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Cardiovascular researchers at the University of Cincinnati (UC)have identified a genetic variant in a cardiac protein that can belinked to heart rhythm dysfunction. This is the first genetic variant in a calcium-binding protein(histidine-rich calcium binding protein) found to be associatedwith ventricular arrhythmias and sudden cardiac death in dilated cardiomyopathy patients,opening up new possibilities for treatment. Dilated cardiomyopathy is a condition in which the heart becomesweakened and enlarged and cannot pump blood efficiently. These findings were presented for the first time at theInternational Society of Heart Research's Pathology and Treatmentof Heart Failure meeting in Banff, Alberta, held May 27 through May31, 2012. The team led by Vivek Singh, PhD, a research scientist under thedirection of Litsa Kranias, PhD, in the department of pharmacologyand cell biophysics at UC, says that sudden cardiac death is a riskfor patients with heart failure who are carriers of this variant in the histidine-richcalcium-binding protein because the calcium inside their heartcells is not properly controlled, possibly leading to thedevelopment of arrhythmias. "The histidine-rich calcium-binding protein (HRC) is a regulator ofcalcium uptake and release in the sarcoplasmic reticulum, a networkof tubes and sacs in heart muscle fibers that plays an importantrole in heart contraction and relaxation by releasing and storingcalcium ions," Singh says. "Recently, our group at UC and Athens, Greece, identified a geneticvariant in HRC, named Ser96Ala, which showed a significantassociation with worsening ventricular arrhythmias and suddencardiac death in a group of patients with idiopathic dilatedcardiomyopathy. In this study, our team characterized themechanisms and pathways that link the HRC variant with arrhythmiascausing sudden death." Researchers first generated animal models with cardiac-specificexpression of the human normal (S96S) or altered (A96A) HRC. "Unexpectedly, we found that contractility of heart cellssignificantly decreased with disturbed calcium regulation in A96Ahearts when compared with S96S hearts," Singh says. "In addition,A96A heart cells showed more arrhythmic behavior under stress conditions." Singh says this data could eventually provide new insights intopathways that control calcium regulation, leading to thedevelopment of new clinical interventions. "Our results showed that the human HRC mutant model displayedaltered intracellular calcium (Ca2+) handling, associated withslowed Ca2+ uptake and increased Ca2+ leak, which may promotearrhythmias under stress," Singh says. "These new findings areimportant because we can use this information to help develop newmethods of screening human patients and preventing arrhythmiadevelopment in the carriers." Additional References Citations. We are high quality suppliers, our products such as China Custom Medical ID Bracelets , China Badge Slot Punch for oversee buyer. To know more, please visits Retractable ID Badge Reels.
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