Handbook of Psychocardiology
Abstract
This handbook brings together the full weight of contemporary evidence bearing on what is now commonly termed "psycho-cardiology". It focuses on the role of psycho-social factors in the genesis and clinical management of cardiovascular disease (CVD). The book constitutes a critically reviewed compendium of current knowledge in the area, coupled with guides to evidence-based best practice in the field of psycho-cardiology. The following categories are covered: Social/demographic risk for CVD, Personality and CVD risk, Stress and CVD risk, Psychopathology (particularly affective disorders) and CVD risk, The psychological management of those with clinical CVD, Psychology in the prevention of CVD. The book integrates the evidence into a compelling argument that clinicians, researchers and those in public health will discount the role of psychological factors in regard to CVD at their own peril. And importantly for clinicians charged with the care of patients with CVD, the book poses the argument that failure to recognize the links between psychological factors and CVD may well be at the considerable peril of those patients under their care. © Springer Science+Business Media Singapore 2016. All rights are reserved.
Chapters (60)
Ideas linking the heart to the brain exist in ancient and of course modern texts. In antiquity, the brain was not given its due! The London physician and neuroanatomist Thomas Willis changed this, correctly attributing the source of emotions to the brain. Contemporary research does establish the existence, and autonomic nervous system mechanisms, of cardiac responses to emotion. Further, it documents the phenomenon of “triggered” heart disease, when the autonomic nervous control of the heart goes awry, producing heart disease of sudden onset, precipitated by acute emotional upheaval.
The term Psychocardiology has achieved prominence quite recently to describe both a field of research and an approach to clinical practice, though the evidence upon which this is based is not at all new. Systematic research linking the heart and the mind has a far longer history – its origins in medical science can be found more than a century ago in, for example, the work of the psychoanalytic movement. And from a more cardiologic space, the speculations of the eminent physician Sir William Osler clearly foreshadowed moves to link personality with diseases of the heart when he said of the person at risk of angina, that … It is not the delicate neurotic person who is prone to angina, but the robust, the vigorous in mind and body, the keen and ambitious man, the indicator of whose engines is always at full speed ahead. This chapter traces the origins of thought linking the heart and mind, commencing with the place of the heart in literature and religion, and ending with a hypothesis that subjective perceptions of cardiovascular activation arising from sympathetic arousal account for the compelling belief among person-kind that diseases of the heart are inextricably linked to afflictions of the mind.
Awareness of the fundamentals of cardiac anatomy, physiology and various disease states is essential to clinicians managing a patient with cardiac pathology. This chapter summarizes the key aspects of cardiac structure and function, as well as providing an overview of the broad range of cardiac pathology. The chapter discusses the various presentations of cardiac disease and the clinical assessment that is performed. Diseases discussed include those of cardiac rhythm, vessels, valves, and muscle as well as congenital heart disease. The various modalities of investigation and basic principles of management are also reviewed.
Impaired cognition following cardiac surgery is a common complication. Estimates of the incidence of postoperative cognitive decline/dysfunction (POCD) vary from 20 % to 70 % of patients in the week after cardiac surgery to 10–40 % by 6 weeks. It has become evident that differences in research design have contributed significantly to these differing estimates of POCD and that greater consistency will be achieved if future studies utilize appropriate control groups. Recent studies have shown that many patients have cognitive impairment prior to undergoing cardiac surgery and furthermore that some of the POCD is associated with surgical procedures in general, rather than with cardiac surgery in particular. The domains of language, concentration, and motor control are commonly affected during the first week after cardiac surgery, and memory and executive function can also be affected. Some individuals are more vulnerable than others. In the future it might be possible to identify these individuals prior to surgery with computer-based cognitive tests and measures of emotional state, so that the factors involved can be managed and the risk of POCD can be reduced.
Noncommunicable diseases such as cardiovascular diseases and cancers are key threats to maintaining health and well-being in the twenty-first century. In 2008, 30 % of global deaths were due to cardiovascular disease, a mortality burden felt by countries across the income/development spectrum. The middle of the twentieth century saw the advent of epidemiological studies which have made significant advances in understanding the factors driving cardiovascular disease risk. Studies such as the Seven Countries Study gathered data from across the globe on clinical and lifestyle factors and their relationship to rates of cardiovascular disease. Other landmark studies such as the Framingham Study set the scene for a detailed understanding of the magnitude of risk conferred by clinical factors.
An increasingly sedentary lifestyle and energy-dense diet facilitated by urbanization have contributed to epidemics of obesity, hypertension, and diabetes, which are all major cardiovascular risk factors. These risks, coupled with aging populations (age being another key risk factor), drive the need to develop and implement prevention strategies that will be effective and accessible for high- and lower-income countries. The worldwide framework for tobacco control and working with the food industry to develop healthier accessible foods are key examples of lifestyle-related strategies for prevention. Low-cost preventive medications such as the multicomponent “polypill” also hold promise as cost-effective strategies to reduce the burden of cardiovascular disease; however further evidence of the efficacy across different population and age groups is required.
Cardiovascular disease (CVD) is the leading cause of death and disability in the developed world. Lifestyle factors are thought to account for up to 90 % of attributable risk of myocardial infarction worldwide. Smoking, dyslipidemia, hypertension, diabetes, abdominal obesity, consumption of fruits and vegetables, psychosocial factors, and physical activity are the key components of this risk. Interventions to reduce risk such as exercise, smoking cessation, and dietary change are valuable in lowering CVD risk at any age; however, instituting the “right” lifestyle choices from childhood or even from conception is likely to have the greatest impact on reducing the long-term burden of disease. The “sitting time” is now recognized to add to the risk of CVD, even in people who are physically active at other times. Sitting more than 10 h per day increases all-cause mortality. TV watching is a strong predictor of CVD risk and is more profound than “screen time” which may include video games. This may relate to increased snacking and poor dietary choices when watching TV. If we are to reduce CVD, a paradigm shift is needed in how our “Western” society operates. Fundamental changes are needed in infrastructure, travel, use of cars, work patterns, food industry, and education from birth to grave.
Smoking is an acknowledged – and significant – risk factor for cardiovascular disease (CVD). Research into the causes of smoking behavior is extensive, but few would disagree that smoking is a discretionary human behavior acquired through the operation of a combination of well-understood psychological mechanisms. This chapter considered the role of psychological stress in its many forms – and including psychological illness – in the genesis of smoking behavior. While the evidence is both widespread and various, the collective view is that stress plays a very clear role in the maintenance of smoking behavior, and in the frequency of tobacco consumption, in well-established adult smokers. More than this, however, there is growing evidence that psychological distress experienced in adolescence is causally related to the onset of smoking behavior in that age group. Public health programs to prevent smoking onset among adolescents – as part of continuing efforts to lower the incidence of CVD in adults – must therefore include components of stress reduction and management in addressing this crucial issue.
Alcohol is a psychoactive substance that has a considerable impact on the physical and mental health of individuals. While there is clear evidence for a wide range of harms associated with alcohol consumption, research has also been conducted into the potential positive effects, including cardiovascular effects. The results of many of these studies are suggestive of a J-shaped association between low levels of regular alcohol intake and a reduction in cardiovascular risk – particularly coronary heart disease risk. This is an association that appears to be affected both by the level and the pattern of alcohol consumption. However, most of this research has consisted of observational and population-based studies, with inherent methodological limitations and difficulties controlling for confounding factors. Consequently, there is still insufficient evidence to suggest a causal relationship between alcohol consumption and a reduction in cardiovascular risk. On a population level, the putative benefits of alcohol intake are more salient for some individuals compared to others – such as older adults with other cardiovascular risk factors. On the other hand, negative health effects can arise from even low levels of alcohol intake. Thus, the provision of advice regarding alcohol consumption needs to be individualized and is best undertaken within a clinical context.
Both major depression and cardiovascular disease are leading causes of burden of disease worldwide. Major depression is common in those suffering cardiovascular disease, and likewise cardiovascular disease is common in those suffering major depression. This chapter aims to look at the association between the two and the underlying biological mechanisms that link them. There now is vast evidence indicating that major depression is a risk factor for the development of coronary heart disease. The mechanisms involved are numerous and certainly multifactorial. These include behavioral and lifestyle factors, the sympathetic nervous system, platelet function, and the autoimmune and inflammatory systems. Of importance is that major depression increases the mortality in those suffering coronary heart disease. Until recently it was thought that this increased mortality could be explained by the increased co-occurrence of classical cardiac risk factors such as hypertension, diabetes, smoking, and dyslipidemia. It has now been shown that major depression is itself an independent risk factor. There is obvious need to understand the neurobiological mechanisms underpinning both of these disease processes. This would hopefully aid the development of better treatments of these diseases.
