SYNCOPE
The role of psychological factors in response to treatment in neurocardiogenic (vasovagal) syncope
1 Department of Psychology, Royal Victoria Infirmary, Newcastle NE1 4LP, UK; 2 Department of Psychology, University of Newcastle, Newcastle, UK; 3 Falls and Syncope Service, Care of the Elderly Offices, Royal Victoria Infirmary, Newcastle NE1 4LP, UK
Manuscript submitted 17 November 2005. Accepted after revision 18 April 2006.
* Corresponding author. Tel: +44 191 2824128; fax: +44 191 2225638. E-mail address: julia.newton{at}nuth.northy.nhs.uk
| Abstract |
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Aims Studies have established a link between vasovagal syncope (VVS) and anxiety, depression, and functional impairment. This study examines the prevalence of psychological problems in patients with VVS and whether non-responders are psychologically different from those whose symptoms respond to conservative treatment.
Methods and results Subjects with tilt-confirmed VVS completed the hospital anxiety and depression scale (HADS) (measures current levels of anxiety and depression) and the syncope functional status questionnaire (SFSQ) (syncope-specific quality-of-life measure) and participated in a semi-structured interview to ascertain potential triggers, thought content, and coping strategies. In this study, 41 subjects participated. There was no difference in gender and age duration of symptoms between responders (n=21) and non-responders (n=20). Non-responders were significantly more anxious (P=0.003) and depressed (P=0.003) and had a higher level of state (P=0.008) and trait (P=0.004) anxiety than responders. Non-responders reported more fear/worry (P=0.02), a significantly higher degree of impairment owing to syncope (P=0.01), and a greater number of perceived triggers (P=0.039); on average, participants reported eight negative thoughts about the consequences of VVS, with particular emphasis on threats of physical harm or death. Non-responders had higher levels of avoidance/protection coping and rumination.
Conclusion This study has confirmed that patients with VVS have a significant degree of psychological distress, which is worthy of consideration in its own right, out with management purely aimed at reducing syncopal or pre-syncopal symptoms. Further, this distress may actually influence the natural history of what is a chronic relapsing condition and may in fact be more relevant to the patient than the number of syncopal episodes that they are experiencing.
Key Words: Vasovagal syncope, Anxiety, Depression, Coping
| Introduction |
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Vasovagal syncope (VVS) accounts for 29% of syncope.1
The difference between the clinicians' perception of important symptoms and the patients' comes from studies carried out in patients with dizziness,7
in which patients' beliefs about the negative consequences of symptoms better predicted disability after 6 months than the severity of those symptoms. Studies have shown that 21% of syncopal patients experience a high degree of worry and fear associated with their symptoms when assessed using a syncope-specific measure of impairment (mixed aetiology).8
Furthermore, heterogeneous groups of patients with recurrent syncope report high rates of anxiety (30%), panic (20%), and depression (15%).9
,10
This is severe enough that people experiencing syncope (of mixed origin) have reduced quality of life, similar to people with severe rheumatoid arthritis or chronic low back pain.11
Studies specifically examining patients with VVS are few. However, case studies and a recent case series of VVS patients from our group suggest that psychological intervention with cognitive behavioural therapy (CBT) results in dramatic improvements in symptoms12
in those with VVS resistant to conventional treatment. However, identifying those who would most benefit from psychological intervention, at what phase in the natural history of this condition, and whether an individual's reaction to their symptoms influences outcome is unclear.
Here we present, to our knowledge, the first study specifically examining the prevalence of psychological problems in patients with a definitive diagnosis of VVS and determine whether non-responders are psychologically different from those who have responded to medical treatment. Specifically, we set out to examine psychological parameters including anxiety, depression, fear/worry, coping strategies, and degree of impairment in those with VVS who had responded to conventional treatment compared with those who had not responded.
| Methods |
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This is an exploratory study employing a descriptive and comparative design. Also, it is a quantitative cross-sectional study. Ethical permission for the study was provided by the Newcastle and North Tyneside Ethical Committee and all participants provided written informed consent. An opportunity or convenience sampling method was used to allow maximum recruitment.13
- A definite diagnosis of VVS/pre-syncope, confirmed by symptom reproduction with hypotension ±bradycardiapositive head-up tilt (HUT) test.14
- Experience of at least one syncopal/pre-syncopal episode in the preceding 6 months.
