Download Type D Personality Is Associated with the Development of Stress

ann. behav. med.
DOI 10.1007/s12160-013-9474-x
ORIGINAL ARTICLE
Type D Personality Is Associated with the Development
of Stress Cardiomyopathy Following Emotional Triggers
Angelo Compare, Ph.D & Riccardo Bigi, MD &
Pedro Silva Orrego, MD & Riccardo Proietti, MD &
Enzo Grossi, MD & Andrew Steptoe, Ph.D
# The Society of Behavioral Medicine 2013
Abstract
Background Stress cardiomyopathy (SCM) can be triggered by emotional events. Recently, type D personality
has been established as an independent predictor of acute
cardiac adverse events.
Purpose We sought to examine whether type D personality
can be identified in SCM patients.
Methods A case–control study with 37 SCM patients, 37
myocardial infarction (AMI) patients, who both experienced
emotional triggering, and 37 SCM patients without emotional triggers was performed. The DS14 and Interview for
Recent Life Events were administered.
Results Twenty-eight (76 %) SCM emotional trigger
patients were categorized as type D compared with 13
(43 %) SCM patients without emotional trigger and 12
(32 %) AMI patients (p<0.001). SCM patients with emotional triggers had higher scores on the social inhibition
subscale than the other patient groups.
A. Compare (*)
University of Bergamo, Bergamo, Italy
e-mail: [email protected]
R. Bigi
Department of Cardiovascular Sciences,
University School of Medicine, Milan, Italy
P. S. Orrego
Interventional Cardiology Unit, Hospital Fatebenefratelli,
Milan, Italy
R. Proietti
Department of Cardiology, Hospital L. Sacco, Milan, Italy
E. Grossi
Centro Diagnostico Italiano, CDI, Milan, Italy
A. Steptoe
Psychobiology Group, Department of Epidemiology and Public
Health, University College London, London, UK
Conclusions The present study highlights the possible link
between type D, with a specific key role for social inhibition
component, and increased biological reactivity to acute
emotional stress.
Keywords Stress cardiomyopathy . Case–control Studies .
Personality traits . Emotional triggering . Type D
Introduction
During the last few years, there has been increasing awareness of specific transient cardiomyopathy, referred to as
takotsubo or stress cardiomyopathy (SCM) [1–3], that has
a clinical presentation indistinguishable from an acute myocardial infarction (AMI). The main features of stress cardiomyopathy are transient apical left ventricular dysfunction
that mimics myocardial infarction, but in the absence of
significant coronary artery disease. Several variants, including mid-ventricle and basal inverted patterns, have also been
reported [4]. An excessive catecholamine-induced sympathetic stimulation of the heart, causing an acute stunning of
the myocardium, has been suggested as a pivotal mechanism in stress cardiomyopathy [2]. This hypothesis is further
supported by the observation that stress cardiomyopathy
patients with pheochromocytoma develop transient reduction in left ventricular systolic function in conjunction with a
rise in plasma catecholamine levels [2, 5]. Despite evidence
that the myocardial stunning of stress cardiomyopathy may
be sympathetically mediated, the precise pathogenesis of
this disorder remains incompletely understood.
Frequently, stress cardiomyopathy may be triggered by
acute emotionally stressful events in the hours preceding
symptom onset. Emotional triggers have been observed in
20–33 % of patients in retrospective studies [6, 7] and 36–
47 % in prospective clinical cohort studies [8, 9]. Since most
people are subjected to repeated emotional and physiologic
ann. behav. med.
acute stressors throughout their lives, the fact that only a
relatively small number develop stress cardiomyopathy suggests that there are likely to be risk factors that increase
individual susceptibility. These risk factors may influence a
person’s physiologic response to acute stress and increase
their vulnerability to the pathophysiologic mechanisms that
result in myocardial stunning. Studies support the role of
hormonal processes [10], endothelial dysfunction [6], and
genetic factors [11] as susceptibility factors for stress cardiomyopathy. In terms of mental health, stress cardiomyopathy patients appear to have a high prevalence of mixed
depression and anxiety, ranging between 21 and 40 %
[12–14]. Studies that have distinguished anxiety and depression have shown rates of 30–56 % for anxiety [15, 16] and
36–48 % for depression [15, 16]. Additionally, a recent
study showed high trait anxiety in 60 % of stress cardiomyopathy subjects [17]. Although some studies have focused
on pre-morbid psychiatric symptoms or disorders, no research to date has specifically investigated the personality
traits of stress cardiomyopathy patients. Investigation of the
characteristic patterns of thoughts, feelings, and behaviors
of stress cardiomyopathy patients would promote understanding of the personality traits that may make some people
susceptible to the deleterious cardiovascular effects of sympathetic stimulation following an acute emotional stressor.
Findings from behavioral genetic studies support the
notion that stable personality traits may play a role in
stress-related autonomic reactions. Specific personality
traits are associated with genotypic variations in hypothalamic–pituitary–adrenocortical (HPA) afferents and seem to
regulate the HPA response to psychological and physiological stressors [18, 19]. One personality trait that may be
particularly relevant is type D personality [20].
