Depressive Symptoms Are Associated With Increased Systemic Vascular
Resistance to Stress
SCOTT C. MATTHEWS, MD, RICHARD A. NELESEN, PHD, AND JOEL E. DIMSDALE, MD
Objective: The deleterious effects of major depressive disorder on cardiovascular (CV) functioning are well known. However, the
etiologic mechanisms underlying this association are incompletely understood. In the current study, subjects with varying degrees
of depressive symptoms performed a stress task while CV reactivity was measured. We hypothesized that high levels of depressive
symptoms would be associated with altered CV reactivity. Methods: Ninety-one healthy volunteer subjects performed reactivity
testing while measures of impedance cardiography and autonomic nervous system function were obtained. Subjects completed the
Center for Epidemiological Studies Depression Scale (CES-D) and were categorized into either the high depressive (i.e., CES-D
>16) or low depressive (i.e., CES-D ?16) symptoms group. Results: Task performance was associated with increases in systemic
vascular resistance (SVR) (p ? .001), mean arterial pressure (p ? .001), and heart rate (p ? .005), and decreases in cardiac output
(p ? .001), heather index (p ? .001), and stroke volume (p ? .05). After controlling for screening mean arterial pressure, an
interaction effect of stress by mood group on SVR (p ? .01) was observed; subjects with high amounts of depressive symptoms
manifested significantly greater SVR at baseline and in response to a stressor task than did subjects with low amounts of depressive
symptoms. Conclusions: These results suggest a mechanism that may partially explain the increased CV morbidity associated with
depressive symptoms. In future studies, it may be useful to examine if treatment of depressive symptoms alters CV reactivity. Key
words: depressive symptoms, systemic vascular resistance, reactivity, mirror star tracing task.
ANS ? autonomic nervous system; CESD ? Center for Epidemio-
logical Studies Depression Scale; CO ? cardiac output; CV ?
cardiovascular; DSM-IV ? Diagnostic and Statistical Manual,
Fourth edition; HI ? Heather index; HR ? heart rate; HRV ? heart
rate variability; HRVhf? high-frequency HRV; MAP ? mean arte-
rial pressure; MDD ? major depressive disorder; MI ? myocardial
infarction; PNS ? parasympathetic nervous system; POMS ? Pro-
file of Mood States; MSTT ? mirror star tracing task; SNS ?
sympathetic nervous system; SV ? stroke volume; SVR ? systemic
events. The adverse impact of these depressive symptoms on
all-cause mortality has been repeatedly described (1–5), al-
though discrepant reports exist (6–13). Numerous studies
have also focused on the impact of depressive symptoms,
specifically on cardiovascular (CV) mortality. Whereas the
majority of this literature indicates that depressive symptoms
are associated with increased CV mortality (14–18), there are
negative studies as well (8,19,20). Two recent metaanalyses
address this issue. In their analysis of 22 published studies,
van Melle et al. report that postmyocardial infarction (MI)
depression is associated with a 2- to 2.5-fold increased risk of
mortality or an adverse cardiac event within 2 years of the MI
(21). Similarly, Barth et al. indicate that depressive symptoms
(as well as clinical depression) have an unfavorable impact on
mortality in patients with coronary heart disease (22). It is
conceivable that depressive symptoms are associated with
increased CV mortality in a dose-dependent fashion, with the
epressive symptoms are associated with major psychiatric
and medical illnesses, and with exposure to stressful life
greatest risk being associated with major depressive disorder
(MDD). In one study of 896 post-MI patients, level of depres-
sion at admission was significantly related to cardiac mortality
at 5-year follow up (23). However, the mechanism that un-
derlies the association between depressive symptoms and CV
mortality is incompletely understood.
Altered hemodynamic and autonomic nervous system
(ANS) functioning have been associated with depressive
symptoms, and such alterations may partially explain depres-
sion’s relationship to increased CV morbidity. MDD has been
associated with ANS dysfunction as reflected by: 1) decreased
overall heart rate variability (HRV); 2) decreased high-fre-
quency HRV (HRVhf), which specifically reflects parasympa-
thetic nervous system (PNS) activity; and 3) increased low-
frequency HRV, which provides an estimate of sympathetic
nervous system (SNS) tone (15,24–26). Related studies have
linked these physiological changes with poor clinical out-
comes. Low overall HRV, which reflects either increased
sympathetic activation and/or decreased PNS tone, is a strong
and independent predictor of post-MI mortality (27,28).