- Had received conservative advice, i.e. increase fluids/salt/caffeine.
- Age over 16 years.
- Not currently consulting a mental health professional for treatment of a psychological problem, or taking anti-depressant medication.
- Previous investigations had ruled out other causes of syncope as described by current syncope guidelines, e.g. postural hypotension, cardiac abnormalities, or other serious medical condition.
Definition of treatment response
All patients attending the clinic follow a standardized management proforma that ensures consistency of management in all patients. All patients are given conservative advice (to increase salt and fluid intake and to avoid precipitating situations, etc.) and if symptoms do not resolve completely with these measures are then treated with incremental doses of fludrocortisone and midodrine as appropriate. At the time of recruitment to the study and after consideration of the current symptoms described by the participants, they were subsequently allocated (by clinician responsible) to responder (following diagnosis, the standardized clinical intervention algorithm has been applied and participant reports a significant or full recovery) or non-responder groups (following diagnosis, the standardized clinical intervention algorithm has been applied, but the symptoms have proved resistant).
Procedure
When participants agreed to take part, they were given a participant information sheet, and contact details were forwarded to the researcher. The researcher contacted participants to provide information about the study and arrange an appointment either at home (n=18) or in the psychology department (n=23). Consent to take part in the study was obtained and then a semi-structured interview was conducted and the following questionnaires were administered.
Measures
Demographic information
This included age, sex, number of months with VVS symptoms, number of months since VVS diagnosis, frequency of syncopal episodes, syncope type (syncope/pre-syncope), past history of fainting, whether the participant experienced prodromal symptoms or not, and stage of medical intervention (conservative advice/medication).
Psychological questionnaires
Subjects completed the following self-administered questionnaires:
- The hospital anxiety and depression scale (HADS)15
measures current levels of anxiety and depression (14 items).
- The syncope functional status questionnaire (SFSQ)8
is a syncope-specific quality-of-life measure consisting of an 11-item matrix of yes/no questions, assessing the ways that syncope interferes with the respondent's life, and three Likert-scale questions that assess the patient's fear and worry about syncope. The SFSQ is reported in three sections, the fear/worry score, impairment score, and the overall syncope dysfunction score, which is a composite of the first two measures.
Semi-structured interview
A semi-structured interview (based on Figure 1) was used to ascertain potential triggers, thought content, and coping strategies. This interview was based on the cognitive intrusions questionnaire,16
the dizziness beliefs scale, and the vertigo coping questionnaire.17
,18
The first author developed the interview through expert consensus from three supervisors in the fields of psychological research in anxiety, clinical health psychology, and the medical field of VVS (other authors). It was piloted on three clinical patients. The interview comprised eight sections:
- description of symptoms;
- perceived triggers for symptoms;
- thought content;
- impact of key thought;
- coping strategies;
- helpfulness of key strategy to cope with symptoms;
- helpfulness of key strategy to cope with thought;
- impact on mood.
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A funnel approach (starting with broad questions and progressively narrowing down to more specific and closed questions) reduced the risk of researcher suggestion.13
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Perceived triggers
Participants were asked to rate whether they perceived that each of 17 items triggered their symptoms as never, sometimes, or always (scored 0, 1, 2). The overall reliability of the scale was adequate (Cronbach's alpha=0.80).
Coping
Three coping scales were identified from the semi-structured interview, including:
- Conservative advice (four items, Cronbach's alpha coefficient 0.64),
- Avoidance and protection (five items, Cronbach's alpha coefficient 0.71),
- Fighting spirit (seven items, Cronbach's alpha coefficient 0.62).
Thoughts
A 19-item scale of negative thoughts related to the possible consequences of VVS [Cronbach's alpha coefficient of 0.82 was scored as to whether the participant experienced the thought (1) or not (0)].
