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A Meta-Analytic Examination of Basal Cardiovascular Activity in Posttraumatic Stress Disorder

From the National Center for PTSD–Behavioral Science Division, Boston VAMC, and Boston University School of Medicine, Boston, Massachusetts.

Address reprint requests to: Todd C. Buckley, PhD, National Center for PTSD (116B-2), VA Boston Healthcare System, 150 South Huntington Avenue, Boston, MA 02131-4817. Email: Todd.Buckley{at}med.va.gov

	ABSTRACT

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OBJECTIVE: The objective of this meta-analytic study was to determine whether individuals with posttraumatic stress disorder (PTSD) have higher levels of basal cardiovascular activity relative to comparable groups of individuals without PTSD.

METHODS: Meta-analytic data methods were applied to 34 studies that gathered indicators of basal cardiovascular activity including: heart rate (HR), systolic blood pressure, and diastolic blood pressure on subjects diagnosed with PTSD and two types of comparison groups. In total, cardiovascular measures were analyzed for 2670 subjects across all studies.

RESULTS: Results indicate that individuals with a current PTSD diagnosis have higher resting HR relative to both trauma-exposed individuals without a PTSD diagnosis and non–trauma-exposed individuals. The results also suggest that PTSD is associated with elevations in blood pressure; however, the effect sizes were smaller in magnitude than those obtained for heart rate. A subset analysis revealed that the effect sizes for comparisons on basal HR were greatest in studies with the most chronic PTSD samples.

CONCLUSION: The meta-analysis supports previous qualitative reviews, finding a positive association between PTSD and basal cardiovascular activity. The discussion addresses possible mechanisms of action and the health-related implications of these findings.

Key Words: posttraumatic stress disorder • cardiovascular • heart rate • blood pressure

Abbreviations: PTSD = posttraumatic stress disorder; HR = heart rate; RR = respiration rate; EEG = electroencephalograph; SBP = systolic blood pressure; DBP = diastolic blood pressure; CI = confidence interval.

	INTRODUCTION

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Since 1980, the formal diagnostic criteria for PTSD have included symptoms of excessive autonomic nervous system arousal (1), with more recent versions of the DSM nosology adding, "physiological reactivity to trauma related cues" (2). Even before 1980, experts on traumatic stress recognized that individuals exposed to the horrors of combat or other human atrocity (eg, violent sexual assault) often experienced marked autonomic arousal long after the traumatic experience. Conditions known as irritable heart, shellshock, and war neurosis were all characterized by elevated autonomic arousal as part of the symptom profile (3).

Dobbs and Wilson (4) provided the first laboratory-based demonstration of this phenomenon when they examined HR, RR, and EEG responses of World War II and Korean War combat veterans to auditory presentations that simulated combat sounds. Although the majority of the veterans found the protocol too aversive to complete, those who did showed both higher baseline levels of HR and RR and greater magnitude of cardiac response to the auditory stimuli relative to the comparison group of university students. This study showed that humans exposed to strong aversive conditioning events during combat (ie, traumatic stress) produce patterns of autonomic reactivity like those seen in research on fear acquisition with infrahumans—a notion that has been increasingly accepted in recent years (5).

The past 2 decades have witnessed a tremendous increase in research examining both phasic and tonic changes in the autonomic profile of individuals exposed to severe trauma, especially those subsequently diagnosed with PTSD (6). A corresponding increase in the precision of physiological measurement has resulted in a large number of high-quality laboratory-based studies that have examined the autonomic responses of patients with PTSD (7, 8).

These studies have used two primary laboratory paradigms. The first, often referred to as the cue-reactivity paradigm, involves assessment of physiological response to narrative descriptions of trauma (9), pictorial representations (7), or auditory representations of traumatic events (10). The second method, the acoustic startle probe paradigm (11), examines physiological responses evoked by loud and unexpected/unpredictable acoustic stimuli. Both paradigms focus on the direction and magnitude of reactivity of various physiological responses—that is, on phasic changes in physiology on exposure to specific stimuli.

Another important physiological feature of PTSD was identified by Blanchard (12), who noted apparent basal elevations in cardiovascular activity, particularly heart rate, shown by PTSD groups relative to comparison groups during the resting baseline periods of such studies. Blanchard proposed that PTSD might be a risk factor for hypertension or other cardiovascular problems, in light of evidence that links stress-induced cardiovascular reactivity with changes in basal cardiovascular levels (13, 14).

