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 Research & Giving News Article  of Heart Attack Patients This is among the findings of research conducted by NARSAD Distinguished Investigator Alexander H. Glassman, M.D., of the Columbia University College of Physicians and Surgeons and the New York State Psychiatric Institute, and colleagues, and reported in the September issue of Archives of General Psychiatry. Dr. Glassman’s team measured heart rate variability in 290 depressed patients an average of three weeks after they were hospitalized for acute coronary syndrome, a term encompassing heart events such as heart attacks. Heart rate variability refers to the degree to which the heart rate changes from beat to beat in response to normal impulses. Low heart rate variability is statistically linked with death following a heart attack. In non-depressed patients who have an acute coronary episode, heart rate variability drops and then typically recovers substantially, but not completely, during the next few months. Heart rate variability is reduced, comparatively, in depressed patients following a heart attack and it is suspected of being a factor in the higher mortality otherwise associated with depression. On the basis of their new study, Dr. Glassman and colleagues suggest that “patients with depression after myocardial infarction, especially those with prior episodes, should be both carefully watched and aggressively treated, because they are at an elevated cardiac risk and less likely to get better spontaneously.” Patients in the trial were randomly assigned to take either the antidepressant sertraline or placebo for 24 weeks. After 16 weeks, 258 patients returned for a second heart rate variability reading. The severity of each participant’s depression and their clinical response to depression treatment also were measured on previously established scales. At the beginning of the study, previous episodes of depression were associated with lower heart rate variability. At the 16-week follow-up visit, the depressed patients had recovered their heart rate variability more slowly than expected and some even experienced a decrease. Patients who took sertraline had a 9 percent increase in heart rate variability and patients who took placebo had a 10 percent decrease, compared with the 28 to 33 percent increase in recovery of heart rate variability observed in previous studies of non-depressed patients. “Both sertraline treatment and symptomatic recovery from depression were associated with increased heart rate variability compared with placebo-treated and non-recovered post–acute coronary syndrome control groups, respectively, but this results primarily from decreased heart rate variability in the comparison groups,” the authors write. The mechanisms behind the relationship between heart rate variability, depression and cardiac death remain unclear, Dr. Glassman and colleagues note. “What is clear is that depression is associated with biological changes involving increased heart rate, inflammatory response, plasma norepinephrine, platelet reactivity, decreased heart rate variability and now absent post–acute coronary syndrome heart rate variability recovery, all of which is associated with life-threatening consequences. Understanding why these characteristics so strongly associate with depression is crucial to understanding the nature of depression itself,” they conclude. Dr. Glassman, who is chief of clinical psychopharmacology at New York State Psychiatric Institute and professor of psychiatry at Columbia’s College of Physicians and Surgeons, is an authority on depression and antidepressant drugs, and has altered the standard of care for depressed patients. He received NARSAD’s Distinguished Investigator Award in 2005. This article was adapted by NARSAD with permission of JAMA and Archives Journals. |
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