Anxiety disorders tend to be highly prevalent in heart disease, particularly amongst patients recovering from acute cardiac events. Yet, the role of anxiety in heart disease has not received as much attention in the literature as has depression. Epidemiologic studies indicate that there is an increased risk of sudden death and myocardial infarction in patients experiencing panic anxiety. Pathophysiologic correlates of anxiety appear to contribute to an increased cardiac risk, leading to the appreciation that anxiety disorders might in fact constitute a risk to life as exemplified by the cardiovascular disease link. Explanatory mechanisms of cardiac risk point to a link between anxiety and heart disease being mediated by stress giving way to increased cardiac sensitivity and reactivity.
The present chapter reviews the psychobiological link between anxiety and heart disease. It also supports an integrative approach for the analysis of psychogenic heart disease, that cardiac patients can benefit from cardiologists educating them about the influence of psychosocial factors on their cardiac conditions and that further research is required on the development of specific psychologically based therapies which tap into the proposed pathophysiological mechanisms associated with the mind-heart nexus.
Most people harbor some perception of the word “stress.” When one hears someone mention that they are “under a lot of stress,” one has a certain idea of what they mean and experience. Indeed, the word “stress” infuses everyday conversations, providing a term with rich subtexts that explain innumerable problems, ailments, and illnesses of unknown origins. Links between hypertension and stress have for many years constituted the archetypical example of the causal relation between physiological (or clinical) and psychological phenomena. Stressors, both mental and environmental, are today readily identified and reproduced, and one of the most active areas in psychosomatic research has been the investigation of cardiovascular reactivity to mental stress. This chapter addresses the development of various concepts of stress ranging from those of the ancient Greeks to today, as well as how to operationalize and measure stress. Furthermore, the chapter describes models of stress development and how to understand the role of stress in association with health. In this regard, the chapter also focuses on the role of coping and coping resources that influence the stress-health relationship. At the end of the chapter, stress is demonstrably linked to the development of coronary heart disease (CHD).
The effective prevention of cardiovascular disease (CVD) lies with the identification and modification of risk markers known to be causally associated with clinical events of CVD – and the evidence would support the view that the earlier this can take place, the more effective CVD prevention will be. Thus, intervention programs targeting such things as diet and obesity, cigarette smoking, and sedentary physical behavior in children and adolescents have been reported in abundance in the public health literature. A host of risk markers for CVD is now well documented, and their predictive associations with clinical CVD are well established by epidemiological evidence. Among these, psychological risk markers, and in particular psychosocial stress and depression, have recently been prominent in the literature examining CVD risk in adults. It is now clear, however, that children experience both psychosocial stress and depression to a significant degree not really recognized prior to the past two decades. This chapter addresses both stress and depression in children, evident in a large epidemiological study (the LOOK study), which has allowed these psychological states to be related to behavioral, fitness, and metabolic risk markers for future CVD over a 4-year period. The evidence from the LOOK study links both stress and depression in young children (7–8 years old at intake) with fitness deficits 4 years later. It also links stress with unhealthy levels of insulin resistance over the same time course. Both these findings point to the need to address psychosocial stress and depression early in life – along with perhaps more traditionally recognized risk markers for CVD – in the overall public health effort to reduce the incidence of this chronic and potentially life-threatening clinical condition.
Associations between depression, chronic stress, and cardiovascular disease (CVD) are often reported in the literature, suggesting that individuals with poor psychological health are at a higher risk for developing CVD and CVD-related mortality. Much of the research in this area has been carried out among adult populations, but there is growing evidence that the origins of these relationships occur at a much younger age. In the current chapter, the childhood and adolescent literature is reviewed with a focus on the effects of depression and psychosocial stress on a set of intermediary markers for CVD, namely, endothelial function and arterial stiffness. Findings arising from the adolescent phase of the Lifestyle of Our Kids (LOOK) study, a collaborative longitudinal study, are presented. From these findings, it is clear that children as young as 12 years old are already experiencing stress and depressive symptoms and more so in less fit and fatter children. Although we did not uncover any direct impact of psychological health on cardiovascular function, given the risks associated with low fitness and obesity, depression and psychosocial stress in childhood and adolescence may be exerting an early impact on the risk of developing CVD in later life.
PTSD is a disabling mental disorder with health consequences that reach far beyond the neuropsychiatric domain. Growing evidence links PTSD to increased risk of cardiovascular conditions including ischemic heart disease and thromboembolic stroke. Emerging data also suggest that PTSD may be a consequence, in addition to a cause, of acute, life-threatening cardiovascular events. Individuals with PTSD are more likely to engage in adverse lifestyle behaviors, which may predispose to cardiovascular risk factors such as obesity, diabetes, and hypertension. PTSD is also frequently comorbid with other psychiatric conditions which may affect cardiovascular risk, such as depression and substance abuse. However, additional plausible mechanisms exist that go beyond these associated conditions and risk factors. An emerging model of cardiovascular risk in PTSD is that neurobiology plays a role. Specifically, mechanisms such as repeated and heightened physiological activation in association with intrusive memories in PTSD could lead to cumulative long-term damaging effects on the cardiovascular system. This could be mediated through vascular, immune, or other mechanisms. This chapter will review the existing evidence linking PTSD to major cardiovascular disorders, discuss potential underlying pathophysiology, and provide suggestions for future research.
Cardiovascular disease and its risk factors are markedly overrepresented in people suffering with psychotic disorders such as schizophrenia. Adverse sequelae of this association include heightened mortality, worsened quality of life, and course of mental illness. Of further concern are that cardiovascular disease is underreported and neglected in this population as well as low rate of metabolic screening. The relationship of cardiovascular disease to psychosis is a complex one, with core symptoms of psychosis, poor diet, smoking, sedentary lifestyle, and socioeconomic factors predisposing to cardiovascular risk. These factors act in combination with iatrogenically induced risk factors attributed to antipsychotic medication, in particular weight gain. There are also syndromes that predispose to both psychosis and cardiovascular disease, including velocardiofacial syndrome, homocystinuria, and Cushing’s syndrome and possibly pro-inflammatory mechanisms. Psychotic symptoms are also independently associated with coronary artery bypass and valve surgery. Stress plays a role in the negative impact on both psychosis and cardiovascular disease via the hypothalamic-pituitary-adrenal axis.
Regular metabolic monitoring and intervention for identified cardiovascular risk factors in psychosis are mandatory. The latter includes education about diet, exercise, and cardiac risk factors, as well as minimization of weight gain and sedation associated with antipsychotic medication, with switching to more weight-neutral and tolerable medication options. Metformin appears to have a role in ameliorating antipsychotic-related weight gain. While there is a limited evidence base about psychological and psychotherapeutic interventions for primary or secondary prevention of cardiac disease in people with psychoses, behavioral and lifestyle interventions have emerged as showing benefit. Varenicline, a medication not without its propsychotic risks, may also complement these lifestyle interventions via facilitation of smoking cessation.
The response of the cardiovascular system to stressful situations has long been considered to have implications for health outcomes. Both exaggerated and diminished cardiovascular reactivity to acute psychological stressors have serious consequences for health. This chapter will compare and discuss research on both high and low cardiovascular responses to psychological stress. Exaggerated reactions are associated with the development of hypertension, markers of systemic atherosclerosis, and cardiovascular disease. Blunted or low reactivity is related to depression, obesity, and a range of addictions. It has been proposed that an interaction between genetics and the environment contributes to individuals’ reactivity to stress. The objective of this chapter is to explore cutting-edge research on the pathways to the development of disease via alterations in stress reactivity. It will also highlight some of the key environmental, social, and mechanistic pathways from high and low cardiovascular reactivity to health and ill health in later life and potential research and clinical implications.
This chapter reviews the evidence relating occupational stress (OS) to risk and incidence of cardiovascular disease (CVD), from the simple notion of occupational level and type as a risk marker to the more complex and theoretically more sophisticated models of occupational stress as a determinant of cardiovascular risk and disease. It does so by mapping measures of occupational stress against the three related CVD end-points of coronary risk profiles, clinical hypertension, and diagnosed events or episodes of clinical cardiovascular disease. Taken broadly, the evidence is consistently supportive of postulated links. While the evidence from studies following established theoretical models of OS appears to be both stronger and more easily interpretable, evidence from atheoretical studies employing proxy measures of OS – work hours, shift work, or perceived discrimination in the workplace, for example – has also produced evidence which is strongly supportive of the OS/CVD link. The persuasiveness of the evidence, overall, now points to the importance of OS intervention studies in the workplace undertaken according to rigorous clinical trial methodologies as the next major focus of research.
“The doctor died unexpectedly at home. His wife of 45 years passed away 4 days previously. He was known for his professional, surgical expertise, and his compassionate care for patients and their families.” From a notice in a local paper.
The death of a loved one has long been known to convey an adverse health risk, including increased cardiac events, although the mechanisms remain uncertain. While the mortality risk appears to be greatest in the initial weeks following bereavement, it remains significantly elevated during the first 6 months. Despite the difficulties conducting studies at this time, early bereavement has been associated with neuroendocrine activation, hemodynamic and prothrombotic changes, altered sleep, and immune imbalance, all of which may contribute to increased cardiovascular risk. Further research, based on an understanding of the underlying mechanisms and identified physiological changes, is required to pursue the goal of reducing health risk during this major life stress.
