Clinical Heath Psychology and Cardiovascular Disease Essay

Introduction

Cardiovascular disease is one of the leading causes of death globally. The spectrum of cardiovascular diseases includes coronary heart disease, stroke, hypertension, peripheral artery disease, congenital heart disease, rheumatic heart disease, deep vein thrombosis, pulmonary embolism and heart failure. The major causes of cardiovascular disease are smoking, sedentary lifestyle without any exercise, and an unhealthy diet. Heart disease can affect all age groups.

In coronary artery disease, most commonly, there is a fatty deposit in the inner blood vessel lining. These blood vessels are involved in the blood supply of the brain and heart. As a consequence, the blood vessels become narrower and less flexible. This condition is called atherosclerosis. Subsequently, these affected vessels become blocked by blood clots. The end result is the development of myocardial infarction, stroke etc.

Some preventive measures which have been advocated for cardiovascular disease includes not smoking, physical activity, healthy diet, controlling diabetes and blood pressure and a regular health check up.

This essay examines the psychological characteristics and psychosocial factors associated with, or causative of, cardiovascular disease. The essay also addresses some models like the cardio reactivity model, psychoneuroimmunology, the role of the sympathetic nervous system in cardiovascular disease, and the HPA axis. The association of certain psychosocial risk factors like depression leading to medical non-compliance is also dealt with.

Psychological factors associated with or causative of cardiovascular disease

Psychological risk factors for coronary syndromes belong to three categories. These include: chronic, episodic, and acute psychological risk factors (Kop, 1999). Chronic psychological risk factors (like hostility) leads to a gradual progression of coronary artery disease. The temporal relation to coronary syndrome is 10 years and the associated cardiovascular risks include hyperlipidemia, hypertension, and increased sympathetic activation. The pathophysiology involves sympathetic activity and elevated lipids. The primary pathological result is atherosclerosis (Kop, 1999).

Psychological risk factors, which occur episodically (like exhaustion) have a duration, which lasts from few months to two years and can occur again. The temporal relation to coronary syndrome is 2 years and the associated cardiovascular risks include increased blood clotting and inflammation, and a shift of sympatho-vagal balance. The pathophysiology involves sympatho-vagal imbalance, neurohormonal changes, and a procoagulant state. The primary pathological result is altered homeostasis (Kop, 1999).

Acute psychological risk factors (like outbursts of anger or mental activity) can trigger the coronary syndrome within an hour. The associated cardiovascular risks include cardiac demand, coronary supply, and platelet activation, and decreased plasma volume (Kop, 1999). The pathophysiology involves increased catecholamines, increased blood pressure and heart rate, increased platelet activity, increased coagulation and increased inflammation; decreased plasma volume and coronary constriction. The primary pathological result is cardiac ischaemia, arrhythmia, plaque rupture, and thrombosis (Kop, 1999).

Rutledge & Hogan, 2002, presented the first empirical review based on the literature about psychological hypertension, and the results provide statistical data on the effects of psychological factors on the development of hypertension in the future.

According to the study, there is an 8% risk of developing hypertension in the future amongst the high psychological distress group when compared to the low psychological distress group. Variables like anger, anxiety, and depression have the highest relationship with the development of hypertension. The proposed biological pathways include catecholamine release, chronic sympathetic nervous system activation, endothelial dysfunction, and serotonergic dysregulation. The behavioral factors implicated includes obesity and inactivity (Rutledge & Hogan, 2002).

A study by Dimsdale, 2008, discusses the effects of psychological stressors on the human heart. Up to a certain point, there is coordination and a functional response by the cardiovascular system to stress but beyond this point, when the stressor persists or when the patient broods, it begins to affect the heart. Like other cardiac risks, these stressors are capable of being modified either by cardiologists or by behavioral psychologists (Dimsdale, 2008). Many cross-sectional and prospective analyses have shown an increased co-morbidity of depression and cardiovascular disease (Grippo & Johnson, 2002).