Participants were also asked to identify the thoughts they had when they last experienced a VVS episode, and from these, to identify their most frequent thought (Table 2). These key thoughts were coded into categories, which all related to a threat.
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The impact of the participants' key thought was explored in terms of four dimensions of thinking style. Partial correlations were used to explore the relationship between elements of thinking style on the one hand (including rumination; how distressing it would be if the key thought happened, how distressing the thought of their key thought is, and how likely it was to happen) and levels of distress (anxiety and depression, measured by HAD) and functional impairment (as measured by SFSQ) on the other hand. As some of the key thoughts included predictions that had actually happened for a number of participants, the correlation was controlled for frequency of the outcome actually occurring (0, never; 1, occasionally; 2, half the time; 3, most of the time; 4, every time).
Data analysis strategy
Basic assumptions for parametric analyses were examined, and details are reported with the results of the tests. Categorical data were analysed using
2, unless the assumption of having a minimum expected count of 5 per cell was violated, in which case Fisher's exact probability test was reported. The MannWhitney U test was used to test differences in frequency and, due to doubts about the distribution, the number of months with symptoms and with diagnosis. All the analyses were conducted at the conventional significance level of 0.05, unless there were multiple comparisons, when Bonferroni corrections were used to control for type I error. Two-tailed tests were used throughout. The results were analysed using SPSS (version 11). Power calculations suggested that 2025 participants per group was likely to allow the detection of a moderate-to-large effect size. Effect sizes were assessed using Cohen's d, with >0.2 a small effect, >0.5 a medium effect and >0.8 a large effect.
Results
Participants' characteristics
The main characteristics of participants are shown in Table 3. There was no difference in gender (P=0.91), age (P=0.64), number of months with symptoms (P=0.24), past history of fainting (P=0.42), or type of symptom (syncope/pre-syncope; P=0.25) between responders and non-responders.
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However, non-responders had been diagnosed significantly longer than responders (P=0.001) and had a higher frequency of syncopal episodes (P=0.048) as would be expected for non-responders, where non-response is defined by continuing symptoms. Further, there was a significant difference with more prodromal symptoms before syncope reported by non-responders (P=0.05). Non-responders had also been prescribed medication (P<0.001), again as would be expected if they had not responded to conservative advice.
Measure of emotional distress
Mean and standard deviations on the measures of psychological features are shown in Table 2. Non-responders were significantly more anxious (P=0.003) and depressed (P=0.003) and have a higher level of state (P=0.008) and trait (P=0.004) anxiety than responders. The HADS also provides cut-off scores for clinically probable levels of anxiety and depression; hence, the scores were converted to three categories, non-cases, borderline, and cases, and
2 tests were used to compare groups. A significant difference was found, with non-responders reporting higher levels of caseness for anxiety but not depression (Table 4).
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Syncope-specific measure: the SFSQ
Using the SFSQ, non-responders reported more fear/worry related to syncope than responders (P=0.02) and a significantly higher degree of impairment due to syncope (P=0.01); these findings had a medium-to-large effect size (Cohen's d>0.6) (Table 5).
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Semi-structured interview
Perceived triggers
When asked to rate perceived triggers for their symptoms to develop a score, there was a significant difference in trigger score between responders and non-responders (P=0.039), with the latter reporting higher scores, suggesting that non-responders had a higher number of perceived triggers compared with responders (Table 1).
Coping
When considering the three coping scales that were identified from the semi-structured interview (conservative advice, avoidance and protection, fighting spirit), there was a statistically significant difference between responders and non-responders on the combined dependent variables: F(3, 37)=3.74, P=0.019; partial
2=0.23. When the results for the dependent variables were considered separately, the only difference to reach statistical significance using a Bonferroni-adjusted alpha level of 0.017 was avoidance/protection coping; F(1, 39)=11.62, P=0.002, partial
2=0.23, which is considered a large effect size. The mean scores indicate that the non-responders had a higher level of avoidance/protection coping than the responders (Table 1).