Cardiovascular events are a major cause of morbidity and mortality worldwide. Such events can be triggered by both acute and chronic mental stress caused by a number of known stressors, one of these being natural disasters. Triggering of acute mental stress results in increased sympathetic output, disturbed endothelial function, and the creation of a hypercoagulable state. There is then the potential for vulnerable plaque to be ruptured, resulting in thrombosis, and subsequent myocardial infarction, or even death. Chronic mental stress contributes to the atherosclerotic process through increased allostatic load, and related chronic risk factors.
This chapter summarizes what is known about the relationship between natural disasters and cardiovascular disease. A review of the literature relating cardiovascular risk to natural disasters was undertaken and proposed underlying mechanisms of this relationship examined. The review then examines potential management of cardiovascular risk related to natural disasters, particularly focusing on psychological implications and strategies for management of both individual and population health.
Despite decades of effort, one of the greatest mysteries in biology is to understand sleep. Sleep is more than simply rest. Depriving someone of sleep has powerful adverse effects on their mental, metabolic, and cardiovascular health. The timing of sleep also plays an important role in terms of the onset of cardiovascular events. Finally, the effects of sleep on ventilation and the downstream effects of sleep apnea in the pathogenesis of all cardiovascular conditions have come of age in the evidence-based medicine field.
Psychological reactions to a cardiac event differ among patients, impacting upon individual presentation and recovery. Cognitive response to symptoms and resulting coping mechanisms will impact on how quickly a patient will seek help, comprehend, and adjust to their condition and engage in interpersonal relationships. Negative cognitive responses can result in, or be a product of, common mental health issues often seen following acute coronary syndrome including adjustment disorder, depression, anxiety, stress, trauma, anger, or hostility. The increasing recognition of the link between these negative emotions and cardiac disease has increased the focus on whether treatment can mitigate negative outcomes. Findings highlight the importance of elucidating beliefs and understanding around illness and targeting interventions appropriately to modify any maladaptive beliefs. This includes implementing routine screening processes that identify patients at risk of persistent mental health problems.
Introduction: Congenital heart defect (CHD) may be defined as an anatomic malformation of the heart or great vessels which occurs during intrauterine development. CHDs are serious and chronic illnesses. Congenital heart defects may be classified into acyanotic and cyanotic depending on the presence or absence of cyanosis. As survival has improved, evidence has accumulated that CHD touches many aspects of the lives of those affected. Children and adults with CHDs report difficulties in physical, behavioral, and psychiatric abnormalities.
Aim: To emphasize that people with CHDs often need treatment over their life and therefore require specialist review during childhood and adulthood. This is because people with complex heart problems can develop further problems with their heart rhythm or valves over time. Also they may report physical, psychological, and behavioral abnormalities.
Conclusion: A significant proportion of survivors of open-heart surgery for CHD are at risk for physical and psychological maladjustment. This calls for an integrated approach to family support, taking the child’s individual needs into account as well as the needs of the parents.
During the last few decades, the survival rate of adults with congenital heart disease (ConHD) has increased considerably. The psychological characterization of adults with ConHD is very different from patients with acquired cardiac pathologies. Recent guidelines of cardiology associations indicate the necessity for specialized psychosocial support. The majority of the studies in the literature indicate the absence of a relationship between diagnosis, physical functionality, and the presence of residual symptoms and a worse psychological functioning in these patients. The variables which seem to be related to psychological well-being in these patients are the following; negative thoughts, solitude, social support, fear of negative evaluation, imposition of limits, perceived health status, somatic symptoms, perception of an economical difficulty, and restrictions linked to the surgical scar in females. Interestingly, studies, which utilized psychiatric interviews or similar methodologies, outlined that it was common for patients, who were diagnosed with a mood or anxiety disorder, not to have received any appropriate treatment and often they were assumed to be well psychologically. When it comes to the life experiences of adults with ConHD, it has been outlined how these patients feel different from their healthy peers. It has been seen that often there is a struggle to feel normal and also to be perceived by others as being normal. This could lead to denial of the conditions and also efforts to exceed their physical boundaries imposed by their condition. Three main domains in which clinical health psychologists can contribute in the handling of adults with ConHD were identified: provision of clinical services, multidisciplinary research, and professional education.
Valvular heart disease is an increasing health concern in most developed countries due to aging populations resulting in increased prevalence. While there is significant focus on ensuring timely medical care and developing less-invasive procedures to treat the functional valve lesions, there is often little attention given to the psychological impact of valvular heart disease.
Indeed while the impact of ischemic heart disease on psychological health and even the potential causative association between psychological illness and ischemic heart disease have been widely acknowledged, such a link is often not recognized in valvular heart disease. However among this unique population who are often older and frailer, assessment of psychological health may be even more important.
Sudden cardiac arrest is a common and often lethal event, claiming roughly 400,000 lives annually in the United States alone. Implantable cardioverter defibrillators (ICDs) represent a significant technological advance in the medical arena and are the best available intervention for sudden cardiac arrest and subsequent prevention of sudden cardiac death. Over the last two decades, research has increasingly focused on understanding how living with an ICD presents unique and serious psychological challenges for many patients benefiting from this lifesaving technology. Employing a biopsychosocial model in caring for these patients’ psychological health helps address relevant factors that can contribute to their psychologically distressed presentation, including cardiac disease burden, ICD treatment delivery (i.e., shock), psychiatric (s) disorder or symptoms, health behaviors, and disruption of day-to-day life or social functioning. This chapter highlights known, common psychological risks for ICD patients, which include depression, anxiety, and compromised quality of life. It further explores some key considerations or groups that are associated with risk for psychological distress, such as pediatric ICD patients, devices under recall, and end-of-life issues. Several relevant assessment measures are provided to assist providers in identifying which psychological risks are realities for each particular patient. In total, this information is designed to lend knowledge and confidence to consulting mental health providers, leaving them well equipped to deliver state-of-the-art assessment of ICD patients – a medically complex, and often psychologically distressed, group of individuals.
Psychiatric symptoms are common after cardiac surgery, particularly adjustment disorders, major depressive disorder, posttraumatic stress disorder, delirium, and cognitive disorders. Depression has been reported in up to 37 % of patients after coronary artery bypass graft surgery and up to 63 % of patients after cardiac transplantation. PTSD has a prevalence of 15–25 % in postoperative cardiac patients and 10–17 % among posttransplant patients. The reported incidence of delirium among postoperative cardiac patients ranges from 10 % to 50 %. Postsurgical psychopathology confers significant morbidity and mortality. This chapter will review the prevalence, clinical features, and treatment of the most common psychiatric disorders after open-heart surgery (including coronary artery bypass graft and valve repair procedures) and orthotopic heart transplant.
This chapter provides an overview of major attempts to relate personality in the form of stable traits to the development and progression of coronary heart disease (CHD). Among the first attempts to relate personality to CHD was the Type A behavior pattern, a complex of emotion and action tendencies including aggressive competitiveness, free-floating hostility, and time urgency. Although evidence supported the relationship of the Type A pattern to CHD, questions arose concerning the aspects of the Type A pattern that were the active ingredients. Analysis of components of the Type A pattern suggested hostility as the primary active ingredient. This has led to a large number of studies of the relationship of hostility and anger to CHD, mostly with positive results. In addition to this work, there is also a body of literature suggesting that a combination of negative affectivity and social inhibition, a pattern known as the Type D (distressed) personality, is associated with heightened CHD risk. Although some studies have supported this idea, a number of studies have obtained negative findings, and there are concerns about the way in which the Type D personality is conceptualized and measured. Recently, an integrative review has suggested that the personality trait of interpersonal sensitivity, a concern with negative social evaluation, is associated with CHD. This review concludes by considering possible mechanisms by which personality traits are associated with CHD.
The concept and the impact of inadequate social networks and poor social support on health have been intuitively known since long. But it was not until the 1970s that the significance of social relations was demonstrated, for the first time in the Alameda county study in California.
Within a few years, several population-based prospective studies came to the same conclusion: Poor social networks and support increased total and cardiovascular mortality. This was true even in the North Karelia, Eastern Finland, but only in men. In North Karelian women, and also in other groups of women, the function of the social relationships appeared to be more important than the structure. North Karelia is a part of rural Finland, situated directly at the border between Russia and Finland.
In Stockholm, women patients with coronary disease and social isolation modified the role of depression so that only when they exist together, the factors worsen prognosis and accelerate progression of coronary artery disease, as measured by quantitative coronary angiography (QCA). Similarly using QCA methodology, we could show that exhaustion, more clearly than depression, worsened prognosis in women. The stress burden originating from the family was more important than the stress burden of the job, although almost all of the Stockholm women were employed outside home. Therefore, we designed a cognitive behavioral intervention to reduce women’s stress. In a randomized controlled trial, this proved to both prolong women’s lives and attenuate their negative emotions.
