Current drugs used to treat heart failure and irregular heartbeat have limited effectiveness and have side effects. New basic science findings from a University of Iowa and Vanderbilt University study suggest a way that treatments could potentially be refined so that they work better and target only key heart-related mechanisms.

"CaM kinase helps regulate calcium, which is essential to heart function, but CaM kinase's calcium connection also can play a role in electrical problems that lead to irregular heart beats and cell death. This new finding suggests a specific way to keep the wanted CaM kinase effects but at the same time eliminate the bad effects," said Mark E. Anderson, M.D., Ph.D., professor and head of internal medicine at the University of Iowa Roy J. and Lucille A. Carver College of Medicine.
"Most patients with heart failure are at risk of sudden death. Figuring out how and why heart failure happens is a major goal for academic medicine," Anderson said.
"The study showed, surprisingly, the importance of CaM kinase's effect on two particular amino acid targets among the thousands of amino acids that make up protein targets for phosphorylation by CaM kinase. Controlling these targets might prevent the 'ripple effect' of other molecular events that result in arrhythmia and cell death," said Anderson, who also is a member of the University of Iowa Heart and Vascular Center and holds the Francois Abboud Chair in Internal Medicine.
"CaM kinase is needed to maintain calcium channel function, which allows the heart to contract. But too much CaM kinase, and consequently too much calcium entry into heart cells, causes electrical instability and other downstream molecular problems that can lead to cell overload and cell death, which causes heart failure," Anderson said.