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J Am Coll Cardiol, 2006; 48:2215-2217, doi:10.1016/j.jacc.2006.09.007
(Published online 8 November 2006). © 2006 by the American College of Cardiology Foundation |
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,
,*
Department of General Internal Medicine, Division of Psychosomatic Medicine, University Hospital Berne, Berne, Switzerland
Cardiovascular Prevention and Rehabilitation, Psychocardiology Unit, Swiss Cardiovascular Center, University Hospital Berne, Berne, Switzerland.
* Reprint requests and correspondence: Dr. Roland von Känel, Division of Psychosomatic Medicine, Department of General Internal Medicine, Freiburgstrasse 4, University Hospital/INSELSPITAL, CH-3010 Berne, Switzerland. (Email: roland.vonkaenel{at}insel.ch).
Clearly, before another clinical trial of depression treatment is initiated in post-MI populations, we need more information on the "cardiotoxic" subtypes of depression. This is exactly what de Jonge et al. (4) achieved with their groundbreaking investigation presented in this issue of the Journal. They studied a sample of 468 post-MI patients, predominantly men in their early 60s, of whom almost 25% had a recurrent fatal or non-fatal cardiovascular event, defined as cardiovascular mortality, and cardiac-related readmissions during an average follow-up of 2.5 years. Patients who developed depression for the very first time after their MI ("incident post-MI depression") showed the highest risk of a new cardiovascular event. Strikingly, this risk was significantly lower and similar in patients who were depressed before the onset of MI ("non-incident post-MI depression") and in patients without post-MI depression. These findings held when controlled for MI severity, personality factors, and socioeconomic status. One strength of their protocol is that they performed a structured clinical interview to formally diagnose depression. This sound methodology supports another recent study showing that depressive symptom level at the time of, but not before, hospitalization predicted all-cause mortality at 5-year follow-up, even after adjustment for other prognostic indicators (5). Most remarkably, these findings suggest that depression onset before MI may not be causally linked with MI, supporting the most recent notion that this link is partially due to a shared genetic vulnerability (6).
It is of utmost clinical importance to find treatment options for incident post-MI depression. In order to decrease cardiac risk, such treatments must also favorably affect alterations in cardiovascular biology accompanying depression. The ENRICHD trial suggests this treatment may not be standard cognitive behavioral therapy used to treat depression in the general population (3). Also, in the SADHART (Sertraline Antidepressant Heart Attack Trial), sertraline did not reduce depressed mood more than placebo in patients with onset of a major depressive episode after they entered the hospital because of an acute coronary syndrome (7). de Jonge et al. (4) encourage fellow researchers to adopt a more individually tailored approach to treatment. They remind us that current standard diagnostic manuals of psychiatric disorders diagnose depression based on the sum of depressive symptoms adding up to a syndromal diagnosis of depression. Diagnostic manuals exclude concerns about the etiology of depression to arrive at a descriptive type of depressive disorder that can be reliably diagnosed by different investigators across different populations and times. However, if we view post-MI depression as failure to adjust to the traumatic experience of heart attack (7), its origin is of course qualitatively different from depression developing after the loss of a loved one before MI. In the first case, a tailored psychological intervention would focus on coping with the stress of a life-threatening experience and, in the second, on supporting the mourning process.
de Jonge et al. (4) seem to have unraveled incident post-MI depression as one cardiotoxic subtype of depression. What we have not yet resolved and what ought to guide treatment recommendations in the future are the presumably numerous contributing factors to incident post-MI depression. As suggested by the authors, these are best assumed to be both biological and psychosocial in nature. We specifically feel that considering the effect of the subjective experience of an acute MI on onset of depression after MI could teach us another important lesson. Patients who perceived their heart attack as a trauma involving threatened death to which they responded with intense fear or helplessness show substantial levels of post-traumatic stress symptoms. More precisely, approximately 15% of post-MI patients suffer from clinical post-traumatic stress disorder (PTSD) related to their MI (8). The diagnosis of acute PTSD requires that for more than 1 month, patients reexperienced the MI spontaneously in thoughts or dreams, avoided cues related to the MI such as taking cardiac medication, and affirmed symptoms of hyperarousal such as sleeplessness and irritability (9). Post-traumatic stress disorder predicted cardiovascular readmission rate in post-MI patients (10). Symptoms of PTSD substantially overlap with symptoms of depression (9). However, sole treatment of depression will only partially address PTSD-related symptoms and thus might not benefit cardiovascular health in a substantial proportion of depressed post-MI patients.
Regarding accumulated anecdotal evidence from patients who became clinically depressed after they received beta-adrenergic receptor blocking drugs, one factor that could evoke post-MI depression is beta-blocker therapy. In a prospective, carefully conducted case-control study also presented in this issue of the Journal, van Melle et al. (11) investigated whether beta-blocker use during hospitalization for MI predicts the development of depressive symptoms and disorders during the first year post-MI. Their assessment of the beta-blocker regimen before MI and during follow-up is a strength of their study. They did not, however, control for previous episodes of depression, which could have prompted beta-blocker initiation before MI in patients who somatize depressive affect (e.g., in the form of palpitations and trembling) (12). In addition, their analysis considered some patients who were also part of the sample studied by de Jonge et al. (4), but we are not told whether beta-blocker use specifically affected symptom levels of incident post-MI depression at different times of follow-up.
The authors found no significant difference in any depression end point between beta-blocker users and non-users well-matched in terms of demographic factors, baseline depressive symptom level, and MI severity (11). Adjustment for potential confounders, including risk factors for cardiac disease and diseases contraindicative of beta-blocker use, maintained this observation. Although supporting their findings, they did not discuss a previous meta-analysis of randomized trials of beta-blocker therapy in cardiovascular disease—including MI—accumulating data from over 10,000 patients followed up for at least 6 months (13). This meta-analysis showed that overall frequency of depressive symptoms was the same in the beta-blocker and placebo groups and that depressive symptom frequency did not relate differently to either lipophilic or hydrophilic beta-blocking compounds (13).
Beta-blocker therapy belongs to the current guidelines for the management of patients with acute MI and reduces mortality of post-MI patients by approximately 20% (13). In spite of this evidence, beta-blockers are underused in secondary prevention of MI even though post-MI patients with diseases contraindicative for these drugs have clear cardiovascular benefits from carefully monitored beta-blockade (14). Correctly, van Melle et al. (11) state that no population-based study is able to discount individual susceptibility to a depressogenic effect of beta-blockers. Specifically, their study cannot rule out the possibility that post-MI patients taking high-dose beta-blockade might become depressed with a delay of at least half a year after their MI, thereby calling for close monitoring of depressed mood in this particular group of patients. Nevertheless, we agree that the most important lesson to be learned from their study is to abandon the general reluctance in prescribing beta-blockers to post-MI patients who are depressed and do not have any absolute contraindication for this medication.
We conclude with a comment aimed at integrating important aspects of the 2 studies discussed here (4,11). Early in the course of an acute psychological trauma, therapy with propranolol recently prevented storing of traumatic memories in the brain by blocking neurotransmission (15). We feel tempted to encourage an extension of this mesmerizing avenue of research to MI populations. We hypothesize that beta-blocker therapy might similarly benefit patients who experience their heart attack as particularly traumatic, thereby perhaps decreasing onset of incident post-MI depression and related cardiovascular risk.
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1 Dr. von Känel has recently received funding from Pfizer Inc., Switzerland.
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