Type D personality is thought to be a relatively stable
personality trait [21] characterized by high negative affectivity (NA—tendency to experience negative emotions such
as dysphoria, anxiety, irritability, and negative view of self
across time/situations) and social inhibition (SI—tendency
to inhibit the expression of emotions/behaviors in social
interactions to avoid disapproval by others or feeling
inhibited, tense, and insecure when with others). Several
studies have demonstrated that type D is an independent
predictor of major adverse cardiac events in patients with
coronary heart disease [22–25]. The prevalence estimates of
type D personality are between 24 and 31 % in the general
population [26, 27] and ranges between 15 % [28] and 53 %
[29], respectively, in coronary artery disease (CAD) and
hypertensive patients. Recent cross-cultural analyses of coronary heart disease patients have shown that the prevalence
of type D personality ranges between 24 and 37 % [30].
Although these studies have confirmed a significant association between type D personality and mortality and nonfatal
myocardial infarction, heterogeneity between studies was
large and the prognostic effects of type D have decreased
considerably in recent compared with older studies [31–34].
Recent studies [31, 35, 36] have been critical of the
conceptualization of type D as a personality construct based
on the practice of dichotomizing the negative affectivity and
social inhibition scales and defining type D as being in the
upper division of both scales. It has been argued that type D
is better represented as a dimensional than a categorical
construct and that the categorization of variables is not an
appropriate representation of the synergistic combination of
the two dimensions that supposedly underlies the concept
[37]. Our primary analyses were therefore based on continuously distributed scores on the two components and their
interactions, though we also present results based on the
categorization of patients into high and low negative affectivity and social inhibition groups.
There has been no previous research on type D personality
in stress cardiomyopathy patients. However, a recent laboratory study [38] involving healthy women showed that type D
individuals displayed reduced cardiac relative to vascular
responses to acute laboratory stress, consistent with other
studies indicating that type D personality is associated with
modified cardiovascular responses to acute psychological
stress [39, 40]. It is possible, therefore, that type D personality
may make some individuals more susceptible to stress cardiomyopathy reactions following acute emotional stressors.
Accordingly, the aim of this controlled investigation was
to test whether emotion-triggered stress cardiomyopathy
patients differ in type D personality from those without
emotion-triggered stress cardiomyopathy. In order to discover whether any differences were due to emotional triggering per se, we also included a group of acute myocardial
infarction patients who experienced emotional triggering
matched for socio-demographic variables. We hypothesized
that type D would be more common in emotionally triggered
stress cardiomyopathy than in the other two groups of patients.
Method
In this cross-sectional study, 37 stress cardiomyopathy patients
who experienced emotional triggering (4 males, 33 females;
mean age, 66 years, SD=12.8), 37 stress cardiomyopathy
patients who did not experience emotional triggering (4 males,
33 females; mean age, 66 years, SD=11.1), and 37 acute
myocardial infarction patients who also experienced emotional
triggers (4 males, 33 females; mean age, 66 years, SD=10.1)
were enrolled. Both patients with stress cardiomyopathy and
those with acute myocardial infarction were newly diagnosed
and had not previously been treated at the time of study. The
stress cardiomyopathy patients were admitted consecutively to
our hospital-based specialized cardiovascular clinics over a 3
year period. Stress cardiomyopathy was diagnosed according to
ann. behav. med.
the Mayo Clinic diagnostic criteria [41] including: (1) an acute
cardiac event typically presenting with substernal chest pain;
(2) systolic dysfunction with a marked left ventricular contraction abnormality, extending beyond the geographic territory
of a single epicardial coronary artery, assessed with left
ventricular angiography, cardiovascular magnetic resonance
imaging, or two-dimensional echocardiography; and (3) absence of obstructive atherosclerotic coronary artery stenosis
(i.e., ≤50 % luminal narrowing of the epicardial arteries by
angiography). The most common presenting cardiovascular
symptoms were substantial chest pain (n=46), exertional
dyspnea (n=18), and syncope (n=11).
Careful history taking identified whether significant stressful events immediately preceded the presentation of stress
cardiomyopathy. Preliminary assessment of trigger events
was carried out by cardiologists during admission to the emergency unit. Information about trigger events was, where possible, confirmed with the companion (if any) who accompanied
the patient to the emergency unit. Thirty-seven of the 75 stress
cardiomyopathy patients (49.33 %) reported an emotional trigger within the past 48 h, while 38 (50.66 %) experienced a
physical trigger (of which 71 % was acute respiratory infection,
26 % post-surgical/fracture, and 3 % migraine headache) or
else no trigger event. Over the same period of stress cardiomyopathy enrolment, the first consecutive 37 acute myocardial
infarction patients who reported acute emotional triggers, and
who 1:1 matched cases on socio-demographic variables (e.g.,
age, sex, marital status, and living alone condition), were
selected from a larger population of more than 300 acute
myocardial infarction admitted to the emergency unit. Acute
myocardial infarction, hypertension, diabetes, and hypercholesterolemia were defined according to standard criteria [42].
Informed consent was obtained in all cases, except for one
stress cardiomyopathy patient with migraine headache as a
physical trigger who declined to participate.
Psychological Assessment
All patients were interviewed by two clinical psychologists
who were blind to the patients’ group. Interviews involved a
thorough assessment of emotional trigger events that occurred
within 48 h of symptom onset and were performed within 8 h
of initial screening in order to avoid memory distortion effects.
Type D personality assessment was performed by two different clinical psychologists 3 months after initial screening
and without knowledge of the clinical diagnosis of the
patients. The clinical psychologist made sure that all subjects
provided complete data in the questionnaire.
Interview for Recent Life Events
Formal assessment of emotional trigger events in a period of
48 h prior to stress cardiomyopathy symptom onset was
carried out using the Interview for Recent Life Events
[43]. The Interview for Recent Life Events was administrated by two clinical psychologists 8 h after the initial
stress cardiomyopathy assessment by the cardiologist.