Altogether around 800 women patients have been followed for up to 20 years. They have been examined with a variety of psychosocial measures. Of psychosocial measures, vital exhaustion was best fitting to the pattern of coronary artery atherosclerosis progression and also seemed to yield the best fit to the multivariate model of disease progression. Their precise psychobiological mechanisms remain unclear. However, multivariate evaluations suggest that standard coronary risk factors partly “explain” and metabolic, hemodynamic, immunologic, and autonomic imbalances contribute to the final and complete remaining psychobiological pathogenic pathways.
The type A behavior pattern (TABP) showed immense success in predicting coronary heart disease (CHD) incidence for three decades, from the 1960s onward, and was considered a strong and independent risk factor for CHD development. The TABP, or behavior classifications closely related to this pattern, are still used both in practice and in research settings, for this purpose. But due to a number of negative findings and critical commentaries on the relation between type A behavior pattern and CHD from the middle of the 1980s and few positive findings in the same period of time, researchers and practitioners have questioned whether the TABP’s predictability of future CHD development was really quite so well established. This chapter describes the early history of TABP and also scrutinizes the related concept of type A personality, which became the concept to describe what was the underlying personality of TABP. It sums up the research history for the TABP construct by starting with a number of reviews and meta-analyses on the concept from the late 1980s and until now. The chapter is based on a close examination of the research on TABP involving extensive literature searches conducted in 2003, 2010, and 2013 using PubMed, MEDLINE and PsycINFO, and the search term “type behavior and CVD.” While the volume of evidence has declined over time, recent work suggests a continuing utility for the construct.
Anger and hostility are described with special attention to their cognitive-motivational properties. Varying operational definitions related to anger self-report and behavioral observation are presented. The idea that anger can be maladaptive is now widely accepted as in DSM and alternative classifications of dysfunctional anger. The idea that maladaptive anger raises risks for hypertension and coronary heart disease is reviewed with reference to empirical findings on mediators such as atherosclerosis, cardiovascular reactivity, immune system changes, and unhealthy lifestyles. Given that anger is a relational emotion, it is not surprising that it befalls many interpersonal relations including close/intimate relationships. Dimensions of affiliation and control in relationships are presented as a framework for understanding how anger and hostility can develop and persist in these contexts. The further connection between such anger and cardiovascular function is illustrated. Fortunately, maladaptive anger is treatable, as explained with meta-analytic evidence on cognitive behavioral therapy (CBT). Also available are recent enhancements like CBAT that involve sequencing multiple cognitive, behavioral, and affective strategies appropriate to the process of anger from onset, through progression, to offset. Finally, traditional interpersonal therapies and newer therapeutic formulations such as acceptance and commitment therapy may address major themes in interpersonal conflict underlying the onset and maintenance of cardiovascular disease. Yet, many of these potential applications still await research and implementation in the field of psychocardiology.
While coronary heart disease (CHD) for decades was understood as mainly a male disease group, it has through the last years become increasingly evident that it is now an important disease causing premature death also in the female populations throughout the Westernized world. Present paper scrutinizes via literature searches and discussions of relevant data the sex and gender differences in psychological risk factors for CHD with an emphasis on female risk. It is concluded that the risk factor picture in females is, due to limited research, still far from clear, even if there are indications of sex differences in both the risk factors picture and the trajectories of the disease development.
In 2013 there were 51.2 million persons worldwide who had been forcibly displaced as a result of persecution, conflict, generalized violence, or human rights violations. 16.7 million persons, half of whom were children, were refugees. More than 80 % were living in refugee camps and other generally temporary although often long-lasting arrangements, in developing countries. From this massive population, only 98,000 were resettled in refugee-receiving countries. The prevalence of mental disorders, particularly post-traumatic stress disorder, depression, and anxiety, is greater in refugees than in non-refugees, although prevalence estimates vary greatly. As well as having poorer mental health, refugees are also more likely than non-refugee immigrants or host populations to experience poorer physical health, higher all-cause mortality, and higher cardiovascular mortality. Although the severe and persistent stress that is a central element of refugee experience is probably an independent risk factor for cardiovascular disease, it seems likely that the higher cardiovascular risk is mediated by mental disorders, such as post-traumatic stress disorder and depression, which are common in refugees and are clearly associated with increased cardiovascular risk. In addition, refugees are less likely to have access to effective mental health and general health services, resulting in further avoidable risk of cardiovascular morbidity and mortality.
In western societies there is a persistent social patterning of cardiovascular disease (CVD) risk. Social disadvantaged (SD) people are at greater risk of CVD than people in more advantageous positions. Both individual and contextual risk factors are of importance. Several models have been put forward to understand the relationship between social disadvantage and CVD risk. The concept psychosocial reflects psychological processes that are linked to the social environment and directs attention to both behavioral and endogenous biological responses to human interactions. The physical and social environment shapes health behaviors as health behaviors are observed socially patterned. Today, one must expect that clinicians are aware of the fact that SD increases CVD risk and thus manage to think beyond traditional individual-based CVD risk assessment.
The sympathetic nervous system is pivotal in both circulatory and metabolic control. While acute activation of the sympathetic nervous system is important during regular daily activities in order to maintain homeostasis or in times of stress in order to initiate a fight or flight response, chronic activation of the sympathetic nervous system is associated with disease development and end-organ dysfunction. Of particular importance is the role of the sympathetic nervous system in the initiation and maintenance of hypertension and the development of left ventricular hypertrophy, diastolic dysfunction, and insulin resistance. Given the undoubted role of the sympathetic nervous system in generating cardio-metabolic illness, inhibition of the sympathetic nervous system seems a logical choice in order to alleviate disease burden associated with these conditions. Lifestyle changes involving diet, exercise, and cognitive-based therapies as well as pharmacological and device-based interventions directly targeting the sympathetic nervous system are likely to be of benefit.
Recent discoveries supporting a functional and structural link between the brain and the heart emphasize the importance of understanding the cross talk for cardio- and cerebrovascular health. Stress has been shown to play a crucial role in the generation of cardiovascular diseases and has a major impact on neurodegenerative diseases and mental disorders presumably through activation of the sympathetic branch of the autonomic nervous system. It is well established that overactivity of the sympathetic nervous system plays a central role in the development of cardiovascular disease and constitutes an important risk factor for cardiovascular morbidity and mortality. Further, increasing evidence suggests the overactivity of the sympathetic branch is a common phenomenon linking major cardiac pathologies seen in association with several primarily neurological conditions, such as cerebral infarction and subarachnoid hemorrhage. Modulating brain activity in humans for otherwise treatment resistant disorders has been demonstrated to affect cardiovascular parameters. Direct electrical stimulation of specific midbrain areas in humans for pain relief regulates human cardiovascular reflex control and can evoke panic and anxiety, by modulating the activity of the autonomic nervous system.
This chapter examines the connection between the brain and the heart the autonomic nervous system provides. Evidence of a linking between emotional stresses and cardiovascular risk is explored, more specifically, stress-induced cardiomyopathy and a plausible explanation for the female predisposition of the condition.
The clinical relationship between mental disorders and cardiovascular disease and risk factors is highly important with serious consequences for morbidity and mortality. A key biological mechanism in this complex and bidirectional relationship is related to immune dysregulation and inflammation in particular. This review critically evaluates the existing literature on the bidirectional nature of this relationship, the contributing clinical factors, and the role of inflammation in prevalent risk factors for both mental disorders and cardiovascular disease including obesity, endothelial dysfunction, and diabetes mellitus type 2. This chapter outlines the lines of biological mechanisms in the bidirectional relationship between mental disorders and cardiovascular disease by exemplifying this using depression as a common disorder. This focus on the role of immune dysregulation and inflammation in these risk factors and comorbid disease suggests new avenues for identifying and possibly treating early patients at risk, but also it opens up novel and preventive treatments such as the use of anti-inflammatories for both types of conditions.
Precisely how regulated patterns of gene expression under the control of diverse signaling pathways underlie the homeostatic control of neuroanatomical aspects of cardiac function remains unclear. The autonomic nervous system is distinguished by the sympathetic and parasympathetic nervous systems that are under the direct control of transcription factors that function as either activators or repressors of gene expression. While several regulatory determinants are known to coordinate the actions of activators and repressors, how these factors serve to maintain genes implicated in the neurocardiac axis is the subject of review. The discovery of regulatory complexes that serve as a functional linkage between DNA-bound transcription factors and altered chromatin structures indicates that posttranslational modifications of core histones connect aspects of neurocardiac gene function. The complexity of these regulators to alter noradrenaline transporter (NET) gene function is explored here. Recent evidence of chromatin-modifying enzymes regulating NET expression might apply to genes implicated in neurocardiology.
