Psychosocial Risk Factors: Assessment and Management Interventions



Psychosocial Risk Factors: Assessment and Management Interventions


Simone K. Madan

Erika S. Sivarajan Froelicher



Despite extensive research and advances in knowledge about coronary heart disease (CHD) over the past several decades, traditional risk factors and genetics fail to fully explain either the development or the course of the disease. Consistent with biopsychosocial models of health, studies have now shown that psychological and social factors are also related to the development of and recovery from CHD. In health schemas of the mind and body, emotions have often been linked to specific organs. The English language is replete with expressions that describe this assignation. For example, jubilation “makes the heart flutter” or anxiety causes “butter-flies in one’s stomach.” Throughout the ages, the heart has been seen as the “seat of emotions.” William Harvey (1578 to 1657), the English physician who first described the circulatory system, wrote, “Every affliction of the mind that is attended with either pain or pleasure, hope or fear, is the cause of an agitation whose influence extends to the heart.”1 In this chapter, we summarize the evidence that links psychological and social factors to CHD and describe how nurses can assess and manage selected psychosocial risk factors to promote cardiovascular and psychosocial health.


PSYCHOSOCIAL RISK FACTORS FOR CHD

Several psychosocial risk or prognostic factors have been identified for CHD: acute life events, anxiety, depression, hostility, job stress, low-perceived social support, social isolation, socioeconomic status, and Type A personality.2, 3, 4, 5 Of these, depression and low-perceived social support have been well established as independent risk factors for CHD, as shown in Table 33-1.6


Depression

The complex clinical diagnosis of depression, as defined in the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition,7 classifies the disorders as either major or minor based, in part, on the number, frequency, and duration of symptoms and signs. In this chapter, the term depression will be all inclusive. Substantial empirical evidence from well-designed population studies8,9 and review papers2,4,10 have shown that depression is a risk factor for CHD. Furthermore, depression is also a prognostic factor for CHD patients,2,4,10, 11, 12, 13, 14, 15, 16 and high prevalence rates of the disorder have been found in CHD populations. Studies have reported that 16% to 25% of the CHD population has depression, as compared with 6% of the general population.11, 12, 13, 14 Women in the general population are especially at higher risk because they are twice as likely to be depressed than men, thus one would expect the same gender distribution to be observed in the cardiac population,17,18 and their depression leads to worse cardiovascular outcomes, especially in younger women.19 Besides women, individuals with low income and less education experience significantly higher rates of depression.17 Regardless of the severity of CHD, patients with depression are three to four times more likely to die in the first year after a myocardial infarction (MI) than those without depression.20,21 Six months after an MI, patients with depression had a 17% event rate compared with 3% for nondepressed patients20; at 18 months, premature ventricular contractions and mortality were reported for 50% of patients with depression compared with 17% for those without.22

Combined depression and CHD is a significant challenge for patients recovering from a cardiac event. Depression can lead to social withdrawal and less participation in activities such as exercise.23,24 Depressed patients have more difficulty adopting and maintaining healthy lifestyle behaviors,25 and they consistently report higher smoking rates compared with nondepressed CHD patients.11,26 For example, in older patients who suffered an MI, depression scores predicted the performance of risk-reducing, self-care behaviors.27 In patients attending cardiac rehabilitation programs, anxiety, depression, and coping abilities predicted leisure-time activity and higher smoking cessation at 1-year follow up.28 In relation to functional impairments, only 38% of patients with depression returned to work within 3 months of a cardiac event compared with 63% of nondepressed patients.29 Depression is also associated with decreased compliance in taking medications12,30 and a delay in seeking medical treatment, because affected patients often minimize the significance of cardiac symptoms.31,32 Besides the individual health consequences of depression in CHD patients, tremendous economic costs affect society.33 The cost of increased hospitalization admissions for recurrent cardiac events and longer hospital stays are also associated with higher emotional distress. The average hospital cost for a depressed cardiac patient is more than four times the cost of a nondepressed patient.25


Social Support

Social support is defined by the quality of the structure and function of social relationships. Structural support reflects the number and frequency of social interactions, social ties, and networks.34,35 Functional support focuses on tangible aid, emotional comfort and care, and the value an individual places on the support.34,35 Structural and functional support, however, fail to account for individual perceptions and beliefs about the support. Further, they do not account for (a) the social skills needed to elicit support from others; (b) how much support, if any, is needed or acceptable and who should provide it; (c) whether an individual is deserving of support; or (d) the concern of the cost of seeking
support.36 Individual differences must be considered because what one person may consider as valuable support, another person may consider a burden, engendering feelings of obligation or guilt. Gender or ethnic differences may influence attitudes and beliefs about support.37 In the research substantiating the association between social support and CHD, the definition of social support is highly varied, ranging from marital status, or being single to measurement of social support that involves detailed complexity.








