Our lab focuses on understanding how impulse formation and failure in the heart leads to sudden cardiac death in diseases such as Andersen Tawil Syndrome Type 1, Brugada Syndrome, and diabetes.
The mortality rate from heart disease is the number one cause of death. In specific, over 600,000 of the nearly 1 million annual deaths due to heart disease in the United States are ascribed to sudden cardiac death (SCD) presumably due to ventricular arrhythmias. However, many of the mechanisms leading to ventricular arrhythmias are incompletely understood or highly controversial.
My research focuses on the initiation, propagation, and selective failure of cardiac propagation leading to arrhythmias. The initiation of an arrhythmia requires some kind of trigger usually in the form of a premature beat. It is well established that these premature beats are linked to calcium handling dysregulation, but it remains unknown why certain cells or groups of cells are more likely to trigger a premature beat than others. My laboratory seeks to understand the underlying mechanism of premature beats in hopes of developing therapies to target the most at risk cells.
Once the premature beat begins in a group of cells, it must propagate to the remainder of the heart and trigger contraction. If that propagation is slow or stops suddenly, the heart is at risk for a lethal condition called ventricular tachycardia or fibrillation. The mechanisms governing impulse propagation and failure are controversial. We seek to understand how cardiac conditions previously accorded marginal significance in the generation of sudden cardiac death may affect the success or failure of propagation. We are currently engaged in a project that seeks to understand how the amount of water in the heart increases or decreases the success of impulse propagation. This research has potential to lead to more cost-effective strategies for lowering the chances of sudden cardiac death in patients with high blood pressure for example.