Contact:
Christine Guilfoy
Office: (301) 634-7253
Cell: (978) 290-2400
cguilfoy@the-aps.org
Acetaminophen Safe To Use
After Heart Attack
But animal study shows drug doesn’t
protect the heart
BETHESDA, MD. (May 16, 2006) – Acetaminophen is safe to
use as a pain reliever and fever reducer after a heart attack, but it does
not protect the heart muscle, a new study using sheep and rabbits concluded.
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:
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.
Editor’s note: The media may obtain a copy of
Leshnower et al. by contacting
Christine Guilfoy, American Physiological Society, (301) 634-7253, (978)
290-2400 (cell), or
cguilfoy@the-aps.org.
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