Table 33-1 ▪ PSYCHOSOCIAL RISK FACTORS AND CHD: SUMMARY OF PROSPECTIVE STUDIES






































































Number of Reports of Etiological Studies (n = 70)


Number of Reports of Prognostic Studies (n = 92)




0


+


++



0


+


++


Depression


0


8


5


9


0


16


7


11


Social support


0


3


4


2


0


7


4


10


Anxiety


0


4


1


3


1


9


4


4


Type A behavior/hostility


1


11


5


1


3


10


1


1


Work characteristics


0


3


5


5


0


2


2


0


−, Finding counter to hypothesis; 0, lack of clear association; +, moderate association (RR ≥1.50 and <2.00); ++, strong association (RR ≥ 2.00) Borrowed with permission from Hemingway, H., Kuper, H., & Marmot, M. (2003). Psychosocial factors in the primary and secondary prevention of coronary heart disease: A systematic review. In S. Yusuf, J. A. Cairns, E. Fallen, B. J. Gersch, & A. J. Camm (Eds.), Evidence based cardiology. London: British Medical Journal Publishing.


Social support from others decreased the incidence of cardiac events in men without CHD.38 One important form of social support can be derived from a marital relationship. Marital relationships perceived as satisfactory are associated with decreased mortality.39 Conversely, discordant marital relationships may precipitate poor health outcomes because social connections can also lead to stress if perceived needs or expectations are not met. A higher likelihood of mortality in cardiac patients has been associated with low-perceived support or lack of support for unmarried individuals.40, 41, 42 In addition, lack of social support is also a risk factor if cardiac disease is already well established. Case et al.43 examined social networks by comparing recurrent cardiac events in patients who had suffered an MI. Patients who lived alone had a 50% increased risk for subsequent events. In patients who had suffered an MI or were living with congestive heart failure or both, those with no sources of emotional support had a two-fold risk of a subsequent event.44,45 An examination of gender differences discovered that high marital distress in women is associated with three times the risk of recurrent coronary events than in men.46

Low social support seems to blunt the desire for behavioral change in patients following an MI. Unmarried patients with high rates of smoking are less likely to stop smoking than married patients, and marital separation at the time of an MI decreases the likelihood that a patient will give up smoking.47 Men receive more support for their participation in cardiac rehabilitation programs from their spouses than female cardiac patients do from their male partners.48 During or after a hospital admission, distress can surface even in a satisfactory relationship if coping resources are challenged or if spouses become overprotective, which may be stressful for the patient.49 Conversely, an MI can exacerbate distress in a tempestuous relationship if emotional or functional support are lacking, especially when nurturing is so important.50 Researchers have suggested that being separated or divorced is an independent risk factor for MI.9 Perhaps social support influences physiological and behavioral factors that promote “heart-healthy behaviors,” reinforcing them and providing a sense of intimacy, belonging, while promoting competence and self-efficacy.51 How social support protects a patient with CHD is not clearly understood, but it appears such protection exists.


Anxiety

High levels of anxiety are related to increased incidence of heart disease. Men who report two or more symptoms of anxiety are three times more likely to have a fatal CHD event than men without symptoms of anxiety.52 Similar associations have been reported for phobic anxiety symptoms and for high levels of chronic worry among CHD patients.52,53 Symptoms of anxiety during a hospital admission increase the risk of a recurrence of cardiac events independent of depression.21 In patients who have experienced an acute MI, high levels of anxiety were associated with increased hospital complications, including acute ischemia, arrhythmias, functional impairments, reinfarction and sudden cardiac death.52,54, 55, 56 Anxious cardiac patients without adequate support and education are more likely to smoke, to have higher cholesterol, hypertension and diabetes mellitus,52 and can be fearful of physical activity.57