Subclinical depressive symptoms in the absence of psychi-
atric illness are common, and the “normal range” of these
symptoms in the general population is wide. Prior research
supports the notion that subclinical mood symptoms are asso-
ciated with altered CV reactivity both at rest and in response
to stress. In one study that examined resting impedance mea-
sures underlying blood pressure in healthy volunteer subjects
without psychiatric illness, the fatigue–inertia and tension–
anxiety subscales of the Profile of Mood States (POMS) (29)
were negatively correlated with stroke volume (SV). The
study also found that the POMS fatigue–inertia subscale was
negatively associated with cardiac output (CO), and the
POMS fatigue–inertia subscale was positively correlated with
systemic vascular resistance (SVR) (30). Depressive symp-
toms have also been associated with altered hemodynamic
responses to stress. In another study of 60 healthy women with
varying levels of subclinical depressive symptoms, perfor-
mance of a speech task was associated with increased plasma
norepinephrine, CO, heart rate (HR), systolic and diastolic
From the University of California, San Diego, Department of Psychiatry,
San Diego, California.
Address correspondence and reprint requests to Scott C. Matthews, MD,
San Diego VA Health Services, 3350 La Jolla Village Drive, Mail Code
116A, La Jolla, CA 92161. E-mail: email@example.com
Received for publication September 7, 2004; revision received January 20,
This work was supported by grants HL36005, HL44915, RR00827, and
5T32MH18399 from the National Institutes of Health.
509 Psychosomatic Medicine 67:509–513 (2005)
Copyright © 2005 by the American Psychosomatic Society
blood pressure, and a shorter preejection period, suggesting
that subclinical depressive symptoms are associated with in-
creased SNS activity in women performing a speech task (31).
In the current study, two groups of subjects were examined:
1) a group with a high level of depressive symptoms, i.e.,
(CES-D) (32) of ?16, and 2) a group with a low level of
depressive symptoms, i.e., CES-D ?16. The mirror star trac-
ing task (MSTT), which has been shown to induce robust
changes in CV reactivity (33–36), was administered while
various measures of ANS and hemodynamic functioning were
We hypothesized that high levels of depressive symptoms
would be associated with increased SNS (both alpha and beta
adrenergic) output and decreased PNS tone in response to
stress. Support for these hypotheses would add to an existing
body of literature suggesting a relationship between subclin-
ical depression and altered CV reactivity, and may speak to a
putative mechanism that may partially mediate the relation-
ship between subclinical depressive symptoms and CV mor-
Studies Depression Scale
Ninety-one subjects signed informed consent and completed this study
that was approved by the University of California San Diego Human Research
Protection Program. Individuals were coded as Euro-American or black on the
basis of self-report. During the initial screening visit, subjects had a history
and physical examination, and completed the CES-D, a 20-item self-report
instrument that is a valid and reliable measure for assessing level of depres-
sive symptoms. Based on the commonly used cutoff score of 16, subjects
were placed into either the high depressive (i.e., CES-D >16) or low depres-
sive (i.e., CES-D ?16) symptoms group. Subjects were excluded if they had
MDD or another Axis I psychiatric diagnosis, according to the Diagnostic and
Statistical Manual, Fourth edition (DSM-IV).
To decrease the amount of medical comorbidities, all subjects were
between 18 and 50 years old and between 85% to 150% of ideal body weight.
Women who were taking oral contraceptives or hormonal replacement ther-
apy, menopausal women, and those who were pregnant were excluded.
However, restrictions regarding the timing of the menstrual cycle were not
imposed. Hypertensive subjects who were currently receiving antihyperten-
sive medication completed a careful tapering program followed by a 3-week
drug washout. Any patient whose blood pressure was ?180/110 mm Hg while
off treatment left the protocol and returned to active treatment.
Reactivity testing was performed within approximately 2 weeks of the
screening visit. Subjects were tested in a sound-attenuated room at 8:30 AM
while seated in a comfortable reclining chair. On arrival to the laboratory,
subjects rested quietly for 30 minutes. After this acclimatization phase,
subjects rested quietly for an additional 3 minutes (resting baseline) and then
performed the MSTT. The MSTT has been used extensively in psychophys-
iological experiments to probe CV reactivity and has been shown to induce
changes in blood pressure (BP) and SVR (33–36). In this task, subjects trace
the outline of a star using its mirror image for 3 minutes.