Thoughts
The 19-item scale of negative thoughts related to the possible consequences of VVS. The difference in scores was not statistically significant between responders and non-responders (P=0.104). However, the magnitude of the differences was moderate (
2=0.07; 7%). It is worth noting that on average, participants reported eight negative thoughts about the consequences of VVS.
Participants were asked to identify the thoughts they had when they last experienced a VVS episode, and from these, to identify their most frequent (or key) thought. When these key thoughts were coded into categories, all related to a threat. A range of contents was reported, with 12 of the sample (eight of whom were in the non-responders group) reporting threats of physical harm or death (Table 2).
Relationship between key thoughts and emotional distress (HADS) and functional impairment (SFSQ)
The impact of the patients' key thought was explored in terms of thinking style. Partial correlations were used to explore the relationship between elements of thinking style on the one hand (including rumination, how distressing it would be if the key thought happened, how distressing the thought of their key thought is, and how likely it was to happen) and levels of distress (anxiety and depression) and functional impairment (as measured by SFSQ) on the other. As some of the key thoughts included predictions that had actually happened for a number of participants, the correlation was controlled for the frequency of the outcome actually occurring (0, never; 1, occasionally; 2, half the time; 3, most of the time; 4, every time).
There was a strong, positive partial correlation between the level of rumination and both emotional distress (measured using the HADS) and functional impairment (measured using the SFSQ). A medium, positive correlation was also found between how distressing participants predicted their key thoughts would be if it happened and how distressing it is to think about the key thought happening, with the same measures. An inspection of the zero-order correlations suggested that controlling for how often the key thought had actually happened had very little effect on the strength of the relationship between the variables [for example, correlation between rumination and anxiety (HADS), r=0.639]. There were no significant correlations between the perceived likelihood of the event happening and the measures of anxiety, depression, and functional impairment (Table 6). This, therefore, suggests that rumination in those with VVS is associated with increased anxiety, depression, and functional impairment.
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Discussion
This study has explored the ways that people experience and respond to VVS focusing on psychological variables. We have shown that a large number of patients with VVS suffer from anxiety, fear, and worry and are disabled by their condition, and that those who do not respond to conventional interventions have higher levels of psychological distress. These findings will have implications for clinicians managing patients with VVS and may influence the outcomes of clinical trials in VVS.
Why increased anxiety might be associated with non-response to conventional treatment in those with VVS is unclear, and further work is needed to ascertain whether anxiety (and distress) arises as a direct consequence of the symptoms of VVS (and hence leads to non-response) or whether those with high levels of anxiety are destined to be non-responders. A longitudinal study of those with newly diagnosed VVS will be necessary to define further the relationships. Although no specific triggers are known to cause VVS episodes,19
as predicted, non-responders report a significantly higher level of triggering stimuli. Predicting situations that trigger VVS symptoms can lead to an autonomic response, providing evidence to a VVS sufferer that the situation is dangerous and further increase anxiety. A confirmatory cognitive bias in attention to and processing external and internal information in this context could lead to maintenance of distress, as in general anxiety.20
An understanding of thoughts immediately before fainting can be found in a study involving US Air Force flying personnel who experienced syncope.21
Thoughts included catastrophic predictions about potential bodily harm and negative social consequences. In our study, all participants reported at least one negative prediction related to VVS, with the most frequent predictions being negative social consequences, physical injury, and the impact on independence. Other less common intrusions were about dying, loss of certainty, and control, as would be expected from models of anxiety.22
Our study examined the relationship between the rumination experienced by participants and how this impacted on emotional state, and we showed strong relationships between how patients with VVS consider the negative impact of VVS with anxiety and depression. This raises the question of causality: do depression and anxiety cause rumination, or vice versa, or indeed does a bi-directional relationship exist? In addition, a strong relationship was also found between rumination and functional impairment. An indirect relationship is most likely to account for this, as models of rumination suggest that cognitive activity such as ruminating about threat will prompt specific maladaptive coping strategies such as avoidance and precautionary behaviour.23
However, further studies are necessary, as it is difficult in this cross-sectional study (as participants' psychological profiles at the start of their syncopal episodes are unknown) to determine whether the psychological problems such as coping and rumination are the cause of not responding to treatment, or the consequence.