Depressive disorders vary from mild (subclinical) depression to major depression. Statistical data from numerous studies indicate that there is a relationship in the level of depressive symptoms and the occurrence of cardiac disease (Rozanski et al., 2005). The pathophysiology involves the chronic stimulation of the HPA axis due to depression. This leads to diminished HPA activity, hypercortisolemia, and decreased feedback control (Rozanski et al., 2005; Jokinen, Nordström, 2008).

In addition, there is also sympathetic nervous system stimulation along with elevated plasma levels of norepinephrine and increased sympathetic activity in the body. Clinical signs in these patients, therefore, include: higher resting heart rates, decreased variability of heart rate, dysfunction of baroreflex, and increased variability of QT (Rozanski et al., 2005).

The combination of hypercortisolemia along with diminished sex and growth hormone secretion leads to central obesity and increased fatty acids (both peripheral and portal). The other changes, which also results in cardiovascular disease includes development of diabetes, platelet abnormalities, increases in C-reactive protein, interleukin-6, other inflammatory proteins, increased white blood cell counts, increased fibrinogen, and endothelial dysfunction (Rozanski et al., 2005; Barth, Schumacher, Herrmann-Lingen, 2004). Some of the indirect pathways include psychosocial and behavioral mediators like social isolation, maladaptation, and chronic life stress (Barth, Schumacher, Herrmann-Lingen, 2004).

Psychosocial factors

Emotional factors and chronic stressors are the two general psychosocial factors that are considered to lead to atherosclerosis and adverse cardiac events. The emotional factors are affective disorders (major depression and anxiety disorders), hostility, and anger. Chronic stressors are poor socioeconomic status, poor social support, work stress, caregiver strain, and marital stress (Rozanski et al., 2005)

Evidence is available to show that there is a link between coronary artery disease and emotional factors and chronic stressors. However, since these variables interact and have a tendency to cluster together, it is not always possible to isolate the effects of these. In general, the risk of coronary artery disease is higher with a more negative psychosocial profile. The lack of social support is especially associated with a greater risk of coronary artery disease (Strike & Steptoe, 2004).

Numerous research work on both humans and animal have helped to identify the pathways through which stress and negative emotions influence the development of coronary artery disease. A few studies have identified that the prognosis can be improved by psychosocial interventions (Smith & Ruiz, 2002).

The following psychosocial factors have the strongest evidence for a role in the etiology of coronary heart disease: low socioeconomic status, social isolation, work stress, other forms of chronic strain, anxiety, depression, and hostility. Increased psychophysiological stress reactions contribute to heart disease by stimulating plaque rupture and occluding the coronary arteries. Other possible mechanisms include a disruption of the cardiac rhythm, which leads to cardiac arrhythmias. Along with these psychosocial factors, changes in behavior like smoking, alcohol intake etc may also contribute to heart disease (Vedhara & Irwin, 2005).

Cardio reactivity model

The cardio reactivity model is based on a positive feedback loop. This loop includes behavioral factors (stress, high-fat diet, sedentary lifestyle), which increases or promotes the progression of insulin resistance, hyperinsulinemia, and an imbalance in the autonomic-sympathetic drive. As these conditions worsen, it leads to a cascading series of pathophysiological events that may promote or facilitate atherogenesis, diminished left ventricular function, and high blood pressure (McCabe et al., 2000).

Hereditary is a cause for individual differences in cardiac reactivity, and a high reactivity is thought to be a precursor to hypertension (Carroll et al., 1985).

Psychoneuroimmunology

Psychoneuroimmunology deals with the many ways in which health and behavior is related, with an emphasis on the immunological mechanisms behind it (Irwin, 2008). The central nervous, endocrine and immune systems are important regulators of both psychological and physical well-being (Kropiunigg, 1993; Kemeny, 2008). Conditions like stress can alter the immune system function and have effects on the endocrine and nervous system (Lutz, Tarkowski, Dudek, 2001).

