A team of Johns Hopkins and other researchers have found in animal experiments that an antidepressant developed over 40 years ago can blunt and even reverse the muscle enlargement and weakened pumping function associated with heart failure.
In a report to be published in the Jan. 8 edition of the journal Circulation Research, the international team of U.S. and Italian heart experts describes in a dozen key laboratory experiments in rodents how the antidepressant clorgyline, which is no longer in use in humans, blocks the action of enzyme monoamine oxidase-A (MAO-A) and stops its breakdown of a key neurohormone. Norepinephrine, as it is called, controls the pace of blood pumping and makes the heart pump harder and faster in response to stress.
The latest study results, they say, are believed to be the first evidence showing how elevated MAO-A activity biochemically drives heart failure and that its dangerous downstream effects can be stalled by drug therapy.
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