Nonsurgical treatment might prevent mitral valve damage after a heart attack


According to a study published in the Journal of the American College of Cardiology, it is potential to treat or even prevent the heart valve damage that occurs after a heart attack, noninvasively. Losartan reduced mitral valve damage in an animal model of heart attack. The damage usually takes place in heart attack patients (25%), which can result in heart failure and an increased risk of death.   

Robert Levine, said, "Our study supports a new concept on heart valves. They are not just passive tissue flaps, as previously thought, but are biological battlegrounds where medicines can be used to help patients. Patients with the heart valve disease are currently treated with interventions like surgeries or implanted devices late in their illness when the heart is failing. We aim to prevent disease progression at an early stage and keep our patients' hearts healthy."

The mitral valve keeps blood flowing in the right direction. However, Mitral valve regurgitation process decreasing the heart efficiency and increasing stress on the already-damaged organ. The previous study reported that post-heart-attack damage to the mitral valve was due to physical forces exerted by the scarring and stretching of damaged heart muscle.

Jacob Dal-Bianco, describes, the recent study found that the tumor growth factor β (TGF- β) released by immune cells to heal damaged the heart muscle, can over-activate other cells, leading to scarring and stiffening of the mitral valve and reducing its ability to close. Repair of a damaged mitral valve failed in patients (60%) after two years of surgery which caused heart failure.

To understand whether losartan could reduce post-heart-attack mitral valve damage in an animal model, the drug was given to a sheep in which a heart attack had been surgically induced, daily for two months. Considerably less inflammation, thickening, and scarring had developed in the mitral valves of the losartan-treated animals when compared with the control group. The animals had surgical mesh sutured to their left ventricular walls to restrict the stretching and keep the size of the ventricle the same as in the drug-treated animals.

Joyce Bischoff said, "that previously losartan could prevent endothelial cells from responding to TGF-β, we also examined how the endothelial cells lining the mitral valve changed after the heart attack when sheep were treated with losartan or not. We found that losartan reduced the number of endothelial cells that were transitioning into potentially fibrotic cells, which we speculate is part of how losartan reduced mitral valve thickness."

Further, the study is required to identify losartan ability to treat mitral valve disease in human beings. Levine, a professor of Medicine, concluded, it is necessary to check whether treatment during the inflammatory period after a heart attack is sufficient and whether the treatment benefits patients who developed mitral valve regurgitation and heart failure.

The first time, it may be possible with losartan to nonsurgically treat or prevent the post-heart-attack damage to mitral valve, which could improve the patient’s quality-of-life with less heart failure.