Hostility and Anger

After years of research on the relationship between Type A behavior and CHD, hostility and anger have emerged as risk factors for CHD.58 Hostility has been redefined to include affective, behavioral, and cognitive components. Expressive hostility refers to overt anger, aggressive or rude behaviors, or assaultive behaviors.59 Potential for hostility describes the tendency to experience anger and resentment in daily life.59 Hostile cognitions include appraisals and perceptions of others as distrustful and attributions of frustration and mistreatment to others. Studies of hostility in adults have shown an association between hostility and CHD morbidity and mortality. Extremely hostile men, followed for 9 years, had a two-fold risk for an MI, even after controlling for behavioral risk factors such as alcohol use, body mass index, and smoking.60, 61, 62, 63 The link between anger and hostility and cardiac reactivity suggests an important physiologic pathway for triggering cardiovascular events. Expressing acute anger has been reported to lead to a coronary event within 2 hours.64 Increased platelet aggregation and thrombogenesis,65 plaque rupture, and occlusion have been hypothesized as the most likely mechanisms.66 High levels of hostility have also been found predictive of restenosis
after angioplasty.67 If hostility is also a prognostic factor for CHD is not known.4,58


Acute Stress and Stressful Life Events

Convincing evidence exists that acute stress or stressful life events can trigger cardiac events. Observational studies on the incidence of cardiac events examined exposure to sudden stresses such as natural disasters. The incidence of fatal and nonfatal MIs in Los Angeles County significantly increased on the day of the Northridge earthquake compared with rates before and after the earthquake.68 In contrast, mortality rates for other types of heart disease, such as cardiomyopathy or cerebrovascular disease, did not increase. Similar increases were observed after major Japanese earthquakes and the missile attacks on Israel during the 1991 Gulf War. These studies, however, could not exclude the effects of increased physical stress caused by exertion. Data from both the missile attacks against Israel and the Japanese earthquakes suggest that the incidence of MI and CHD mortality was greater in women than in men. Posttraumatic stress scores were also higher in Japanese women than in men, suggesting that mental stress could trigger these coronary events.69,70 Some evidence suggests that in the hour after high levels of negative emotions, the risk for ischemic episodes doubles.71 Some including Krieger72 have suggested that lower socioeconomic groups appear to have increased incidence of CHD because of acute stress and exposure to stressful life events. It has been argued that they have less control over their environment, which leads to stress. Other factors, such as lack of access to medical care or engaging in unhealthy lifestyle behaviors, may be alternative explanations.

Acute stress can also lead to arrthymias and sudden cardiac death in patients with CHD.73 The effects of mental stress have been evaluated during angiography by asking patients to solve arithmetic problems. Investigators found that stenosed coronary artery segments responded by dilating.74 Studies using challenging video games that have a timing aspect have shown similar results. Comparisons of mental and physical activity stress tests found that mental stress produces higher diastolic blood pressure and lower heart rate responses than physical activity.75 These studies suggest that ischemia caused by mental stress might occur because of inappropriate vasoconstrictor responses. Because exposure to severe stress cannot be ethically evaluated in experimental human studies, conclusive statements about its effects cannot be made.


Job Stress

Several observational studies have attempted to link chronic job stress with the precipitation of coronary events. Higher numbers of MIs occur in the early morning hours and are associated with increases in catecholamines. Weekly patterns suggest an approximately 20% increase in the incidence of MIs on Mondays, with the lowest rates occurring on Saturdays and Sundays.76 Some relate this increased incidence with a person’s return to his or her stressful workplace; others have suggested that lifestyle habits at work and at leisure account for this difference. Occupational stress has been posited as the explanation for the increase in CHD risk and mortality in blue-collar workers.77, 78, 79 As more women enter the workforce, some have suggested that women will experience increased cardiovascular events.80,81 When CHD risk factors were examined in middle-aged women in Rancho Bernardo, California, employed women had significantly lower lipids and glucose levels than unemployed women. In the same study, employed women tended to smoke fewer cigarettes and exercised more than unemployed women.82 This suggests that factors other than employment explain observed associations. Low levels of support from coworkers and supervisors have also been associated with elevated blood pressure after accounting for other factors, such as cigarette smoking.83 Such findings have led to the suggestion that workers who endure “job strain” (intense job demands with little control) would be more likely to develop CHD.84 Studies using this assessment of job strain, however, have shown both positive and negative associations with CHD mortality.85,86 Leading researchers suggest that other job factors, for example, little support from coworkers, job insecurity, and juggling family and job demands, likely influence a person’s perception of employment as a stressor. Similarly, what one person experiences as stress, another may view as stimulating and exciting. All things considered, clearly substantiated evidence supporting the causal relationship between job stress and CHD is still absent.2,87


PATHOPHYSIOLOGICAL MECHANISMS FOR PSYCHOSOCIAL RISK FACTORS AND CHD

The neuroendocrine response theory, the behavioral mechanisms theory, or a combination of both offers the most likely explanation for the link between psychosocial risk factors and CHD. According to the neuroendocrine response theory, a state of physiological arousal occurs when a person is confronted by real or imagined threats or stressors.88 “Fight-or-flight” describes these physiologic responses.89 Neuroendocrine response systems are activated, triggering the release of cortisol and catecholamines (epinephrine [adrenaline] and norepinephrine) that initiate several physiologic responses (Fig. 33-1).