Interview for Recent Life Events specifies 64 different
life events in nine areas. For each life event, detailed
information was recorded in order to assess the independence from the illness and objective adverse impact
and to compute the standardized Paykel Stress Index.
We also calculated the hours before symptom onset at which
the event occurred. The reliability coefficient between the two
interviewers was 0.88.
Type D Personality
The Type D Scale (DS14) was used to assess type D personality. The DS14 consists of two subscales, each of seven
items, measuring NA and SI [29]. Items are answered on a
five-point Likert scale, ranging from 0 (false) to 4 (true),
with total scores ranging from 0 to 28 for both subscales.
Considering recent type D literature which suggests that
type D personality is a dimensional construct [44], continuous scores for negative affectivity, social inhibition, and
their interaction, NA×SI, were used in the analysis. We also
analyzed type D personality as a categorical construct, with
negative affectivity and social inhibition components being
dichotomized on the basis of a score ≥10 on both subscales.
In the present study, the internal consistencies, calculated by
Cronbach’s alpha, for negative affectivity and social inhibition subscales were 0.89 and 0.91, respectively.
Statistical Analysis
Using a conditional regression model and Monte Carlo simulation, a minimum of 70 patients (35 cases and 35 acute
myocardial infarction patients) was needed to detect a medium
effect, assuming a 1:1 case–control ratio with an alpha level of
0.05 and power of 0.80. Categorical values are expressed as
frequency and percentage, while continuous values are
expressed as the mean±SD. Differences in categorical variables (sex, marital status, living condition, risk factors, chest
pain, Type D and subscales, social inhibition and negative
affectivity, classifications) between groups were analyzed using the χ2 test. Differences among groups were assessed by
one-way ANOVA for continuous variables followed by
Bonferroni-corrected post hoc tests. Hierarchical logistic regression analyses with z-transformed negative affectivity and
social inhibition scores, entering the main effect terms followed by the NA×SI interaction, were used to test differences
among groups. These analyses were adjusted for diabetes,
history of CAD, systolic blood pressure (SBP), and hypertension since these factors may be particularly relevant to the
development of stress cardiomyopathy, as indicated in Table 1.
ann. behav. med.
The final results are presented as adjusted odds ratios (ORs)
with 0.95 confidence intervals (CI) and exact p values. Statistical analyses were performed with SPSS, version 18.0 (SPSS
Institute Inc., Chicago, IL).
Results
Socio-demographic and clinical characteristics of stress cardiomyopathy and acute myocardial infarction patients are
reported in Table 1. Patients with stress cardiomyopathy and
acute myocardial infarction were not significantly different
with regard to age, sex, marital status, living alone, and ST
segment elevation (Table 1). As expected, patients with
acute myocardial infarction had significantly higher levels
of troponin T, creatine kinase-MB fraction, white cell count,
hypertension, and systolic blood pressure compared with
stress cardiomyopathy patients. Moreover, acute myocardial infarction patients had a higher prevalence of diabetes
and history of coronary artery disease compared with the
other groups.
Emotional Trigger Events
The acute emotional events experienced by patients in this
study are summarized in Table 2. Loss experiences
through death or separation from someone close (son,
father/mother, husband, friend, etc.) were the most prevalent emotional triggers in both the stress cardiomyopathy
and acute myocardial infarction groups (Table 2). Ten
(27.0 %) stress cardiomyopathy patients and nine
(24.3 %) acute myocardial infarction patients had severe
loss experiences within 12 h of cardiac symptom onset.
Other common events were job loss, a serious quarrel, and
the unexpected hospitalization of someone close. The
overall severity score for emotional triggers (Paykel Stress
Index) and their timing did not differ significantly between the two groups.
Table 1 Comparison of patients with SCM, patients with AMI, and healthy controls in terms of demographic and clinical characteristics
Variables
SCM-t (n=37)
SCM-nt (n=38)
AMI (n=37)
p value
Age, mean (SD)
Male, n (%)
Marital status, n (%)
Married
Single
Divorced
Living alone, n (%)
Cardiac risk factors
Smoking, n (%)
Diabetes, n (%)
History of CAD, n (%)
Hypertension, n (%)
BMI, mean (SD)
Clinical presentation
Chest pain, n (%)
EF, mean (SD)
TT, mean (SD)
CK-MB, mean (SD)
66 (12.8)
4 (10.1)
66 (11.1)
4 (10.8)
66 (10.1)
4 (10.8)
0.81
0.92
0.78
22 (59.5)
13 (35.1)
2 (5.4)
6 (16.2)
20 (54.1)
14 (37.8)
3 (8.1)
7 (18.9)
21 (56.8)
11 (29.7)
5 (13.5)
8 (21.6)
5 (13.5)
4 (10.8)
5 (13.5)
4 (10.8)
23.8 (3.3)
4 (10.8)
2 (5.4)
4 (10.8)
2 (5.4)
23.1 (2.4)
7 (18.9)
18 (48.6)
19 (51.4)
10 (27.0)
23.6 (3.1)
0.58
0.64
0.36
0.04c
0.03c
0.03c
0.37
32 (86.0)
24.0 (5.6)
2.6 (3.7)
11.8 (5.9)
0 (0.0)
26.3 (4.4)
0.0 (0.0)
0.0 (0.0)
32.0 (86.0)
27.0 (4.4)
9.4 (4.1)
28.5 (6.3)
0.74
0.83
0.04a,b
0.03a,b
7.3 (4.2)
90.2 (5.3)
117.2 (2.1)
4.7 (3.1)
89.4 (3.4)
115.2 (2.3)
12.4 (5.6)
95.3 (2.3)
124.1 (3.8)
0.02c
0.54
0.02c
WBCC, mean (SD)
HR, mean (SD)
SBP, mean (SD)
CAD coronary artery disease, SBP systolic blood pressure
(in millimeters of mercury), HR heart rate (in beats per minute), WBCC white blood cell count (×103 /μL), EF ejection fraction (in percent), BMI
body mass index (in kilograms per square meter), CK-MB Creatine kinase-MB fraction (in nanograms per milliliter), TT troponin T (in nanograms
per milliliter), SCM-t stress cardiomyopathy patients with emotion triggers, SCM-nt stress cardiomyopathy patients without emotion triggers, AMI
acute myocardial infarction
a
p<0.01, SCM-t and AMI vs. SCM-nt
b
p<0.01, SCM-nt and AMI vs. SCM-t
c
p<0.01, SCM-t and SCM-nt vs. AMI
ann. behav. med.
