Johns Hopkins, and his team of researchers, did some experiments on animals to find that an antidepressant developed more than 40 years ago can affect and even reverse the muscle enlargement and weak pumping function related to heart failure.

The report will be published in the Jan edition of the journal, “Circulation Research”. The team of US and Italian researchers explained, through experiments on rodents, how the antidepressant stops the action of enzyme monoamine oxidase-A.

The experiments also revealed how the antidepressant, called clorgyline, stops its breakdown of a key neurohormone. It is no longer used in humans.

Norepinephrine controls the flow of blood pumping and makes the heart pump harder and faster in response to stress.

This is the first evidence showing how elevated MAO-A activity drives the heart failure biochemically. It also shows that its dangerous downstream effects can be stalled by drug therapy.

Senior study investigator and cardiologist Nazareno Paolocci, M. D. says, “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.”