Circulating levels of plasma lipids are also increased and platelet and macrophage cells are activated to release chemotactic and cytotoxic substances. Cardiovascular responses include increased heart rate, blood pressure, muscle and myocardial oxygen demands, and accelerated blood flow. Increased blood flow triggers a cascade of endothelial vascular responses, including release of nitric oxide to promote vasodilation, stimulation of platelets to release chemoattractants and promote thrombosis, and activation of macrophages. Activated macrophages enhance phagocytic activity and have been implicated in the development of atherosclerotic foam cells and the destabilization and rupture of the fibrous cap surrounding atherosclerotic plaque.90,91

The neuroendocrine response theory has led to speculation about the connection between affective states and physiological responses. An association has been found between depression and increased nervous system activity,92 which in turn can increase cardiovascular-disease-related death. Depressed cardiac patients have increased platelet reactivity,93,94 and depressed patients following an MI have shown decreased heart rate variability.95 The risk of sudden death after an MI is significantly higher in patients with a decrease in heart rate variability.96 Lower heart rate variability and decreased parasympathetic nervous system activity in depressed patients has been associated with ventricular fibrillation.22 Carney et al.97 examined a subsample of ENRICHD patients and showed that low heart rate variability partially mediates
the effect of depression on survival after an acute MI. Thus, treatment that improves depression and heart rate variability can also improve survival. Those with hostile traits usually have high blood pressure, heart rate, and neuroendocrine responses, such as cortisol release, in frustrating or harassing situations.59 When the negative emotions of depression, anger, and anxiety were simultaneously evaluated in the same group of patients who suffered an MI, both depression and anxiety were significant independent predictors of subsequent cardiac events.14 Dividing events into thrombogenic events (infarction or unstable angina) and arrhythmic events, the authors in this study found that anxiety and a history of depression were associated with thrombogenic events, while current depression and anger were associated with arrhythmic events. The authors speculate that mechanisms such as enhanced platelet adhesion leading to plaque instability and thrombosis might account for these results. These biologic pathways have yet to be tested.






Figure 33-1 Physiologic mechanisms linking stress and coronary heart disease.

Behavioral mechanism theories such as negative affective states also perpetuate behaviors such as social withdrawal, lack of pleasurable activities, chronic angry outbursts, and disconnection from support, which can adversely affect cardiac physiology. Also, patients who experience psychosocial risk factors may be less compliant with risk-reduction strategies, and their noncompliant behaviors may be the mechanism associated with the development of CHD and its prognosis. Longstanding negative behaviors, such as a high-calorie diet, inadequate self-care, inadequate sleep, lack of exercise, and smoking, are likely to contribute to the development of CHD and, unless modified following an MI, increase the susceptibility toward future events. Both of these theories may explain the link between psychosocial risk factors and CHD.


ASSESSMENT OF PSYCHOSOCIAL RISK FACTORS RELATED TO CHD

Nurses in any practice setting are encouraged to evaluate patients not only for the traditional risk factors but also for psychosocial risk factors. In the following discussion of subjective and objective assessment of depression, low-perceived social support, anxiety, and hostility and anger, note that several of these psychosocial risk factors may be present concurrently.


Screening for Depression

Depression has a complex variable definition, and measurement can often be difficult in patients with coexisting medical problems.98 Jiang et al.99 have questioned the sensitivity of the screening instruments for depression and have highlighted the difficulty of differentiating a normal grief response from a diagnosis of significant depression. Although the diagnosis of depression often requires the skill of a licensed mental health practitioner, nurses,
given their extensive contact with cardiac patients, are in a pivotal role to recognize or screen for depression. Several brief and reliable screening tools for clinical purposes can be used by nurses to identify patients at high risk for depression:

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Jan 10, 2021 | Posted by in NURSING | Comments Off on Psychosocial Risk Factors: Assessment and Management Interventions
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