Metformin, the go-to drug for patients diagnosed with type 2 diabetes mellitus (T2DM), may help control glycated hemoglobin (A1C) levels, but it does not help prevent heart failure in heart attack patients who do not have the disease, according to a new study from the Netherlands.
Metformin, the go-to drug for patients diagnosed with type 2 diabetes mellitus (T2DM), may help control glycated hemoglobin (A1C) levels, but it does not help prevent heart failure in heart attack patients who do not have the disease, according to a new study from the Netherlands.1
The study, presented Monday at the late-breaking session of the 63rd Scientific Sessions of the American College of Cardiology (ACC), which concluded in Washington, DC, answered a question that some researchers have wondered about, given that some studies have suggested metformin’s protective effects go beyond its ability to lower glucose levels.
Although Monday’s session was jointly sponsored by the ACC and the New England Journal of Medicine, the metformin study was simultaneously published in the Journal of the American Medical Association.1
Lead author and presenter, Chris P.H. Lexis, MD, of the University Medical Center Groningen, Netherlands, said the study was designed to find out whether metformin would benefit patients who had suffered a heart attack, but who would not be candidates for metformin because they did not have diabetes. Animal studies had shown that after myocardial infarction (MI), metformin preserved the ability of the heart to pump blood through the body, which left researchers wondering if the same was true in humans. If so, metformin could be prescribed for heart attack patients to prevent heart failure after MI.
In the study, 380 patients who had suffered MI and had percutaneous coronary intervention (PCI) were randomized to receive either 500 mg of metformin twice daily or placebo, in addition to normal standard of care. Patients who were already diagnosed with T2DM or who were coronary bypass candidates were excluded. The median age of patients was 59 years.
The primary end point of the study was left ventricular ejection fraction, a measurement that describes the percentage of blood leaving the heart each time it contracts. This measure is key after MI, which often injures the muscle that pumps blood and can reduce the left ventricle’s ability to pump blood through the body. The measurement was taken by magnetic resonance imaging, 4 months after each patient’s MI. Results showed that the metformin group’s fraction was 53.1%, compared with 54.8% for the placebo group, which Dr Lexis said was not statistically significant.
Dr Lexis said that while the results will not change clinical practice for patients without diabetes, they do show that metformin is safe for patients who have suffered ST-elevated myocardial infarction, or STEMI. “It is noteworthy that metformin started early after heart attack did not adversely affect kidney function and was well-tolerated. So, our findings do not preclude the use of metformin to treat diabetes in this setting,” he said.2