Foundations for
Polaris-CV development
Development of Polaris-CV is grounded in extensive research
on the significance of depression as a risk factor for cardiovascular
disease. CVD is the most common cause of death in the western
world. Depression is often co-morbid with CVD. It adversely
effects prognosis, increasing both mortality and morbidity.
Prevalence of Depression among CVD Patients
The most recent review of research on the relationship of
depression to CVD (12) found that researchers consistently
report major depression prevalence rates in the 15% - 23%
range. Prevalence rates can be considerably higher among patients
undergoing specific procedures. Studies which report subsyndromal
symptoms of depression have also found higher rates. For example,
a study of 200 patients who had recently undergone cardiac
catheterization and angiography found that 17% met DSM IV
criteria for major depression, and an additional 17% for minor
depression (8). Prevalence rates for major and minor depression
among 283 patients who were hospitalized following a heart
attack were 18% and 27% respectively (14). Presumably, additional
subjects in these studies suffered from depressive symptoms
which, though subsyndromal, may be clinically significant.
Thus the proportion of CVD patients suffering from serious
symptoms of depression is in the range 20% - 50%.
While serious symptoms of depression are commonly found in
CVD patients, depression is rarely diagnosed by either primary
care physicians or cardiologists, and “…..when
it is diagnosed, it is apparently often left untreated…….A
significant first step in the treatment of patients with CVD
is increasing the ability and willingness of cardiologists…..to
detect and treat depression.” (5; pg. 119).
Finally, it is important to note that these symptoms do not
refer to the transitory feelings of depression normally associated
with chronic or potentially life-threatening illness. Rather,
they are persisting cognitive and somatic conditions having
a powerful impact upon cardiac prognosis.
Impact upon Morbidity, Mortality and Costs
Depression significantly impacts morbidity and mortality
in CVD patients; its impact may exceed that of physiological
risk factors (5). Frasure-Smith et al. (1993) found that major
depression was a significant predictor of mortality six months
after myocardial infarction (MI). The effect of depression
persisted after controlling for left ventricular function
and history of prior MI. Its impact was found to be at least
equivalent to the impact of these conditions.
Major depression is the best predictor of adverse cardiac
events (e.g., MI, death) among patients who undergo cardiac
catheterization; the risk of an adverse event is twice as
great for depressed patients (4). Research during the past
20 years has repeatedly documented the importance of depression,
social isolation and loss of purpose in life as major risk
factors for CVD morbidity and mortality. Dozens of studies,
covering many thousands of patients in the U.S. and other
Western countries (13), consistently find that their impact
is at least equal to known physiological risk factors (blood
pressure, cholesterol, family history of CVD etc.). Mortality
rates for CVD patients who are depressed, isolated, and feel
that their life lacks purpose, are two to six times higher,
after controlling for age and physiological risk factors.
Medical costs of untreated depression in CVD patients are
high. Increased morbidity leads to higher medical utilization
for depressed patients, whose rehospitalization expenses alone
have been found to be more than four times those of undepressed
CVD patients (1).
Treating Depression
Can treatment for depression improve CVD prognosis? There
is growing evidence that psychosocial and pharmacological
treatment of depression in CVD patients results not only in
improved quality of life and psychosocial functioning, but
also in reduced cardiac morbidity and mortality, and lower
costs. A recent meta-analysis of 23 randomized, controlled
studies (10) that evaluated the incremental impact of psychosocial
treatment as part of Coronary Artery Disease (CAD) rehabilitation
found large (46% improvement in 2 year follow up) and nearly
universally positive results. Even modest psychosocial interventions
may have pronounced effect. A review of 34 controlled studies
covering 2,000 surgical or coronary patients (11) found that,
among other positive impacts upon morbidity and quality of
life, emotional support reduced hospitalization by an average
of two days (20%). The interventions were quite modest (e.g.,
brief psychotherapy; educational) but nonetheless produced
substantial cost savings.
Depression complicates treatment for CVD. One hypothesis
is that since depression adversely effects compliance with
medical therapy (3), as patients become less depressed they
are more likely to take the steps necessary to recovery (e.g.,
compliance with medication, exercise, diet). Also, researchers
have begun to identify physiological changes that occur as
depressive symptoms decline; these in turn improve CVD prognosis.
This work has implications for the choice of anti-depressants
for the treatment of depression in CVD patients. Serotonin,
for example, “has been implicated both in platelet aggregation
and coronary artery vasoconstriction, it is of primary importance
to determine whether the SSRIs (e.g., Prozac), widely used
to treat depression produce effects on platelet function”
(12; pg. 587). In their review of research on biological mechanisms
mediating depression and CVD prognosis; Musselman et al. (1998)
report that several investigators have found increased platelet
5HT2 binding density (implicated in atherosclerosis, thrombosis
and vasoconstriction) which decreased to control values only
in patients whose depression improved.
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