Obesity is a known risk factor for cardiovascular disease (CVD). With the progress of obesity, there is also an increase of adipokines like plasminogen activator inhibitor type I, TNF-α, leptin and resistin, which contributes to type 2 diabetes and atherosclerosis. In particular, adinopectin, which decreases with visceral fat accumulation, is important in the development of CVD. An atherogenic lipid profile is usually associated with low adinopectin level. Leptin is also implicated in CVD (Ader, 2007).

Acute stress can result in an alteration in many biological factors that are crucial to inflammation and atherosclerosis. Platelets get activated and there is an increase in the circulating levels of inflammatory cytokines. Plasma levels of IL-10, TNF-α, IL-10, IL-1β, norepinephrine, and cortisol are elevated. In addition, haemostatic factors that are associated with inflammation and atherosclerosis may also be activated in acute stress (Vedhara & Irwin, 2005.)

The involvement of the sympathetic nervous system

The sympathetic nervous system plays an important role in the response of the cardiovascular system to increased circulatory requirement during periods of acute stress. The cardiac rate and contractility are augmented while the peripheral vascular tone changes. However, these responses can lead to detrimental effects in the long-term like renal, systemic, and coronary vasoconstriction, altered myocardial function, left ventricular hypertrophy and ventricular arrhythmias, in patients with cardiovascular disease (Cohn, 1989).

1. There are many different ways by which coronary artery disease and myocardial ischaemia are related with the sympathetic nervous system. By the process of platelet activation, formation of platelet-derived growth factor and by inducing mechanical injury to the vascular wall as a result of increased blood pressure and increased flow velocity, the sympathetic nervous system contributes to the development of atherosclerosis (Remme, 1998).
2. During normal living conditions, the influence of the sympathetic nervous system on the coronary vasomotor tone is not that important. However, once endothelial dysfunction develops after coronary artery disease, this becomes an important factor. At this time, the increase in the sympathetic adrenergic tone leads to coronary vasoconstriction along with an increase in the myocardial oxygen demand; eventually, ischaemia of the myocardium develops (Remme, 1998). Another mechanism, which could happen, is the activation of the sympathetic nervous system and the renin-angiotensin system due to myocardial ischaemia. As a result, systemic and coronary vasoconstriction develops leading to more myocardial ischaemia (Remme, 1998).

When cardiac failure develops, there is a specific stimulation of the sympathetic nerves of the heart. Without any treatment, at this point, there is an excess release of noradrenaline by the failing heart (Esler & Kaye, 2000). Although this release of noradrenaline gives the required adrenergic support to the failing heart, it eventually leads to the development of cardiac arrhythmia and progressive deterioration of the myocardium. In essential hypertension also, there is activation of the sympathetic system (Esler & Kaye, 2000).

The HPA axis

The hypothalamic-pituitary-adrenal (HPA) axis plays a crucial role in the regulation of energy metabolism through the actions of the glucocorticoids and in the homeostatic processes (Rosmond & Björntorp, 2000; Farag et al., 2008). Cortisol has a circadian rhythm, i.e. there is a peak secretion early in the morning and a low during the first half of the sleep cycle. The peak secretion early in the morning provides a circadian signal to the body cells, and thereby regulates gene expression and cellular activity. In conditions like hypertension and diabetes, there are disturbances in this circadian rhythm (Farag et al., 2008).

In persons suffering from chronic stress, there is a dysregulation of the HPA axis. There is an elevation of cortisol levels, which leads to overeating. This in turn, triggers a cascade of events, eventually leading to obesity and conditions like type 2 diabetes and cardiovascular disease (Farag et al., 2008).

