Congestive heart failure (CHF) is a chronic, degenerative condition that impairs the heart's ability to pump blood at normal filling pressures to adequately meet the energy requirements of the body. Multidrug treatment regimens that include diuretics, vasodilators and inotropic agents such as angiotensin-converting enzyme inhibitors, can slow the progression of CHF and reduce the number of acute episodes. However, treatment remains directed at symptoms and is most effective in the early stages of CHF. In later stages of the disease, mechanical devices can play an important role. Left ventricular pacemakers can improve the heart's function as a pump, while cardiac assist devices may be used to help support the failing heart.
Dartmouth researchers have now found that an increase in the endothelial cell mass in the normal heart in the absence of hemodynamic load can induce myocyte hypertrophy and result in a stronger, more efficiently functioning heart. The increase in the endothelial mass precedes the onset of myocardial enlargement by several weeks and the process stops when the capillary density per unit gram of myocardial tissue has returned to the baseline level. This endothelium-driven myocardial hypertrophy was achieved by cardiac-specific overexpression of angiogenic proline/arginine-rich peptide PR39. PR39 was found to increase myocardial mass by 50% and cause a marked increase in both systolic and diastolic performance as well as ejection fraction and cardiac output of the heart. Accordingly, agents which increase cardiac levels of PR39 can be used to enhance cardiac mass or performance and in the treatment of heart disease or disorders such as congestive heart failure and cardiomyopathies.
This technology is claimed in the published PCT Application No. PCT/US2006/016621. We are seeking an industrial partner interested in its commercialization. (Ref: J305)
Last Updated: 7/24/12