Mydicar

Administration of Mydicar occurs via an intracoronary injection of the drug. Mydicar delivers the SERCA2a gene to cardiomyocytes using an adeno-associated viral-vector (AAV).^[6] In the cardiomyocytes, the viral vector can insert itself into the genome and increase expression of the SERCA2a protein. Delivering the gene via an AAV is beneficial because it readily infects cardiac tissue and can produce stable, long-term expression of the delivered gene.^[7] AAVs also produce less of an immune response than alternative viral vehicles, such as adenoviruses.^[7] AAVs have been studied in multiple patients and have not been known to cause human disease.^[5]

Proper relaxation of the heart in preparation for the next contraction depends largely on the decline of Ca²⁺ in the cytosol of cardiomyocytes during diastole. Along with impaired contractility, an increased level of cytosolic Ca²⁺ increases the risk of arrhythmias and remodeling of the heart.^[8] Excess Ca²⁺ found in the cytosol leads to asynchronous contractions of cardiomyocytes causing tachyarrhythmias. The unusual increase in contraction and faster beating of the heart leads to hypertrophy by increasing the size of the cardiac myocytes in the heart. Excess hypertrophy of the cardiac myocytes leads to further dysfunction of the heart by affecting their ability to relax and contract properly.^[5] Administration of Mydicar increasing functioning SERCA2a can assist in lessening these negative effects of an increase in cytosolic Ca²⁺ during diastole by increasing reuptake into the SR.^{[citation needed]}