Depression is one of the most prevalent disorders worldwide, with high comorbidity with cardiovascular disease (CVD). Despite significant heritability, robust genetic associations are yet to be identified in depression. Multiple factors are accountable for this, including that genetic studies have not widely considered environmental factors, despite their established association with depression. One such factor is stress, a robust risk factor for depression; many genetic studies have failed to include nurture in their research into depression. The first gene-environment interaction (GxE) study in depression was published in 2003, reporting a significant interaction between a functional polymorphism in the serotonin transporter gene (5-HTTLPR) and recent stressors to predict depression. Many studies aimed to replicate this finding, as well as investigate other candidate genes (i.e., CRHR1, GR, FKBP5, BDNF). Initially, findings appeared not to reach a clear consensus; however, a closer analysis of the literature has shown that there are consistencies when specific methodological aspects are considered (i.e., timing of stressors). While there are some exciting and strongly evidenced findings, GxE research continues to face some significant challenges. This includes recognition of the importance of subtle method differences and also sample size. Samples are relatively small due to the time required to ascertain high-quality environmental data relative to standard genetic association studies, compromising power. Ascertaining large samples must therefore be made a priority in GxE research to enable further discoveries. GxE studies in depression have the potential to inform disease mechanisms that may be relevant to CVD, informing future CVD-depression research.
In searching for biological evidence that essential hypertension is caused by chronic mental stress, a disputed proposition, parallels are noted with panic disorder, which provides an explicit clinical model of recurring stress responses: (i) There is clinical comorbidity; panic disorder prevalence is increased threefold in essential hypertension. (ii) Plasma cortisol is elevated in both. (iii) In panic disorder and essential hypertension, but not in health, single sympathetic nerve fibers commonly fire repeatedly within an individual cardiac cycle (these salvoes of nerve firing constituting a stress “signature”). (iv) For both, adrenaline cotransmission is present in sympathetic nerves, as is seen in experimental models of stress. (v) There is induction of the adrenaline synthesizing enzyme, PNMT, in sympathetic nerves, an explicit indicator of mental stress exposure. Patients with essential hypertension exhibit a further manifestation of mental stress: there is activation of noradrenergic brainstem neurons, most likely of the Al and AS nuclei, projecting rostrally to the hypothalamus and amygdala. Activation of the renal sympathetic outflow is pivotal in hypertension development. In the presence of high dietary sodium intake, endemic in contemporary life, this activation of the renal sympathetic nerves provides concurrent “neural,” “renal,” and “sodium” mechanisms of hypertension development. Relaxation and stress reduction measures lower blood pressure, but less than anticipated, and not sufficient for BP control in severe grades of hypertension. A modern and commonly successful development in the therapeutics of severe and resistant hypertension is the targeting of the final common pathway in the hypertension pathogenesis, with ablation of the renal sympathetic nerves by radiofrequency energy delivered as a one-off procedure, using a specially engineered catheter sited in the renal arteries, the procedure of endovascular renal denervation.
Diabetes and depression are major public issues that often co-occur. Both diseases affect a growing number of people worldwide and are projected to be among the five leading causes of disease burden in 2030. Approximately 10–30 % of the people with type 1 (5–10 % of all diabetes cases) or type 2 diabetes is affected by depression. There is ample evidence that the association between type 2 diabetes and depression is bidirectional. Depression is likely to increase the risk of cardiovascular complications and mortality in people with diabetes. Several behavioral mechanisms (e.g., treatment nonadherence, physical inactivity, and poor diet) and biological mechanisms (e.g., deregulation of the hypothalamic–pituitary–adrenal axis and the sympathetic nervous system, vascular pathology, and central obesity) explain the link between depression and cardiovascular risk in diabetes patients. It has been postulated that treatment of depression could improve cardiovascular outcomes. Due to limited number of studies, there is currently no convincing evidence that pharmacological or psychological treatment of depression improves cardiovascular outcomes. Various organizations suggest screening for depression in their guidelines or recommendations for diabetes care. At present, there is no substantial evidence of the effectiveness of screening for depression among diabetes patients and is therefore not recommended. Future trials should focus on (a) the development of innovative interventions that can help to prevent depression, type 2 diabetes, and cardiovascular diseases in a cost-effective way and (b) long-term prospective studies that disentangle the mechanisms that link depression with unfavorable cardiovascular risks in diabetes patients.
In recent years, a novel syndrome of transient cardiac dysfunction and heart failure precipitated by emotional or physical stress has been described. Because patients with “stress cardiomyopathy” (SCM) typically present with chest pain, electrocardiographic abnormalities, elevated cardiac biomarkers and focal left ventricular wall motion abnormalities, it is perhaps not surprising that this condition was mistaken for many years for an acute coronary syndrome (ACS). It has become increasingly clear over the past decade, however, that both the clinical features and pathophysiology of SCM are distinct from those of an ACS. In contrast to the plaque rupture physiology of ACS that results in permanent myocardial necrosis, SCM is characterized by the absence of obstructive coronary disease in most cases and by completely reversible cardiac dysfunction. There is considerable evidence to suggest that the mechanism underlying this stress related “stunned” myocardium is enhanced sympathetic stimulation. Elevated plasma levels of catecholamines have been found in patients with SCM, and the syndrome has been associated with other conditions of catecholamine excess such as central neurologic injury and pheochromocytoma. Further, SCM can be precipitated by the intravenous administration of catecholamines and beta agonists. The precise mechanism in which enhanced sympathetic stimulation causes myocardial stunning in SCM remains unknown, but possibilities include either catecholamine mediated microcirculatory dysfunction or direct myocyte inhibition due to cyclic AMP mediated calcium overload. This chapter will review the clinical and diagnostic features of SCM, and the evidence supporting a sympathetically mediated pathogenesis will be presented. In addition, risk factors will be highlighted that may increase individual susceptibility to SCM by modulating myocyte and microvascular sensitivity to catecholamines.
Close causative relationship between psychological stresses and cardiovascular morbidity is now well documented. Research on humans has been attempting to unravel the significance of this association by investigating psychological and social characteristics in relation to cardiovascular health. However, this research is limited by the difficulty to control and standardize for the individual social history, the impossibility to apply psychosocial stress stimuli for mere experimental purposes, as well as the long time span of cardiovascular pathogenesis in humans. Animal studies controlling for social environment and adverse social episodes allow for partially overcoming these limitations. The aim of this review is to provide an up-to-date reference of the experimental evidence so far collected on the link between psychosocial factors and cardiovascular dysfunction in rodents, with special emphasis on modeling stress-induced sudden cardiac death, cardiac arrhythmias, stress cardiomyopathy, and psychogenic hypertension and with focusing on acute and chronic psychological and social stresses, aggressiveness, and negative mood states as causative factors.
The nonlinear dynamics of heart action are such as to generate and to support irregular nonrandom variations in the main output parameters of pulse and pressure, in response to external stimulation such as stressors (Pearson 1972; Gregson 2009; Herbert 1995; Mezentseva et al. 2002; Rao and Yeragani 2001; Shiferaw and Karma 2006). These dynamic complexities have serious implications for the analysis and treatment of hypertension, as the probabilities of misdiagnosis of state, dysfunction, and potential morbidity cannot with certainty be based on the linear or Gaussian statistics usually employed in epidemiological and related studies. A Bayesian analysis of decision probabilities is used to point up ambiguities in reported results. There is gradual recognition of this situation, but so far little established linkage between nonlinear dynamical modeling and clinical practice, except perhaps in some recent biomedical physics modeling.
A large body of evidence links depression and coronary artery disease and includes findings that patients who experience depression at the time of an acute cardiac event die sooner than their nondepressed counterparts. Although cardiac rehabilitation programs addressing medical, lifestyle, and psychosocial issues have positive effects on behavioral change, significantly reduce the risk of having future cardiac events, and reduce mortality, depressed mood and social isolation can compromise the positive effects of these programs. Systematic reviews have shown the effectiveness of psychological interventions for cardiac patients; however, comparison of interventions is difficult due to variation in target population, severity of depression, “dose” and mode of delivery of the intervention delivered, variation in outcome measures used, varied follow-up periods, and lack of detail on intervention content. Brief interventions have been shown to be effective in reducing depression, as has Internet-delivered cognitive-behavioral therapy for adults with high CVD risk. Interventions comprising psychological and social support-enhancing components, when compared with usual care, are also effective in reducing depressive symptoms in cardiac patients. Although effect sizes reflect a small benefit of these psychosocial interventions, it appears that they improve social support and possibly mental health quality of life, but no firm conclusions can be drawn as to whether these interventions impact on cardiac mortality and morbidity. Notwithstanding methodological limitations and the modest effects achieved, psychological and psychosocial interventions are worth implementing, post-cardiac event, as unresolved depression is a major cause of death and disability in cardiac patients.
This chapter will provide a definition of anxiety and describe methods for assessing it within cardiac practice. Next the epidemiology of anxiety disorders and prevalence of anxiety disorders in cardiovascular disease will be reviewed followed by literature on anxiety and cardiovascular disease. Subsequently, different treatment options including pharmacotherapy and different psychological approaches will be evaluated. Other treatment measures discussed in this chapter include breathing retraining, relaxation, and exercise therapy. The chapter concludes with recommendations for treatment of anxiety in heart disease along with future directions for research.