Table 2 Emotional trigger events on the Interview for Recent Life Events in SCM and AMI patients
Emotional trigger categories
N (%)
PSI, mean (SD)
Hours before symptom onset, mean (SD)
SCM-t
AMI
SCM-t
AMI
SCM-t
AMI
Loss
Sudden hospitalization—others
Diagnosis of illness
Judicial notification
Quarrel
10 (27.0)
7 (18.9)
3 (8.1)
1 (2.7)
6 (16.2)
9 (24.3)
6 (16.2)
4 (10.8)
1 (2.7)
8 (21.6)
18.1
15.3
14.6
13.8
12.1
(0.8)
(0.0)
(0.0)
(0.0)
(0.0)
17.1 (1.3)
15.3 (0.0)
14 (0.0)
13.8 (0.0)
12.1 (0.0)
6.3
5.7
6.7
6.0
6.0
7.7
5.0
6.5
7.0
6.9
Job loss
Eviction from home
Total
6 (16.2)
4 (10.8)
7 (18.9)
2 (4.4)
11.7 (1.1)
8.5 (0.0)
14.1 (3.1)
13.6 (1.6)
8.5 (0.0)
14.6 (2.0)
6.0 (2.5)
6.3 (2.6)
6.1 (1.9)
(2.3)
(1.8)
(1.2)
(0.0)
(2.1)
(3.4)
(0.6)
(3.3)
(0.0)
(2.4)
6.6 (3.5)
8.0 (1.4)
6.7 (2.7)
SCM-t stress cardiomyopathy patients with emotion triggers, AMI acute myocardial infarction, PSI Paykel Stress Index
Type D Personality
In the statistical analysis of the continuous score of two components of Type D (Table 3), the three groups differed on the
social inhibition subscale (p<0.001), but not on the negative
affectivity scale. Subsequent tests indicated that social inhibition scores were higher in patients with emotionally triggered
stress cardiomyopathy than non-emotionally triggered stress
cardiomyopathy or acute myocardial infarction (p<0.01),
while the SCM without emotional triggers and acute myocardial infarction groups did not differ. Additionally, analysis of
type D as a categorical construct showed that of the 37 SCM
patients with emotional triggers, 28 (76 %) were categorized
as type D compared with 13 (43 %) SCM patients without
emotional triggers and 12 (32 %) acute myocardial infarction
patients. The difference among the three groups was significant (χ2 =15.12; see Table 3 and Fig. 1). The differences
between the three groups were also significant for social
inhibition (χ2 =11.89) and for negative affectivity (χ2 =
9.93). Post hoc analyses revealed that for type D classification,
the difference was significant between SCM with emotional
triggers and both SCM without emotional triggers and acute
myocardial infarction, and between SCM without emotional
triggers and acute myocardial infarction. For negative affectivity, the differences were significant between SCM with
emotional triggers and SCM without emotional triggers in
comparison with acute myocardial infarction patients, but
did not differ from each other. For social inhibition, the differences were significant between SCM with emotional triggers
and SCM without emotional triggers, and between SCM with
emotional triggers and acute myocardial infarction, but not
between SCM without emotional triggers and acute myocardial infarction.
Results of the hierarchical logistic regressions are summarized in Table 4. The negative affectivity and social inhibition
scales were z-transformed for these analyses so that the interaction between negative affectivity and social inhibition gave
equal weight to the two components. After adjusting for diabetes, history of CAD, SBP, and hypertension, the NA×SI interaction term distinguished stress cardiomyopathy from acute
Table 3 Comparison between SCM, with and without emotional triggers, and AMI patients on Type D and subscales in terms of categorical and
continuous variables
Variables
SCM-t (n=37)
SCM-nt (n=37)
AMI (n=37)
p value
14.3 (2.1)
25.4 (2.4)a
13.2 (3.4)
13.4 (2.1)
14.8 (2.6)
11.1 (3.2)
0.44
<0.001
28 (76)a
29 (78)b
34 (92)a
16 (43)c
27 (74)c
17 (44)
12 (32)
14 (38)
15 (41)
<0.001
0.04
0.01
Continuous variables
Type D-NA, mean (SD)
Type D-SI, mean (SD)
Categorical variables
Type D classification, n (%)
Type D-NA ≥10, n (%)
Type D-SI ≥10, n (%)
NA negative affectivity, SI social inhibition, SCM-t stress cardiomyopathy patients with emotion triggers, SCM-nt stress cardiomyopathy patients
without emotion triggers, AMI acute myocardial infarction
a
p<0.01, SCM-t vs. AMI and SCM-nt
b
p<0.01, SCM-t vs. AMI
c
p<0.01, SCM-nt vs. AMI
ann. behav. med.