During resting baseline and during performance of the MSTT, electrocar-
diography (ECG; model 78352C; Hewlett Packard; Andover, MA), imped-
ance cardiography (Minnesota Impedance Cardiograph 304B; Surcom, Min-
neapolis, MN), and BP (Colin Pilot, Houston, TX) were monitored
continuously to obtain dependent measures of ANS and hemodynamic func-
tioning. To record the impedance cardiography measures, impedance cardio-
graphic tape was applied in a standard tetrapolar configuration. A BP cuff and
ECG electrodes in a modified lead I or lead II configuration that maximized
the R wave were then applied. The ECG, BP, and impedance waveform
signals were recorded and relayed to an analog-to-digital converter (DT2801;
Data Translation; Marlboro, MA), sampling at 1 kHz per channel and stored
in a computer for subsequent review, artifact rejection, and calculation. These
data were collected in 3-minute epochs. The review and calculation of HRV
were performed using a program developed at the University of Miami,
Behavioral Medicine Research Center (37,38). This program calculated the
variables of LF power and HF power from spectral analyses. Stroke volume
(SV), SVR, and Heather index (HI) were calculated using standard formulas
from BP, ECG, and impedance cardiography data (39). Details of the instru-
mentation and calculation (40) of the physiological variables have been
previously described in detail. SVR and HI provide sensitive and reliable
measures of alpha and beta SNS activity, respectively (39). Parasympathetic
activation is reflected in HRVhf(41).
The dependent variables were HR, HRVhf, HI, SV, MAP, CO, and SVR.
To examine main effects of stress and interaction effects of stress by depres-
sion on these dependent variables, a two (task, i.e., baseline versus stress) by
two (mood group, i.e., high/low depression) repeated-measures analysis of
variance (SPSS for Windows 9.0; SPSS, Chicago, IL (42)) was performed.
Then, to control for the potential confounding variables of gender and eth-
nicity, data were analyzed using a two (task, i.e., baseline versus stress) by
two (gender, i.e., male versus female) by two (ethnicity, i.e., Euro-American
versus black) by two (mood group, i.e., high/low depression) repeated-
measures analysis of variance.
A post-hoc analysis of simple effects was then performed. Independent-
samples t tests were performed to compare SVR during the baseline condition
between the high and low depressive symptoms groups, and to compare SVR
during performance of the MSTT between the high and low depressive
symptoms groups. Paired t tests were performed to compare SVR during
baseline with SVR during performance of the MSTT within the high and low
depressive symptoms groups.
The sociodemographic characteristics and values for rele-
vant physiological measures during screening of study partic-
ipants are outlined in Table 1. At initial assessment, the high
and low depressive symptoms groups were not significantly
different in age, gender, ethnicity, screening MAP, or body
mass index (Table 1).
The repeated-measures analysis revealed a main effect of
stress on several variables of interest. Task performance was
associated with significant increases in SVR (p ? .001), MAP
(p ? .001), and HR (p ? .005), and significant decreases in
TABLE 1. Sociodemographic and Baseline Physiological Variables for
Depressed and Nondepressed Subjects
Mean arterial pressureb
Body mass indexb
bMean (standard deviation).
S. C. MATTHEWS et al.
510Psychosomatic Medicine 67:509–513 (2005)
SV (p ? .05), CO (p ? .001), and HI (p ? .001). More
interestingly, an interaction effect of stress by mood was
observed on SVR (F[1,88] ? 7.43, p ? .01). Subjects with
high depressive symptoms responded to stress with a partic-
ularly pronounced increase in SVR (Fig. 1). This interaction
remained significant after controlling for ethnicity, gender,
and screening MAP (F[1,82[rsqb ? 7.87, p ? .01). The
analysis of simple effects revealed significant increases in
SVR from baseline to task within the high depressive symp-
toms (p ? .0001) and within the low depressive symptoms
(p ? .0001) groups. Independent-samples t tests revealed
significant differences in SVR between the high and low
depressive symptoms groups both during baseline (p ? .05)
and during performance of the MSTT (p ? .005). There were
no significant interactions of ethnicity by stress or gender by
stress on SVR. No significant interactions of stress by mood
group on HR, HRVhf, HI, MAP, CO, or SV were observed
In the current study, a high level of depressive symptoms
was related significantly to increased SVR. Specifically, an
interaction effect of depression level (high/low) by stress
(task/baseline) on SVR was observed such that a high level of
depression was associated with significantly greater SVR at
rest and, particularly so, during performance of the MSTT.
