595–605.[Medline]
  34. Spielberger CD. State-Trait Anger Inventory, Research edition, professional manual. Odessa, FL: Psychological Assessment Resources; 1986.
  35. Taylor GJ, Ryan DB, Bagby RM. Toward the development of a new self-report alexithymia scale. Psychother Psychosom 1985; 44: 191–9.[Medline]
  36. Kronholm E. Sleep and daytime vigilance: a psychophysiological community study [in Finnish, with an English summary]. Turku, Finland: Social Insurance Institution ML:121; 1993.
  37. American Society of Hypertension. ASH public policy position paper: recommendations for routine blood pressure measurement by indirect cuff sphygmomanometry. Am J Hypertens 1992; 5: 207–9.[Medline]
  38. Omboni S, Parati G, Frattola A, Mutti E, Di Rienzo M, Castiglioni P, Mancia G. Spectral and sequence analysis of finger blood pressure variability: comparison with analysis of intra-arterial recordings. Hypertension 1993; 22: 26–33.[Abstract/Free Full Text]
  39. Imholtz BPM, Wieling W, Montfrans GA, Wesseling KH. Fifteen years experience with finger arterial pressure monitoring: assessment of the technology. Cardiovasc Res 1998; 38: 605–16.[Abstract/Free Full Text]
  40. Robbe H, Mulder L, Rüddel H, Langewitz W, Veldman J, Mulder G. Assessment of baroreceptor reflex sensitivity by means of spectral analysis. Hypertension 1987; 10: 538–43.[Abstract/Free Full Text]
  41. Airaksinen KEJ, Huikuri HV, Huhti L, Kuusela TA, Tahvanainen KUO, Tulppo M, Mäkikallio T, Eckberg DL. Effects of noradrenaline on human vagal baroreflexes. Ann Med 2001; 33: 193–200.[Medline]
  42. Sloan RP, Shapiro PA, Bagiella E, Myers MM, Gorman JM. Cardiac autonomic control buffers blood pressure variability responses to challenge: a psychophysiologic model of coronary artery disease. Psychosom Med 1999; 61: 58–68.[Abstract/Free Full Text]
  43. Laude D, Girard A, Consoli S, Mounier-Vehier C, Elghozi JL. Anger expression and cardiovascular reactivity to mental stress: a spectral analysis approach. Clin Exp Hypertens 1997; 19: 901–11.
  44. Siegel JM, Matthews KA, Leitch CJ. Blood pressure variability and the type A behavior pattern in adolescence. J Psychosom Res 1983; 27: 265–72.[CrossRef][Medline]
  45. Januzzi JL, Stern TA, Pasternak RC, DeSanctis RW. The influence of anxiety and depression on outcomes of patients with coronary artery disease. Arch Intern Med 2000; 160: 1913–21.[Free Full Text]
  46. Haynes SG, Feinleib M, Kannel WB. The relationship of psychosocial factors to coronary heart disease in the Framingham Study: III. Eight-year incidence of coronary heart disease. Am J Epidemiol 1980; 111: 37–58.[Abstract/Free Full Text]
  47. Barefoot JC, Dahlstrom WG, Williams RB. Hostility, CHD incidence, and total mortality: a 25-year follow-up study of 255 physicians. Psychosom Med 1983; 45: 59–63.[Abstract/Free Full Text]
  48. Shekelle RB, Gale M, Ostfeld AM, Paul O. Hostility, risk of coronary heart disease and mortality. Psychosom Med 1983; 45: 109–14.[Abstract/Free Full Text]
  49. Barefoot JC, Larsen S, von der Lieth L, Schroll M. Hostility, incidence of acute myocardial infarction, and mortality in a sample of older Danish men and women. Am J Epidemiol 1995; 142: 477–84.[Abstract/Free Full Text]
  50. Everson SA, Kauhanen J, Kaplan GA, Goldberg DE, Julkunen J, Tuo-milehto J, Salonen JT. Hostility and increased risk of mortality and acute myocardial infarction: the mediating role of behavioral risk factors. Am J Epidemiol 1997; 146: 142–52.[Abstract/Free Full Text]
  51. McCranie EW, Watkins LO, Brandsma JM, Sisson BD. Hostility, coronary heart disease (CHD) incidence, and total mortality: lack of association in a 25-year follow-up study of 478 physicians. J Behav Med 1986; 9: 119–25.[CrossRef][Medline]
  52. Koskenvuo M, Kaprio J, Rose RJ, Kesäniemi A, Sarna S, Heikkilä K, Langinvainio H. Hostility as a risk factor for mortality and ischemic heart disease in men. Psychosom Med 1988; 50: 330–40.[Abstract/Free Full Text]
  53. Toska K, Eriksen M. Respiration-synchronous fluctuations in stroke volume, heart rate and arterial pressure in humans. J Physiol 1993; 472: 501–12.[Abstract/Free Full Text]
  54. Nathan MA, Reis DJ. Chronic labile hypertension produced by lesions of the nucleus tractus solitarii in the cat. Circ Res 1977; 40: 72–81.[Abstract/Free Full Text]
  55. Nathan MA, Tucker LW, Serverini WH, Reis DJ. Enhancement of conditioned arterial pressure responses in cats after brainstem lesions. Science 1978; 201: 71–3.[Abstract/Free Full Text]
  56. Ferrario CM, Barnes KL, Bohonek S. Neurogenic hypertension produced by lesions of the nucleus tractus solitarii alone or with sinoaortic denervation in the dog. Hypertension 1981; 3 (6 Pt 2): II112–8.