Fig. 1 Prevalence of type D personality and subscales among groups.
NA negative affectivity, SI social inhibition, SCM-t stress cardiomyopathy patients with emotion triggers, SCM-nt stress cardiomyopathy
patient without emotion triggers, AMI acute myocardial infarction
(**p<0.01; *p<0.05)
myocardial infarction (OR=1.72, 95% CI=1.21–2.11, p=
0.03), indicating that the interaction between the two components is crucial. Within stress cardiomyopathy, the odds of
belonging to the SCM with emotional triggers compared with
SCM without emotional triggers group were 1.11 (p=0.04) for
every unit increase in the NA by SI interaction and 1.86
(p=0.02) in comparison with the acute myocardial infarction
group. Scores on the social inhibition component also distinguished SCM with emotional triggers from acute myocardial
infarction (OR=1.92, p=0.01) and SCM with emotional triggers from SCM without emotional triggers (OR=1.53, p=0.04).
Discussion
The results of this study document for the first time a higher
prevalence of type D personality in stress cardiomyopathy
patients, both with and without emotional triggers, compared
with emotion-triggered acute myocardial infarction patients. In
particular, the social inhibition component of type D personality
seems to represent a trait which differs between stress cardiomyopathy patients who experience emotional triggers and
matched stress cardiomyopathy patients without emotional triggers and acute myocardial infarction patients. The prevalence of
type D in stress cardiomyopathy patients was not only higher
than the comparison group tested in this study but also higher
than the levels observed in other studies of acute myocardial
infarction patients [28] and in general populations [26, 27].
As noted in the introduction, there have been criticisms of the
categorical approach to type D personality. However, it is worth
noting the prevalence of type D as conventionally defined in
comparison with rates in different cardiac groups. General
population studies have reported a prevalence of 22 % [45] of
type D personality. Within the cardiac patient population, the
prevalence rate has ranged from 29 % [46] in general cardiac
patients to 37 % in acute myocardial infarction patients [30].
Our findings show a prevalence rate of type D personality
within the acute myocardial infarction group of 32 %, similar
to that shown elsewhere in the literature. The prevalence of type
D in the group of stress cardiomyopathy patients was 59.5 %, a
greatly elevated level. There are no other data in the literature on
stress cardiomyopathy with which to compare our results.
Our research underscores some differences in results between considering type D as a dimensional rather than a
categorical construct, as has been suggested by others [31,
35, 36]. Both the analyses of continuous scores on the two
dimensions and the categorical analyses show that the differences in the prevalence of type D personality between groups
were primarily attributable to social inhibition, with the synergistic interaction between social inhibition and negative affectivity being driven in large part by elevated social inhibition
scores in the stress cardiomyopathy patients (SCM) with emotional triggers group. As shown in Table 2, patients who
experienced emotionally triggered stress cardiomyopathy had
a substantially higher rate of elevated social inhibition (92 %)
compared with stress cardiomyopathy patients without emotional triggers (44 %). The difference between these two
Table 4 ORs and 95% CIs between groups
SCM vs. AMIa
Type D-NA (z score)
Type D-SI (z score)
NA by SI
SCM-t vs. SCM-ntb
SCM-t vs. AMIa
SCM-nt vs. AMIa
OR
95% CI
p
OR
95% CI
p
OR
95% CI
p
OR
95% CI
p
1.01
1.04
1.72
0.82–1.15
0.92–1.21
1.21–2.11
0.11
0.13
0.03
1.05
1.53
1.11
0.54–1.23
1.12–2.28
1.09–2.02
0.21
0.04
0.04
1.00
1.92
1.86
0.89–1.12
1.22–2.45
1.12–2.53
0.38
0.01
0.02
1.22
0.99
1.18
0.97–1.87
0.72–1.04
0.89–1.68
0.21
0.32
0.33
NA negative affectivity, SI social inhibition, SCM-t stress cardiomyopathy patients with emotion triggers, SCM-nt stress cardiomyopathy patients
without emotion triggers, AMI acute myocardial infarction
a
AMI is the reference group
b
SCM-nt is the reference group
ann. behav. med.
groups in elevated negative affectivity was much smaller (78
vs. 74 %). Denollet [29] defines social inhibition as the “tendency to inhibit expression of emotions/behaviors in social
interaction to avoid disapproval of others” and the tendency
to “feel inhibited, tense, and insecure when with others” (p.
89). Social inhibition, a construct conceptually related to emotional inhibition and suppression, has been linked to cardiovascular reactivity to acute stress [47]. Findings from theories
of emotion and self-regulation indicate that expressive suppression increases sympathetic activation of the cardiovascular
system [48, 49]. Indeed, the tendency not to share negative
thoughts and feelings, such as those resulting from stressful
emotional events, has been shown to be associated with exaggerated sympathetic and cardiovascular responses in response
to later events [50, 51]. Additionally, high dispositional negative affectivity may serve to amplify negative emotional
responses following stressful events, and this may have biological correlates that stimulate cardiac dysfunction.
Emotional triggering is recognized as a significant phenomenon in a proportion of acute myocardial infarction
cases [52]. The acute myocardial infarction comparison
group was selected on the basis of reporting emotional
triggers, so the prevalence of triggers is not representative
of patients with acute myocardial infarction in general.