When compared on the coping methods' scales, non-responders did not differ on use of conservative advice or fighting spirit but did report more avoidance and protection. Research into anxiety disorders has demonstrated that avoidance, reassurance seeking, and other self-protecting behaviours reinforce predictions that particular situations are dangerous, and prevent the development of more adaptive ways of coping.23
,24
These indicate that non-responders, like responders, may also use adaptive measures to cope, but their use of avoidance and protection may prevent functional exposure or challenge the negative predictions that maintain distress.25
A caveat to the findings of this study is the possibility that the participants in the non-response group have a more severe level of disease, as there is a significant difference between groups for the current frequency of syncopal/pre-syncopal episodes. Additionally, non-responders do not report as many warning symptoms, potentially leading to VVS being viewed as more unpredictable than the responder group. Thus, greater distress and disability may both have a contributory role, and be a consequence of, more severe or non-response in VVS. Interestingly, however, in our previous case, a series of patients with treatment resistant VVS,12
with psychological intervention the frequency of syncopal episodes dramatically reduced, suggesting that psychological factors may also play a role in the frequency of symptoms.
To date, psychological research has predominantly involved groups of patients with syncope of mixed origin, including VVS.8
,11
,26
Participants in these studies have been mainly diagnosed by medical evaluation and symptom pattern recognition,21
rather than specific diagnostic testing. In our current study, all the subjects had a diagnosis of VVS on the basis of exact symptom reproduction in association with hypotension with or without bradycardia during a head-up tilt test (the recognized diagnostic test for VVS14
). Although well identified and accurately diagnosed, this study recruited a diverse range of participants with VVS. It is particularly important to note the heterogeneity of participants with regard to treatment stage, frequency, duration of symptoms, and symptom type (syncope, pre-syncope, or both). There may be important differences in cognitions and coping between people at different stages of their VVS experience and symptom severity. An increase in these factors may cause more distress; alternatively, they may allow habituation to occur. In this study, we did not consider the haemodynamic response to head-up tilt in each individual with VVS. It is interesting to speculate that perhaps responders represent a different physiological response to tilt than non-responders, suggesting a different phenotype.
This study has several potential limitations. We used a convenience sample in order to ensure adequate numbers. This may have introduced potential bias into the study. We felt, however, that the groups studied were representative of the majority of patients with VVS, which we see in our clinical practice. We excluded those who were taking antidepressants and those seeing a mental health practitioner; we chose to do this in order to ensure reduction of confounding features and would suggest that the inclusion of this group would have only increased the proportion with significant psychopathology. The assignment of patients into responders and non-responders by the clinician could be argued, which does not take into consideration the patients' perspective of their symptoms and may have underestimated the importance of pre-syncope as part of the symptom burden.
In conclusion, this study has confirmed that patients with VVS have a significant degree of psychological distress. We would suggest that this is worthy of consideration in its own right, out with management purely aimed at reducing syncopal or pre-syncopal symptoms. Further, this distress may actually influence the natural history of what is a chronic relapsing condition and may in fact be more relevant to the patient than the number of syncopal episodes that they are experiencing. It is vital that clinicians managing patients with VVS recognize the potential role that psychological factors may have in the manifestation of symptoms in VVS, and when seeing patients, consider not only the number of episodes patients have experienced but also how they are coping with their symptoms and whether these symptoms (or fear of them) are influencing how they live their lives. Clinicians can intervene to reinforce those specific coping strategies that have proved useful to VVS patients, while removing others that although plausible may play an unhelpful role in maintaining distress and symptoms. Simple psychological interventions such as CBT have been of benefit in those with severe symptoms of VVS12
and it may be that those with milder symptoms could also benefit. By considering this, we will potentially prevent entrenchment of symptoms which will have major implications for quality of life in those with VVS.
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