Three hypotheses have been advanced to explain why PTSD may be associated with elevated basal cardiovascular activity. First, elevations at baseline may reflect systemic changes in cardiovascular function that result from repeated cardiovascular responses to stress (13, 14). Indeed, numerous studies show that, relative to traumatized subjects without PTSD, those with PTSD show exaggerated cardiovascular responses to trauma reminiscent cues in laboratory challenge studies (6). It is likely that these cardiovascular responses to trauma cues are mediated by the sympathetic branch of the autonomic nervous system, because individuals diagnosed with PTSD show elevated catecholamine levels, relative to comparison subjects without PTSD, after exposure to stressors (15, 16). Such repeated autonomic reactivity may produce structural and/or functional changes in the cardiovascular system. For example, chronic, stress-related sympathetic activation has been linked to down-regulation of beta-adrenergic receptors in the heart and peripheral vasculature, which increases peripheral vascular resistance and can ultimately lead to an increase in blood pressure (17, 18).

The second hypothesis attributes baseline differences in cardiovascular activity to either emotional priming or apprehension. Priming can occur when exposure to trauma-relevant cues takes place just before physiological assessment and lowers the threshold for subsequent responding. Anticipatory anxiety is a state of arousal shown by participants awaiting exposure to aversive stimuli in cue-reactivity studies (19). Some investigations have used ambulatory monitoring or other procedural maneuvers to reduce the likelihood of either trauma-specific emotional priming or anticipatory anxiety. Findings from these studies are mixed, with some demonstrating elevated basal levels of heart rate and blood pressure in subjects with PTSD, relative to control groups (20–22) and others not doing so (23–25).

A third hypothesis proposes that the association between PTSD and basal cardiovascular activity is mediated through variables known to have direct effects on cardiovascular health. For example, it is relatively well documented that alcohol consumption of >3 drinks per day is associated with increased blood pressure and heart rate, as well as increased mortality from coronary artery disease and stroke (26–28). PTSD is associated with higher rates of alcohol abuse/dependence (29), with especially high rates occurring in some high-risk trauma populations such as Vietnam veterans (30). PTSD also is associated with elevated rates of smoking (31), which is known to adversely affect cardiovascular health. These influences and others like them (eg, lower aerobic fitness) point to ways in which PTSD can have an indirect impact on basal cardiovascular levels.

To date, no meta-analytic examination of baseline cardiovascular indices in persons with PTSD has been conducted to quantify the magnitude of baseline differences. Therefore, we sought to address three questions with this set of meta-analyses. (1) Are observed differences in basal cardiovascular activity found between PTSD and non-PTSD comparison samples statistically reliable? (2) If such differences are reliable, do they vary in relation to chronicity of the disorder? This question aims to addresses the hypothesis that repeated cardiovascular reactions to stress over long periods of time can have an adverse impact on cardiovascular health. (3) Are differences in baseline cardiovascular levels dependent on emotional priming or anticipatory anxiety? This final question allows us to examine whether certain study methodologies result in artificially high basal cardiovascular measurement in PTSD groups because of emotional priming or anticipatory anxiety. Our meta-analysis was not able to address the potential contribution of other specific health habits on effect size outcome, because the individual studies did not provide data on which such information could be coded.

	METHODS

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Candidate studies were identified by means of PsycLit, Medline, and PILOTS database searches with the use of the following terms: PTSD, along with one of the following: heart rate, blood pressure, physiology, or psychophysiology. In addition, an issue-by-issue search was conducted on 10 journals that often publish empirical articles with content relevant to the current analyses. The literature search was conducted from 1980 forward, that being the first year PTSD was recognized in the psychiatric nomenclature (1). The reference sections of relevant review articles and identified empirical articles also were examined for potential candidate studies. Studies were included in the meta-analyses if they met all of the following criteria. (1) There was at least one dependent variable in the study that was a measure of resting heart rate, SBP, or DBP. (2) The physiological measures were collected by use of reliable devices and methods that corresponded to published recording guidelines (32). (3) Either the study report contained enough information such that group means and standard deviations on the dependent variables could be directly determined, calculated from test statistics (33), or relevant means and standard deviations could be obtained from study authors. (4) There was at least one analysis comparing a PTSD-diagnosed group with either a trauma-exposed non-PTSD group or a nontrauma control group (which were comparable in age and gender). (5) Diagnosis for the groups was established via a structured or clinical interview that corresponded to formal diagnostic criteria from DSM-III, DSM-IIIR, or DSM-IV (1, 2, 34). The most common interview formats were the Structured Clinical Interview for DSM-IV (35), The Clinician Administered PTSD Scale (36), and the Anxiety Disorder Interview Schedule (37).

