Type A Behavior in Cardiovascular Disease
Our study found that type A behaviour is significantly more prevalent in cardiovascular disease compared with other medical disorders and it was found to frequently occur together with some psychosomatic syndromes. Some limitations might affect the interpretation of the results. First, the cross-sectional design did not allow to examine the stability of psychiatric and psychosomatic diagnoses over time. We also used a sample of convenience and not a random sample and our definition of 'cardiac patient' was based on current findings and did not include past history of cardiac diseases. However, our study has the merit to assess type A behaviour in a large sample size with subjects coming from different settings. Furthermore, type A behaviour was identified by means of a structured research interview that displayed excellent inter-rater reliability and reflected the original description of the syndrome, and was not based on self-rating scales. The Review Panel on Coronary-Prone Behavior and Coronary Heart Disease suggested that type A behaviour could be associated not only with coronary endpoints but also with non-cardiovascular conditions, but a direct comparison was missing from the literature. Furthermore, the studies examining type A behaviour in non-cardiac diseases relied mostly on self-rating instruments and were characterised by small sample sizes.
In the present study, the prevalence of type A behaviour in our population of patients with cardiovascular disease was 36.1%. This means that the expectation of finding it in every patient with cardiovascular disease is unrealistic, whereas it may mark a subtype of illness. The difference in prevalence between cardiovascular and non-cardiovascular disease was significant and the multivariate analysis confirmed the association between type A behaviour and the cardiac setting.
Mood disorders occurred in conjunction with type A behaviour in only about 7% of patients with cardiovascular disease. Demoralisation, a subclinical form of mood disorder according to the DCPR, was more common, as it occurred in a quarter of patients. It derives from the convergence of psychological distress and subjective sense of incompetence (the idea that one is not able to deal with a stressful situation), with particular reference to feelings of hopelessness and helplessness. The DCPR showed that demoralisation and major depressive disorder are distinct and not hierarchically related phenomena. Demoralisation frequently precedes the onset of serious diseases, such as myocardial infarction, and it is significantly associated with both a worse clinical outcome and a diminished quality of life. In a previous study, DCPR demoralisation was found to characterise one third of patients with DSM-IV adjustment disorder. In our study, demoralisation was far more frequent than DSM-IV adjustment disorder probably because the former sensitively identifies subsyndromal psychosocial distress.
The most distinctive characteristic significantly associated with type A behaviour was irritable mood according to the DCPR. This finding seems to confirm the strong relationship between irritability and cardiovascular diseases. Since the 1980s, hostility emerged as one of the components of type A behaviour most associated with increased cardiac risk. The predictive role of clinical phenomena linked to irritability (i.e. cynical hostility and trait anger) on the onset and course of cardiovascular diseases has been indicated by many studies. Increased levels of irritability also independently predicted mortality among heart transplanted patients.
The relationship between type A behaviour and irritable mood was significant both in cardiac and non-cardiac patients. This suggests that irritability is one of the core features of type A behaviour, regardless of the setting of occurrence. However, irritable mood did not occur in almost half (45.5%) of type A subjects with a cardiac condition and in two of three (72.1%) of those with another medical diagnosis. Although type A behaviour and irritable mood are significantly associated, they are not hierarchically related: the latter may occur even outside the type A behavioural pattern and not all the type A subjects satisfy the DCPR criteria for irritable mood.
Furthermore, cardiac patients with type A behaviour were significantly more likely to have a DSM-IV anxiety disorder than non-cardiac patients. Most of the literature on the link between psychiatric disorders and increased cardiovascular risk concerned mood disorders; yet, in recent years several studies are pointing to a detrimental effect of anxiety on the cardiovascular system. Both physiological (e.g. sympathetic activation) and behavioural (i.e. unhealthy health habits) mechanisms have been proposed to explain how high levels of anxiety may increase the risk of onset and progression of CHD.
