Washington, Feb 11: Researchers have identified and tweaked a specific protein molecule, parvalbumin, to prevent diastolic heart failure when its pumping mechanism goes haywire.
Diastolic heart failure arises when peak calcium levels, required for heart’s sqeezing action, don’t drop off quickly enough to permit the organ to relax. Then the lower left heart chamber (left ventricle) does not fill with enough blood to be pumped out to the body.
University of Minnesota researchers, led by Joseph M. Metzger, professor of integrative biology and physiology, optimised the parvalbumin protein as ParvE101Q, to soak up excess calcium at a precise instant, allowing the heart to relax efficiently after contraction, the journal Nature Medicine reports.
The advance offers a solid conceptual step forward in solving the puzzle of diastolic heart failure.
The next step will be determining the best possible small molecule or gene delivery mechanism for the protein, which should allow the discovery to be used in clinics, according to a Minnesota statement.
“We’ve discovered that our optimised variation of parvalbumin can fulfil that role by treating diastolic heart failure,” adds Metzger.
The researchers believe they may have found a unique clinical application to treat diastolic heart failure.
“Heart disease and heart failure rates are growing, especially as our population ages. We hope this type of discovery may one day help pave the way to a better way to treat patients,” said Metzger.