Emotional triggering of acute myocardial infarction has
previously been associated with chronic life stress and depression in the post-hospitalization period [53], so the elevated negative affectivity scores of the acute myocardial
infarction group were anticipated. However, it is striking
that social inhibition scores were not raised in the acute
myocardial infarction group, suggesting a specific association
of social inhibition with stress cardiomyopathy pathology.
Our findings lead to the hypothesis that there is a vulnerable personality profile for stress cardiomyopathy reactions
after emotional triggers. A possible explanation is that type
D personality is associated with heightened cardiovascular
reactivity to acute stress [39] and that social inhibition is
associated with higher cardiovascular reactivity [54], lower
cardiovascular recovery and heart rate variability [55], and
with overactivity of the sympathetic nervous system [56]. In
our stress cardiomyopathy sample, the prevalence of conventional cardiac risk factors was lower than that of acute myocardial infarction patients. This finding confirms previous
reports [57] which indicate that the pathophysiology of the
syndrome differs from that of coronary heart disease. Current
evidence emphasizes the pathophysiological importance of
extreme sympathetic nervous system activation in stress cardiomyopathy and suggests that endothelial dysfunction is
involved [6]. Thus, type D personality traits could be conceptualized as contributing to individual differences in cardiovascular reactivity to acute emotional stressors through
sympathetic outflow to the heart, with cardiac noradrenaline
spillover potentially achieving very high values [58].
The emotional trigger data collected in this study show that
27 % of stress cardiomyopathy patients experienced the death
of someone close between 3 and 12 h of symptom onset. This
finding is analogous with data from previous retrospective
studies where rates of grief/loss trigger events in stress cardiomyopathy patients varied from 23 % [59] to 28 % [7].
Strengths and Limitations
Emotional triggers were assessed with thorough systematic
procedures and established questionnaires rather than impressionistic clinical observations, as in much previous
work. The three groups were carefully characterized and
well matched socio-demographically. The proportion of
male emotion-triggered stress cardiomyopathy patients
(10.8 %) was similar in our study and others [7, 60],
strengthening the possibility of generalizing the results of
the present study to the emotion-triggered stress cardiomyopathy population. But since other studies have found different proportions of patients experiencing emotional
triggers, the results cannot necessarily be generalized to all
stress cardiomyopathy. However, the sample size was small
in this cross-sectional observational study and causal conclusions cannot be drawn. A limitation to the study is the
timing of the personality assessment. This was performed
3 months after hospitalization to allow the stabilization
of the patient’s emotional condition. We do not know whether
ratings would have been similar if the assessment had
taken place before the clinical episode. However, if the
social inhibition and negative affectivity effects were secondary to cardiac disease, one might have expected a worse
profile in the acute myocardial infarction group since they
suffered from more sustained myocardial damage. This is
not the pattern that we observed.
Conclusions
In conclusion, the present study shows for the first time a
link between type D personality and emotionally triggered stress cardiomyopathy. Our results highlight the
possible link between type D personality and increased
biological reactivity to acute emotional stress. They are
in keeping with findings from experimental studies
showing that the cardiovascular effects of acute stress
may be amplified by the presence of chronic psychosocial stress [61, 62]. The key role of social inhibition of
negative emotions as a characteristic of type D personality in emotionally triggered stress cardiomyopathy
patients emphasizes the importance of emotional regulation processes in biological reactions to acute emotional
stress. This implies that the risk of a stress
ann. behav. med.
cardiomyopathy event may depend not only on the
individual’s cardiovascular vulnerability following stress
exposure but also on his or her coping mechanisms.
Further investigation may shed light both on these emotional regulatory processes and on the protective role of
coping mechanisms in the links between personality and
susceptibility to stress cardiomyopathy following acute emotional events.
15.
16.
17.
Conflict of Interest Statement The authors have no conflict of
interest to disclose. Andrew Steptoe is supported by the British Heart
Foundation.
18.
19.
References
20.
1. Satoh H, Tateishi H, Uchida T, et al. Takotsubo-type cardiomyopathy due to multivessel spasm. In: Kodama K, Haze K, Hon
M, eds. Clinical aspect of myocardial injury, from ischemia to
heart failure. Tokyo: Kagakuhyouronsya Co.; 1990:56–64 (in
Japanese).
2. Wittstein IS, Thiemann DR, Lima JA, et al. Neurohumoral features
of myocardial stunning due to sudden emotional stress. N Engl J
Med. 2005;352:539–548.
3. Wittstein IS. Stress cardiomyopathy: A syndrome of catecholaminemediated myocardial stunning? Cell Mol Neurobiol. 2012;32:847–
857.
4. Hurst RT, Askew JW, Reuss CS, et al. Transient midventricular
ballooning syndrome: A new variant. J Am Coll Cardiol.
2006;48:579–583.
5. Brotman DJ, Golden SH, Wittstein IS. The cardiovascular toll of
stress. Lancet. 2007;370:1089–1100.
6. Martin EA, Prasad A, Rihal CS, Lerman LO, Lerman A.
Endothelial function and vascular response to mental stress are
impaired in patients with apical ballooning syndrome. J Am Coll
Cardiol. 2010;56:1840–1846.
7. Singh NK, Rumman S, Mikell FL, Nallamothu N, Rangaswamy C.
Stress cardiomyopathy: Clinical and ventriculographic characteristics in 107 North American subjects. Int J Cardiol. 2010;141:
297–303.
