Targets of psychosocial intervention
Target 1
Target 2
Target 3
Target 4
Target 5
Psychological reducing symptoms
Depression
Anxiety
Hostility
Pain
Exhaustion
Changing personality traits
Self-esteem
Salutogenesis
Type A
Type D
Changing attitudes to disease and life
Coping abilities
Behavioral changing behavior
Adaption of illness behavior
Smoking, alcohol
Eating habits vegetables and low fat
Physical activity
Sociological gaining social support
Social activities
Going to work
Better relationship with partner/spouse
Better relationship to other family members
Better relationship to friends and neighbors
Biological targets
Harmonize the autonomic imbalance
Influence biological risk factors (BP, cholesterol etc.)
Influence the psycho-endocrinological stress response
Influence the psycho-immunological psychoinflammatory mechanism
Influence cerebral regulation of the stress response
Disease-oriented management
Information about disease
Make regulatory doctor visits
Behavior according disease management needs
Take regulatory drugs
There are different psychosomatic possibilities and measures to influence these individual biological, psychological, and sociological targets (Table 14.2). Treating individuals or groups of individuals with CHD? The differentiation in same sex groups of men and women with CHD was more successful (Orth-Gomér et al. 2009; Gulliksson et al. 2011), if they integrated some of the abovementioned factors. Until now there are few studies, which demonstrate which treatment suggestion is helpful for which target in CHD. Some authors focus in their intervention only on one important factor. Here the technique of the behavioral intervention seems successful in targeting the important influencing factor, like depression, hostility, or anxiety in studies with CHD (Table 14.2, see below). But what are the convincing targets of a treatment: psychological symptom reduction, minimizing cardiovascular events, preventing patients from dying, or healing CHD?
Table 14.2
Psychosocial interventions and their aims in coronary heart disease (modified from Deter 2012)
Psychosocial interventions | ||||||||
|---|---|---|---|---|---|---|---|---|
Aims of intervention | CBT individual, group | Psychodynamic therapy Individual, group | Relaxation | Physical exercise | Family, social therapy | Mentalization | Cardiological drug therapy | Psycho pharmaceuticals |
Psychological reducing of symptoms | +++ 2,3 | +++ 4,7 | ++7 | + | + 7 | + 1,2,3,4,5,6,7 | ++ 2,3,4 | |
Changing personality traits | ++ 1 | +++ 4,7 | ||||||
Changing attitudes to disease and life | ++ 1,5,6 | ++ 4,7 | + | |||||
Behavioral changing behavior | +++ 1,3,5,6 | +7 | ++ | + | + | |||
Sociological gaining social support | ++ 3,5,6 | ++ 4,7 | + | +++ | ||||
Biological targets harmonize the autonomic imbalance | + 3,5,6 | +7 | +++ | + | ? | ? | ? | ? |
Biological risk factors; e.g., hypertension | + 5,6 | 7 | + | ++ | ? | ? | +++ | |
Influence pathogenic psychoinflammatory mechanism | +? | +? | ++? | ? | ? | ? | ? | |
Influence cerebral regulation of the stress response | ? | ? | ? | ? | ++? | ? | +? | |
Disease-oriented measurements | ++ 3,5,6 | +7 | ++ | +++ | + | |||
Another important aspect is the kind and dose of a psychosomatic intended psychosocial therapy (Linden 2013). Is it sufficient to treat depression in CHD with pharmaceuticals alone? Or it is necessary to apply additional psychosocial interventions. If so, what dose of psychotherapy is helpful: 10 min more conversation with the physician compared to therapy as usual (TAU)? Or 1, 2, or 16 h more than TAU, and more over which psychotherapeutic strategy seems necessary: cognitive behavioral therapy, insight therapy, or relaxation? And in which therapeutic setting should be administered: individual therapy, group therapy, a combined therapeutic program? The basis for all these interactions seems a trustful relationship between patient and therapist and that means the therapist has to acknowledge the needs and the low self-esteem of patients and to give hope and trust in the future according professional activity, good relations with the own family and with friends, and in minimizing psychic symptoms.
