Treating the Patient as a Whole Person
Treating the Patient as a Whole Person
(This is the first part of a series of articles addressing interdisciplinary treatment of psychiatric disorders in patients with comorbid medical illness-Ed.)
Collaboration and communication among psychiatrists, primary care doctors and other physicians are becoming increasingly critical, as both research and anecdotal data are lending empirical credibility to the interdependence of body and mind. Comorbid depression with major medical illnesses may be particularly dangerous, and evidence is accumulating that failure to address this depression can impede medical treatment and increase mortality.
"I'm not sure that people -- meaning consumers, mental health professionals and non-mental health professionals -- realize what the numbers are," David Kupfer, M.D., explained in an interview with Psychiatric Times. "They're epidemic and scary. We're not talking about feeling somewhat down and mildly dysphoric, we're talking about major depression."
Kupfer, chair of the University of Pittsburgh department of psychiatry, recently moderated a conference titled "The Unwanted Co-Traveler: Depression's Toll on Other Illnesses." Sponsored by the National Institute of Mental Health, the conference comprised specialists in cardiovascular disease, cancer, diabetes, HIV/AIDS, Parkinson's disease (PD) and other neurological diseases. Psychiatrists and primary care physicians "can learn a lot from each other," Kupfer continued. He believes that depression frequently is undertreated in patients with comorbid medical illness because of the mistaken belief that it is a normal response to the latter, particularly in the case of elderly patients. In fact, major depression does not occur in the majority of patients with other medical illnesses. However, when it does, neurovegetative symptoms associated with depression can substantially interfere with patients' ability to follow through with treatment recommendations. The following is a look at the latest research and treatment recommendations for depression that accompanies cardiovascular disease, stroke and PD.
Estimates indicate that roughly one-fifth of post-myocardial infarction patients meet diagnostic criteria for major depression. Research indicates that the prevalence of depression among patients who have not had heart attacks but have angiographically documented coronary artery disease runs around 18% (Carney et al., 1987, as cited in Robinson and Krishnan, in press), compared to about 10% in the general American population. The risk of dying within six months is three to four times greater for depressed survivors of myocardial infarction (MI), compared to their nondepressed peers (NIMH, 1999).
In another study, Canadian researchers found that the significantly higher risk of cardiac mortality at the one-year mark among depressed patients was largely independent of the severity of cardiac disease (Frasure-Smith et al., 1999). Equally, if not more, concerning are recent findings indicating that depression can actually foreshadow the development of heart disease (Moon, 2001).
"Depression is a chronic illness and contributes to chronic stress," Lawson Wulsin, M.D., coordinator of the family medicine and psychiatry residency training program at the University of Cincinnati, told PT. "We know that stress is taxing to the cardiovascular system in particular, because it can increase blood pressure, decrease heart rate variability and may suppress immune function in subtle ways that contribute to inflammatory processes, and cardiovascular disease is an inflammatory disease."
In addition, higher smoking rates among depressed individuals put them at higher risk of developing heart disease, said Wulsin, who presented findings suggesting the link between depression and subsequent heart disease at the American Psychiatric Association's 2000 annual meeting (Wulsin and Singal, 2000). In a recent interview, Wulsin reiterated his recommendation that depressed patients over the age of 40 be referred for a full medical checkup to screen for potential cardiovascular problems: "Psychiatrists should be taking better cardiovascular histories of their depressed patients, and primary care [doctors] and cardiologists should be taking good histories of depression in their patients with heart disease."
Wulsin said that prophylactic use of antidepressants may be justified in patients with cardiovascular disease who have a history of major depression or a strong family history of the mood disorder. He added, however, that too many questions remain regarding the treatment of depression, and its effect on cardiovascular outcomes, to recommend that all patients with cardiovascular disease receive prophylactic antidepressant treatment.
Despite the high incidence of depression among patients with cardiovascular disease, information on how to safely and effectively treat such patients remains limited. Tricyclic antidepressants generally are not used, due to documented side effects that include cardiac conduction delays and orthostatic hypotension. To date, sertraline (Zoloft) has been shown safest and most effective in post-MI patients (Goodnick and Hernandez, 2000; Robinson and Krishnan, in press).
A number of studies have shown that the selective serotonin reuptake inhibitors are safe and effective for depressed patients with ischemic heart disease, and this class of antidepressants is generally preferred by clinicians due to its more favorable side-effect profile. Still, when choosing an SSRI -- particularly for post-MI patients -- psychiatrists should take into account factors such as platelet activation, as well as the usual drug interaction caveats. Concerning the latter, University of Miami mood disorders director Paul J. Goodnick, M.D., clearly remembers hearing about a patient who was put on paroxetine (Paxil), along with a ß-blocker, digoxin and other medications by cardiac care unit staff after being hospitalized for chest pain. The patient, who was not being treated for depression, was released and then emergently re-hospitalized after an interaction between the paroxetine (a potent 2D6 inhibitor) and the ß-blocker significantly lowered his heart rate.