Obese people with accumulation of fat intraabdominally have an increased risk of developing cardiovascular disease. This intra-abdominal accumulation of fat is attributed to the presence of a great number of glucocorticoid receptors in the abdominal region, which becomes sensitive to the high cortisol levels (Farag et al., 2008). Although there is an altered HPA axis activity in men with systemic hypertension, the exact role of the HPA axis here is not fully understood (Wirtz et al., 2007).

Association of psychosocial risk factors with certain health behaviors

The association of certain psychosocial risk factors with certain health behaviors like depression can lead to medical non-compliance. DiMatteo et al., 2000 sought to study and understand why depressed and anxious patients are linked to poor adherence to treatment recommendations and poorer medical care outcomes.

They made the observation that such people are noncompliant and cancel or do not attend appointments, refuse to take medication correctly, do not exercise as advised, do not follow a diet, and persist in unhealthy lifestyles (DiMatteo et al., 2000). This results in worsening of the disease, and negative treatment outcomes. Some of the reasons why such people are noncompliant include: not believing in treatment efficacy, adverse effects of the drugs, financial constraints, and poor or lack of support from family members (DiMatteo et al., 2000).

Conditions like anxiety and depression also impair the patient’s cognition, energy, and motivation, which in turn, make them noncompliant. There is no clarity on whether treating depression can help patient compliance. However, knowing this fact can improve health care outcomes (DiMatteo et al., 2000).

Wang et al., 2002, performed a cross-sectional study on the use of antihypertensives medication. The results indicated that in spite of patient knowledge of hypertension, health beliefs, satisfaction with care, and other psychosocial variables there still could be noncompliance. They also concluded that depression could be an unknown but modifiable risk factor for poor compliance with antihypertensive medications. It has also been found that depressed patients are at least three times more noncompliant with medical treatment when compared to nondepressed patients (DiMatteo, Lepper, Croghan, 2000).

Conclusion

There are three categories of psychological risk factors, which have been recognized for coronary syndromes: chronic, episodic, and acute. Anger, anxiety, and depression have the highest relationship with the development of hypertension.

The two general psychosocial factors that can lead to atherosclerosis and cardiac disease are emotional factors and chronic stressors. Low socioeconomic status, social isolation, work stress, other forms of chronic strain, anxiety, depression, and hostility are the psychosocial factors that are strongly implicated in the etiology of coronary heart disease.

The cardio reactivity model is based on a positive feedback loop, which includes behavioral factors like stress, high-fat diet, and sedentary lifestyle, which eventually leads to cardiovascular disease. Psychoneuroimmunology deals with the different ways in which health and behavior is related, with an emphasis on the immunological mechanisms behind it. The sympathetic nervous system is also involved in cardiovascular disease. Some of the effects include augmentation of cardiac rate and contractility with peripheral vascular tone changes.

The HPA axis too lays a role in cardiovascular disease. In conditions like hypertension and diabetes, there are disturbances in the circadian rhythm of cortisol, while in those with chronic stress, there is a dysregulation of the HPA axis. The association of certain psychosocial risk factors with certain health behaviors like depression is also known to lead to medical non-compliance.