8. Previtali M, Repetto A, Camporotondo R, et al. Clinical characteristics and outcome of left ventricular ballooning syndrome in a
European population. Am J Cardiol. 2011;107:120–125.
9. Sharkey SW, Windenburg DC, Lesser JR, et al. Natural history and
expansive clinical profile of stress (tako-tsubo) cardiomyopathy. J
Am Coll Cardiol. 2010;55:333–341.
10. Lavi S, Nevo O, Thaler I, et al. Effect of aging on the cardiovascular regulatory systems in healthy women. Am J Physiol Regul
Integr Comp Physiol. 2007;292:R788–R793.
11. Spinelli L, Trimarco V, Di Marino S, et al. L41Q polymorphism of
the G protein coupled receptor kinase 5 is associated with left
ventricular apical ballooning syndrome. Eur J Heart Fail.
2010;12:13–16.
12. Vidi V, Rajesh V, Singh PP, et al. Clinical characteristics of takotsubo cardiomyopathy. Am J Cardiol. 2009;104:578–582.
13. Regnante RA, Zuzek RW, Weinsier SB, et al. Clinical characteristics and four-year outcomes of patients in the Rhode Island
Takotsubo Cardiomyopathy Registry. Am J Cardiol. 2009;103:
1015–1019.
14. Mudd JO, Kapur NK, Champion HC, Schulman SP, Wittstein IS.
Patients with stress-induced (takotsubo) cardiomyopathy have an
21.
22.
23.
24.
25.
26.
27.
28.
29.
30.
31.
32.
increased prevalence of mood disorders and antidepressant use
compared to patients with acute myocardial infarction. J Card
Fail. 2007;13:S176.
Sobnosky S, Shah A, Aharonian VJ, et al. Abstract 20134:
Frequency of psychiatric disorders in persons with stress induced
cardiomyopathy. Circulation. 2010;122:A20134.
Summers MR, Lennon RJ, Prasad A. Pre-morbid psychiatric and
cardiovascular diseases in apical ballooning syndrome (tako-tsubo/
stress-induced cardiomyopathy): Potential pre-disposing factors? J
Am Coll Cardiol. 55:700–701
Del Pace S, Parodi G, Bellandi B, et al. Anxiety trait in patients
with stress-induced cardiomyopathy: A case–control study. Clin
Res Cardiol. 2011;100:523–529.
Uhart M, McCaul ME, Oswald LM, Choi L, Wand GS. GABRA6
gene polymorphism and an attenuated stress response. Mol
Psychiatry. 2004;9:998–1006.
Wittstein IS. Apical-ballooning syndrome. Lancet. 2007;370:545–
547.
Molloy GJ, Perkins-Porras L, Strike PC, Steptoe A. Type-D personality and cortisol in survivors of acute coronary syndrome.
Psychosom Med. 2008;70:863–868.
Kupper N, Boomsma DI, de Geus EJ, Denollet J, Willemsen G.
Nine-year stability of type D personality: Contributions of genes
and environment. Psychosom Med. 2011;73:75–82.
Denollet J, Sys SU, Stroobant N, et al. Personality as independent
predictor of long-term mortality in patients with coronary heart
disease. Lancet. 1996;347:417–421.
Denollet J, Vaes J, Brutsaert DL. Inadequate response to treatment
in coronary heart disease: Adverse effects of type D personality
and younger age on 5-year prognosis and quality of life.
Circulation. 2000;102:630–635.
Martens EJ, Mols F, Burg MM, Denollet J. Type D personality
predicts clinical events after myocardial infarction, above and
beyond disease severity and depression. J Clin Psychiatry.
2010;71:778–783.
Denollet J, Pedersen SS, Vrints CJ, Conraads VM. Usefulness of
type D personality in predicting five-year cardiac events above and
beyond concurrent symptoms of stress in patients with coronary
heart disease. Am J Cardiol. 2006;97:970–973.
Grande G, Romppel M, Glaesmer H, Petrowski K, HerrmannLingen C. The Type-D Scale (DS14)—Norms and prevalence
of type-D personality in a population-based representative
sample in Germany. Personal Individ Differ. 2010;48:935–
939.
Hausteiner C, Klupsch D, Emeny R, Baumert J, Ladwig KH.
Clustering of negative affectivity and social inhibition in the community: Prevalence of type D personality as a cardiovascular risk
marker. Psychosom Med. 2010;72:163–171.
Spindler H, Kruse C, Zwisler AD, Pedersen SS. Increased anxiety
and depression in Danish cardiac patients with a type D personality: Cross-validation of the Type D Scale (DS14). Int J Behav Med.
2009;16:98–107.
Denollet J. DS14: Standard assessment of negative affectivity,
social inhibition, and type D personality. Psychosom Med.
2005;67:89–97.
Kupper N, Pedersen SS, Höfer S, et al. Cross-cultural analysis of
Type D (distressed) personality in 6222 patients with ischemic
heart disease: A study from the International HeartQoL Project.
Int J Cardiol. 2011. doi:10.1016/j.ijcard.2011.10.084
Grande G, Romppel M, Barth J. Association between type D
personality and prognosis in patients with cardiovascular diseases:
A systematic review and meta-analysis. Ann Behav Med.
2012;43:299–310.
Grande G, Romppel M, Vesper JM, et al. Type D personality and
all-cause mortality in cardiac patients—data from a German cohort
study. Psychosom Med. 2011;73:548–556.
ann. behav. med.
33. Coyne JC, Jaarsma T, Luttik ML, et al. Lack of prognostic value of
type D personality for mortality in a large sample of heart failure
patients. Psychosom Med. 2011;73:557–562.