From time immemorial, the mind and the body have been closely linked, and research continues to show a high association of depression and anxiety with heart disease. Depression is a risk factor for heart disease as well as risk for poor recovery after a cardiac event. The Whole Person Model described here integrates thinking about thoughts, emotions, bodily symptoms, and health behaviors, and can form the foundation of a powerful rehabilitation or disease management program. For real functional recovery to occur, patients need to take control of their lives, and for this to occur considerable behavioral change is often required. Integrating psychological care with physical health care will facilitate this.
Psychosocial challenges for ICD patients have been well established in research and clinical practice. Anxiety secondary to disease management and/or fear of ICD shock is among the most common concerns that lead to development and maintenance of psychological distress in ICD patients. Researchers and clinicians have developed a broad range of cognitive-behavioral, pharmacological, and nontraditional approaches to address the unique needs of ICD patients. Findings from two recent meta-analyses suggest that cognitive-behavioral interventions of high intensity were effective in reducing anxiety and depressive symptoms (effect sizes ranging from small to moderate large). However, the high degree of heterogeneity in treatment duration and content across studies has made it difficult to formulate broad conclusions on the feasibility and effectiveness of existing interventions. The purpose of this chapter is to highlight the evidence and breadth of empirically supported psychological treatments for ICD patients and their families. A list of resources for ICD patients and mental health professionals is also provided at the end of the chapter.
Many patients experience significant psychological distress after admission to hospital following acute coronary syndrome or to undergo percutaneous coronary angioplasty, coronary artery bypass surgery, or other cardiac surgery. Anxiety and depression are common emotional responses to these acute cardiac events and may be preexisting conditions. Symptoms of cognitive impairment, post-traumatic stress disorder, delirium, and major denial may also be present in hospitalized cardiac patients. Although gaps in knowledge exist concerning the impact and course of these disorders, there is now sufficient evidence showing their detrimental effects upon patients’ recovery. The importance of early detection and management of depression, in particular, is essential to help prevent unwarranted psychological disability. Screening of patients is recommended in hospital and at appropriate intervals during follow-up. Brief screening tools are available which can be routinely administered. In addition, doctors and other health professionals should be aware of the clinical features of common psychological reactions of hospitalized patients to ensure prompt recognition and assessment. The important role of doctors in the clinical management of patients with anxiety and depression symptoms is stressed. However, referrals for the management of acutely distressed patients should be made to health professionals who have specific training in the treatment of psychological problems. Past studies have reported benefits from some depression treatments, especially those based on cognitive behavioral therapy. However, further rigorous research is required to develop, implement, and evaluate interventions for the early alleviation of symptoms of depression and other psychological conditions. Coordinated care of patients by a multidisciplinary team is essential. Encouragement of patients to attend a group cardiac rehabilitation program is highly recommended.
The chapter opens with an account from an American physician of a meeting with a Tibetan Buddhist practitioner for whom mindful awareness was central to resolving a cardiological diagnostic question, and rather more than that.
After a note on the quality and level of evidence base in this area, a general introduction to mindfulness and other meditative traditions follows, including something of relevant history and cultural origins and the range of interventions that may be considered related in contemporary healthcare.
The role of mindfulness- and meditation-based approaches will briefly be considered as they may be relevant for the practicing clinician and as they have been introduced into a number of medical educational settings.
This leads to considering the role of mindfulness-based interventions in reducing risk factors (Yusuf et al. Lancet 364(9438):937–952, 2004), particularly behavior and lifestyle factors but also psychiatric disorders, particularly depression (Rosengren et al. Lancet 364(9438):953–962, 2004) as shown substantially to influence risk for cardiac conditions.
In the context of treatment of specific cardiac disorders, studies that involve the application of mindfulness- or meditation-based approaches will be considered.
As the chapter considers specific disorder contexts, there will in each case be a drawing of the evidence together by the authors into some suggestions for how mindfulness-based interventions may be relevant for clinical management.
Cardiac illness is frequently comorbid with psychiatric disorders, and patients with heart disease are often prescribed psychotropic medications. Although psychotropics are in general well tolerated and efficacious in patients with cardiac disease, physicians need to be aware of key concerns related to side effects and safety. Among the antidepressants, selective serotonin reuptake inhibitors (SSRIs) have the most established track record for safety in cardiac patients, although atypical antidepressants, such as mirtazapine and bupropion, are also largely considered safe for use in these patients. Mood stabilizers, such as lithium and carbamazepine, have been associated with arrhythmias. Typical antipsychotics, such as haloperidol and chlorpromazine, increase the risk of QTc prolongation; however, the degree of such prolongation varies significantly among agents. Atypical antipsychotics, with the exception of ziprasidone, are considered safer in this regard, but some are associated with metabolic side effects that can increase the risk for coronary artery disease. The use of benzodiazepines is generally safe in patients with cardiac disease, and these agents may mitigate symptoms of acute coronary syndrome (ACS) by reducing catecholamine surges. Finally, stimulants, though relatively contraindicated in those with various heart conditions, may be used cautiously to rapidly treat depression and anergia in cardiac patients.
Up to 80 % of the risk for cardiovascular disease (CVD) in the general population is attributable to lifestyle factors. Hence, the modification of lifestyle behaviors is important for reducing cardiovascular risk in the context of primary and secondary CVD prevention. However, initiating and sustaining changes in lifestyle behaviors remains challenging, particularly for patients who have experienced a potentially life-threatening CVD event. This chapter reviews the evidence base for changing lifestyle behaviors that contribute most to the etiology, progression, and outcomes of CVD, that is, nutrition and dietary behaviors, physical activity, and smoking. Furthermore, the evidence in relation to the effectiveness of behavioral interventions and key factors to consider in the implementation of effective behavior and lifestyle change programs in clinical and non-clinical settings are discussed. Finally, the implications of these findings for future research and practice in the field are considered.
Lack of physical activity is a key risk factor for the development of coronary heart disease, yet activity is decreasing in the modern world. Once cardiovascular disease is present, physical activity is an essential ingredient of recovery and rehabilitation. Heart patients who are regularly active have a much smaller risk of dying compared with inactive patients. Several factors have been found to be associated with the uptake and maintenance of physical inactivity in cardiovascular patients, including psychological, social, and socioeconomic factors. This chapter will first describe the effects of physical activity on post-MI survival and will subsequently examine issues which act as barriers to exercise in this population.
Modern lifestyles are increasingly sedentary yet lack of physical activity is a key risk factor for cardiovascular disease. Moderate to high activity levels offer significant protection against developing CHD via multiple pathways. Furthermore physical activity is an essential ingredient of recovery and rehabilitation after myocardial infarction (MI), with heart patients who participate in cardiac rehabilitation having far greater odds of survival. However, less than 50% of post-MI patients engage in cardiac rehabilitation. Maintaining an active lifestyle is often challenging with many factors involved, and around half of people who begin an exercise program will not continue. Several barriers to physical activity in heart patients are discussed here, including depression, low socioeconomic status, poor sense of coherence, anxiety and social support.
The serious worldwide challenge posed by the prevalent, and increasing, problem of obesity is well known. Obesity places a substantial health burden on affected individuals, including cardiovascular disease, although the complex biopsychosocial pathways linking obesity with cardiovascular disease have yet to be fully explicated. Three primary approaches have been investigated as treatments for obesity, namely, behavioral (lifestyle) weight-loss programs, pharmacotherapy, and bariatric surgery. Behavioral weight-loss programs (and pharmacotherapy) have been found to result in modest weight losses and reductions in cardiovascular risk factors (e.g., a significantly reduced rate of type 2 diabetes). However, the impact of these programs on cardiovascular morbidity and mortality has been inadequately investigated, with the few studies conducted yielding inconsistent results. Any capacity of behavioral weight-loss programs to reduce cardiovascular disease end points is likely to be limited by the transient nature of treatment-induced weight losses, with weight regain the normative response to these programs. Bariatric surgery has been found to yield large and sustained weight losses and, importantly, improved cardiovascular outcomes and yet is limited by its expense and the fact that it is associated with a risk of surgical complications (including the need for operative re-intervention in a sizable number of patients). While the obesity treatment outcome research has elicited pessimistic responses from some researchers and obese patients alike, innovative approaches (e.g., maximizing the support available to obese individuals for sustained weight loss) and integrative responses (that entail shared responsibility for promoting healthy dietary behaviors and physical activity at the individual, interpersonal, and societal levels) are likely needed to meet the obesity challenge.
Psychological adjustment following acute cardiac events such as acute myocardial infarction (AMI) and coronary artery bypass graft surgery (CABGS) has received increasing attention in the last three decades. While physical recovery remains the highest priority, psychological recovery is now considered a primary concern for health professionals working in cardiac rehabilitation and secondary prevention. The prevalence of anxiety and depression in people who have had a cardiac event is up to four times higher than in the general population. Post-event anxiety and depression both confer an increased mortality risk, highlighting the importance of identifying these patients early in order to ensure appropriate treatment. In recent years it has been recommended that all cardiac patients be screened for depression after a cardiac event. However, there are some inherent problems with routine depression screening, particularly if undertaken soon after the event. There are risks of both unnecessary treatment of patients with transient symptoms and non-identification of patients whose symptoms appear later after physical recovery. This chapter outlines evidence regarding the prevalence and impacts of anxiety and depression in cardiac patients and issues regarding depression screening. Some alternative ways of identifying patients at risk of depression are discussed.
