Nursing Care for Cardiovascular Disease
Depression and Cardiovascular Diseases
Over the past 10 years, there has been growing interest in the relationship between depression and cardiovascular diseases. These are two of the most widespread public health problems in the United States, and are among the leading sources of functional impairment and disability.
Recent research findings linking
depression and cardiac disease will therefore be discussed, along with
implications for future research.
Depression and Adverse Cardiac Outcomes
In response to the growing awareness of the magnitude of the interaction between depression and adverse cardiac outcomes, several large scale community based studies have been conducted.
Penninx and others (2001) followed a cohort of 2,847 men and women aged 55 to 85 years for 4 years. These investigators examined the effect of minor depression (ie, Center for Epidemiologic Studies-Depression scale [CES-D] score of 216) and major depression (ie, using DSM-III criteria) on heart disease mortality.
They found that patients with major depression had significantly higher risk for cardiac mortality compared with those who had minor depression. These findings suggest that the severity of depression is related to higher cardiac mortality.
In another study, Schulz and others (2000) studied a total of 5,201 men and women aged 65 years and older enrolled in the Cardiovascular Health Study.
Controlling for sociodemographic variables and common comorbid conditions, individuals with higher scores of depressive symptoms were more likely to die than those who had lower scores.
Depressed participants with heart failure at baseline had the highest mortality risk (adjusted RR = 2.44, RR = 1.62 for stroke patients, RR=1.60 for intermittent claudication, RR 1.30 for angina pectoris, and RR = 1.15 for myocardial infarction).
Furthermore, Cox proportional hazards regression model demonstrated that depressive symptoms were an independent predictor of mortality.
In an other study of the relationships among depression, coronary heart disease (CHD) incidence, and mortality, Ferketich , Schwartz baum , Frid , and Moeschberger (2000) found that depressed men and women were at increased risk for incident CHD events.
Compared with nondepressed counterparts (RR
1.73 (1.11-2.68), RR = 1.71 (1.14-2.56), correspondingly). Furthermore, unlike
depressed women, depressed men had an increased risk of cardiac mortality with
adjusted RR = 2.34 (1.54-3.56).
Population Studies Community Based
Prospective population-based studies of depression also found an increased risk for CHD due to depression, Mendes de Leon and others (1998) conducted a cohort study and found a slight increase in risk for CHD events, RR=1.03 (1.01-1.05), in fairly healthy older women.
However, de Leon failed to find support for depression as an independent risk factor for CHD events in elderly men and women in the aggregate. Another prospective study used data from the Yale Health and Aging Project (Williams, SA, et al., 2002).
The sample consisted of 2,501 men and women, with a mean age of 74 years who were disease-free elders and were followed for up to 14 years.
In comparison with nondepressed individuals, depressed individuals demonstrated a 69% increase in the risk for incident heart failure. In addition, depressed participants were more likely to be women; Consequently, depression was a significant risk factor of heart failure among women but not among men.
Using a randomized clinical trial, Berkman and others (2003) assessed the preventive effect of cognitive behavioral therapy (CBT) on depression in 2,481 myocardial infarction (MI) men and women.
Although CBT reduced depression and decreased social isolation, it failed to reduce mortality or recurrent infarction events after a 6-month intervention period. In short, research findings from community-based studies suggest that depression is a risk factor for cardiac morbidity and mortality.
However, interventions that may reduce depression have failed to reduce depression related cardiac outcomes (eg, see Berkman et al., 2003).
It is essential to note that many of
these studies have controlled for demographic variables and medical comorbidity
that might otherwise explain the reported findings.
Depression and Cardiovascular Disease Biobehavioral Mechanisms
Recognition of the overlap between depression and cardiovascular disease has led to increased interest in finding plausible biobehavioral mechanisms which link them to gather. In fact, there is evidence to indicate that depression may contribute to increased incidence of cardiovascular events.
This effect may be mediated by other behavioral and biological factors that play major roles in the development of negative cardiac outcomes. There are several known behavioral risk factors (eg, sedentary lifestyle, smoking, high-fat dietary intake) among depressed individuals that may contribute to the development of cardiac disease.
In addition, recent research findings suggest that several biomarkers are involved in both depression and cardiac disease pathogenesis. First, research showed that the hypothalamic pituitary adrenocortical (HPA) axis is activated during depression, which increases sympathoadrenal activity.
Consequently, some risk markers such as catecholamines, cortisol, and serotonin are clavated in both depression and some cardiac diseases. Second, depressed patients are at increased risk for rhythm disorders.
Recent evidence indicates that cardiac patients who are depressed exhibit reduced heart rate variability, a known risk factor for sudden death in patients with CVD (Carney et al., 1995).
Third, depressed patients are more likely to have platelet dysfunction that may have a negative impact on the development and prognosis of cardiovascular disease such as atherosclerosis, acute coronary syndromes, and thrombosis.
Finally, the research demonstrated a close relationship among proinflammatory cytokines, such as IL-6 and TNF-a, depression, and incidents of negative cardiac outcomes.
Briefly, any single mechanism will fall short of
capturing the underlying pathogenesis processes of depression and cardiac
disease. Therefore, several mechanisms are needed to account for the
development and progression of the two.
Conclusion
This overview from a biopsychosocial perspective reveals that there is sufficient evidence to support an important association between depression and cardiac disease. It also suggests a number of significant directions for future research.
Large, randomized clinical trials are needed to determine whether early detection of depression coupled with early intervention can prevent the development of cardiac disease or reduce the risk for incidents of negative cardiac events.
Another research priority is to elucidate the potential mediating factors related to depression, such as failure to comply with medical care, sedentary lifestyle, eating habits, and smoking.
Also, biological studies are needed to quantify the latent effect of the alterations in the level of risk biomarkers (eg, homocysteine, IL-6, TNF-α, IL-2, serotonin, dopamine, cortisol, heart rate variability, and platelet activation), which could have a negative effect on cardiac function. Furthermore, depression seems to be more of a problem for women with cardiac disease than for men.
Therefore, future studies are needed that focus on whether there is a disproportionate weight of comorbid depression and cardiac outcomes among women.
Designing large-scale clinical trials that test biobehavioral research models, along with considering both physiological and behavioral outcomes, are essential to better understanding of the depression-cardiac disease communication.
In addition, studies designed to develop a clearer account of psychosocial risk factors to cardiac disease are urgently needed.
Finally, in an era of genetic research,
identifying genes or gene expression mechanisms that may link depression and
cardiac disease may pave the path for ultimate under-standing of the link
between depression and cardiovascular diseases.
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