Cognitive Behavioral Therapy, Psychodynamic Therapy, and Interpersonal Interaction: Different Treatment Rationale and Procedures in Men and Women with CHD
Beside cardiologic and psychiatric drugs the most common therapeutic principles to treat psychosomatic or behavioral targets in CHD are behavioral or psychodynamic treatment strategies (Table 14.2).
The target depression in CHD
Recent meta-analyses have shown that depressive symptoms and depressive disorders both increase the risk of incident CAD (Wulsin and Singal 2003) and the mortality in patients with established CAD (Barth et al. 2004; van Melle et al. 2004). In average women coronary patients have higher level of depressive as well as anxiety symptoms compared to men (Deter et al. 2013; Frasure-Smith et al. 1997).
Increased risk seems mediated by direct effects of depressive symptoms on physiological risk markers such as neuroendocrine and inflammatory activation, coagulation, and autonomic cardiovascular control and by poor health behavior (Rozanski et al. 2005). But there is also a correlation of somatic depressive symptoms with disease severity (Roest et al. 2010). Cognitive behavioral therapy (ENRICHD (Berkman et al. 2003), PROTeCD (Barth et al. 2005)) as well as interpersonal psychotherapy (CREATE; Lesperance et al. 2007) and other studies (Rutledge et al. 2013) yielded only small effects on depressive symptoms in CHD or cardiovascular outcome. In women, when depressive symptoms were found together with lack of emotional support and social isolation, the combination was a significant predictor, not only of the clinical outcome recurrent coronary events (Horsten et al. 2000) but also of the underlying pathogenic process of progression of the coronary artery atherosclerotic disease (Wang et al. 2006).
The target anxiety in CHD
Symptoms of anxiety are common in patients with coronary artery disease (Herrmann-Lingen and Buss 2002) and they result in increased subjective suffering and decreased functioning as well as in increased health care consumption and health care costs. They can be interpreted as maladaptive coping processes used by patients facing a situation of real threat to their lives (Frasure-Smith et al. 2002). Anxiety has been linked to incidence of fatal CHD in healthy subjects (Kawachi et al. 1994), inhospital cardiac complications after acute myocardial infarction (Huffman et al. 2008) as well as an increased risk of mortality in patients with established CHD (Januzzi et al. 2000). Increased levels of anxiety are associated with higher levels of depression (Frasure-Smith and Lespérance 2008). There is a high evidence for anxiety as a prognostic risk factor in CHD (Roest et al. 2010).
Mechanism: Clinical and preclinical studies have gathered evidence that stress response alterations play a major role in the pathophysiology and therapy of anxiety disorders. Changes in the hypothalamic pituitary adrenocortical (HPA) system and its modulation by CRH, ACTH, corticosteroids and their receptors are suggested to mediate the adverse effects of anxiety disorders on CHD (Ströhle and Holsboer 2003, see also Theorell in this book). Whereas several peptides are known to act synergistically with CRH, the only peptide candidate in humans that inhibits the HPA system at all regulatory levels of the system seems to be atrial natriuretic peptide (ANP). ANP has been shown to inhibit the stimulated release of CRH and ACTH in vitro and in vivo. ANP receptors and immunoreactivity have been found to be critically involved in the modulation of anxiety-related behavior. Pro-ANP concentrations are correlated with low anxiety in patients with severe heart failure (Herrmann-Lingen et al. 2003). Also the sympatho-adrenal-medullary system mediate CNS-generated stress signals to the periphery. It is hypothesized that patients with anxiety disorders inherit an especially sensitive central nervous system fear mechanism that has in its center the central nucleus of the amygdale and is of influence for patients autonomic inbalance. So psychosomatic pathways linking anxiety and coronary heart disease seem to be: arrhythmic mechanism (Watkins et al. 2006), dysfunction of the autonomic nervous system, such as reduced baroreflex cardiac control and reduced heart rate variability (Fleet et al. 2000).