Prior studies have shown that gender (34,43) and race (44–
48) can contribute significantly to physiological reactivity and
SVR in particular. However, in the current study, no signifi-
cant interactions of gender by depression or ethnicity by
depression on SVR were observed, indicating that these fac-
tors were not confounding the relationship between depression
These results are consistent with a study by Yu et al., which
reported that SVR at rest was positively correlated with scores
on the POMS fatigue–inertia subscale (30). Our study pro-
vides complementary evidence that extensive depressive
symptoms, as revealed by the CES-D, are associated with
increased SVR at rest. Reservations have been raised about the
validity of using baseline measures of CO and therefore SVR
(49). The current study extends our previously noted obser-
vations of baseline differences to differences observed when
subjects are stressed, an area in which impedance cardiogra-
phy measures are on firmer ground. In this context, we found
that depressive symptoms are associated with greater SVR
Interestingly, we observed no significant interactions of
stress by mood group on MAP, CO, HR, HRVhf, HI, or SV.
Additionally, when the high and low depressive symptom
groups were analyzed together, MSTT performance was as-
sociated with decreased HI, a sensitive measure of beta-
adrenergic tone. Additional research using multiple tasks in a
large sample of patients with various degrees of depressive
symptoms is needed to fully explain this finding. Perhaps
MDD is associated with central ANS changes that result in
dysfunction across a broad range of CV measures, whereas the
presence of subsyndromal symptoms affects peripheral ANS
changes reflected in increased SVR. Also of note is the fact
that the MSTT has been previously shown to affect primarily
SVR through increased alpha-adrenergic tone (36,50), and
additional research using multiple different tasks is needed to
understand the role that specific tasks may play in selective
activation of the alpha adrenergic nervous system.
The current study suggests a mechanism whereby subclin-
ical levels of depression may have deleterious CV effects.
Prior research has described a dose-response relationship be-
tween depressive symptom severity and CV events. In one
cohort study of generally healthy outpatients, an increase in
depressive symptoms over time was significantly associated
with MI, stroke, and death (51). In a related study, increased
depressive symptoms were associated with an increased risk
of subsequent cardiac mortality. In that study, cardiac patients
with a CES-D score of >16 relative to cardiac patients with a
CES-D score of ?16 had a relative risk of subsequent cardiac
mortality of 1.6, and noncardiac patients with a CES-D score
of >16 relative to noncardiac patients with a CES-D score of
?16 had a relative risk of subsequent cardiac mortality of 1.5
Although the underlying mechanism that explains the re-
lationship between depressive symptoms and CV morbidity
remains incompletely understood, some of the same physio-
logical alterations that have been proposed to contribute to CV
morbidity in MDD have also been described in patients with
subclinical levels of depression. For example, altered platelet
function has been demonstrated in patients with subclinical
depressive symptoms (53). Although the current study sug-
gests that depressive symptoms are associated with alterations
in CV reactivity, further research is needed to replicate this
finding and to understand whether altered CV reactivity is
associated with adverse CV outcomes in patients with sub-
clinical depressive symptoms.
There are a number of next steps suggested by this study.
First, a research diagnostic interview was not administered.
Although subjects were excluded if they had a MDD or other
DSM-IV Axis I psychiatric illness, a standardized diagnostic
cular resistance. The interaction of stress (base versus task) and mood (high
depressive symptoms versus low depressive symptoms) on systemic vascular
resistance was significant at p ? 0.01.
Interaction of depressive symptoms and stress on systemic vas-
DEPRESSIVE SYMPTOMS AND PERIPHERAL RESISTANCE
511 Psychosomatic Medicine 67:509–513 (2005)
measure was not used, and we cannot definitively rule out the
presence of MDD. Second, only 24 subjects had high levels of
depression. In future research, it would be useful to study a
larger group of subjects that includes both a subgroup of
subjects with MDD as well as a subgroup of subjects with a
broad range of subsyndromal depressive symptoms. Addition-
ally, because there is ample research showing the values
obtained from a single reactivity paradigm administered at a
single time have limited reproducibility, future studies might
also profitably compare the hemodynamic and autonomic
effects of depressive symptoms in terms of responses elicited
by multiple stressors on several occasions (54). What is
needed to interpret and understand the biologic significance of
the current findings is a study in three groups of subjects (i.e.,
MDD, subclinical depressive symptoms, and healthy volun-
teers) that implements multiple tasks (i.e., one task such as the
MSTT that probes alpha adrenergic functioning, as well as a
second task that perturbs the beta adrenergic system) on
several occasions. Although the current data do not support
general statements about the effects of depressive symptoms
on cardiovascular reactivity, and the specific biologic signif-
icance of the observed depression by stress interaction on
SVR remains uncertain, our study does provide a useful
groundwork for follow-up studies that may examine how the
presence, and potentially treatment, of depressive symptoms
affects CV reactivity.
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Systemic vascular resistance
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SD ? standard deviation; NS ? not significant; HRV ? heart rate variability.
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