Can Diabetes Drug Aid Post-Heart Attack Patients?

A new study finds that metformin, a drug commonly used to treat diabetes, can be used to assist recovery from a heart attack.

A team including investigators from Newcastle University and Queen Elizabeth Hospital in the United Kingdom sought to explore the mechanism behind the drug, using stem cells from cord blood and cells from umbilical cords to construct a model that would simulate a heart attack. Metformin reverses the effects of a lack of oxygen in the presence of high glucose levels, a process that occurs during a diabetic individual’s heart attack, as the authors point out, noting that outcomes of heart disease interventions in patients with diabetes is typically worse when compared to non-diabetic individuals.
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Lead author Jolanta Weaver, MD, senior lecturer in diabetes medicine at Newcastle University, and colleagues determined that metformin affects several new genes that are instrumental in the growth of new blood vessels, and boosts the physiological process that enables new blood vessels to form. The formation of new blood vessels is critical for recovery after a heart attack, the authors note, adding that they believe this study is the first to describe the effect of the physiological concentration of metformin as seen in patients.

“The study showed that, in a test tube model of heart attack, we can define the mechanism behind the cardioprotective effect of metformin,” says Weaver. “This confirmed that metformin has cardioprotective effects in diabetes during hypoxia.”

As other studies have suggested, “metformin should be recommended to as many type 2 diabetes patients who can tolerate it,” says Weaver, “and in whom its use is safe.”

—Mark McGraw

Reference:

Bakhashab S, Ahmed F, et al. Metformin improves the angiogenic potential of human CD34 cells co-incident with downregulating CXCL 10 and TIMP1 gene expression and increasing VEGFA under hyperglycemia and hypoxia within a therapeutic window for myocardial infarction. Cardiovascular Diabetology. 2016.