Therapeutic aspects to control pathogenic brain mechanism: Cognitive behavioral and other effective psychotherapies most likely operate upstream from the amygdala, “reducing phobic avoidance by deconditioning contextual fear learned at the level of the hippocampus and decreasing cognitive misattributions and abnormal emotional reactions by strengthening the ability of the medial prefrontal cortex to inhibit the amygdala” (see Table 14.2; Gorman et al. 2000; Bishop et al. 2004). New therapeutic strategies like mentalization are promising tools to influence different brain mechanism of the disturbed heart brain axis in the future.
We assume that persisting anxiety after MI could be responsible for both the development of depression and CHD, but intervention studies have focused on reducing depression or underlying personality factors more than on treating anxiety. A Cochrane review (Rees et al. 2004) found only little effects on anxiety symptoms and no survival benefit. This might be due to the fact that most interventions were rather unspecific and not adjusted to the individual needs of anxious patients with CHD. According to aforementioned systematic reviews and a systematic review by Herrmann-Lingen and Buss (2002), no other large-scale studies of psychotherapy for anxious patients with CHD have been conducted so far. But both cognitive behavioral therapy and short psychodynamic therapy have been shown to be effective in treating anxious patients without CHD (e.g., Leichsenring (2002).
One limitation of previous studies might explain these contradictory findings: the inclusion of coronary patients independent of their psychological status. In a study by Lie et al. (2007), for instance, the effects of the intervention became only apparent when analyzed for a subgroup of distressed patients. They investigated the benefits of a home-based intervention program regarding anxiety and depression in patients after coronary artery bypass grafting. At 6 month follow-up both groups had improved significantly but there were no significant differences between the groups. However, in a second step Lie et al. analyzed the effects of the intervention in a subgroup of distressed patients and found that among patients who experienced high levels of anxiety and depression at baseline the intervention did result in significant improvements compared to the control group.
Targets of complex psychopathology in CHD
The type A pattern could be isolated as an important combined psychological category and risk factor in CHD, which could be treated very effective (Friedman et al. 1984). Hostility (Chida and Steptoe 2009) as well as negative affectivity (a sum score of depressive and anxiety symptoms; Strik et al. 2003; Sullivan et al. 2000) and social inhibition (type D; Denollet et al. 2006) are also valid constructs of CHD psychopathology as well as a low real or self rated social support (Berkman et al. 2003), which influenced the outcome of this disease. Each of the symptoms depression, anxiety, or hostility have been identified as risk factors for the course of coronary heart disease, but there is an overlap in these psychological dimensions (Suls and Bunde 2005), which can for some reasons (p.e., treating different CHD mechanism) be separated. In the prospective quantitative coronary angiography study (Wang et al. 2006) depression promotes progression of CHD in Swedish women only in the presence of lack of social support.
Stress reduction and psychosocial adjustment to disease as target
Psychological interventions in CHD patients, which focused on stress management, psychosocial adjustment, and the special needs of CHD women or men, but did not aim only on one psychological dimension (depression or anxiety), found beneficial effects in terms of biological risk markers, reduced morbidity, and mortality (Orth-Gomér et al. 2009; Gulliksson et al. 2011, see Schneiderman in this book).
Cognitive Behavioral Therapy (CBT)
If we look on the treatment procedures in cognitive behavioral therapy (CBT) of CHD patients, psychological symptoms, risk behavior, and inappropriate cognitive attitudes seem to be the focus of most group treatment activities through cognitive training and relaxation. There is often a special program with teaching phases, patients communication about the given information, and sometimes integration of information in the own life situation of patients. Cognitive learning, repeating of information and behavioral modification of the patients within a good group atmosphere are the main targets of this kind of intervention (see also Schneiderman and Orth-Gomér in this book). Orth-Gomér (2012) stated: “Each session focused on a special subject (see below) and was accompanied by relevant home work tasks. At the beginning of the following session the home-work from the previous session was reviewed. One such home work task could require that the participant was to observe and record his/her stress behavior-pattern during a whole week. Cognitive behavioral strategies were used in an attempt to alter the participant’s stressful and angry responses. One strategy, “the Hook,” had been specially designed to attenuate irritation and anger. Participants were asked to go home and exercise how to avoid “biting the hooks.” At the next session they were to report about their experiences. Each patient was asked to speak at the order of priority—and the others were expected to listen and be supportive.