The 34 studies selected for the meta-analyses had an average sample size of 82 and included 20 laboratory-based cue-reactivity studies, 6 acoustic startle studies, and 8 nonreactivity studies (eg, ambulatory blood pressure studies or medical clinic basal cardiovascular examinations). Because the majority of phasic reactivity studies to date have been conducted with combat veterans, 59% of the studies in our analysis had exclusively male samples. The length of time since trauma for the PTSD groups ranged from a low of 1 month to a high of >20 years. Additional procedural and sample characteristics, as well as effect sizes for individual studies, are summarized in Table 1. All studies had age- and gender-comparable (relative to the PTSD samples) control groups for comparison purposes.

	RESULTS

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The first step in the analysis was an examination of overall mean differences between the PTSD group and both comparison groups. Table 2 presents both unweighted and weighted effect sizes (with associated 95% CI), which show that PTSD is associated with elevated basal levels of heart rate and diastolic blood pressure relative to the two comparison groups. The results for SBP were slightly different, with the PTSD groups showing elevated basal levels relative to the nontrauma comparison group but not the traumatized non-PTSD comparison group. As suggested by meta-analytic methodologists (40), our distributions of effect sizes were examined for outliers. For 5 of the 6 comparisons that appear in Table 2 (excepting the comparison between PTSD and trauma-exposed non-PTSD on DBP), the amount of variance in the data set explained by sampling error was >75%, and the corresponding tests of homogeneity were nonsignificant, which suggested that the data set was sufficiently homogenous to conduct a meta-analysis (ie, no outlying values had undue influence on the effect size analyses; 40). The average amount of variance explained by sampling error across the six comparisons was 86%.

The comparison between the PTSD samples <8 years posttrauma and age-comparable trauma-exposed non-PTSD samples produced statistically significant unweighted (d = 0.24) and weighted effects (d = 0.23, 95% CI = 0.04–0.43) across 9 studies (409 subjects). The same effect size comparisons for the PTSD samples >12 years posttrauma were larger in magnitude (unweighted d = 0.53, weighted d = 0.39, 95% CI = 0.29–0.49) and were statistically significant across 17 studies (1802 subjects). The amount of variance in the underlying data for these subset analyses explained by sampling error was 90% and 82% respectively, which suggests sufficient homogeneity of effect size across studies (40).

Similar analyses based on the distinction between PTSD samples along the chronicity continuum were also conducted with age-comparable nontrauma control groups. For the PTSD sample <8 years posttrauma vs. nontrauma control group comparison, the unweighted (d = 0.46) and weighted effects (d = 0.32, 95% CI = 0.07–0.58) were statistically significant (5 studies with 247 subjects). Repeating this comparison with the PTSD samples >12 years posttrauma revealed a larger weighted effect size (unweighted d = 0.44, weighted d = 0.52, 95% CI = 0.22–0.82; 6 studies with 178 subjects). The amount of variance in the underlying data for these subset analyses explained by sampling error was 91% and 100% respectively, which suggests sufficient homogeneity of effect size across studies (40).

The third set of analyses controlled for the potential influences of both emotional priming and anticipatory anxiety by using only studies that did not include either PTSD diagnostic assessment or other study-related trauma reminders within the 48 hours preceding the physiological assessment or study procedures involving exposure to trauma-related aversive stimuli after basal measurement. Studies selected for this secondary meta-analysis have been indicated with double asterisks in the Reference section.¹ Again, analysis was limited to heart rate data because too few studies with blood pressure measures fit these criteria.

Relative to trauma-exposed non-PTSD samples, those with PTSD continued to show elevated HR in this subset of 7 studies containing 415 subjects (unweighted d = 0.33, weighted d = 0.26, 95% CI for weighted d = 0.06–0.46). The comparison to the non–trauma-exposed control samples involved 5 studies with 150 subjects and also revealed higher resting HR for the PTSD samples (unweighted d = 0.53, weighted d = 0.60, 95% CI for weighted d = 0.26–0.93). The amount of variance in these two analyses attributed to sampling error was 70% and 79%, respectively. Again, the corresponding tests of homogeneity were nonsignificant, indicating sufficient homogeneity for a meta-analytic examination (40).

In order to convey the distribution of cardiovascular measures across groups, we have provided a graphical representation of the group mean values for each individual study on the heart rate and blood pressure variables in Figures 1 and 2, respectively. It is important to note that some studies only reported test statistics (eg, F ratios and degrees of freedom), without group mean data for the diagnostic groups in question. Thus, the number of data points that appear in the graphs is slightly lower than the number of data points that comprised the studies which went into the data analysis. The graphs do however, represent the vast majority of the studies and nicely display the shapes of the distributions of data.

