Congestive heart failure (CHF) is an increasingly frequent cause of cardiovascular morbidity and mortality. CHF occurs as a result of systolic dysfunction, diastolic dysfunction, or a combination of both. Approximately 40% of CHF diagnoses involve diastolic dysfunction in the absence of systolic dysfunction. Diastolic dysfunction is largely related to impaired intracellular calcium sequestration resulting in prolonged calcium transients and delayed myocardial relaxation. Recent evidence has suggested parvalbumin gene transfer may correct diastolic dysfunction by acting as a delayed calcium buffer. However, limitations are associated with this approach, including systolic dysfunction. This study examines the use of genetically modified parvalbumin to limit these limitations while improving diastolic function by testing the following hypotheses: 1. Mutations that increase the magnesium affinity will limit parvalbumin mediated systolic dysfunction and preserve enhanced relaxation kinetics in normal myocytes. 2. Parvalbumin mutants exhibiting enhanced relaxation kinetics with little or no effect on contractile kinetics will restore relaxation performance in isolated myocytes from failing myocardium.