- Overview
   - What CV Measures
   
- Development Foundation
   - Procedures for using CV
   - Benefits
   - Differentiators
   - System Components
   - References   
   - Grant Award Announcement


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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