Improving cardiac function with either a biologic (MYDICAR) or small molecule (CDN) has been shown to significantly improve cardiac contractility & relaxation, metabolism and/or survival in: - At the cellular level, explanted myocytes from patients or animals with heart failure undergoing cardiac transplantation (CDN & MYDICAR)
- In vivo, aortic-banded pressure overloaded rats with hypertrophy transitioning to failure (MYDICAR)
- Normal animals after intravenous administration (CDN)
- Porcine model of mitral regurgitation induced heart failure. In this model, damage to the mitral valve generates progressive heart failure. Animals treated with the SERCA2a gene showed long-term improvement in stroke volume and other measures to levels nearly double those of untreated animals. Heart function was restored to levels nearly identical to those of healthy control animals. (MYDICAR)
- Ovine model of pacing induced heart failure. In this model, continuous pacing induces moderate to severe heart failure. Left ventricular ejection fractions in the paced animals are approximately 25 percent, levels similar to NYHA Class III heart failure patients. Despite continued pacing, animals treated with the SERCA2a gene not only arrested their progression of heart failure, but showed restoration of left ventricular ejection fractions and other hemodynamic parameters to normal levels. (MYDICAR)
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