View larger version (8K): [in this window] [in a new window]   Fig. 1. Individual study group mean values for heart rate as a function of diagnostic group.

View larger version (9K): [in this window] [in a new window]   Fig. 2. Individual study group mean values for systolic and diastolic blood pressure as a function of diagnostic group

	DISCUSSION

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The second meta-analysis indicates that the effect size is larger for comparisons of basal HR involving the most chronic PTSD samples. Although our analysis does not allow for causal inferences, it is worthy to note that this pattern is consistent with the cardiovascular reactivity hypothesis whereby the association between PTSD and elevated basal cardiovascular activity is a result of cardiovascular adaptation to repeated stress responses over many years.

The results of the third meta-analysis are not entirely consistent with the hypothesis that that PTSD-related elevation in basal cardiovascular activity is attributable to anticipatory anxiety and/or emotional priming that is often present in laboratory studies of cue-reactivity. The HR difference for this subanalysis were of smaller magnitude than for the omnibus analysis but were still consistent with the general finding of higher resting HR for PTSD groups relative to non-PTSD groups. Although we excluded studies that involved exposure to explicit trauma-related threat cues, it is possible that PTSD samples are more reactive to a variety of stressors, which could also influence the baseline measures. Indeed, there is preliminary evidence that PTSD samples may be more reactive to seemingly "neutral" demands (ie, demands without explicit threat cues related to traumatic experiences; Ref. 41).

Most subjects were in the normotensive range, even though the effect size analyses show that the PTSD samples have greater basal blood pressure than the comparison groups. The preponderance of nonpathologic levels is at least partially attributable to selection criteria applied by the individual studies, which typically excluded individuals taking hypertensive medications (eg, beta-adrenergic blocking agents). The likely impact of this medication exclusion is selective enrollment of subjects with the lowest basal levels of both heart rate and blood pressure. This sampling bias complicates interpretation of PTSD-related elevations in basal cardiovascular activity (eg, 5 mm Hg difference in DBP) as a substantive health risk. It is apparent however, that an elevation of 5 mm Hg in DBP in hypertensive populations does constitute a health risk, given literature reviews that conclude that long-term DBP elevations of this magnitude resulted in increased probability of stroke and coronary heart disease in prospectively studied hypertensive samples (42). Furthermore, a recent large-scale study found that PTSD was associated with an increased risk (relative to a comparable group of veterans without PTSD) of myocardial infarction and atrioventricular conduction problems in a cohort of prospectively followed combat veterans (43). For these reasons, the effect of PTSD on basal cardiovascular activity in the hypertensive spectrum is especially worthy of further exploration.

The elevated HR found in PTSD samples is also worthy of further study, given both infrahuman and human research on cardiac reactivity to stress, which shows that repeated phasic increases in cardiac activity and sustained elevated HR as a function of chronic stress can facilitate atherosclerotic buildup and contribute to coronary artery disease (13, 44). Also, several large-scale cohort studies have found higher resting heart rate to be positively associated with early mortality from cardiovascular diseases. For example, the Chicago Heart Association Detection Project prospectively followed thousands of study participants and found such an association in both men and women (45). Although not all studies support such an association (46), the majority of studies that have examined this issue have (45).

If repeated cardiovascular reactivity to stress accounts for the relationship between PTSD and elevated basal cardiovascular activity, one would expect the probability of HR and blood pressure elevations to increase along with the chronicity of PTSD because of functional and/or structural changes in the cardiovascular system due to repeated stress that occurs over long periods of time (47). Our results are partially consistent with this hypothesis, in that studies with the most chronic PTSD samples tended to show the largest differences in basal heart rate relative to trauma-exposed comparison samples. Unfortunately, we could not address this question with analyses on blood pressure measures. Examination of Table 1 reveals that the most chronic samples were often exclusively men, relative to the less chronic samples, which more often included both genders or all women. Thus, it may be tempting to attribute our chronicity findings to a gender confound. However, women tend to have higher resting heart rates than men (48) and, therefore, the fact that more male samples were in the most chronic samples would run counter to our noted effects.

Future investigations of the relationship between PTSD and basal cardiovascular functioning would benefit from less restrictive sampling so that more variables known to affect cardiovascular functioning can be measured. For example, it is well documented that PTSD is associated with high rates of substance use involving agents known to influence cardiovascular functioning (29, 31). Unfortunately, as was noted earlier, the range of potential mediating variables was restricted because most of the studies contributing to the meta-analysis excluded individuals on the basis of substance use. In addition, smoking, body mass, and aerobic fitness level have not been routinely assessed, so important indicators of health behavior were not available for our analyses. It is also the case that the extant research has examined fairly "gender-specific" traumas. Specifically, the combat studies have included exclusively male samples, whereas the rape survivor studies have examined exclusively female samples. Thus, examination of the effects of gender and trauma types on such outcomes is not possible, given the gender by trauma confound. More research on traumas proportionally common to both genders (eg, motor vehicle accidents; Ref. 49) is needed to address these important questions.

By including the aforementioned measures in future research, multivariate procedures such as structural equation modeling (50) might then be used to evaluate the contribution of PTSD as a risk factor for conditions such as hypertension in the context of a multivariate model that accounts for other well-known risk factors for cardiovascular problems. An advantage of that type of analysis is that it allows for concurrent examination of direct, mediating, and moderating effects of PTSD on cardiovascular functioning such as those outlined in the present article. Longitudinal designs that follow patients diagnosed with acute PTSD and assess the covariation between PTSD status and basal cardiovascular functioning would also be an area worthy of investigation. To date, no such comprehensive studies have been conducted. Future investigations might also use ambulatory blood pressure monitoring, which is a fairly common methodology used in cardiovascular research but has not been used frequently with PTSD samples (22). The use of such methodology will allow for more accurate assessment of basal heart rate and blood pressure because it rules out the potential confounds of anticipatory anxiety and emotional priming.

	NOTES

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¹References marked with a single or double asterisk indicate studies included in the first meta-analysis. Those with double asterisks were included in the second meta-analysis.

Received for publication July 27, 2000.

	REFERENCES

TOP ABSTRACT INTRODUCTION METHODS RESULTS DISCUSSION NOTES REFERENCES

 

1. American Psychiatric Association. Diagnostic and statistical manual of mental disorders. 3rd ed. Washington DC: APA; 1980.
2. American Psychiatric Association. Diagnostic and statistical manual of mental disorders. 4th ed. Washington DC: APA; 1994.
3. Kardiner A The traumatic neuroses of war. New York: Harper & Row Publishers, Inc.; 1941.
4. Dobbs D, Wilson WP. Observations on persistence of war neurosis. Dis Nerv Syst 1960; 21: 1–6.
5. Foa EB, Zinbarg R, Rothbaum BO. Uncontrollability and unpredictability in post-traumatic stress disorder: an animal model. Psychol Bull 1992; 112: 218–38.[Medline]
6. Blanchard EB, Buckley TC. Psychophysiological assessment and PTSD. In: Saigh P, Bremner D, editors. Post-traumatic stress disorder: a comprehensive text. Needham: Allyn & Bacon; 1999.
7. *Keane TM, Kolb LC, Kaloupek DG, Orr SP, Blanchard EB, Thomas RG, Hsieh FY, Lavori PW. Utility of psychophysiological measurement in the diagnosis of posttraumatic stress disorder: results from a Department of Veterans Affairs cooperative study. J Consult Clin Psychol 1998; 66: 914–23.[Medline]
8. *Orr SP, Pitman RK, Lasko NB, Herz LR. Psychophysiological assessment of posttraumatic stress disorder imagery in World War II and Korean combat veterans. J Abnorm Psychol 1993; 102: 152–9.[Medline]
9. *Pitman RK, Orr SP, Forgue DF, de Jong JB, Claiborn JM. Psychophysiological assessment of posttraumatic stress disorder imagery in Vietnam combat veterans. Arch Gen Psychiatry 1987; 44: 970–5.[Abstract/Free Full Text]
10. Blanchard EB, Kolb LC, Prins A. Psychophysiological responses in the diagnosis of posttraumatic stress disorder in Vietnam veterans. J Nerv Ment Dis 1991; 179: 99–103.
11. *Shalev AY, Orr SP, Peri T, Schreiver S, Pitman RK. Physiological responses to loud tones in Israeli patients with posttraumatic stress disorder. Arch Gen Psychiatry 1992; 49: 870–5.[Abstract/Free Full Text]
12. Blanchard EB. Elevated basal levels of cardiovascular responses in Vietnam veterans with PTSD: a health problem in the making? J Anxiety Disord 1990; 4: 233–7.
13. Fredrikson M, Matthews KA. Cardiovascular responses to behavioral stress and hypertension: a meta-analytic review. Ann Behav Med 1990; 12: 30–9.
14. Georgiades A, Fredrikson M. Hyperreactivity (cardiovascular). In: Fink G, editor. Encyclopedia of stress. Vol. II. San Diego: Academic Press; 2000. p. 421–5.
