Myocardial gene transfer of β-adrenergic signaling components as a potential therapy for heart failure
Cardiovascular disease accounts for nearly 40% of all deaths annually in the U.S. Prevention management and advances in medical treatments have dramatically reduced the overall mortality rate due to heart disease. However, death due to chronic HF continues to rise, and effective therapy - particularly for end-stage HF - has been elusive. The myocardial βAR system is critical not only in chronic HF, but also in acute settings where cardiac function is compromised. Moreover, the drugs which act by altering βAR signal transduction are at the forefront of conventional HF therapeutic strategies. Accordingly, the ability to genetically manipulate βAR signaling in the heart is of great interest because it may provide unique inotropic support and improve existing therapeutic strategies for HF.
