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.