Research

Atrial fibrillation (AF) is a cardiac arrhythmia that increases the risk of stroke five- to seven-fold and mortality two-fold. AF is age-related, affecting >10% of the population over age 80.

AF can occur in the absence of structural heart disease (lone AF) or in conjunction with coronary artery disease, hypertension, valvular heart disease and congestive heart failure. Risks of stroke and death are related to the extent of endothelial and ventricular dysfunction accompanying arrhythmia. Systemic inflammatory markers such as C-reactive protein are elevated in patients with AF, tending to increase in patients with persistent rather than with paroxysmal forms of AF. Inflammatory mechanisms may contribute to atrial remodeling associated with increased persistence and increased risk of morbidity.

To evaluate the mechanisms that underlie AF, we study the cellular and biochemical properties of atrial tissues from surgical patients and in animal models. We study expression and function of ion channels that underlie atrial excitation-contraction coupling, using microarrays to evaluate the signaling pathways and genes that are altered in AF.

Histologic techniques are used to explore the distribution of inflammatory mediators, inflammatory cellular infiltration, and the links to altered atrial architecture. Animal models allow us to explore the impact of high-rate electrical activity and inflammation post cardiac surgery.

This combination of approaches helps us to identify and evaluate novel pathways for intervention, in an effort to decrease the incidence and complications associated with AF.