Cardiovascular disease is the leading cause of death in both men and women around the globe, taking the lives of more than 17 million people per year. For physicians and researchers alike, the symptoms of acute myocardial infarction (heart attack) and congestive heart failure pose significant problems. The heart muscle is damaged during a heart attack, rendering it less effective at circulating blood across the body. Since the heart has a limited capacity to heal, scar tissue replaces the lost muscle. This results in decreased cardiac output, which often leads to heart failure, in which the heart is unable to satisfy the body’s need for blood supply. Current heart disease therapies rely on treating complications (such as lowering blood pressure) rather than addressing the underlying issue: a heart that has destroyed so many functional heart muscle cells. Despite significant advancements in the treatment of heart failure, it continues to improve. The body cannot repair heart cells after they have been destroyed. Instead of managing this persistent condition, new therapeutic methods are needed to regain work.

What is the concept of congestive heart failure?

Heart failure is a disorder in which the heart’s ability to pump blood is impaired. Blood circulates more slowly, heart rate rises, and the heart is unable to pump adequate oxygen and nutrients across the body as a result. To compensate, the heart’s chambers can expand to accommodate more blood, or the chamber walls can thicken and stiffen. The kidneys eventually absorb more water and salt as a result of the reduced blood pumping activity, and fluid will build up in the bodies, thighs, knees, feet, and also around the lungs. Congestive heart disease is the term for this general clinical image.

Congestive heart disease may be caused by a variety of factors. Heart attacks, elevated blood pressure, valve dysfunction, and hereditary disorders such as cardiomyopathies are among the most common.

What role could stem cells play in heart repair?

To find a response to this query, scientists are learning more about how stem cells are directed to become advanced cells. The cardiomyocyte, a heart muscle cell that contracts to expel blood from the heart’s main pumping chamber, is one essential form of cell that can be formed (the ventricle). The vascular endothelial cell, which forms the inner lining of fresh blood vessels, and the smooth muscle cell, which forms the membrane of blood vessels, are two other cell types essential to a healthy heart. This advanced cells are vital for forming a new network of arteries to deliver nutrients and oxygen to the cardiomyocytes after a heart has been weakened because the heart has a high demand for blood flow. The capacity of both embryonic and adult stem cells to turn into these cell types in the injured heart is now being investigated as part of a campaign to help patients who have suffered heart problems or who have congestive heart failure regain heart function. It’s important not to mix up stem cell research with recent findings that human cardiac myocytes will divide after a myocardial infarction [1]. This research indicates that damaged heart cells may change their condition from dormant to active cell division. This is similar to the tendency of a variety of other cells in the body to differentiate after being injured. There is also no proof that the heart contains real stem cells that will proliferate and divide.

The cells that make up your core come in a variety of shapes and sizes. Researchers typically concentrate on three forms of cardiac cells when it comes to repairing injured heart tissue:

• Cardiomyocytes, which are the beating muscle cells that make up the atria, which are the chambers where blood reaches the nucleus, and the ventricles, which are where blood is pushed out. Cellular treatments for heart failure are currently focusing on cardiomyocytes.

• Pacemaker cells in your heart, which transmit and receive electrical signals to maintain your heart pumping in time.

• Endothelial cells, which line blood vessels and support cardiomyocytes get oxygen.