Acetaminophen Safe To Use After Heart Attack But Doesn't Protect The Heart

The study, using rabbits and sheep, could have implications for people who have suffered heart attacks, about a million people in the U.S. each year, said researcher Robert C. Gorman, a medical doctor and associate professor of surgery at the University of Pennsylvania. "It's a high volume problem," he said.

People who suffer heart attacks need to know which pain relievers are safe to use. Some studies have suggested there is an increased risk of stroke and heart attack among patients taking non-steroidal anti-inflammatory drugs (NSAIDs), Gorman said. And a recent clinical study from Denmark suggested that NSAIDS may increase mortality if taken after a heart attack. NSAIDs are a major class of pain reliever and fever reducer that includes ibuprofen.

Acetaminophen is a popular over-the-counter pain medication that is an alternative to NSAID and aspirin. It is the active ingredient in Tylenol. Some classify aspirin as an NSAIDs, although Gorman said it is more common to place aspirin in its own separate category.

The study "Role of acetaminophen in acute myocardial infarction," by Bradley G. Leshnower, Hiroaki Sakamoto, Ahmad Zeeshan, Landi M. Parish, Robin Hinmon, Theodore Plappert, Benjamin M. Jackson, Joseph H. Gorman III and Robert C. Gorman, University of Pennsylvania School of Medicine, Philadelphia, will appear in the June issue of the American Journal of Physiology-Heart and Circulatory Physiology published by The American Physiological Society.

Is it safe; does it protect?
The researchers wanted to find out if acetaminophen can be used after a heart attack. In particular, they wanted to know if it is safe to use after subjects have undergone reperfusion therapy, a procedure to restore blood flow to the heart.

Reperfusion therapy is used as soon as possible following a heart attack to get the blocked artery open and to save as many heart muscle cells as possible. Reperfusion therapy, which may use balloon angioplasty, surgery, or clot dissolving drugs, is used in about 40% of heart attack patients, and its use is becoming increasingly common, Gorman said.

If acetaminophen does no harm, it could be used to relieve pain or reduce fever by people who have had heart attacks. Gorman and his team also wanted to know if acetaminophen could be used in conjunction with reperfusion therapy to salvage heart muscle cells damaged by the heart attack or to improve the heart's ventricular function.

The research was done within the context of a recent study on humans that reported an increased risk of death among those who had suffered a heart attack and subsequently took NSAIDs. Other studies have suggested that using NSAIDs may increase the risk of stroke and heart attacks, Gorman said.

Safe, but not protective
The researchers assigned eight sheep and 11 rabbits to a group that received acetaminophen, and an equal number of sheep and rabbits to a control group that did not receive any drug. The researchers surgically induced the heart attack and then restored blood flow -- 30 minutes later for rabbits and 60 minutes later for sheep.

They found that acetaminophen had no effect on:

• amount of blood flow to the heart muscle
• how much heart muscle was saved
• blood pressure
• ventricular function
• heart rate

The results are at odds with a previous study using dogs, which concluded that acetaminophen reduced the area affected by a heart attack by 22%. Gorman said the difference may be due in part to the abundance of blood vessels dogs have compared to humans, rabbits and sheep.

Next step
The researchers will compare animals treated with NSAIDS and those treated with acetaminophen over a longer period of time after a heart attack to see if there is a difference in cardiac function, Gorman said.

Source and funding
"Role of acetaminophen in acute myocardial infarction," by Bradley G. Leshnower, Hiroaki Sakamoto, Ahmad Zeeshan, Landi M. Parish, Robin Hinmon, Benjamin M. Jackson, Joseph H. Gorman III and Robert C. Gorman, Harrison Department of Surgical Research, University of Pennsylvania School of Medicine, Philadelphia, and Theodore Plappert, Division of Cardiology, University of Pennsylvania School of Medicine, will appear in the June issue of the American Journal of Physiology-Heart and Circulatory Physiology published by the American Physiological Society. Leshnower and Sakamoto contributed equally to this study.

Research was supported by grants from the National Heart Lung Blood Institute, National Institutes of Health and from McNeil Consumer and Specialty Pharmaceuticals.