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Depression severely impairs the recovery of heart rate variability after acute coronary syndrome, reported Dr. Alexander H. Glassman of Columbia University, New York, and his associates.
In addition, heart rate variability (HRV) continues to decline in patients whose depression does not respond to sertraline (Zoloft), while it ceases to decline in those who do respond to sertraline. It is not yet known whether this cardiac benefit is attributable to a pharmacologic effect of the antidepressant, to improvement of the depressive illness, or to a combination of both, the researchers said.
“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-ACS-HRV recovery, all of which [are] associated with life-threatening consequences,” said Dr. Glassman and his associates.
“From a clinician's point of view, patients with depression after myocardial infarction … should be both carefully watched and aggressively treated, because they are at an elevated cardiac risk and less likely to get better spontaneously,” they noted (Arch. Gen. Psychiatry 2007;64:1025–31).
The researchers used data from 258 subjects who participated in the SADHART study to examine the effects of depression and of antidepressant therapy on heart rate variability. SADHART (Sertraline Antidepressant Heart Attack Randomized Trial), which took place in 1997–2001, compared sertraline with placebo in patients with major depressive disorder who were hospitalized after ACS.
In the general population, HRV falls abruptly during acute coronary episodes and recovers gradually but incompletely in the following weeks. However, Dr. Glassman and his associates found that HRV failed to recover in ACS patients with major depression.
The decline in HRV leveled off or improved slightly in those who responded to sertraline and in those whose mood improved spontaneously, but continued to decline in patients who received placebo or who failed to respond to sertraline, the investigators said.
Even patients who responded to sertraline showed only one-third as much HRV recovery as is reported in the literature among ACS patients who do not have depression. Thus, even successful selective serotonin reuptake inhibitor therapy “may not fully eliminate the autonomic risk associated with major depressive disorder,” the investigators added.
Dr. Glassman served as a member of the steering committee for SADHART. He also has been a consultant for and has received honoraria from Pfizer Inc., which markets sertraline and provided partial support for the study.
Depression severely impairs the recovery of heart rate variability after acute coronary syndrome, reported Dr. Alexander H. Glassman of Columbia University, New York, and his associates.
In addition, heart rate variability (HRV) continues to decline in patients whose depression does not respond to sertraline (Zoloft), while it ceases to decline in those who do respond to sertraline. It is not yet known whether this cardiac benefit is attributable to a pharmacologic effect of the antidepressant, to improvement of the depressive illness, or to a combination of both, the researchers said.
“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-ACS-HRV recovery, all of which [are] associated with life-threatening consequences,” said Dr. Glassman and his associates.
“From a clinician's point of view, patients with depression after myocardial infarction … should be both carefully watched and aggressively treated, because they are at an elevated cardiac risk and less likely to get better spontaneously,” they noted (Arch. Gen. Psychiatry 2007;64:1025–31).
The researchers used data from 258 subjects who participated in the SADHART study to examine the effects of depression and of antidepressant therapy on heart rate variability. SADHART (Sertraline Antidepressant Heart Attack Randomized Trial), which took place in 1997–2001, compared sertraline with placebo in patients with major depressive disorder who were hospitalized after ACS.
In the general population, HRV falls abruptly during acute coronary episodes and recovers gradually but incompletely in the following weeks. However, Dr. Glassman and his associates found that HRV failed to recover in ACS patients with major depression.
The decline in HRV leveled off or improved slightly in those who responded to sertraline and in those whose mood improved spontaneously, but continued to decline in patients who received placebo or who failed to respond to sertraline, the investigators said.
Even patients who responded to sertraline showed only one-third as much HRV recovery as is reported in the literature among ACS patients who do not have depression. Thus, even successful selective serotonin reuptake inhibitor therapy “may not fully eliminate the autonomic risk associated with major depressive disorder,” the investigators added.
Dr. Glassman served as a member of the steering committee for SADHART. He also has been a consultant for and has received honoraria from Pfizer Inc., which markets sertraline and provided partial support for the study.
Depression severely impairs the recovery of heart rate variability after acute coronary syndrome, reported Dr. Alexander H. Glassman of Columbia University, New York, and his associates.
In addition, heart rate variability (HRV) continues to decline in patients whose depression does not respond to sertraline (Zoloft), while it ceases to decline in those who do respond to sertraline. It is not yet known whether this cardiac benefit is attributable to a pharmacologic effect of the antidepressant, to improvement of the depressive illness, or to a combination of both, the researchers said.
“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-ACS-HRV recovery, all of which [are] associated with life-threatening consequences,” said Dr. Glassman and his associates.
“From a clinician's point of view, patients with depression after myocardial infarction … should be both carefully watched and aggressively treated, because they are at an elevated cardiac risk and less likely to get better spontaneously,” they noted (Arch. Gen. Psychiatry 2007;64:1025–31).
The researchers used data from 258 subjects who participated in the SADHART study to examine the effects of depression and of antidepressant therapy on heart rate variability. SADHART (Sertraline Antidepressant Heart Attack Randomized Trial), which took place in 1997–2001, compared sertraline with placebo in patients with major depressive disorder who were hospitalized after ACS.
In the general population, HRV falls abruptly during acute coronary episodes and recovers gradually but incompletely in the following weeks. However, Dr. Glassman and his associates found that HRV failed to recover in ACS patients with major depression.
The decline in HRV leveled off or improved slightly in those who responded to sertraline and in those whose mood improved spontaneously, but continued to decline in patients who received placebo or who failed to respond to sertraline, the investigators said.
Even patients who responded to sertraline showed only one-third as much HRV recovery as is reported in the literature among ACS patients who do not have depression. Thus, even successful selective serotonin reuptake inhibitor therapy “may not fully eliminate the autonomic risk associated with major depressive disorder,” the investigators added.
Dr. Glassman served as a member of the steering committee for SADHART. He also has been a consultant for and has received honoraria from Pfizer Inc., which markets sertraline and provided partial support for the study.