A team of cardiology researchers at Thomas Jefferson University has determined that GRK2, a protein that plays an important regulatory role in heart failure, is elevated in patients with failing hearts when compared to patients with normal heart function.
"These findings add to the growing evidence that GRK2 is a biomarker for heart failure," says Walter Koch, Ph.D., director of the Center for Translational Medicine in the Department of Medicine at Jefferson Medical College of Thomas Jefferson University in Philadelphia. Dr. Koch previously demonstrated that GRK2 is critically important in heart function. It is increased in failing human hearts and contributes to the loss of the heart's contractile strength during the development of heart failure.
In the current study, to be reported September 11, 2006 at the 10th Annual Scientific Meeting of the Heart Failure Society of America in Seattle, Amit Mittal, M.D., heart failure research fellow in the Department of Medicine at Jefferson Medical College, and his co-workers recruited patients at either Thomas Jefferson University Hospital when they were being treated, or during outpatient visits to their physicians. Heart failure patients who often have poor left ventricular function were compared to patients with normal left ventricular function who were taking no heart medications.
White blood cells from 20 heart failure patients were compared with white blood cells from 30 patients who didn't have heart disease to determine the presence of the GRK2 protein. "We have confirmed that GRK2 in white blood cells is elevated in human patients with failing hearts when compared to subjects with normal left ventricular function," Dr. Mittal said. "The GRK2 levels in heart failure patients were three to four times higher."
"Future studies will compare GRK2 levels in heart failure patients treated with standard prescription drug and device therapy to test our hypothesis that GRK2 can be a surrogate marker for determination of a given patient's response to treatment," Dr. Koch explains.
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