The Body and Mind Connection: The Latest Evidence
The third speaker was Dr Steven Roose, professor of psychiatry, New York State Psychiatric Institute, Columbia University Medical Center, New York, whose topic was treatment of depression in heart disease. He noted that depression causes vascular damage through increased sympathetic activity, increased platelet aggregation, increased hypothalamic-pituitary-adrenal axis activity and cortisol, and proinflammatory cytokines.
Depression increases the risk for coronary artery disease fourfold for syndromal depressive episodes and 1.5-fold to twofold for subsyndromal depressive symptoms. In addition, childhood depression leads to a 12-fold increased risk for smoking. Furthermore, depression (but not anxiety or anger) increased cardiac mortality after myocardial infarction (MI). Inflammation and increased platelet activity could be important mechanisms of this effect, he noted. Overall, there is about fourfold increased risk for mortality after MI in patients with depression, with the risk being highest in the first 6 months.
Dr Roose examined the classic SADHEART study, which looked at sertraline (mean dosage, 68.8 mg/d) in 260 patients vs placebo. At 16 weeks, MI was reduced by an odds ratio of 0.70 (95% confidence interval, 0.23-2.16). The composite cardiovascular events score was somewhat reduced as well (odds ratio, 0.77; 95% confidence interval, 0.51-1.16).
The benefit of sertraline for depressive symptoms was greater among patients with preexisting depression before MI (73% with sertraline vs 43% with placebo) than among those whose depression began after MI (63% with sertraline vs 57% with placebo).
That study was followed up by another larger trial, ENRICHD, which was powered for mortality in over 2000 patients. Patients were randomly assigned to receive cognitive-behavioral therapy (CBT) for 6 months or no CBT, and serotonin reuptake inhibitors (SRIs) were allowed. Overall, there was no effect of CBT on mortality. But in the SRI group (n = 353), there was benefit, with about a 50% reduction in cardiovascular mortality (4.5% vs 9.8% with no SRI). However, because participants were not randomly assigned to receive SRI treatment vs no SRIs, this benefit cannot be known definitively to be causal.
If SRIs do provide some benefit for cardiovascular mortality, Dr Roose noted that we cannot assume that the mechanism involves anti-inflammatory effects. Instead, a mechanism could involve direct antiplatelet effects of SRIs; platelets contain most of the body's serotonin. He noted that this effect also is related to the fact that SRIs can cause upper gastrointestinal bleeding in older patients.
These presentations at the recent American Psychiatric Association meeting summarize recent evidence that inflammation is important for some aspects of mood illnesses—but the relationships are complex, and easy solutions don't appear to exist, at least for now.
Depression and Heart Disease
The third speaker was Dr Steven Roose, professor of psychiatry, New York State Psychiatric Institute, Columbia University Medical Center, New York, whose topic was treatment of depression in heart disease. He noted that depression causes vascular damage through increased sympathetic activity, increased platelet aggregation, increased hypothalamic-pituitary-adrenal axis activity and cortisol, and proinflammatory cytokines.
Depression increases the risk for coronary artery disease fourfold for syndromal depressive episodes and 1.5-fold to twofold for subsyndromal depressive symptoms. In addition, childhood depression leads to a 12-fold increased risk for smoking. Furthermore, depression (but not anxiety or anger) increased cardiac mortality after myocardial infarction (MI). Inflammation and increased platelet activity could be important mechanisms of this effect, he noted. Overall, there is about fourfold increased risk for mortality after MI in patients with depression, with the risk being highest in the first 6 months.
Dr Roose examined the classic SADHEART study, which looked at sertraline (mean dosage, 68.8 mg/d) in 260 patients vs placebo. At 16 weeks, MI was reduced by an odds ratio of 0.70 (95% confidence interval, 0.23-2.16). The composite cardiovascular events score was somewhat reduced as well (odds ratio, 0.77; 95% confidence interval, 0.51-1.16).
The benefit of sertraline for depressive symptoms was greater among patients with preexisting depression before MI (73% with sertraline vs 43% with placebo) than among those whose depression began after MI (63% with sertraline vs 57% with placebo).
That study was followed up by another larger trial, ENRICHD, which was powered for mortality in over 2000 patients. Patients were randomly assigned to receive cognitive-behavioral therapy (CBT) for 6 months or no CBT, and serotonin reuptake inhibitors (SRIs) were allowed. Overall, there was no effect of CBT on mortality. But in the SRI group (n = 353), there was benefit, with about a 50% reduction in cardiovascular mortality (4.5% vs 9.8% with no SRI). However, because participants were not randomly assigned to receive SRI treatment vs no SRIs, this benefit cannot be known definitively to be causal.
If SRIs do provide some benefit for cardiovascular mortality, Dr Roose noted that we cannot assume that the mechanism involves anti-inflammatory effects. Instead, a mechanism could involve direct antiplatelet effects of SRIs; platelets contain most of the body's serotonin. He noted that this effect also is related to the fact that SRIs can cause upper gastrointestinal bleeding in older patients.
Summary
These presentations at the recent American Psychiatric Association meeting summarize recent evidence that inflammation is important for some aspects of mood illnesses—but the relationships are complex, and easy solutions don't appear to exist, at least for now.
SHARE
