BACKGROUND: Heart failure (HF) remains a major cause of morbidity and mortality in North
America. With an aging population and an unmet clinical need by current pharmacologic
and device-related therapeutic strategies, novel treatment options for HF are being explored.
One such promising strategy is gene therapy to target underlying molecular anomalies in the
dysfunctional cardiomyocyte. Prior animal and human studies have documented decreased
expression of SERCA2a, a major cardiac calcium cycling protein, as a major defect found in …