This article has been cited by other articles:


Home page
 Psychosom. Med.Home page
A. K. Mattila, E. Kronholm, A. Jula, J. K. Salminen, A.-M. Koivisto, R.-L. Mielonen, and M. Joukamaa
Alexithymia and Somatization in General Population
Psychosom Med, July 1, 2008; 70(6): 716 - 722.
[Abstract] [Full Text] [PDF]

Home page
 Psychosom. Med.Home page
M. E. Bleil, P. J. Gianaros, J. R. Jennings, J. D. Flory, and S. B. Manuck
Trait Negative Affect: Toward an Integrated Model of Understanding Psychological Risk for Impairment in Cardiac Autonomic Function
Psychosom Med, April 1, 2008; 70(3): 328 - 337.
[Abstract] [Full Text] [PDF]

Home page
 Psychosom. Med.Home page
A. K. Derrickson, J. R. Baber, and A. Agarwal
A CASE OF ACUTE STRESS-INDUCED VENTRICULAR TACHYCARDIA
Psychosom Med, October 1, 2007; 69(8): 825 - 825.
[Full Text] [PDF]

Home page
 Psychosom. Med.Home page
T. Ritz and B. Dahme
Implementation and Interpretation of Respiratory Sinus Arrhythmia Measures in Psychosomatic Medicine: Practice Against Better Evidence?
Psychosom Med, July 1, 2006; 68(4): 617 - 627.
[Abstract] [Full Text] [PDF]

Home page
 Occup. Environ. Med.Home page
M Elovainio, M Kivimaki, S Puttonen, H Lindholm, T Pohjonen, and T Sinervo
Organisational injustice and impaired cardiovascular regulation among female employees
Occup. Environ. Med., February 1, 2006; 63(2): 141 - 144.
[Abstract] [Full Text] [PDF]

Home page
 Biol Res NursHome page
M. J. Rice and K. Records
Cardiac response rate variability in physically abused women of childbearing age.
Biol Res Nurs, January 1, 2006; 7(3): 204 - 213.
[Abstract] [PDF]

Home page
 Psychosom. Med.Home page
M. E. Alvarenga, J. C. Richards, G. Lambert, and M. D. Esler
Psychophysiological Mechanisms in Panic Disorder: A Correlative Analysis of Noradrenaline Spillover, Neuronal Noradrenaline Reuptake, Power Spectral Analysis of Heart Rate Variability, and Psychological Variables
Psychosom Med, January 1, 2006; 68(1): 8 - 16.
[Abstract] [Full Text] [PDF]

Home page
 Psychosom. Med.Home page
M. M. Burg, R. Lampert, T. Joska, W. Batsford, and D. Jain
Psychological Traits and Emotion-Triggering of ICD Shock-Terminated Arrhythmias
Psychosom Med, November 1, 2004; 66(6): 898 - 902.
[Abstract] [Full Text] [PDF]

This Article
Right arrow Abstract Freely available
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
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Virtanen, R.
Right arrow Articles by Airaksinen, J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Virtanen, R.
Right arrow Articles by Airaksinen, J.
Related Collections
Right arrow Parasympathetic Nervous System
Right arrow Sympathetic Nervous System
Right arrow Blood Pressure
Right arrow Health Psychology
Right arrow Personality

HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS