Journal of Traumatic StressFebruary 2013, 26, 169–172

BRIEF REPORT

The Impact of Posttraumatic Stress Disorder on Blood Pressureand Heart Rate in a Veteran Population

Eric J. Paulus,1 Tami R. Argo,2 and Jason A. Egge2

1Advocate Medical Group, Clinical Pharmacy Department, Chicago, Illinois, USA2Veterans Affairs Healthcare System, Clinical Pharmacy Department, Iowa City, Iowa, USA

Hyperarousal is a hallmark of posttraumatic stress disorder (PTSD). PTSD has been associated with increased blood pressure (BP) andheart rate (HR) in veteran populations. We retrospectively identified male patients consulted to outpatient psychiatry at the Iowa CityVeterans Affairs Healthcare System. Patients were divided into PTSD (n = 88) and non-PTSD (n = 98) groups. All PTSD patients anda subset of non-PTSD patients had documented blast exposure during service. The study investigated whether patients with PTSD hadhigher systolic blood pressure (SBP), diastolic blood pressure (DBP), and heart rate (HR) than patients without PTSD. The effect of traumaexposure on BP was also examined. Mean SBP (133.8 vs. 122.3 mm Hg; p < .001), DBP (87.6 vs. 78.6 mm Hg; p < .001), and HR (78.9vs. 73.1 bpm; p < .001) were all significantly higher in the PTSD group. Trauma-exposed patients without PTSD had significantly higherBP than nonexposed patients. The prevalence of hypertension (HTN) was 34.1% (diagnosed and undiagnosed) among PTSD patients.Patients with PTSD had higher BP and HR compared to patients without PTSD. Trauma exposure may increase BP in this population.These findings will increase awareness about the cardiovascular implications of PTSD.

Hyperarousal is a hallmark of posttraumatic stress disorder(PTSD). Physiological response to reminders of trauma is partof the Diagnostic and Statistical Manual of Mental Disorders(4th ed., text rev.; DSM-IV-TR; American Psychiatric Asso-ciation, 2000) definition of PTSD, with the responses beingmore exaggerated than those observed in otherwise ordinarytrauma survivors. Although not included in the diagnostic cri-teria, two physiological responses commonly associated withPTSD include increased blood pressure (BP) and heart rate(HR; Blanchard, 1990).

Several studies have investigated the relationship betweenPTSD and elevated BP and HR, although study design, popula-tion, PTSD etiology, and results have been variable. Regardingdifferences in study design, an important distinction is tonic(no stimulus) versus phasic (stimulus applied) physiologicalmeasurements. A recent meta-analysis included over 50 rest-ing baseline studies and concluded PTSD is associated withsignificantly elevated resting HR (Pole, 2007). Although eleva-tions in resting BP were also observed, the difference reached

Correspondence concerning this article should be addressed to Eric J. Paulus,Advocate Medical Group, 2545 South King Drive, Chicago, IL 60610. E-mail:ejpaulus@gmail.com

Published 2013. This article is a US Government work and is in the publicdomain in the USA. View this article online at wileyonlinelibrary.comDOI: 10.1002/jts.21785

significance with unweighted effect sizes only (Pole, 2007).Patients with increased BP may have increased risk for de-veloping hypertension (HTN) and subsequent cardiovasculardisease (CVD), as observed in retrospective studies for vet-eran populations with PTSD (O’Toole & Catts, 2008; Schnurr,Spiro, & Paris, 2000).

The association between PTSD and elevated BP and HR hasbeen specifically investigated among veteran populations, al-though studies have primarily focused on older veterans (WorldWar II, Korean war, Vietnam war). Limited information is avail-able regarding this association in younger veteran populations,such as those having served in Afghanistan/Iraq (OperationEnduring Freedom/Operation Iraqi Freedom [OEF/OIF]).

The estimated prevalence of HTN for the general popula-tion over 20 years of age is 33.5%. For males aged 20–34years, the estimated prevalence is 11.1% (American Heart As-sociation, 2012). Most OEF/OIF veterans fall within this agegroup, with an average age of 27 years (Lapierre, Schwegler, &LaBauve, 2007). A recent study found increased prevalence ofdiagnosed HTN among younger veterans (average age 34 years)with PTSD compared to those without PTSD (15.5% vs. 7.5%;Kibler, Joshi, & Ma, 2009).

The exact biological mechanism(s) responsible for poten-tially elevated BP and HR in veterans with PTSD is un-known. Evidence suggests the sympathetic nervous system(SNS) and hypothalamic–pituitary–adrenal (HPA) axis are

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involved with the pathogenic processes of chronic PTSD(Pervanidou & Chrousos, 2010). There is evidence for increasedurinary epinephrine (EPI) and norepinephrine (NE) levels inpatients with PTSD (Kosten, Mason, Giller, Ostroff, & Hark-ness, 1987). Hyperactivity of the SNS might contribute to CVDthrough the effects of chronically elevated norepinephrine (NE)levels on the heart, vasculature, and platelet function (Bedi &Arora, 2007). It has been suggested that PTSD leads to struc-tural/functional changes and cardiovascular adaptation to re-peated stress responses, supported by a meta-analysis that ob-served a correlation between PTSD duration and resting HRelevations (Buckley & Kaloupek, 2001). Other proposed expla-nations for increased BP and HR among veterans with PTSD in-clude increased rates of smoking, alcohol, and substance abuseassociated with PTSD (Beckham et al., 1998; Kessler, Sonnega,Bromet, Hughes, & Nelson 1995).

The purpose of this study was to investigate the relation-ship between combat-related PTSD and resting BP and HR inyounger male veterans, using tonic (no stimulus) physiologi-cal measurements. In addition, we attempted to determine iftrauma exposure, independent of PTSD, influences BP in thispopulation.

Method

Procedures and Participants

This study was a retrospective cohort design, utilizing electronicchart review through the Iowa City Veterans Affairs HealthcareSystem (ICVAHCS). The study was approved by the VeteransAffairs Research and Development Institutional Review Board.

We retrospectively identified all patients consulted to IC-VAHCS outpatient psychiatry between January 1, 2008 andJanuary 1, 2010. The index date was defined as the consultdate. All patients were required to be male, aged < 55 years,and have two documented BP and HR measurements within30 days of the index date. Patients in the PTSD group musthave been diagnosed within 3 months of the index date. Sub-jects in the PTSD group were required to have a history ofdocumented trauma exposure, defined as blast exposure duringOEF/OIF service. A proportion of the non-PTSD group alsohad documented trauma exposure.

We identified 3,529 patients consulted to outpatient psychi-atry between January 1, 2008 and January 1, 2010. There were1,357 subjects with diagnosed PTSD and 2,172 subjects with-out diagnosed PTSD. Within the PTSD group, 88 patients metcriteria for inclusion. We identified 52 patients without PTSDbut with trauma exposure; 27 met criteria for inclusion. Due tothe larger sample size in the group without PTSD and withouttrauma (n = 2,120), we randomly selected 150 patients basedon numerically ordered Social Security number. In this group,71 patients met criteria for inclusion.

Study questions included whether patients with PTSD hadhigher SBP, DBP, and HR compared to patients without PTSD.In addition, we examined the relationship between trauma ex-

posure and BP, independent of PTSD diagnosis. The frequencyof HTN (both diagnosed and undiagnosed) was also recorded.To determine BP and HR at index date, we recorded the averageof two outpatient, resting BP and HR measurements closest tothe index date, within 30 days of the index date.

Baseline characteristics and potentially confounding diag-noses were recorded from the medical record: age, gender, bodymass index, HTN, antihypertensive medication use, diabetes,chronic kidney disease, other anxiety disorders, depression,mood disorder, smoking status, and substance abuse (includingalcohol abuse).

Data Analysis

Comparisons between the PTSD and non-PTSD groups fordescriptive variables were performed using χ2 or Fisher’s exacttests for categorical variables and unpaired two-sample t testsor Mann Whitney tests for continuous variables.

We used unpaired two-sample t tests to report the differencesin mean resting SBP, DBP, and HR between the PTSD andnon-PTSD groups. Statistically significant variables identifiedby bivariate analyses in this sample included age, HTN, otheranxiety disorders, depression, mood disorder, substance abuse,smoking status, and antihypertensive medication use. We thenused an analysis of covariance (ANCOVA) to compare SBP,DBP, and HR in the two groups with these variables in themodel.

A one-way analysis of variance (ANOVA) was used to assessthe relationship between trauma exposure and SBP and DBPafter dividing the sample into three groups based on PTSDdiagnosis and trauma exposure. Tukey post hoc comparisonswere generated to evaluate between group differences.

Results

The study sample consisted of 88 patients with PTSD and 98patients without PTSD. Baseline demographics were similarbetween the two groups. The average age was significantlylower among patients with PTSD (26.0 vs. 32.0 years; p <

.001). Depression, mood disorders, and other anxiety disor-ders were significantly more common in the non-PTSD group(p < .001, p < .04, p < .02, respectively). Rates of documentedsmoking (27% vs. 33%) and substance abuse (6% vs. 9%)were similar between the PTSD and non-PTSD groups. Ratesof diagnosed HTN were comparable between the PTSD andnon-PTSD groups (13.6% vs. 14.3%), respectively, althoughthe PTSD group had much higher rates of undiagnosed HTN(20.5% vs. 2.0%). No significant differences were observed inrates of antihypertensive medication use.

Results for study questions are displayed in Tables 1 and 2.Mean resting SBP, DBP, and HR were all significantly higherin the PTSD group. Among patients without PTSD, those withtrauma exposure had significantly higher resting SBP and DBPthan those without trauma exposure. Findings were unchanged

Journal of Traumatic Stress DOI 10.1002/jts. Published on behalf of the International Society for Traumatic Stress Studies.

Effect of PTSD on Blood Pressure and Heart Rate 171

Table 1Levels of DBP, SBP, and HR Between Study Groups

PTSD Non-PTSD(n = 88) (n = 98)

Variable M SD M SD d

DBP, mmHg 87.6 6.3 78.4 7.2 1.36***

SBP, mmHg 133.8 8.6 122.3 9.6 1.27***

HR, bpm 78.9 9.8 73.1 8.0 0.65***

Note. DBP = diastolic blood pressure; SBP = systolic blood pressure; HR =heart rate; PTSD = posttraumatic stress disorder; mmHg = millimeters mercury;bpm = beats per minute.

***p < .001.

when adjusted for the following variables: age, HTN, diabetes,anxiety, depression, mood disorder, substance abuse, smokingstatus, and antihypertensive use.

Discussion

The results of this study suggested male veterans with combat-related PTSD have higher resting BP and HR compared to vet-erans without PTSD. This is the first study, to our knowledge, tohave identified higher resting BP and HR in a younger veteranpopulation with PTSD (average age 26 years). The primaryclinical application of these findings may be more medical thanpsychiatric. Veterans with PTSD and elevated BP may have in-creased risk for developing HTN and subsequent CVD, whichis supported by retrospective studies (O’Toole & Catts, 2008;Schnurr et al., 2000) as previously mentioned. These conse-quences may contribute to increased heart disease mortality(Boscarino, 2008) and all-cause mortality (Boscarino, 2006)associated with PTSD. Although these studies were conductedin older veteran populations (World War II, Korean war, Viet-nam war), similar findings might be predicted for current andfuture veterans with PTSD based on our findings of increasedBP in a younger veteran population. We must also recognizeour finding of elevated HR among patients with PTSD. A largepopulation-based study found higher resting HR in men aged

