Washington: An anti-depressant developed over 40 years ago can blunt and even reverse the muscle enlargement and weakened pumping function associated with heart failure, research says.
A team of Johns Hopkins and other researchers stumbled on the discovery during animal experiments.
The latest study results, they say, are believed to be the first evidence showing how elevated MAO-A (enzyme monoamine oxidase-A) activity biochemically drives heart failure and that its dangerous downstream effects can be stalled by drug therapy.
The team of US and Italian heart experts have shown how, in a dozen key mice experiments, clorgyline, an anti-depressant, no longer prescribed, blocks the action of 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.
"Our study helps describe heart failure as a vicious chemical circle of stimulant norepinephrine overload and breakdown, and it offers a disease blueprint with monoamine oxidase-A as the target for drugs similar to clorgyline to rein in the disease," says senior study investigator and cardiologist Nazareno Paolocci.
Notable side-effects from clorgyline, Paolocci says, include insomnia and agitation, or high blood pressure, said a Johns Hopkins release.