Promising New Treatment For Heart Failure

An anti-depressant drug developed over 40-years ago has been found to dull, even reverse muscle enlargement and weakened pumping function connected to heart failure, in animal experiments carried out by a team of researchers from Johns Hopkins.

Publishing their report in the journal Circulation Research, the heart experts describe how the no longer in use anti-depressant clorgyline, blocked enzyme monoamine oxidase-A (MAO-A) from breaking-down a key neurohormone in a dozen key laboratory experiments on rodents. The enzyme norepinephrine is responsible for controlling the the pace of blood pumping and in response to stress, it makes the heart pump harder and faster.

These findings are the first evidence showing how elevated MAO-A activity that bio-chemically drives heart failure can be stalled by drug therapy.

Insomnia, agitation, high blood pressure after ingesting foods containing the amino acid tyramine, a protein that stimulates a surge of stored stimulatory hormones, specifically, norepinephrine are some of the notable side effects from clorgyline.

Patients taking clorgyline and whose chemical binding to MAO-A is irreversible, should avoid tyramine-rich foods, such as, chocolate, red wine, certain beans, aged cheeses and meat.

An estimated 5.7-million American men and women suffer from chronic heart failure, which killed an estimated 290,000 people in 2005.

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