Table 2Levels of DBP and SBP Between Study Groups

PTSD No PTSD No trauma(n = 88) (n = 27) (n = 71)

Variable M SD M SD M SD F

SBP, mm Hg 133.8 8.6 128.3 9.0 120.1 8.9 50.13*DBP, mm Hg 87.6 6.3 81.9 7.2 77.1 6.8 48.48*

Note. Tukey’s post hoc comparisons were significant at p < 0.05 for both variableswhen comparing the PTSD group with each of the other groups. DBP = diastolicblood pressure; SBP = systolic blood pressure; PTSD = posttraumatic stressdisorder.

*p < .05.

18–39 years was associated with increased mortality from bothcardiovascular (CV) and non-CV causes over 20 years later(Greenland et al., 1999).

We found patients with trauma exposure, but without diag-nosed PTSD had significantly elevated BP compared to non-exposed patients. Although the magnitude of BP elevation wasless than patients with both diagnosed PTSD and trauma ex-posure, these findings suggested veterans with combat-relatedtrauma exposure may be at risk for increased BP without de-veloping PTSD.

Within the PTSD group, 34.1% of patients had HTN (13.6%diagnosed and 20.5% undiagnosed), compared to 16.3% ofpatients without PTSD (14.3% diagnosed and 2.0% undiag-nosed). This observation in the PTSD group is similar to theprevalence of HTN (33.5%) in the general population over20 years of age, but the average age of our patients with PTSDwas only 26 years. In comparison, the estimated prevalenceis 11.1% for males aged 20–34 years (American Heart As-sociation, 2012). This suggests younger veterans with PTSDmay be at increased risk for developing HTN compared toage-matched controls without PTSD. In this study, we had toexclude twice as many PTSD patients (n = 177) than wereincluded in the study (n = 88) due to lack of having two docu-mented BP and HR measurements within 30 days of the indexdate. It is imperative to improve BP monitoring among youngerveterans with PTSD and trauma history to allow earlier inter-vention and minimize the potential consequences of chronic,elevated BP.

We must address certain unexpected baseline demographics.First, rates of documented depression, other anxiety disorders,and mood disorders were significantly more common in thenon-PTSD group. Second, the rate of documented substanceabuse (6%) in the PTSD group was much lower than expected.These findings are likely explained by lack of adequate as-sessment within the health care system. Many PTSD patientswere relatively new to the health care system; thus, patients andproviders may have been reluctant to report or diagnose withinthe first few assessments.

The retrospective design is inherently associated with lim-itations involving incomplete and incorrect documentation inthe medical record. This study has low external validity tothe general population, as we studied only male veterans withcombat-related PTSD. Substantial heterogeneity was present inregards to trauma frequency and severity. The sample size wasrelatively small (n = 186). Finally, we were unable to distin-guish the potential confounding effects of HTN diagnosis orantihypertensive treatment on BP from the inherent effects ofPTSD.

We did not exclude potentially confounding diagnoses. De-spite the small sample size, the results were statistically signifi-cant, suggesting the study was adequately powered. We studieda younger veteran population than most currently published lit-erature regarding PTSD and BP and HR. Finally, we examinedthe relationship between trauma exposure and BP, independentof PTSD.

Journal of Traumatic Stress DOI 10.1002/jts. Published on behalf of the International Society for Traumatic Stress Studies.

172 Paulus, Argo, and Egge

Our results indicated male veterans with combat-relatedPTSD have significantly elevated resting BP and HR comparedto those without PTSD. Patients with a history of trauma ex-posure, regardless of PTSD diagnosis, had elevated resting BP.The prevalence of HTN among younger veteran populationsis concerning and should be more accurately monitored, diag-nosed, and treated. Larger prospective studies are needed tofurther clarify the association between PTSD and trauma expo-sure with elevated BP and HR.

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Journal of Traumatic Stress DOI 10.1002/jts. Published on behalf of the International Society for Traumatic Stress Studies.