34. Pelle AJ, Pedersen SS, Schiffer AA, et al. Psychological distress
and mortality in systolic heart failure. Circ Heart Fail. 2010;3:
261–267.
35. Bacon SL, Moullec G. Type-D personality and heart disease: It
might be ‘one small step’, but it is still moving forward: A
comment on Grande et al. Ann Behav Med. 2012;43:280–281.
36. de Voogd JN, Sanderman R, Coyne JC. A meta-analysis of spurious associations between type D personality and cardiovascular
disease endpoints. Ann Behav Med. 2012;44:136–137.
37. Kupper N, Denollet J. Type D personality as a prognostic factor in
heart disease: Assessment and mediating mechanisms. J Pers
Assess. 2007;89:265–276.
38. Howard S, Hughes BM, James JE. Type D personality and hemodynamic reactivity to laboratory stress in women. Int J
Psychophysiol. 2011;80:96–102.
39. Habra ME, Linden W, Anderson JC, Weinberg J. Type D personality is related to cardiovascular and neuroendocrine reactivity to
acute stress. J Psychosom Res. 2003;55:235–245.
40. Williams L, O’Carroll RE, O’Connor RC. Type D personality and
cardiac output in response to stress. Psychol Health. 2009;24:489–
500.
41. Bybee KA, Kara T, Prasad A, et al. Systematic review: Transient
left ventricular apical ballooning: A syndrome that mimics STsegment elevation myocardial infarction. Ann Intern Med.
2004;141:858–865.
42. Thygesen K, Alpert JS, White HD, et al. Universal definition of
myocardial infarction. Circulation. 2007;116:2634–2653.
43. Paykel ES. The interview for recent life events. Psychol Med.
1997;27:301–310.
44. Ferguson E, Williams L, O’Connor RC, et al. A taxometric
analysis of type-D personality. Psychosom Med. 2009;71:981–
986.
45. Beutel ME, Wiltink J, Till Y, et al. Type D personality as a
cardiovascular risk marker in the general population: Results from
the Gutenberg Health Study. Psychother Psychosom. 2012;81:
108–117.
46. Svansdottir E, Karlsson HD, Gudnason T, et al. Validity of
type D personality in Iceland: Association with disease severity and risk markers in cardiac patients. J Behav Med. 2012;
35:155–166.
47. Westmaas JL, Jamner LD. Paradoxical effects of social support on
blood pressure reactivity among defensive individuals. Ann Behav
Med. 2006;31:238–247.
48. Gross JJ. Emotion regulation: Affective, cognitive, and social
consequences. Psychophysiology. 2002;39:281–291.
49. Muraven M, Baumeister RF. Self-regulation and depletion of limited resources: Does self-control resemble a muscle? Psychol Bull.
2000;126:247–259.
50. Elfant D, Pal BZ, Emptage N, Capogna M. Specific inhibitory
synapses shift the balance from feedforward to feedback inhibition
of hippocampal CA1 pyramidal cells. Eur J Neurosci. 2008;
27:104–113.
51. Quartana PJ, Burns JW. Emotion suppression affects cardiovascular responses to initial and subsequent laboratory stressors. Br J
Health Psychol. 2010;15:511–528.
52. Mittleman MA, Mostofsky E. Physical, psychological and chemical triggers of acute cardiovascular events: Preventive strategies.
Circulation. 2011;124:346–354.
53. Steptoe A, Molloy GJ, Messerly-Burgy N, et al. Emotional triggering and low socio-economic status as determinants of depression
following acute coronary syndrome. Psychol Med. 2011;41:1857–
1866.
54. Gross JJ, Levenson RW. Hiding feelings: The acute effects of
inhibiting negative and positive emotion. J Abnorm Psychol.
1997;106:95–103.
55. Brosschot JF, Thayer JF. Anger inhibition, cardiovascular recovery, and vagal function: A model of the link between hostility and
cardiovascular disease. Ann Behav Med. 1998;20:326–332.
56. Roberts NA, Levenson RW, Gross JJ. Cardiovascular costs of
emotion suppression cross ethnic lines. Int J Psychophysiol.
2008;70:82–87.
57. Madhavan M, Rihal CS, Lerman A, Prasad A. Acute heart failure
in apical ballooning syndrome (takotsubo/stress cardiomyopathy):
Clinical correlates and Mayo Clinic risk score. J Am Coll Cardiol.
2011;57:1400–1401.
58. Baumert M, Lambert GW, Dawood T, et al. Short-term heart rate
variability and cardiac norepinephrine spillover in patients with
depression and panic disorder. Am J Physiol Heart Circ Physiol.
2009;297:H674–679.
59. Elesber AA, Prasad A, Lennon RJ, et al. Four-year recurrence rate
and prognosis of the apical ballooning syndrome. J Am Coll
Cardiol. 2007;50:448–452.
60. Pilgrim TM, Wyss TR. Takotsubo cardiomyopathy or transient left
ventricular apical ballooning syndrome: A systematic review. Int J
Cardiol. 2008;124:283–292.
61. Chida Y, Hamer M. Chronic psychosocial factors and acute physiological responses to laboratory-induced stress in healthy populations: A quantitative review of 30 years of investigations. Psychol
Bull. 2008;134:829–885.
62. Compare A, Proietti R, Del Forno D, et al. Vulnerable personality and takotsubo cardiomyopathy consequent to emotional
stressful events: A clinical case report. Monaldi Arch Chest
Dis. 2011;76:99–103.