New Drug Aids Heart Patients

Cardiac myosin activators improve heart failures

(RxWiki News) Standard heart failure drugs are designed to force the heart to beat more often. A new class of medication that prompts longer heart contractions instead may prove to be a novel treatment.

Cardiac myosin activators target motor proteins that prompt muscle contractions, increasing the blood volume pumped with each beat.

"Ask your cardiologist if you should stick with your current heart drug."

John Cleland, study leader and a professor from the University of Hull, said a trial has proven that the intravenous drug can safely be given to heart failure patients, and that at the correct dose and blood plasma concentrations can improve heart function and aid the heart in contracting more effectively.

Cardiac myosin activators can successfully lengthen the interaction between motor proteins and prolong the contraction of the left ventricle, which is the chamber of the heart responsible for pumping oxygenated blood to the remainder of the body.

During a second phase double-blind placebo clinical trial, researchers tested the effectiveness of the drug in 45 heart failure patients who had impaired function of the left ventricle. It was found that the drug successfully increased the contraction duration of the left ventricle and the amount of blood pumped, showing that the heart was working more efficiently and effectively.

Previously the drug was successfully tested with healthy volunteers, but this was the first test of the drug on heart failure patients. The drug was given through infusion into a vein, but an oral capsule is currently under development.

Cleland called the initial findings "promising," and said additional larger-scale studies already are underway. He said those trials will examine whether the improvements found in heart function would provide real benefits for patients in terms of symptoms, quality of life and impact on mortality rates.

The research was published in Lancet.

Reviewed by: 
Review Date: 
August 20, 2011