The link between heart and mind is now so well established that it can no longer be considered a farfetched speculation; rather there is now a robust body of respectable empirical and clinical evidence which strongly asserts the nature of this relationship as both congruous and complimentary. It is now clear that strong emotional distress, whether in the context of acute or chronic stress or from mental illness, is commonly reciprocated by elevated risk factors for cardiovascular disease (CVD) and increased cardiac morbidity and even cardiac mortality. The Handbook of Psychocardiology is the first fully comprehensive volume examining this now accepted heart/mind nexus. The book showcases a unique collaboration between research scientists and clinicians across the fields of behavioral medicine and psychology, neuroscience, cardiology, and psychiatry. It was by bringing together such a seemingly diverse and eclectic mix of scientists and practitioners that we have been able to fully highlight the commonalities and complimentary aspects of this relationship.
The concepts of quality of life and health-related quality of life (HRQoL) are wildly used in literature but lack agreed formal definitions. It is however broadly accepted that they are complex, multidimensional, and dynamic constructs, which should be assessed on the basis of positive and negative indicators. The term HRQoL is used to clarify the health-disease context of the analyzed QoL. Both generic and disease-specific instruments are used for HRQoL measurement.
Results of the studies on the level and changes in HRQoL after MI are inconsistent. Some studies show HRQoL as being minimally affected by MI, while others indicate major reduction in at least some of its dimensions. Moreover, minor fluctuations to significant changes in HRQoL’s different dimensions are reported. The dynamic of these changes varies depending on the period since an MI and between different dimensions of HRQoL.
A number of clinical, sociodemographic, and psychosocial characteristics are recognized as predictors of HRQoL in MI survivors. Among sociodemographic characteristics, age, gender, and education are of a special interest with higher education predicting better HRQoL, but age and gender’s role being unclear. Among psychosocial resources, e.g., self-esteem and various social resources were recognized as strong predictors of HRQoL, with higher levels of psychosocial resources predicting better HRQoL.
More work still needs to be performed to fully understand the dynamics and complexity of quality of life in the context of myocardial infarction and CVD in general. But the results support a need for a comprehensive and patient-centered medical practice.
The following chapter details current understanding of interactions between insulin, or insulin resistance, obesity, and mood and affect as key mediators of this association. The functions of insulin in the periphery and central nervous system are reviewed, and insulin resistance is explained. Three different levels of affective states are defined: pure affect, mood, and emotion, although it is noted that more research currently focuses on mood and mood disorders. Insulin crosses the blood-brain barrier using saturable transporters, whereupon it influences a range of functions ranging from memory to the regulation of mood and reward-seeking behaviors including eating. The review notes striking similarities between the neurological consequences of diabetes and depressive illness, including decreases in hippocampal formation volume. Hence, the development of insulin resistance would appear to disrupt these systems, contributing to the development of mood disorders such as major depressive disorder and the overconsumption of calorie-dense foods. The precise mechanisms for these processes remain unclear and are likely to be highly complex and multifaceted. Possible mechanisms for these relationships are outlined, including insulin resistance, HPA-axis dysfunction, autonomic nervous system imbalance, endothelial dysfunction, platelet overactivity, inflammation responses, and chronic psychosocial distress. Any or all of these systems offer plausible explanations, and there is no reason to suppose that there is only one correct option from those listed. In addition to studying the cellular and physiological levels of analysis, research must incorporate consideration of the subjective experiences generated by these systems. In particular, there may be explanatory value in examining the less stable short-term experiences of emotions, as well as more stable mood states.
Cardiac medications including β-blockers, cardiac glycosides, and antiarrhythmics have long been known to have CNS effects including alterations in mood, emotion state anxiety, and depression. While the predominant effects come from those with higher lipophilicity and when used at high doses, the evidence is actually quite mixed. At cardiac therapeutic doses, lipophilic β-blockers like propranolol have actually few CNS effects on mood. The effectiveness of β-blockers is established for relieving performance anxiety, but the actions involve more a peripheral relief of somatic symptoms rather than a central effect. By contrast the reduction in consolidation of aversive and stressful memory by propranolol appears to involve altering the functioning of the amygdala and hippocampus directly. While evidence suggests that β-blockers reduce aggressive behaviors associated with various psychological conditions such as schizophrenia, they are now used relatively rarely. Cardiac glycosides such as digoxin have been implicated in causing a variety of mental dysfunctions including depression, yet quality prospective trials are lacking and evidence is largely anecdotal. The difficulty is that the patients likely to receive either β-blockers or digoxin are often suffering heart failure which in itself causes mood alterations such as depression. The current review analyzes the evidence of mood-altering side effects for the various pharmacological agents used to treat cardiac disease.
Syncope is a transient and abrupt loss of consciousness and postural tone due to a transient reduction in cerebral blood flow, typically due to a fall in blood pressure. There are many causes of syncope, and some people may suffer from recurrent and unexplained episodes. Recurrent t syncope can be challenging to diagnose and treat with the potential for severe psychosocial morbidity.
Work to mitigate the increased risk of cardiovascular disease (CVD) brought about by cigarette smoking compels primary and secondary prevention activity among adolescents. Personality plays a prominent role among the variables associated with adolescent onset and maintenance of smoking. The role of personality in adolescent smoking is examined by contrasting results from research exploring association versus causality and then evidence from studies examining onset versus maintenance in relation to models of personality, risk, smoking beliefs/knowledge, self-esteem/self-efficacy, locus of control, and religiosity. Analysis using the two comparisons demonstrates the need for research in the area to consider dynamical approaches to explain changes in adolescent smoking behavior more deeply. For example, advances in the mathematical sophistication of adolescent smoking research make it possible to understand how changes in knowledge about the health consequences of smoking influence the onset or maintenance of smoking among adolescents. The development of more dynamical explanations of adolescent behavior may prove valuable explanations of behavior among adults trying to quit smoking to reduce the risk of CVD.
... These events represent instances of exceptionally high stress that may persist over time. Significant negative life events (NLEs) are likely associated with heightened physiological distress, leading to diminished CVR and subsequent health complications (Alvarenga and Byrne 2016). The perception of NLEs is influenced by individuals' perspectives and coping mechanisms, both of which are closely tied to personality traits (Oshio et al. 2018). ...
Blunted cardiovascular reactivity (CVR) is associated with adverse health outcomes such as depression, obesity, and increased carotid intima-media thickness. Research indicates that significant negative life events (NLE) contribute to reduced CVR and related health issues, with individual perceptions and coping mechanisms playing a crucial role. Optimism, which is linked to fewer reported NLEs and better cardiovascular health, may improve coping processes, thereby reducing NLE's impact on CVR. This study investigated how NLEs mediate the relationship between optimism and CVR. The sample consisted of 199 adults recruited from universities in Ecuador. Participants completed psychological assessments prior to a controlled 45-min experimental session, which included baseline cardiac activity measurements followed by the PASAT task. The findings indicated that the number of NLEs mediates the relationship between optimism and diastolic blood pressure (DBP) reactivity, while optimism also exerts a direct effect on CVR beyond this mediation. Specifically, a significant inverse relationship was observed between the number of NLEs and DBP reactivity, alongside a positive relationship between optimism and DBP reactivity. Additionally, pessimism was associated with reduced systolic blood pressure (SBP) reactivity, though neither pessimism nor NLEs showed any effect on heart rate. These results highlight the protective role of optimism in modulating stress-related impacts on CVR and align with previous research suggesting that low CVR might be a result of maladaptive stress responses.
... It is the most important risk factor for many chronic non-communicable diseases resulting in morbidity, and mortality, and medical costs globally [2][3][4]. With the development of the economy and improvement of living standards, more and more people suffer from atherosclerotic cardiovascular diseases which constitute the leading cause of death [5]. ...
Background
Serum lipid profile abnormalities are major predictors for coronary artery diseases. The relationship between demographic factors and dyslipidemia in Ethiopia is not completely explored. Thus, this study aimed to assess the prevalence and predictors of dyslipidemia among hypertensive patients in Lumame Primary Hospital.
Methods
A cross-sectional study was conducted from June to August 30, 2020, on the hypertensive patients in Lumame Primary Hospital. All adult hypertensive patients who visited the adult hypertensive care services during the study period were included. Interview-guided self-administered questionnaire and a chart review were used for data collection. Statistical Package for the Social Sciences (SPSS) software version 24.0 was used for data analysis.