Type A behaviour may share some features with hypomania, which frequently results in an over-optimistic view of one's own ability to cope with a stressful situation (as a life-threatening disease is) and in the minimisation of vulnerability to future difficulties (e.g. medical complications). According to Barrick, type A behaviour also overlaps with cyclothymia and hyperthymic temperament. Two investigations seem to confirm this hypothesis. In a study by Oedegaard and colleagues, bipolar II patients had higher speed and impatience than those with unipolar depression. The same component of type A behaviour was significantly associated with cyclothymic temperament. Wang and colleagues found a significant relationship between type A behaviour and hyperthymic temperament, which may characterise a subtype of bipolar disorder named 'bipolar IV' (depression in subjects with hyperthymic temperament). As suggested by Wang et al., the close association between type A behaviour and the bipolar spectrum, especially its subsyndromal manifestations, may explain the increased risk of cardiovascular mortality in patients with bipolar disorders. It is conceivable, even though yet to be tested, that type A behaviour may be part of an atypical form of the bipolar disorder. An innovative characterisation of cyclothymia, essentially based on abnormal reactivity to social environment, could shed some light on this intriguing relationship.
Type A behaviour may have important clinical consequences as to both the awareness of allostatic load and illness behaviour, which may adversely affect the rehabilitation process. Allostatic load reflects the cumulative effects of long-standing stressful experiences in daily life. It may result from both the frequent and/or prolonged activation of the stress response system and the inability to shut off allostatic responses after a stress is terminated. The toxic effects of both allostatic load and stress in general on the cardiovascular system have been documented and type A behaviour may mediate the relationship between stress and cardiovascular morbidity. Subjects with type A behaviour respond to laboratory mental tasks with a greater activation of the sympathetic nervous system than type B subjects. A chronic activation of both the sympathetic nervous system and the hypothalamic-pituitary-adrenal axis in type A subjects was also outlined. Type A features (e.g. excessive work involvement even during weekends, lack of leisure activities, competitiveness even in recreational activities) may expose subjects to daily stressful events, but also decrease their ability to interrupt the stress response.
As to illness behaviour, in our study, cardiac patients with type A behaviour had fewer DCPR syndromes concerning worries about one's own health than non-type A patients. Type A behaviour may be associated with a tendency to minimise both the psychological impact of a life-threatening medical illness and the vulnerability to its possible consequences. This may lead patients to underestimate the need to modify unhealthy lifestyles.
Point biserial correlation allowed to further examine whether type A behaviour was modestly but significantly associated with DSM-IV and DCPR comorbidity. We found that only the presence of DCPR comorbidity was significantly related to type A behaviour. This result seems to extend to the total sample the lack of significant associations between type A behaviour and DSM-IV psychiatric diagnoses, except for a significant lower prevalence of mood disorders, found among cardiac patients. Furthermore, the low correlation with DCPR comorbidity suggests that type A behaviour may be clinically relevant in cardiology regardless of the extent to which it is influenced by other psychosomatic syndromes (see Table 2).
In the past decade, studies on the psychosocial aspects of cardiovascular diseases emphasised the role of depression and hostility/irritability, neglecting other psychosocial variables, such as type A behaviour. The presence of comorbidity (especially anxiety disorders and irritable mood) and of detrimental lifestyle attitudes in conjunction with a major depressive disorder were found to have considerable clinical implications. Resolution of the depressive episode is unlikely to entail solution to the complex clinical configuration. Not surprisingly successful treatment of depression in cardiovascular diseases was not associated with cardiovascular benefits. In psychiatric settings, a sequential approach (pharmacotherapy of depression followed by psychotherapy addressed to the comorbid symptomatology) was found to entail significant benefits in terms of relapse rate. Similar considerations and strategies may potentially apply to cardiovascular illness, when type A behaviour is found to accompany the depressive symptoms. Its lifestyle connotations may be important also when type A behaviour is not accompanied by depressed and irritable mood. Indeed, targeting lifestyle modification was found to entail significant benefits in prognosis of coronary artery disease.