Topics discussed at the group sessions:
Presentation of group members and their heart condition. Atherosclerosis, coronary risk factors, and psychological consequences in relation to the cardiac event. Psychosocial stress and physiological stress reactions. Individual assessment of standard coronary risk factors—and identification of the problem areas of the group. Anger and hostility in response to daily stress exposure, problem-solving and cognitive strategies, e.g., the “hook.” Coronary prone stress behavior. Reviewing and testing patient’s individual stress behavior. Worry, depression, anxieties, low-spiritedness, depression, and social inhibition (type D). Communication training—improving communication skills by passive and active approach. Everyday conflict situations. The patients are introduced to examples of conflict situations and asked to deal with them. Positive and negative emotions. An exercise book with daily, concrete cognitive exercises is started and maintained throughout the course. Daily practice of relaxed behavior. Patterns/roles of life, roles of social relations, stress, and personality. Defining one’s own life-situation.”
This program was somewhat specified for anxiety (BAT): “The initial sessions focused on CHD and its treatment and on symptoms of anxiety and stress and its effects on the body. As a next step, patients were taught to monitor and register signs of stress and techniques of stress management were applied, including the regular use of relaxation training. One major element of the program was changing the patients distorted beliefs and interpretations by teaching techniques of cognitive restructuring. This intended to help the patients to find alternative interpretations of threatening symptoms and life situations” (Merswolken et al. 2011).
Psychodynamic Therapy (PDT)
The efficacy of psychodynamic psychotherapy in depressed or anxious CHD patients has not been addressed in a randomized trial, although psychodynamic psychotherapy is frequently used in the routine treatment of depression. It has shown to be highly effective in the treatment of depressed patients without heart disease in a meta-analysis by Leichsenring (2002). Support for using psychodynamic psychotherapy arises from the fact that chronic traits like negative affectivity or social inhibition may even be better predictors of adverse outcomes in CHD patients than “depression.” So a modified treatment approach could be of importance in patients with persistent depression, anxiety or stress exposure (Albus et al. 2011).
Psychodynamic group therapy in diseased patients (Deter 1986; Deter and Schüffel 1988) modified for patients with coronary heart disease (Hahn and Leisner 1970; Albus et al. 2009) focused on the individual, his or her thinking, feeling and social adaptation in his/her social environment, and focused also on the behavioral and social interaction during a group session. The person and his development in childhood and later course of time, the experiences of an individual in different phases of life, especially during traumatic life events and the kind of coping strategies are in the focus of treatment and the basis for an understanding of present psychic symptoms and CHD risk behavior. Modification of symptoms and behavior depends not only from the cognitive thinking and restructuring of the patients but also from emotions and motivations growing up during the therapeutic process in the group. The understanding of psychic symptoms as an emotional conflict between different tendencies in an individual is also a basis of psychodynamic understanding and treatment.
The person of therapist and the expectations and former experiences with these person or profession is important (unspecific therapeutic component, similar to a placebo effect (Enck et al. 2008)), but also the expectations and real experiences with other group members with the same diagnosis CHD (Orth-Gomér 2012). Trust in relations to the therapist and his competence (Barber and Crits-Christoph 1996) depends also from the attachment style developed in the earlier life. This seems also a predictor for changing risk behavior, for example, in obese patients (Kiesewetter et al. 2012). In the meantime there is a tendency to coordinate important principles of CBT with important principles of psychodynamic therapy (PDT).
