Examining Illness Invalidation and Illness Perception in Relation to Physical Functioning in the Context of Cardiovascular Disease

Invalidation is defined as the perception of cognitive, affective, and behavioral responses of others that are experienced as denying, lecturing, overprotecting, not supporting, and not acknowledging with the respect to the condition of the patient (Kool, 2012). Invalidation has also been suggested to negatively impact patients’ physical health (Kool, 2012). One specific type of invalidation is illness invalidation (II), defined as attitudes of distrust, suspicion, lack of support for, or acknowledgement that a patient is suffering from an illness (Blom et al., 2011). In addition to II, illness perception (IP) is another construct that has been linked to negative physical health (Arran, Carufurd, & Simpson, 2013). IP is a process through which an individual constructs a cognitive representation of an illness and has also been shown to influence symptom severity and physical functioning (Arran et al., 2013). Although the relationships between II, IP, and physical health have been observed previously, more extensive research is needed to determine the specific mechanisms of these relationships and what other psychological factors may play a role. Previous studies indicate that coping behaviors and depressive symptoms may be factors that influence these relationships (Shen, McCreay, & Myers, 2003). The present study used a regression analysis to reveal that depression was the only significant predictor of physical functioning. The present study also used PROCESS (Hayes, 2013) to reveal that depression mediated the relationship between IP and physical functioning, but did not mediate the relationship between II and physical functioning. The present study also revealed that coping did not mediate the relationship between IP and physical functioning, nor did coping mediate the relationship between II and physical functioning. Lastly, the present study revealed that II and IP were both significantly related to depression, and IP was significantly related to II. II AND IP IN THE CONTEXT OF CARDIOVASCULAR DISEASE 3 Examining II and IP in Relation to Physical Functioning in the Context of Cardiovascular Disease Cardiovascular disease is currently the leading global cause of death, accounting for 17.3 million deaths per year (American Heart Association, 2015). Since 1921, cardiovascular disease has been the leading cause of death in the United States and currently accounts for over 375,000 American deaths per year (Howarter, Bennett, Barber, Gessner, & Clark, 2014). By the year 2020, the World Health Organization predicts that cardiovascular disease and major depression will become the two leading contributors to the global burden of disease, and that cardiovascular disease alone will account for more than 23.6 million deaths per year by the 2030 (Ali, Rollman, & Berger, 2010). A widespread amount of recent literature has established that psychosocial factors significantly contribute to the pathogenesis of coronary artery disease (Rozanski, Blumenthal, & Kaplan, 2014). The prevalence of comorbid mental health conditions in cardiac patients is well documented with many studies associating psychological risk factors with a poor prognosis for heart diseases (Ali et al., 2010). This extensive knowledge has also contributed to the illumination of the basic pathophysiology that underlies the relationship between psychosocial factors and development and severity of heart disease (Rozanski et al., 2014). However, the identification of psychological predictors for coronary heart disease has produced inconsistent results (Rugulies, 2002). Despite many encouraging findings, there has been insufficient research exploring the interrelationships among some of these conceivable related psychosocial variables and how they may affect the outcomes of coronary heart disease (Shen et al., 2003). Depression and Cardiovascular Disease Prognosis Perhaps the most widely studied psychosocial factor in relation to cardiovascular disease is depression. In this paper, depression refers to unipolar clinical depression as diagnosed by II AND IP IN THE CONTEXT OF CARDIOVASCULAR DISEASE 4 clinical assessment, and depressed mood as measured by standardized self-report scale. Depression has been found to be an independent risk factor in the etiology of coronary heart disease and the risk of coronary heart disease has been found to be directly related to the severity of depression (Goldston & Baillie, 2008). Comorbid depression is relatively common in patients with coronary heart disease, as approximately one in five patients with newly diagnosed heart disease has major depression (Carney, Freedlan, Miller, & Jaffe, 2002). The prevalence of major depression is similar in patients recovering from acute myocardial infarction and other acute cardiac stresses and once coronary heart disease is established, depression has a negative overall impact on the prognosis of the disease, increasing