References

1. Ader, R, 2007. Psychoneuroimmunology. Academic Press.
2. Barth, J, Schumacher, M, Herrmann-Lingen, C, 2004. Depression as a Risk Factor for Mortality in Patients With Coronary Heart Disease: A Meta-analysis. Psychosomatic Medicine 66:802–813.
3. Cohn, JN, 1989. Sympathetic nervous system activity and the heart. Am J Hypertens.
4. Carroll, D, Hewitt, JK, Last, KA, Turner, JR, Sims, J, 1985. A twin study of cardiac reactivity and its relationship to parental blood pressure. Physiology & Behavior. 34 (1).
5. Dimsdale, JE, 2008. Psychological Stress and Cardiovascular Disease. Journal of the American College of Cardiology. 51 (13).
6. DiMatteo, MR, Lepper, HS, Croghan, TW, 2000. Depression is a risk factor for noncompliance with medical treatment: meta-analysis of the effects of anxiety and depression on patient adherence. Arch Intern Med. 160(14): 2101-7.
7. Esler, M, Kaye D, 2000. Sympathetic nervous system activation in essential hypertension, cardiac failure, and psychosomatic heart disease. J Cardiovasc Pharmacol.
8. Farag, NH, Moore, WE, Lovallo, WR, Mills, PJ, Khandrika, S, Eichner, JE, 2008. Hypothalamic-Pituitary-Adrenal Axis Function: Relative Contributions of Perceived Stress and Obesity in Women. Jounral of Women’s Health. 17(10).
9. Grippo, AJ, Johnson, AK, 2002. Biological mechanisms in the relationship between depression and heart disease. Neuroscience and Biobehavioral Reviews 26: 941–962.
10. Irwin, MR, 2008. Human psychoneuroimmunology: 20 years of discovery. Brain Behav Immun. 22(2): 129-39.
11. Jokinen, J, Nordström, P, 2008. HPA axis hyperactivity and cardiovascular mortality in mood disorder inpatients. J Affect Disord.
12. Kemeny, ME, 2008. Psychobiological responses to social threat: evolution of a psychological model in psychoneuroimmunology. Brain Behav Immun. 23(1): 1-9.
13. Kropiunigg, 1993. Basics in psychoneuroimmunology. Ann Med. 25(5): 473-9
14. Kop, WJ, 1999. Chronic and Acute Psychological Risk Factors for Clinical Manifestations of Coronary Artery Disease. Psychosomatic Medicine 61:476–487.
15. Lutz W, Tarkowski M, Dudek B, 2001. Psychoneuroimmunology. A new approach to the function of immunological system. Med Pr. 52(3): 203-9.
16. McCabe, PM, Schneiderman, N, Field, TM, Wellens, AR, 2000. Stress, Coping, and Cardiovascular Disease. Lawrence Erlbaum Associates.
17. Rutledge, T, Hogan, BE, 2002. A Quantitative Review of Prospective Evidence Linking Psychological Factors With Hypertension Development. Psychosomatic Medicine 64:758–766.
18. Rozanski, A, Blumenthal, JA, Davidson, KW, Saab, PG, Kubzansky, L, 2005. The Epidemiology, Pathophysiology, and Management of Psychosocial Risk Factors in Cardiac Practice. Journal of the American College of Cardiology. 45(5).
19. Remme, WJ, 1998. The sympathetic nervous system and ischaemic heart disease. Eur Heart J.
20. Rosmond, R, Björntorp, P, 2000. The hypothalamic-pituitary-adrenal axis activity as a predictor of cardiovascular disease, type 2 diabetes and stroke. J Intern Med. 247(2): 188-97.
21. Strike, PC, Steptoe, A, 2004. Psychosocial Factors in the Development of Coronary Artery Disease. Progress in Cardiovascular Diseases. 46 (4).
22. Smith, TW, Ruiz, JM, 2002. Psychosocial Influences on the Development and Course of Coronary Heart Disease: Current Status and Implications for Research and Practice. Journal of Consulting and Clinical Psychology. 70 (3). 548–568.
23. Vedhara, K, Irwin, M, 2005. Human Psychoneuroimmunology. Published by Oxford University Press.
24. Wirtz, PH, von Känel, R, Emini, L, Ruedisueli, K, Groessbauer, S, Maercker, A, Ehlert, U, 2007. Evidence for altered hypothalamus–pituitary–adrenal axis functioning in systemic hypertension: Blunted cortisol response to awakening and lower negative feedback sensitivity. Psychoneuroendocrinology. 32 (5).
25. Wang PS, Bohn RL, Knight E, Glynn RJ, Mogun H, Avorn J, 2002. Noncompliance with antihypertensive medications: the impact of depressive symptoms and psychosocial factors. J Gen Intern Med. 17(7): 504-11.