Interpersonal Interactions
The German Stepwise Intervention in Risk Reduction in Coronary Artery Disease (SPIRR-CAD, Albus et al. 2011) tried to bring in (25 sessions—2 h) CBT (information about disease and life skills, working on the “hook”-problem (Powell 1996) and on other dangerous risk behaviors (Williams and Williams 1997, see also Williams V. in this book) and PDT elements (open discussion, important and emotional individual experiences from actual living or from the personal history; clearing of individual conflicts, actual emotional interactions in the group, which would interpreted by the group leader) to gain the effect of group therapy in CHD (Before the group starts three sessions of psychodynamic individual therapy were administered. One therapeutic session took place with the partner/spouse of patient to examine problems in the partnership, to find solutions for it, and to gain social support for the patient and his/her partner).
The interaction between individuals during the individual and the group therapy reflect social interactions in life (see Chap. 15). Patient’s expectations, the social environment, where the group take place, the atmosphere and coherence in the group are significant predictors for a good treatment process. So the emotional adaptation to the group and to the group leader are important conditions for patient’s effective learning and emotional benefit.
Gender Aspects
Gender aspects, especially “women’s Coronary Heart Disease” are not completely understood. Evidence suggests that psychosocial risk factors and response to treatment differ between men and women with CHD (Orth-Gomer et al. 2000; Frasure-Smith et al. 1997; Cossette et al. 2002; Burell and Granlund 2002; Bankier and Littman 2002; Wang et al. 2006). If specific subgroups of depressed or anxious CHD women patients benefit differentially from psychotherapy remains unclear (Schneiderman et al. 2004; Orth-Gomér et al. 2009).
The proposal by Orth-Gomér (2012) to organize same sex groups with CHD females or CHD males seems an interesting tool. Often a group with only men (Friedman et al. 1984) or six men and one or two women focused mostly on masculine topics, there is an overweight of male (speeching-) activities and an disadvantage in women’s interests, topics, and experiences (Berkman et al. 2003). A homogenous women’s group gives more space for women needs, more understanding between women and more emotional cohesion between women group members. In male groups perhaps women topics and women views on special problems are missing. This kind of treatment seems often too cognitive and focused on men topics “work, sports and cars.”
The Berlin Anxiety trial (BAT): Gender and Biological Factors in CHD Psychosocial Interventions
H.C. Deter, M. Merswolken, K. Orth–Gomér and Ch. Walldin.
Berlin Anxiety Trial
Although the concept of anxiety coexists with other psychological concepts including depression (Frasure-Smith and Lespérance 2008) that has been addressed in several intervention trials (Frasure-Smith et al. 1997; Berkman et al. 2003), to our knowledge few randomized controlled study have primarily addressed the group of CHD-patients with elevated levels of anxiety. Therefore, the purpose of this study was to investigate whether the course of disease with TAU or an additional psychosocial (pilot-) intervention or a specific psychotherapeutic intervention in a RCT design would reduce the level of anxiety in anxious patients with a medically stable CHD. In these studies additional severity-of-disease-related factors of influence as well as gender-specific differences should be examined.
The Berlin Anxiety Trial (BAT) included 120 patients with CHD over 4 years and started 2007 as a visibility study for a psychosomatic RCT in Germany. It should detect in the first step the natural course of diseased patients with coronary heart disease and symptoms of depression and/or anxiety. These “therapy as usual” conditions should be analyzed and then influenced by a psychosocial intervention. The aim of this psychosocial intervention focused on anxiety symptom reduction.
We had the following hypotheses: (1) Anxiety remains on the same level in high and low anxiety CHD patients without psychosocial treatment in the course of disease. (2) After a first phase without intervention patients with a remaining high level of anxiety (HADS > 8), who are willing to be treated should get a psychosocial group intervention to reduce their anxiety (clinical decision of patient and physician). They should compared with patients without intervention (pilot intervention). (3) In a RCT another CHD sample with high levels of anxiety should get a psychosocial intervention to reduce anxiety compared to a control group with TAU.
