Not all diseases need novel medicines; in fact, some of them could be treated with already existing medicines initially designed for another disease. The pre-existing drugs can get approval more quickly as compared to the newly developed drug as it is mostly, never tested in patients.
Scientists used this fast-tracking approach to treat the common heart failure called heart failure with preserved ejection fraction (HFpEF). The approach is valuable and lifesaving for heart patients. Shortness of breath is seen among the patients of HFpEF when they subjected to physical exertion.
This is because the heart muscles get weak and are not strong enough to pump all the blood across the whole body, so it has to work more to meet the needs of the body. The condition of heart failure patients worsens with time and their quality of life declines which often leads to death.
Scientists at the Lewis Katz School of Medicine at Temple University (LKSOM) carried out new research on already available drugs for checking their healing effects on HFpEF patients. The drugs that are used for some types of cancer can be used to reverse the symptoms of HEpEF and soon be available in the market for treatment. In HFpEF animal model, the drug improves the ability of the heart to pump the blood across the whole body.
Steven Houser who is Senior Associate Dean of Research, Vera J. Good friend Endowed Chair of Cardiovascular Research and the Professor of Physiology and Medicine at the Cardiovascular Research Center at LKSOM said that currently, no FDA approved treatment is available in the market for the HFpEF patients as many people suffer from this problem. The study was published in the journal “Science Translational Medicine”.
He further added previous research had shown that there are abnormalities in the heart cells of the HFpEF patients. The abnormalities are results of mutations in the genes of the heart cell and function of the proteins that encode the genes.
A group of enzymes called histone deacetylase (HDACs) is involved in bringing the changes in the genes and protein function of heart cells. The drugs that block the activity of these enzymes are already available in the market that is used for treating the many diseases such as cancer.
Timothy A. McKinsey LaConte Chair in Cardiovascular Research, associate Cardiology Division Head for Translational Research, Professor of Medicine and Director of the Consortium for Fibrosis Research and Translation at the University of Colorado Anschutz Medical Campus suggested to Houser and Mckinsey team to investigate the effect of drug SAHA, it is a HDAC inhibitor that were used in the HFpEF animals for testing. The market name for SAHA is Zolinza and is approved for treating the type of cancer called cutaneous T-cell lymphoma.
The drug SAHA were tested in animal models with HFpEF which slowly developed the signs of disease such as shortness of breath and loss of exercise tolerance. Tissues changes have also been seen in animals which are similar to human especially heart remolding.
Hypertrophy and thickening of the left ventricle are the main characteristics involved in heart remolding. The left ventricle is the main chamber that pumps the blood to all the body parts through the aorta. Hypertrophy is the response of the heart in chronic cardiovascular disease e.g. high blood pressure.
Animals with HFpeEF showed great improvements when treated with SAHA particularly reducing the hypertrophy of the left ventricle. In treated animals, the muscles of the left ventricle are much relaxed as compared to non-treated animals. It restores the capacity of the heart to pump blood effectively and improves its function and structure.
Dr. Houser said that it is amazing that today the therapy could be tested in human patients with HFpEF.
He further added that now researchers’ team is planning to investigate the factors that cause the changes in the genes of heart cells. These changes bring alternations in cell and they function abnormally. If we were able to find the exact reason, then it will help us in the future for developing the more targeted treatments for HFpEF.