Heart failure (HF), the final common stage of many diseases of the heart, continues to be a major health concern in the United States, affecting nearly 6 million people. Each year, about 550,000 individuals are diagnosed with HF. Although advances in managing HF continue to grow, about half of those diagnosed will die within five years.
Those who are 65 and older account for about 80 percent of the deaths in the U.S. and Europe. A number of risk factors, including ischemic heart disease, hypertension, smoking, obesity, and diabetes, predict both the incidence of HF as well as the severity.
The American Heart Association (AHA) recommends the importance of physical activity in maintaining a healthy heart, suggesting at least 30 minutes of moderate intensity aerobic activity at least five days each week for a total of 150 minutes or at least 25 minutes of vigorous aerobic activity at least three days per week for a total of 75 minutes. To lower blood pressure or cholesterol, the AHA recommends 40 minutes of aerobic exercise of moderate to vigorous intensity three to four times a week to lower the risk for heart attack and stroke.
We all want to be healthy and avoid HF, but exercising is often pushed to the side because of our busy schedules. Now, however, researchers have discovered that a protein, cardiotrophin 1 (CT1), may be able to trick the heart into growing and pumping more blood, exactly as it does in response to exercise.
Dr. Lynn Megeney, senior author of the study and a senior scientist at The Ottawa Hospital and professor at the University of Ottawa, and colleagues conducted a variety of studies in mice, rats and cells growing in the lab. CT1 was originally identified as a promising hypertrophic agonist in vitro, but its expression has been more recently linked to myocardial pathology, systemic elevated blood pressure, and cardiac failure in both animals and humans.
Despite observational data implicating CT1 in certain cardiovascular diseases, this cytokine is known to bind and engage gp130 receptor complexes, a known pro-survival signal for cardiomyocytes. The researchers hypothesized that elevated expression of CT1 in human cardiac pathologies may simply reflect a compensatory response, which attempts to curtail disease progression through the biologic remodeling activity of CT1. In addition to CT1, some of the studies involved phenylephrine (PE), known to cause the bad kind of heart growth.
In this study, the researchers observed that heart muscles treated with CT1 become longer, healthier fibers. Those treated with PE just grow wider. CT1 causes blood vessels to grow beside the new heart muscle tissue and increases the heart's ability to pump blood. When CT1 treatment stops, the heart reverts back to its original condition, similar to when exercise ends, while the dysfunctional heart growth caused by PE is irreversible.
CT1 improved heart function in two animal models of HF, one cause by a heart attack and one cause by pulmonary hypertension. Both CT1 and PE stimulate heart muscle growth via a molecular pathway that has been associated with promoting apoptosis, but CT1 has better ability to control this pathway.
Currently, transplant is the only treatment for right HF. Drugs for left HF only reduce the symptoms and over time, and left HF often leads to right HF. The researchers are hopeful that this experimental therapy shows promise in treating both left and right HF.
