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Treating depression may improve recovery of heart rate variability following coronary syndromes

Patients with depression appear to have an impaired ability to recover their heart rate variability following acute coronary syndromes such as heart attack, a factor that could increase their risk of coronary death, according to a report in the September issue of Archives of General Psychiatry, one of the JAMA/Archives journals. However, patients who are treated with antidepressants or whose mood lifts may experience more of an improvement in heart rate variability than those who are untreated or remain depressed.

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 predicts death after myocardial infarction [heart attack], the authors write as background information in the article. It is reduced in depressed compared with non-depressed patients after myocardial infarction and has been proposed to be a mediator of the increased mortality associated with depression. In non-depressed patients who have an acute coronary episode, heart rate variability drops and then recovers substantially but not completely during the next few months.

Alexander H. Glassman, M.D., of the Columbia University College of Physicians and Surgeons and the New York State Psychiatric Institute, New York, and colleagues 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 attack. The patients were then 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 participants 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 postacute 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, the authors 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 postacute 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.

From a clinicians point of view, 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.


Contact: Dacia Morris
JAMA and Archives Journals

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