Results
Out of 372 hypertensive patients, 190(51.1%) were females and the mean age of the study participants was 43.56 years (SD ± 4.31). The overall prevalence of dyslipidemia in this study was 48.4%. Besides the overall prevalence, the prevalence of TC, TG, LDL-c, and HDL-c was 73(19.6%), 91(24.5%), 60(16.1%), and 115(30.9%), respectively. Females were at higher risk for having high levels of TC (AOR = 2.31, 95% CI = 1.54–3.13), TG (AOR = 1.70, 95% CI = 1.34–3.79), LDL-c (AOR = 2.15, 95% CI = 1.56–2.86), and HDL-c (AOR = 2.67, 95% CI = 1.44–5.67) than males. Respondents who were from urban were at higher risk for having high levels of TC (AOR = 1.98, 95% CI = 1.04–6.83), TG (AOR = 1.78, 95% CI = 1.09–2.86), LDL-c (AOR = 3.01, 95% CI = 1.45–7.43), and HDL-c (AOR = 2.01, 95% CI = 1.94–4.55) than respondents who were from rural. Similarly, obese respondents were at higher risk for having high levels of TC (AOR = 2.03, 95% CI = 1.64–2.00), TG (AOR = 3.78, 95% CI = 1.06–6.42), LDL-c (AOR = 1.92, 95% CI = 1.66–2.12), and HDL-c (AOR = 4.23, 95% CI = 2.84–4.32) than to respondents who were underweight.
Conclusion
The prevalence of dyslipidemia among hypertensive patients was high. Independent variables such as age, gender, residence, family history of HTN, smoking, alcohol drinking, fruit diet habits, physical activity, DM, and BMI were significant determinants of dyslipidemia.
... HR can be analyzed both in terms of beats per minute and in terms of the inter-beat interval (IBI). The mathematical analysis of HRV is based on the variation of the IBI interval [33], and can be divided in the amount of parasympathetic or mixed (both parasympathetic and sympathetic) activity that is reflected [9,13,[34][35][36]. HRV can be calculated in both time domains and frequency domains [37] (and nonlinear analysis, but this was not included in the current review). ...
This systematic review examines the relationship between sympathetic and parasympathetic activity on the one hand and job stress and burnout on the other, and is registered at PROSPERO under CRD42016035918. Background: Previous research has shown that prolonged job stress may lead to burnout, and that differences in heart rate variability are apparent in people who have heightened job stress. Aims: In this systematic review, the associations between job stress or burnout and heart rate (variability) or skin conductance are studied. Besides, it was investigated which–if any–guidelines are available for ambulatory assessment and reporting of the results. Methods: We extracted data from relevant databases following the PRESS checklist and contacted authors for additional resources. Participants included the employed adult population comparing validated job stress and burnout questionnaires examining heart rate and electrodermal activity. Synthesis followed the PRISMA guidelines of reporting systematic reviews. Results: The results showed a positive association between job stress and heart rate, and a negative association between job stress and heart rate variability measures. No definite conclusion could be drawn with regard to burnout and psychophysiological measures. No studies on electrodermal activity could be included based on the inclusion criteria. Conclusions: High levels of job stress are associated with an increased heart rate, and decreased heart rate variability measures. Recommendations for ambulatory assessment and reporting (STROBE) are discussed in light of the findings.
Background: This study aimed to examine whether dyadic coping (DC) is associated with relationship satisfaction (RS) among couples facing cardiac diseases. Furthermore, the moderating role of both partners' anxiety and depression was tested. Methods: One hundred cardiac patients (81.5% men) and their partners (81.5% women) completed a self-report questionnaire during hospitalization. The Actor-Partner Interdependence Model (APIM) and moderation analyses were used to assess the above associations. Results: Results showed that positive DC was significantly related to higher levels of RS, and negative DC was related to lower levels of RS. Furthermore, patient and partner psychological distress significantly moderated the link between DC and RS: patient-perceived positive DC was associated with higher partner RS when partner depression was high; partner-perceived positive DC was associated with higher patient RS when patient anxiety was low; patient-perceived negative DC has associated with lower patient RS when patient anxiety and depression were high. Conclusion: This study showed that positive DC is associated with a more satisfying relationship and identified under what conditions of cardiac-related distress this can happen. Furthermore , this study underlined the importance of examining DC in addition to the individual coping skills as a process pertaining to personal well-being and couple's outcomes.
The life course development of cardiovascular diseases (CVDs) and the undergoing epidemiological transition in Mozambique highlight the importance of monitoring the cardiovascular risk profile in young adults. Therefore, this study aims to estimate the prevalence of CVD risk factors in a population aged 18–25 years living in Mozambique. A total of 776 young adults from a nationally representative sample were evaluated in 2014/2015 following the World Health Organization’s STEPwise approach to chronic disease risk factor surveillance. Current smoking was the most prevalent among rural men (10.8%, 95%CI: 6.3–17.8), and drinking was most prevalent among urban men (38.6%, 95%CI: 29.3–48.8). The proportion of young adults not engaging in at least 75 min of vigorous physical activity per week ranged between 14.5% in rural men and 61.6% in urban women. The prevalence of being overweight/obese and hypertension were highest among urban women (21.6%, 95%CI: 14.7–30.6) and urban men (25.2%, 95%CI: 15.9–37.6), respectively. Education >8 years (vs. none) was independently associated with lower odds of being a current smoker, and increased monthly household income was associated with increased odds of low levels of physical activity. This study shows that important CVD risk factors are already common in the young adult population of Mozambique.
The heart and cardiovascular system in general are intimately related to emotional states. Tension, anxiety, and fear can intensely alter the cardiac rate and blood pressure even in acute situations. If the child or adolescent lives under constant stress, some further alterations are possible. Syncope is a possible manifestation of overwhelming fear and a way of coping with difficult life circumstances. It is related to sudden lowering of blood pressure. Cardiac anxiety, unexplained chest pain, and some episodic tachycardias may also be related closely to emotional situations and constant stress. The circulatory system can be altered in terms of a higher rate of hypertension and hardening of arteries due to chronic stress. Some adolescents manifest heart-focused anxiety often as a “concretized metaphor” of suffering and tension. We describe the “broken heart syndrome” (Takotsubo), which can occur as a manifestation of a sudden loss or acute frightening situation. The chapter outlines general principles of management with complex and multimodal interventions that address the child’s emotional life, psychic function, interpersonal relationships, and family tensions and stressors that may be at the root of the problems.KeywordsFunctional cardiovascular symptomsPsychogenic syncopeEpisodic faintingTilting table testCardiac-focused anxietyNon-specific chest painGorlin-Likoff syndromeSomatoform autonomic dysfunctionTakotsubo myopathyBroken heart syndrome
Mental stress has been recognized as an essential risk factor for hypertension. Therefore, experts specializing in cardiology, psychiatry, and Traditional Chinese Medicine organized by the Psycho-Cardiology Group of College of Cardiovascular Physicians of Chinese Medical Doctor Association and Hypertension Group of Chinese Society of Cardiology proposed the expert consensus on the diagnosis and treatment of adult mental stress-induced hypertension in March 2021, which includes the epidemiology, etiology, diagnosis, and treatment of the mental stress-induced hypertension. This consensus will hopefully facilitate the clinical practice of this disorder. In addition, the COVID-19 pandemic has become one of the primary global sources of psychosocial stressors since the beginning of 2020, and the revision of this expert consensus in 2022 has increased the relevant content. This consensus consists of Part A and Part B. Part A includes (I) Background and epidemiological characteristics, (II) Pathogenesis, and (III) Diagnosis and Part B includes (IV) Treatment recommendations and (V) Prospects. This part presents the content of Part A.
There is inconsistent evidence that healthy dietary interventions can effectively mitigate the risk of adverse outcomes associated with elevated insulin resistance in pregnancy, suggesting that other moderating factors may be at play. Maternal psychological state is an important factor to consider in this regard, because stress/mood state can directly influence glycemia and a bidirectional relationship may exist between nutrition and psychological state. The objective of this study was to examine the interaction between maternal negative affect and diet quality on third trimester insulin resistance. We conducted a prospective longitudinal study of N = 203 women with assessments in early and mid-pregnancy, which included an ecological momentary assessment of maternal psychological state, from which a negative affect score (NAS) was derived, and 24-h dietary recalls, from which the Mediterranean Diet Score (MDS) was computed. The homeostasis model assessment of insulin resistance (HOMA-IR) was computed from third trimester fasting plasma glucose and insulin values. Early pregnancy MDS was inversely associated with the HOMA-IR, but this did not maintain significance after adjusting for covariates. There was a significant effect of the mid-pregnancy MDS*NAS interaction term with the HOMA-IR in the adjusted model, such that a higher negative affect was found to override the beneficial effects of a Mediterranean diet on insulin resistance. These results highlight the need to consider nutrition and affective state concurrently in the context of gestational insulin resistance.
The article is on the discussion of the article by Drobizhev M. Yu., Kikta S. V., Machilsky O. V. "Cardiopsychiatry. Translation issues", published in Cardiovascular Therapy and Prevention 2016; 15(4): 88-97. The authors propose classification of cardiopsychiatric disorders which is based only on literary data and is itself just a reductionist attempt to relate neurophysiological mechanisms with complex psychopathological and psychosomatic compounds being reified at the level of cardiovascular system. Also, it cannot be agreed, the publication part on psychopharmacotherapy of psychiatric disorders cardiological practice, where the authors position is just an application of one single medication.
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