15. Blanchard EB, Kolb LC, Prins A, Gates S, McCoy GC. Changes in plasma norepinephrine to combat-related stimuli among Vietnam veterans with posttraumatic stress disorder. J Nerv Ment Dis 1991; 179: 371–3.[Medline]
16. Bremner JD, Southwick SM, Charney DS. The neurobiology of posttraumatic stress disorder: an integration of animal and human research. In: Saigh P, Bremner D, editors. Post-traumatic stress disorder: a comprehensive text. Needham: Allyn & Bacon; 1999. p. 103–43.
17. Amerena J, Julius S. The role of the autonomic nervous system in hypertension. Hypertens Res 1995; 18: 99–110.[Medline]
18. Hocking-Schuler JL, O’Brien WH. Cardiovascular recovery from stress and hypertension risk factors: a meta-analytic review. Psychophysiology 1997; 34: 649–59.[Medline]
19. Prins A, Kaloupek DG, Keane TM. Psychophysiological evidence for autonomic arousal and startle in traumatized adult populations. In: Friedman MJ, Charney DS, Deutch AY, editors. Neurobiological and clinical consequences of stress: from normal adaptation to PTSD. Philadelphia: Lippincott-Raven; 1995. p. 291–314.
20. **Cohen H, Kotler M, Matar MA, Kaplan Z, Miodownik H, Cassuto Y. Power spectral analysis of heart rate variability in posttraumatic stress disorder patients. Biol Psychiatry 1997; 41: 627–9.[Medline]
21. **Gerardi RJ, Keane TM, Cahoon BJ, Klauminzer GW. An in vivo assessment of physiological arousal in posttraumatic stress disorder. J Abnorm Psychol 1994; 103: 825–7.[Medline]
22. **Muraoka M, Carlson JG, Chemtob CM. Twenty-four hour ambulatory blood pressure and heart rate monitoring in combat related posttraumatic stress disorder. J Trauma Stress 1998; 11: 473–84.[Medline]
23. **McFall ME, Veith RC, Murburg MM. Basal sympathodadrenal function in posttraumatic stress disorder. Biol Psychiatry 1992; 31: 1050–6.[Medline]
24. **Orr SP, Meyerhoff JL, Edwards JV, Pitman RK. Heart rate and blood pressure resting levels and responses to generic stressors in Vietnam veterans with posttraumatic stress disorder. J Trauma Stress 1998; 11: 155–64.[Medline]
25. **Shalev AY, Bleich A, Ursano RJ. Posttraumatic stress disorder: somatic comorbidity and effort tolerance. Psychosomatics 1990; 31: 197–203.[Abstract/Free Full Text]
26. Camargo CA, Rimm EB. Epidemiological research on moderate alcohol consumption and blood pressure. In: Zakhari S, Wassef M, editors. Alcohol and the cardiovascular system. Bethesda: National Institutes of Health; 1996. p. 25–62.
27. Hillbom M, Juvela S. Alcohol and risk for stroke. In: Zakhari S, Wassef M, editors. Alcohol and the cardiovascular system. Bethesda: National Institutes of Health; 1996. p. 63–83.
28. Kunos G, Varga K. Alcohol effects on autonomic control of the cardiovascular system. In: Zakhari S, Wassef M, editors. Alcohol and the cardiovascular system. Bethesda: National Institutes of Health; 1996. p. 243–61.
29. Kessler RC, Sonnega A, Bromet E, Hughes M, Nelson CB. Posttraumatic stress disorder in the National Comorbidity Survey. Arch Gen Psychiatry 1995; 52: 1048–60.[Abstract/Free Full Text]
30. Kulka RA, Schlenger WE, Fairbank JA, Hough RL, Jordan BK, Marmar CR, Weiss DS Trauma and the Vietnam War Generation: report of findings from the National Veterans Readjustment Study. New York: Brunner/Mazel; 1990.
31. Beckham JC, Moore SD, Feldman ME, Hertzberg MA, Kirby AC, Fairbank JA. Health status, somatization, and severity of postraumatic stress disorder in Vietnam combat veterans with posttraumatic stress disorder. Am J Psychiatry 1998; 155: 1565–9.[Abstract/Free Full Text]
32. Shapiro D, Jamner LD, Lane JD, Light KC, Myrtek M, Sawada Y, Steptoe A. Blood pressure publication guidelines. Psychophysiology 1996; 33: 1–12.[Medline]
33. Hunter JE, Schmidt FL. Methods of meta-analysis. Newbury Park, Sage Publications, Inc. 1990.
34. American Psychiatric Association, Diagnostic and statistical manual of mental disorders. 3rd edition, revised. Washington, D.C.: APA; 1987.
