Depression can stop heart failure
Heart failure can effectively be reversed by a commonly-prescribed antidepressant, scientists have claimed.
The discovery, made in mice, has excited researchers who believe it could pave the way to revolutionary new treatments for the condition.
A side effect of the drug, paroxetine, is thought to be responsible for its ability to overcome symptoms of heart failure, which occurs when the organ is too weak to pump sufficient blood around the body.
US lead researcher Dr Walter Koch, from Temple University Health System in Philadelphia, said: "This may open the way for a new class of therapies for a disease for which we lack effective interventions."
Paroxetine, used to treat depression, anxiety disorders and obsessive compulsive disorder (OCD), was found to inhibit an enzyme that plays a crucial role in heart failure.
Previous research has shown that heart failure in animals can be reversed by using genetic engineering to lower levels of the enzyme GRK2 (G protein-coupled receptor kinase-2).
In the new study, mice were given induced heart attacks which caused their hearts to fail over a period of two weeks.
When the heart failure was well developed, they were treated with paroxetine, fluoxetine (Prozac) or an inactive dummy.
Only paroxetine restored function to near-normal levels, proving that its effect was unrelated to antidepressant properties shared with fluoxetine.
Paroxetine was also tested against the beta-blocker drug metoprolol, a standard treatment for heart failure.
"The beneficial effects of paroxetine were far greater than beta-blocker therapy," Dr Koch said.
GRK2 appears to be important for the unhealthy "remodeling" of a heart responding to damage caused by a heart attack.
The maladaptive adjustments cause the heart to grow larger, weaker and less efficient.
The research was reported in the journal Science Translational Medicine.
About half of people diagnosed with heart failure die within five years.