Kentucky Physiological Society 1 st Inaugural Meeting University of Kentucky March 25 , 2013 Introducing Physiology From Around

(See registration table for assigned poster # and parking validation for free exit of parking garage for out of town guests) 12:00-1:30PM: Box lunches provided (free) for people submitting abstracts or preregistering with a notice of attending (can pay when arriving). The $10 registration fee will give you a one-year membership to KY-PHYS, and will help defray meeting expenses. Further details on the KY-PHYS inaugural meeting and program are available: Hot link: The ordered electrical excitation of the heart coordinates the efficient pumping of blood. Electrical impulses normally originate in the sinoatrial node and then propagate through the atria and into the ventricles. Arrhythmias are electrical disturbances that disrupt the normal initiation or propagation of the cardiac impulse. They can cause abnormally slow or fast heart rates, block impulse propagation, or initiate the impulse to circle in a " reentry " loop. Atrial arrhythmias can result in the formation of blood clots and increase the risk of stroke, and ventricular arrhythmias can cause inefficient pumping of blood, loss of consciousness, and sometimes death. Long QT syndrome (LQT) is one of the most common congenital arrhythmia syndromes. LQT patients have a delay in the repolarization of their ventricles and are at increased risk for polymorphic ventricular tachycardia (torsades de pointes), which can cause a loss of cardiac output, syncope, and sudden death. LQT typically follows a dominant inheritance pattern and is linked to mutations in three different genes that encode cardiac potassium and sodium channels. Testing for genetic variants in LQT-susceptibility genes is helping to identify mutations that might cause the syndrome, but the considerable genetic variability among suspected LQT patients, as well as seemingly healthy individuals, makes accurately diagnosing and managing LQT difficult. A missed LQTS diagnosis can result in preventable sudden death, whereas a false LQT diagnosis can lead to unnecessary family stress, lifestyle restrictions, β-blocker therapy, and the expensive and sometimes painful implantation of cardioverter defibrillator. Our research program studies the mechanisms that underlie the dysfunction for LQT-linked mutations. Our goal is to identify strategies that improve the diagnostic, prognostic and therapeutic value of a genotype positive test for LQT, as well as identify novel strategies for the treatment of cardiac arrhythmias. returned to the University of Kentucky Physiology Department as an Assistant Professor, and he is funded with an R01 from the National Heart Lung and Blood Institute. Since rejoining the Physiology Department, he has been awarded …