NYITCOM Researchers Discover Potential New Treatment for Heart Attack Patients
April 17, 2018
Since the 1960s, beta blockers have been a staple prescription drug for recovering heart attack patients. However, these blood pressure-reducing medications cannot be tolerated by many high-risk patients, including those with chronic obstructive pulmonary disease (COPD) and asthma, the elderly, and diabetics. In the March 26 issue of Thyroid, a team of NYIT College of Osteopathic Medicine (NYITCOM) researchers led by Martin Gerdes, Ph.D., professor and chair of biomedical sciences, offers a new treatment for patients with beta blocker intolerance: thyroid hormone therapy.
During a heart attack, also known as myocardial infarction or MI, increased adrenaline raises pressure in the arteries and increases the heart rate to compensate for the sudden loss of contractile tissue. Unfortunately, this places stress on the surviving muscular tissue of the heart. This damage may cause the organ to be less effective in pumping blood to the rest of the body, a condition that can eventually lead to heart failure and death.
Beta-adrenergic blocking agents (beta blockers) work by blocking the neurotransmitters norepinephrine and epinephrine (adrenaline) from binding to receptors in the heart. Consequently, heart rate and blood pressure are lowered, allowing the heart to beat with less force and more easily deliver circulation to the body.
“While beta blockers have been viewed as the gold standard in MI treatment for years, a significant population at risk for heart failure is unable to tolerate these drugs,” explained Gerdes. “If given beta blockers, these patients’ conditions can, in fact, worsen—heart rate may fall too low and heart function could deteriorate.”
The NYITCOM researchers studied the thyroid hormone triiodothyronine (T3), which controls many aspects of cardiovascular function and is a powerful regulator of beta receptor function, to determine how it could provide an effective alternative treatment.
“Preclinical studies have shown thyroid hormone treatment to be a safe and effective method for managing cardiovascular disorders, and may offer a better option for these patients,” said Gerdes, whose team, including world-class cardiovascular experts from Beijing’s FuWai Heart Hospital, put their theory to the test. They compared the effectiveness of T3 and metoprolol, a commonly prescribed beta blocker, in female laboratory rats. Immediately following MI, the rats were provided either a low dose of T3 or the beta blocker in their drinking water for eight weeks. At the end of that period, the thyroid hormone proved to be as good, if not better, than metoprolol at improving heart function. In fact, T3 provided all the benefits of the beta blocker plus some unique to thyroid hormones, such as improved expression of genes related to better contraction and relaxation of the heart.
“Both treatments provide comparable results and similar long-term benefits, including improved function in the left ventricle, an area often damaged during heart attack, as well as reduced infarction size and improved vessel function,” said Gerdes, who has studied the cardiovascular benefits and effects of thyroid hormone treatment for more than a decade. “Overall, these results suggest that T3 is capable of providing a safe alternative for beta blocker-intolerant patients following MI.”