both the risk of occurrence of future cardiac events and higher risk of mortality (Goldston & Baillie, 2008). The presence of depressive symptoms even in the absence of diagnosed major depressive episodes is associated with increased risk for cardiac events, and a number of studies confirm a relationship between the magnitude of depression and future cardiac events (Rozanski et al., 2014). This data suggests that risk for future cardiac disease associated with depression exists along a continuum relative to the magnitude of depressive symptoms (Rozanski et al., 2014). There are many proposed mechanisms to explain the relationship between depression and severity of physical symptoms in patients with cardiac disease. Some plausible explanations for the relationship between depression and cardiac mortality and morbidity include biological mechanisms such as antidepressant cardiotoxicity and dysregulation of autonomic, neuroendocrine, and seratonergic systems (Carney et al., 2002). More specifically, depression has been associated with hyperactivity of the hypothalamic-pituitary-adrenocortical (HPA) axis, which results in over-stimulation of the sympathetic nervous system, which then increases circulating catecholamines and serum cortisol (Goldston & Baillie, 2008). These neurohormonal II AND IP IN THE CONTEXT OF CARDIOVASCULAR DISEASE 5 abnormalities contribute to an imbalance in sympathetic and parasympathetic activity, which results in surges in heart rate and systolic blood pressure, increasing the risk of atherosclerotic plaque rupture and acute coronary thrombosis (Goldston & Baillie, 2008). According to Rozanski et al. (2014), direct pathophysiological effects of depression involve at least three mechanisms. The first is that depression is accompanied by hypercortisolemia, which is associated with attenuation of the adrenocorticotropin hormone response to corticotropin-releasing factor administration, non-suppression of cortisol secretion after dexamethasone administration, and elevated corticotropin releasing factor concentrations in the cerebrospinal fluid, all of which contribute to more severe symptoms of heart disease. A second mechanism proposed by Rozanski et al. is that due to the association between depression and unhealthy lifestyle behaviors, depressed patients may develop substantial impairment in platelet function. This impairment can include augmented platelet reactivity and release of platelet products including platelet factor 4 and b-thromboglobulin, which are associated with adverse cardiovascular events. The mixture of hypercortisolemia and enhanced platelet function establishes the theoretical basis to explain the proatherogenic effects of depression (Rozanski et al., 2014). Lastly, reduced heart rate variability (HRV) and impaired vagal control have been reported in cardiac patients suffering from depression. HRV is a widely used noninvasive measure that reflects the autonomic regulation of the heart and is measured by beat-to-beat changes in a patient’s heart rate (Hoogwegt et al., 2014). Reduced HRV is a well-known predictor of cardiac mortality, including sudden cardiac death resulting from ventricular fibrillation. This finding also supports the assertion that depressed patients may be subject to increased risk for cardiac arrhythmia, further contributing to severity of cardiac related II AND IP IN THE CONTEXT OF CARDIOVASCULAR DISEASE 6 symptoms. Therefore, HRV might be an important explaining mechanism of the relationship between psychological distress and prognosis (Hoogwegt et al., 2014). Depression may also contribute to the onset or worsening of cardiovascular disease by triggering recurrent endothelial injuries (Carney et al., 2002). The endothelium is the key regulator of homeostasis in the vascular tissue, and alteration in endothelial function precedes the development of atherosclerosis in patients (Deanfield, Halcox, & Rabelink, 2015). This could occur via promotion of maladaptive health processes, triggering dysregulation of the neurohormonal systems responsible for cortisol and catecholamine secretion, or increasing susceptibility to infection with latent pathogens that colonize the vessel wall (Herbert & Cohen, 1993; Miller, Cohen, & Herbert, 1999; Plotsky, Owens, & Nemeroff, 1995). Furthermore, in consideration of behavioral mechanisms, depression is associated with unhealthy lifestyle behaviors including smoking and poor compliance with medication, which have been shown to contribute to the worsening function of these biological processes and, thus, increased rates of morbidity and mortality in patients with cardiovascular disease (Rozanski et al., 2014). In order to investigate the relationship between depression and physical function in the present study, a regression analysis was used. Coping and Cardiovascular Disease Prognosis As previously mentioned, psychological interventions for cardiac patients have mostly focused on depression factors, selecting patients for treatment based on the type and severity of symptoms displaye