Discussion
Our study found that type A behaviour is significantly more prevalent in cardiovascular disease compared with other medical disorders and it was found to frequently occur together with some psychosomatic syndromes. Some limitations might affect the interpretation of the results. First, the cross-sectional design did not allow to examine the stability of psychiatric and psychosomatic diagnoses over time. We also used a sample of convenience and not a random sample and our definition of 'cardiac patient' was based on current findings and did not include past history of cardiac diseases. However, our study has the merit to assess type A behaviour in a large sample size with subjects coming from different settings. Furthermore, type A behaviour was identified by means of a structured research interview that displayed excellent inter-rater reliability and reflected the original description of the syndrome, and was not based on self-rating scales. The Review Panel on Coronary-Prone Behavior and Coronary Heart Disease suggested that type A behaviour could be associated not only with coronary endpoints but also with non-cardiovascular conditions, but a direct comparison was missing from the literature. Furthermore, the studies examining type A behaviour in non-cardiac diseases relied mostly on self-rating instruments and were characterised by small sample sizes.
In the present study, the prevalence of type A behaviour in our population of patients with cardiovascular disease was 36.1%. This means that the expectation of finding it in every patient with cardiovascular disease is unrealistic, whereas it may mark a subtype of illness. The difference in prevalence between cardiovascular and non-cardiovascular disease was significant and the multivariate analysis confirmed the association between type A behaviour and the cardiac setting.
Mood disorders occurred in conjunction with type A behaviour in only about 7% of patients with cardiovascular disease. Demoralisation, a subclinical form of mood disorder according to the DCPR, was more common, as it occurred in a quarter of patients. It derives from the convergence of psychological distress and subjective sense of incompetence (the idea that one is not able to deal with a stressful situation), with particular reference to feelings of hopelessness and helplessness. The DCPR showed that demoralisation and major depressive disorder are distinct and not hierarchically related phenomena. Demoralisation frequently precedes the onset of serious diseases, such as myocardial infarction, and it is significantly associated with both a worse clinical outcome and a diminished quality of life. In a previous study, DCPR demoralisation was found to characterise one third of patients with DSM-IV adjustment disorder. In our study, demoralisation was far more frequent than DSM-IV adjustment disorder probably because the former sensitively identifies subsyndromal psychosocial distress.
The most distinctive characteristic significantly associated with type A behaviour was irritable mood according to the DCPR. This finding seems to confirm the strong relationship between irritability and cardiovascular diseases. Since the 1980s, hostility emerged as one of the components of type A behaviour most associated with increased cardiac risk. The predictive role of clinical phenomena linked to irritability (i.e. cynical hostility and trait anger) on the onset and course of cardiovascular diseases has been indicated by many studies. Increased levels of irritability also independently predicted mortality among heart transplanted patients.
The relationship between type A behaviour and irritable mood was significant both in cardiac and non-cardiac patients. This suggests that irritability is one of the core features of type A behaviour, regardless of the setting of occurrence. However, irritable mood did not occur in almost half (45.5%) of type A subjects with a cardiac condition and in two of three (72.1%) of those with another medical diagnosis. Although type A behaviour and irritable mood are significantly associated, they are not hierarchically related: the latter may occur even outside the type A behavioural pattern and not all the type A subjects satisfy the DCPR criteria for irritable mood.
Furthermore, cardiac patients with type A behaviour were significantly more likely to have a DSM-IV anxiety disorder than non-cardiac patients. Most of the literature on the link between psychiatric disorders and increased cardiovascular risk concerned mood disorders; yet, in recent years several studies are pointing to a detrimental effect of anxiety on the cardiovascular system. Both physiological (e.g. sympathetic activation) and behavioural (i.e. unhealthy health habits) mechanisms have been proposed to explain how high levels of anxiety may increase the risk of onset and progression of CHD.
