Thursday, June 09, 2005

From Science News, Vol. 167, No. 22, May 28, 2005, p. 341.

Positive Jolt: Electroshock therapy may have side benefit
Nathan Seppa

People with depression have high concentrations of norepinephrine, a nervous system hormone that signals blood vessels to constrict and ratchets up blood pressure, researchers report. Treating these individuals with electroshock therapy lowers their norepinephrine concentrations—and their heart rate and blood pressure too, scientists find.

A fast pulse, vessel constriction, and high blood pressure are valuable tools in a person's fight-or-flight response. But if high norepinephrine concentrations chronically keep a person in that state, it puts a strain on the heart, says Mitchel A. Kling, a psychiatrist at the National Institute of Mental Health in Bethesda, Md. Excess norepinephrine, he says, could partly explain the long-standing connection between depression and heart failure, which is a weakening of the heart. Depression doubles the risk of death in people with heart failure, as do high norepinephrine concentrations.

"Depression is not good for your heart, basically," says Kling.

He and his colleagues conducted standard clinical tests on 22 people with the most severe form of depression and 23 people free of depression. The groups were similar in age. Volunteers with depression had a higher average pulse rate and higher blood pressure than did people in the comparison group. Blood and spinal-fluid samples revealed higher concentrations of three stress hormones—norepinephrine, cortisol, and epinephrine—in study participants with depression than in the others. The stress-hormone differences showed up even during sleep.

Next in the study, eight of the depressed patients volunteered to receive a series of electroshock treatments, which are also called electroconvulsive therapy. Among psychiatrists, electroshock treatment remains controversial. Many depressed people show gains from it, but some complain of memory loss and other side effects. Its benefit sometimes lasts only a few days and, at other times, endures for months or years, Kling says.

The eight patients in Kling's study averaged nine electroshock treatments apiece over roughly 3 weeks. Four weeks after the last treatment, the patients again provided blood and spinal-fluid samples. These showed a clear drop in the concentration of norepinephrine, but not cortisol or epinephrine, the researchers report in an upcoming Proceedings of the National Academy of Sciences.

"To my knowledge, no one has ever looked at the effect of electroconvulsive therapy on the levels of norepinephrine," says cardiologist Inder S. Anand of the Veterans Affairs Medical Center and University of Minnesota in Minneapolis. Combined with other work, this research is "pretty convincing" that stress chemicals such as norepinephrine are being overproduced in the depressed brain, he says.

Even more interesting, he says, is that electroshock can change conditions in the brain to the point of reversing norepinephrine's oversupply.

Made by nerve cells, norepinephrine carries signals between the cells. Electroshock therapy might "reset" overzealous nerve cells in the brain and reduce their norepinephrine production, Kling hypothesizes. But the therapy's long-term benefits in this regard are unknown, he says.

Suppressing norepinephrine might nevertheless offer benefits for patients with heart failure, Kling says. Some of the many antidepression drugs on the market may reduce norepinephrine concentrations too, he says, "but there is surprisingly little data on that."
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References:

Gold, P.W. . . . and M.A. Kling. In press. Cardiac implications of increased arterial entry and reversible 24-h central and peripheral norepinephrine levels in melancholia. Proceedings of the National Academy of Sciences. Abstract available at http://www.pnas.org/cgi/doi/10.1073/pnas.0503069102.

Further Readings:

Aggarwal, A., et al. 2002. Norepinephrine turnover is increased in suprabulbar subcortical brain regions and is related to whole-body sympathetic activity in human heart failure. Circulation 105(March 5):1031-1033. Available at http://circ.ahajournals.org/cgi/content/full/105/9/1031.

Anand, I.S., et al. 2003. Changes in brain natriuretic peptide and norepinephrine over time and mortality and morbidity in the Valsartan Heart Failure Trial (Val-HeFT). Circulation 107(March 11):1278-1283. Available At http://circ.ahajournals.org/cgi/content/full/107/9/1278.

Carney, R.M., et al. 1999. Major depression, heart rate, and plasma norepinephrine in patients with coronary heart disease. Biological Psychiatry 45(Feb. 15):458-463. Abstract available at http://dx.doi.org/10.1016/S0006-3223(98)00049-3.


Sources:

Inder S. Anand
University of Minnesota, Minneapolis
Veterans Affairs Medical Center
1 Veterans Drive
Minneapolis, MN 55417

Mitchel A. Kling
National Institute of Mental Health
National Institutes of Health
Building 10, Room 2D-46
10 Center Drive
Bethesda, MD 20892-1284

Friday, June 03, 2005

Someone sent me this article, which is interesting because I've been taking medication for an underactive thyroid for more than 20 years before my heart failure was diagnosed:

Researchers discover thyroid, heart failure connection
Plain Talk ^ | May 27,2005

Researchers at The University of South Dakota School of Medicine believe they are on the verge of changing the way physicians view the treatment of heart disease.

Along with several colleagues, A. Martin Gerdes, director of the School of Medicine's Cardiovascular Research Institute in Sioux Falls, has recently published groundbreaking research in a nationally recognized medical journal for establishing a connection between low functioning thyroid glands and the development of heart disease. Although treatment on human patients may be some time away, the team is excited at the prospect of standing on the cutting edge in a new trend in the field of heart medicine research.

The study, titled "Thyroid Hormones Induce Unique and Potentially Beneficial Changes in Cardiac Myocyte Shape in Hypertensive Rats Near Heart Failure," appears in the May issue of the American Journal of Physiology-Heart and Circulatory Physiology, published by the American Physiological Society. During the course of his study, Gerdes and his colleagues established that not only can a poorly functioning thyroid contribute to congestive heart failure; it also indicates a reduced likelihood of recovery, and an increased chance of death.

This study builds upon earlier work at the institute which showed researchers that whatever leads to heart failure is always preceded by changes in the shape heart cells. As pressure within the heart increases, stress causes the heart cells to stretch and flatten, and thereby weaken. The new study demonstrates that a moderate dose of thyroid hormones (TH) over 30 days "normalizes" the shape of the cardiac cells (myocytes) and reduces stress on the heart's wall nearly 40 percent.

The research team was pleased not only because the hormone therapy appeared to have a positive effect upon the distorted heart cells, but also because this research involves a new treatment approach.

"This is the first study to look at the implications of thyroid hormone therapy on hypertensive heart failure," Gerdes said.

Based on these encouraging findings, the authors of the paper feel that this new avenue of treatment warrants further study. However, Gerdes warned since "this is the first study to disclose these positive effects with TH, we don't yet have enough information to do this intelligently in humans. Care should be taken in administering TH to humans for heart disease since there is so little information available from animal studies," Gerdes said.

However, Gerdes was optimistic that the successes he and his research team have enjoyed will someday be applied to the treatment of heart disease in humans.

"We're really just looking at the tip of the iceberg here, but we believe this could be the beginning of the next big thing in the treatment of heart disease," Gerdes said.


http://www.plaintalk.net/stories/05...0526050167.html

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