Heart failure is a common cardiovascular condition with more than 500,000 new cases each year and requiring close to 1 billion dollars in health care expenses [1]. During the last decade or so, several publications have noted the prevalence and unfavorable effects of conduction abnormalities in heart failure [2–5]. Conduction delay, most often in the lateral wall, results in early activation and contraction of the septum at a time when the lateral wall is quiescent, and thus in early systole stretches. Subsequent late activation and contraction of the lateral wall occur as the septum is initiating deactivation, resulting in septal bulging. This ventricular dyssynchrony and its associated mechanical abnormalities result in inefficient global contraction and reduced stroke volume [6–8]. Stress is highest in lateactivated myocardial regions because of exaggerated prestretch in early systole (secondary to septal contraction) and late systolic contraction against increased afterload [9]. These mechanical perturbations appear to be associated with significant regional molecular changes. Spragg and colleagues [10] demonstrate the regional expression disparities of key proteins involved with stress response (mitogen-activated kinase), calcium handling (eg, phospholamban), and electrophysiology (connexin 43). Dyssynchrony