Type A behaviour may share some features with hypomania, which frequently results in an over-optimistic view of one's own ability to cope with a stressful situation (as a life-threatening disease is) and in the minimisation of vulnerability to future difficulties (e.g. medical complications). According to Barrick, type A behaviour also overlaps with cyclothymia and hyperthymic temperament. Two investigations seem to confirm this hypothesis. In a study by Oedegaard and colleagues, bipolar II patients had higher speed and impatience than those with unipolar depression. The same component of type A behaviour was significantly associated with cyclothymic temperament. Wang and colleagues found a significant relationship between type A behaviour and hyperthymic temperament, which may characterise a subtype of bipolar disorder named 'bipolar IV' (depression in subjects with hyperthymic temperament). As suggested by Wang et al., the close association between type A behaviour and the bipolar spectrum, especially its subsyndromal manifestations, may explain the increased risk of cardiovascular mortality in patients with bipolar disorders. It is conceivable, even though yet to be tested, that type A behaviour may be part of an atypical form of the bipolar disorder. An innovative characterisation of cyclothymia, essentially based on abnormal reactivity to social environment, could shed some light on this intriguing relationship.
Type A behaviour may have important clinical consequences as to both the awareness of allostatic load and illness behaviour, which may adversely affect the rehabilitation process. Allostatic load reflects the cumulative effects of long-standing stressful experiences in daily life. It may result from both the frequent and/or prolonged activation of the stress response system and the inability to shut off allostatic responses after a stress is terminated. The toxic effects of both allostatic load and stress in general on the cardiovascular system have been documented and type A behaviour may mediate the relationship between stress and cardiovascular morbidity. Subjects with type A behaviour respond to laboratory mental tasks with a greater activation of the sympathetic nervous system than type B subjects. A chronic activation of both the sympathetic nervous system and the hypothalamic-pituitary-adrenal axis in type A subjects was also outlined. Type A features (e.g. excessive work involvement even during weekends, lack of leisure activities, competitiveness even in recreational activities) may expose subjects to daily stressful events, but also decrease their ability to interrupt the stress response.
As to illness behaviour, in our study, cardiac patients with type A behaviour had fewer DCPR syndromes concerning worries about one's own health than non-type A patients. Type A behaviour may be associated with a tendency to minimise both the psychological impact of a life-threatening medical illness and the vulnerability to its possible consequences. This may lead patients to underestimate the need to modify unhealthy lifestyles.
Point biserial correlation allowed to further examine whether type A behaviour was modestly but significantly associated with DSM-IV and DCPR comorbidity. We found that only the presence of DCPR comorbidity was significantly related to type A behaviour. This result seems to extend to the total sample the lack of significant associations between type A behaviour and DSM-IV psychiatric diagnoses, except for a significant lower prevalence of mood disorders, found among cardiac patients. Furthermore, the low correlation with DCPR comorbidity suggests that type A behaviour may be clinically relevant in cardiology regardless of the extent to which it is influenced by other psychosomatic syndromes (see Table 2).
In the past decade, studies on the psychosocial aspects of cardiovascular diseases emphasised the role of depression and hostility/irritability, neglecting other psychosocial variables, such as type A behaviour. The presence of comorbidity (especially anxiety disorders and irritable mood) and of detrimental lifestyle attitudes in conjunction with a major depressive disorder were found to have considerable clinical implications. Resolution of the depressive episode is unlikely to entail solution to the complex clinical configuration. Not surprisingly successful treatment of depression in cardiovascular diseases was not associated with cardiovascular benefits. In psychiatric settings, a sequential approach (pharmacotherapy of depression followed by psychotherapy addressed to the comorbid symptomatology) was found to entail significant benefits in terms of relapse rate. Similar considerations and strategies may potentially apply to cardiovascular illness, when type A behaviour is found to accompany the depressive symptoms. Its lifestyle connotations may be important also when type A behaviour is not accompanied by depressed and irritable mood. Indeed, targeting lifestyle modification was found to entail significant benefits in prognosis of coronary artery disease.
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