35. First MB, Spitzer RL, Gibbon M, Williams JBW. Structured clinical interview for DSM-IV, patient edition (SCID-I/P). Version 2.0. New York, Biometrics Research Department-New York State Psychiatric Institute 1996.
36. Blake D, Weathers F, Nagy L, Kaloupek D, Klauminzer G, Charney D, Keane T. Clinician-administered PTSD scale (CAPS). Boston, National Center for Post-Traumatic Stress Disorder, Behavioral Science Division-Boston VA 1997.
37. DiNardo PA, Barlow DH, Cerny J, Vermilyea BB, Vermilyea JA, Himadi W, Waddell M. Anxiety disorders interview schedule—revised (ADIS-R). Albany (NY): Phobia and Anxiety Disorders Clinic, State University of New York at Albany; 1985.
38. Cohen J. Statistical power analysis for the behavioral sciences. 2nd ed. New York: Academic Press; 1988.
39. Hedges LV, Olkin I. Statistical methods for meta-analysis. Orlando, Academic Press 1985.
40. Hunter JE, Schmidt FL, Jackson GB. Meta-analysis. Cumulating research findings across studies. Beverly Hills, Sage Publications, Inc. 1982.
41. Grillon C, Morgan CA. Fear-potentiated startle conditioning to explicit and contextual cues in Gulf War veterans with posttraumatic stress disorder. J Abnorm Psychol 1999; 108: 134–42.[Medline]
42. Collins R, Peto R, MacMahon S, Hebert P, Fiebach N, Eberlein KA, Godwin J, Qizilbash Taylor JO, Hennekens CH. Blood pressure, stroke, and coronary heart disease. Part 2, short-term reductions in blood pressure: overview of randomised drug trials in their epidemiological context. Lancet 1990; 335: 827–37.[Medline]
43. Boscarino JA, Chang J. Electrocardiogram abnormalities among men with stress-related psychiatric disorders: implications for coronary heart disease and clinical research. Ann Behav Med 1999; 21: 227–34.[Medline]
44. Manuck SB, Kaplan JR, Clarkson TB. Behaviorally induced heart rate reactivity and atherosclerosis in cynomolgus monkeys. Psychosom Med 1983; 45: 95–108.[Abstract/Free Full Text]
45. Greenland P, Daviglus ML, Dyer AP, Liu K, Huang C, Goldberger JJ, Stamler J. Resting heart rate is a risk factor for cardiovascular and noncardiovascular mortality. Am J Epidemiol 1999; 149: 853–62.[Abstract/Free Full Text]
46. Gillman MW, Kannel WB, Belanger A, et al. Influence of heart rate on mortality among persons with hypertension: the Framingham study. Am Heart J 1993; 125: 1148–54.[Medline]
47. Light KC, Sherwood A, Turner JR. High cardiovascular reactivity to stress: a predictor of later hypertension development. In: Turner JR, Sherwood S, Light KC, editors. Individual differences in cardiovascular response to stress. New York: Plenum Press; 1992. p. 281–93.
48. Saab PG, Llabre MM, Schneiderman N, Hurwitz BE, McDonald PG, Evans J, Wohlgemuth W, Hayashi P, Klein B. Influence of ethnicity and gender on cardiovascular responses to active coping and inhibitory-passive coping challenges. Psychosom Med 1997; 59: 434–46.[Abstract/Free Full Text]
49. *Blanchard EB, Hickling EJ, Buckley TC, Taylor AE, Vollmer AJ, Loos WR. The psychophysiology of motor vehicle accident related posttraumatic stress disorder: replication and extension. J Consult Clin Psychol 1996; 64: 742–51.[Medline]
50. Bollen KA. Structural equations with latent variables. New York, John Wiley & Sons 1989.
51. *Beckham JC, Feldman ME, Barefoot JC, Fairbank JA, Helms MJ, Haney TL, Hertzberg MA, Moore SD. Ambulatory cardiovascular activity in Vietnam combat veterans with and without posttraumatic stress disorder. J Consult Clin Psychol 2000; 68: 269–76.[Medline]
52. *Blanchard EB, Kolb LC, Pallmeyer TP, Gerardi RJ. A psychophysiological study of posttraumatic stress disorder in Vietnam veterans. Psychiatr Q 1982; 54: 220–9.[Medline]
53. *Blanchard EB, Kolb LC, Gerardi RJ, Ryan P, Pallmeyer TP. Cardiac response to relevant stimuli as an adjunctive tool for diagnosing posttraumatic stress disorder in Vietnam veterans. Behav Ther 1986; 17: 592–606.