The results of our study showed aspects of the course of disease, the results of a psychosocial intervention, and the impact of biological factors, which were different between genders. In the first study (Merswolken et al. 2008) we contacted in the hospital 100 CHD patients after MI or acute coronary syndrome with an interest for a psychosocial intervention. We included 58 patients in the study with HADS depression score > 7 (Herrmann et al. 1995) and focused our study on anxiety. So we could demonstrate that anxiety remained stable in high (>7) and low (7 and below) anxiety CHD patients or increased over 12 month.
After this phase 38 patient again filled out the HADS (20 of 58 patients did not adhere to the entire program in this phase). Twenty-one patients had a high anxiety level (>7) and were interested to participate in the psychosocial intervention, but out of these only seven participated in the therapy. Interestingly these were 4 of 6 women (66 %), but only 3 of 15 men (20 %). Seventeen (4 of 10 women (40 %), 13 of 28 men (46 %)) were further interested in the psychosocial intervention, but had low HADS anxiety level < = 7. Patients were treated with a psychosocial group therapy (modified from Orth-Gomér 2012)—13 sessions (2 h) 1/per week and three booster session 1/month). This led to a significant, 60 % reduction of anxiety in this small treatment group (n = 7, t0:11.2, t1:12.0, t2:4.9) while anxiety scores (as well as depression) in the two control groups (HA (n = 14); t0:8.2, t1:9.8, t2:8.6 and LA (n = 17); t0:4.2, t1:2.5, t2:2.7) remained stable (Fig. 14.1a, b).
Fig. 14.1
(a, b) Course of CHD patients with high (HA) and low anxiety (LA) symptoms in the first phase (0–12 month; n = 58) without and in the second phase with psychosocial intervention difference TG vs. CG HA anxiety: p = 0.005; depression: p = 0.002; Merswolken et al. 2008). Twenty of 58 patients did not adhere to the entire program in phase 2
Then 62 new patients with CHD and elevated levels of A (HADS-A score of 8 or higher; age lower 75 years) were recruited for a psychosomatic RCT (Merswolken et al. 2011). At 6 months follow-up significant reductions (intervention group: −2.0 ± 2.3; control group: −1.8 ± 2.8; p < 0.01) were found in both groups in the HADS anxiety scale but no significant differences between the groups were observed (Fig. 14.2). Adjustment for baseline differences and disease severity did not change these results.
Fig. 14.2
Psychodiagnostic course of anxiety and depression in intervention and control patients of a RCT (differences between groups are not significant; Merswolken et al. 2011)
If the phase after the myocardial infarction is 3 months and first coping processes of a patient have finished, it is possible to compare anxiety over 6 month in the treatment and TAU group of a RCT which includes many control examinations and a lot of care giving security (and anxiety reduction?) in both study groups? Anxiety as a trait and a state emotion can react very sensitive on such kind of different interventions. In the pilot study there was a minimum of therapeutic intervention (filling out the HADS-questionnaires only two times within 12 months) and we found a remaining of high anxiety levels in the high anxiety group.
In the RCT a small trend towards a beneficial effect of the intervention for low active-coping patients could be calculated (Merswolken et al. 2011). Active problem-orientated coping strategies (e.g., seeking information about the disease) are associated with more positive outcomes (Van Elderen et al. 1999). Depressive coping seems close to a negative outcome (Fritzsche et al. 2007). The relevance of anxiety for the patients’ psychological and physical well-being suggest that interventions should try to reduce anxiety and to improve the coping abilities of the patients as well as stimulating stress management and social support. A number of studies have demonstrated beneficial effects of cardiac rehabilitation and psychological interventions on emotional distress and quality of life in patients with CHD (Michalsen et al. 2005; Mittag et al. 2006), as confirmed in a meta-analysis by Linden (2000). The focusing of one psychological symptom like anxiety fails to understand all the psychological processes, which are happening in a psychosocial intervention of CHD patients.
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