54. *Blanchard EB, Kolb LC, Taylor AE, Wittrock DA. Cardiac response to relevant stimuli as an adjunct in diagnosing post-traumatic stress disorder: replication and extension. Behav Ther 1989; 20: 535–43.
55. *Blanchard EB, Hickling EJ, Taylor AE, Loos WR, Gerardi RJ. The psychophysiology of motor vehicle accident related posttraumatic stress disorder. Behav Ther 1994; 25: 453–67.
56. *Carson MA, Paulus LA, Lasko NB, Metzger LJ, Wolfe J, Orr SP, Pitman RK. Psychophysiological assessment of post-traumatic stress disorder in Vietnam nurse veterans who witnessed injury or death. J Consult Clin Psychol 2000; 68: 890–7.[Medline]
57. *Davis JM, Uddo M, Vasterling JJ, and Orr SP. Psychophysiological assessment of Persian Gulf war veterans with PTSD. Boston: 11th annual meeting of the International Society for Traumatic Stress Studies; 1995.
58. *Davis JM, Adams HE, Uddo M, Vasterling JJ, Sutker PB. Physiological arousal and attention in veterans with post-traumatic stress disorder. J Psychopathol Behav Assess 1996; 18: 1–20.
59. *Gerardi RJ, Blanchard EB, Kolb LC. Ability of Vietnam Veterans to dissimulate a psychophysiological assessment for post-traumatic stress disorder. Behav Ther 1989; 20: 229–43.
60. *Kinzie JD, Denney D, Riley C, Boehnlein J, Mcfarland B, Leung P. A cross-cultural study of reactivation of posttraumatic stress symptoms: American and Cambodian psychophysiological response to viewing traumatic video scenes. J Nerv Ment Dis 1998; 186: 670–6.[Medline]
61. *Litz BT, Orsillo SM, Kaloupek D, Weathers F. Emotional-processing in posttraumatic stress disorder. J Abnorm Psychol 2000; 109: 26–39.[Medline]
62. *Malloy PF, Fairbank JA, Keane TM. Validation of a multimethod assessment of posttraumatic stress disorders in Vietnam veterans. J Consult Clin Psychol 1983; 51: 488–94.[Medline]
63. *McFall ME, Murburg MM, Ko GN, Veith RC. Autonomic responses to stress in Vietnam combat veterans with posttraumatic stress disorder. Biol Psychiatry 1990; 27: 1165–75.[Medline]
64. **Metzger LJ, Orr SP, Berry NJ, Ahern CE, Lasko NB, Pitman RK. Physiological reactivity to startling tones in women with posttraumatic stress disorder. J Abnorm Psychol 1999; 108: 347–52.[Medline]
65. **Murburg MM, McFall ME, Lewis N, Veith RC. Plasma norepinephrine kinetics in patients with posttraumatic stress disorder. Biol Psychiatry 1995; 38: 819–25.[Medline]
66. **Orr SP, Lasko NB, Shalev AY, Pitman RK. Physiologic responses to loud tones in Vietnam veterans with posttraumatic stress disorder. J Abnorm Psychol 1995; 104: 75–82.[Medline]
67. *Orr SP, Lasko NB, Metzger LJ, Pitman RK. Physiologic responses to non-startling tones in Vietnam veterans with post-traumatic stress disorder. Psychiatry Res 1997; 73: 103–7.[Medline]
68. *Orr SP, Solomon Z, Peri T, Pitman RK, Shalev AY. Physiologic responses to loud tones in Israeli veterans of the 1973 Yom Kippur War. Biol Psychiatry 1997; 41: 319–26.[Medline]
69. *Orr SP, Lasko NB, Metzger LJ, Berry NJ, Ahern CE, Pitman RK. Psychophysiological assessment of women with posttraumatic stress disorder resulting from childhood sexual abuse. J Consult Clin Psychol 1998; 66: 906–13.[Medline]
70. *Pallmeyer TP, Blanchard EB, Kolb LC. The psychophysiology of combat-induced post-traumatic stress disorder in Vietnam veterans. Behav Res Ther 1986; 24: 645–52.[Medline]
71. *Shalev AY, Orr SP, Pitman RK. Psychophysiological assessment of traumatic imagery in Israeli civilian patients with posttraumatic stress disorder. Am J Psychiatry 1993; 150: 620–4.[Abstract/Free Full Text]
72. *Shalev AY, Peri T, Orr SP, Bonne O, Pitman RK. Auditory startle responses in help-seeking trauma survivors. Psychiatry Res 1997; 69: 1–7.[Medline]
73. *Shalev AY, Peri T, Gelpin E, Orr SP, Pitman RK. Psychophysiological assessment of mental imagery of stressful events in Israeli civilian posttraumatic stress disorder patients. Comp Psychiatry 1997; 38: 269–73.

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