Acid Reflux Drug May Cause Heart Disease Sat Jul 13, 2013
http://www.prnewswire.com/news-releases/acid-reflux-drug-may-cause-heart-disease-214931981.html
Acid Reflux Drug May Cause Heart Disease
HOUSTON, July 10, 2013 /PRNewswire-USNewswire/ -- Drugs that help
millions of people cope with acid reflux may also cause cardiovascular
disease, report scientists from Houston Methodist Hospital and two other
institutions in an upcoming issue of Circulation (now online). It is the
first time researchers have shown how proton pump inhibitors, or PPIs,
might cause cardiovascular problems. In human tissue and mouse models,
the researchers found PPIs caused the constriction of blood vessels. If
taken regularly, PPIs could lead to a variety of cardiovascular problems
over time, including hypertension and a weakened heart. In the paper,
the scientists call for a broad, large-scale study to determine whether
PPIs are dangerous.
"The surprising effect that PPIs may impair vascular health needs
further investigation," said John Cooke, M.D., Ph.D., the study's
principal investigator. "Our work is consistent with previous reports
that PPIs may increase the risk of a second heart attack in people that
have been hospitalized with an acute coronary syndrome. Patients taking
PPIs may wish to speak to their doctors about switching to another drug
to protect their stomachs, if they are at risk for a heart attack."
Commonly used proton pump inhibitors in the United States are
lansoprazole and omeprazole, and these drugs are purchasable over the
counter as brands or generics. The FDA estimates about 1 in 14 Americans
has used them. In 2009, PPIs were the third-most taken type of drug in
the U.S., accounting for $13 billion in sales. PPIs are used to treat a
wide range of disorders, including gastroesophageal reflux disease, or
GERD, infection by the ulcer-causing Helicobacter pylori,
Zollinger-Ellison syndrome, and Barrett's esophagus.
Recent studies of proton pump inhibitors use by people who've already
experienced severe cardiovascular events have raised concern about the
anti-reflux drugs, at least for this subgroup of patients, said Cooke,
chair of the Department of Cardiovascular Sciences and director of the
Center for Cardiovascular Regeneration at Houston Methodist DeBakey
Heart & Vascular Center.
PPIs are initially inert. After oral consumption, they are activated by
specialized cells in the stomach. Once active, the molecules suppress
the movement of protons into the intestine, which reduces the amount of
acid present there and in the stomach.
In mouse models and cultures of human endothelial cells, Cooke and lead
author Yohannes Ghebremariam, Ph.D., found that PPIs suppressed the
enzyme DDAH, dimethylarginine dimethylaminohydrolase. That caused an
increase in the blood levels of ADMA (asymmetric dimethylarginine), an
important chemical messenger. They found ADMA in turn suppressed the
production of another chemical messenger, nitric oxide, or NO, proven by
1998 Nobel Prize winners Furchgott, Ignarro, and Murad to impact
cardiovascular function. Quantitative studies in mouse models showed
animals fed PPIs were more likely than controls to have tense vascular
tissue.
"We found that PPIs interfere with the ability of blood vessels to
relax," said Ghebremariam, a Houston Methodist molecular biologist.
"PPIs have this adverse effect by reducing the ability of human blood
vessels to generate nitric oxide. Nitric oxide generated by the lining
of the vessel is known to relax, and to protect, arteries and veins."
The researchers found PPIs led to an approximately 25 percent increase
in ADMA in mouse and tissue cultures, and reduced the ability of mouse
blood vessels to relax by over 30 percent on average.
Also contributing to this report were Paea LePendu, Ph.D., Jerry Lee,
Daniel Erlanson, Ph.D., and Nigam H. Shah, Ph.D. (Stanford University)
and Anna Slaviero, Ph.D., and James Leiper, Ph.D. (Imperial College
London). Work was funded with grants from the National Institutes of
Health, the American Heart Association, the Stanford SPARK program, and
the Stanford Translational Research and Applied Medicine (TRAM) program.
Circulation is published by the American Heart Association.
The Methodist Hospital recently changed its name to Houston Methodist
Hospital.
To speak with Ghebremariam or Cooke, please contact David Bricker,
Houston Methodist, at 832-667-5811 or dmbricker@tmhs.org
<mailto:dmbricker@tmhs.org>.
Media Contact: David Bricker Houston Methodist 832-667-5811
dmbricker@tmhs.org <mailto:dmbricker@tmhs.org>
SOURCE Houston Methodist
RELATED LINKS
http://www.methodisthealth.com
http://www.prnewswire.com/news-releases/acid-reflux-drug-may-cause-heart-disease-214931981.html
Acid Reflux Drug May Cause Heart Disease
HOUSTON, July 10, 2013 /PRNewswire-USNewswire/ -- Drugs that help
millions of people cope with acid reflux may also cause cardiovascular
disease, report scientists from Houston Methodist Hospital and two other
institutions in an upcoming issue of Circulation (now online). It is the
first time researchers have shown how proton pump inhibitors, or PPIs,
might cause cardiovascular problems. In human tissue and mouse models,
the researchers found PPIs caused the constriction of blood vessels. If
taken regularly, PPIs could lead to a variety of cardiovascular problems
over time, including hypertension and a weakened heart. In the paper,
the scientists call for a broad, large-scale study to determine whether
PPIs are dangerous.
"The surprising effect that PPIs may impair vascular health needs
further investigation," said John Cooke, M.D., Ph.D., the study's
principal investigator. "Our work is consistent with previous reports
that PPIs may increase the risk of a second heart attack in people that
have been hospitalized with an acute coronary syndrome. Patients taking
PPIs may wish to speak to their doctors about switching to another drug
to protect their stomachs, if they are at risk for a heart attack."
Commonly used proton pump inhibitors in the United States are
lansoprazole and omeprazole, and these drugs are purchasable over the
counter as brands or generics. The FDA estimates about 1 in 14 Americans
has used them. In 2009, PPIs were the third-most taken type of drug in
the U.S., accounting for $13 billion in sales. PPIs are used to treat a
wide range of disorders, including gastroesophageal reflux disease, or
GERD, infection by the ulcer-causing Helicobacter pylori,
Zollinger-Ellison syndrome, and Barrett's esophagus.
Recent studies of proton pump inhibitors use by people who've already
experienced severe cardiovascular events have raised concern about the
anti-reflux drugs, at least for this subgroup of patients, said Cooke,
chair of the Department of Cardiovascular Sciences and director of the
Center for Cardiovascular Regeneration at Houston Methodist DeBakey
Heart & Vascular Center.
PPIs are initially inert. After oral consumption, they are activated by
specialized cells in the stomach. Once active, the molecules suppress
the movement of protons into the intestine, which reduces the amount of
acid present there and in the stomach.
In mouse models and cultures of human endothelial cells, Cooke and lead
author Yohannes Ghebremariam, Ph.D., found that PPIs suppressed the
enzyme DDAH, dimethylarginine dimethylaminohydrolase. That caused an
increase in the blood levels of ADMA (asymmetric dimethylarginine), an
important chemical messenger. They found ADMA in turn suppressed the
production of another chemical messenger, nitric oxide, or NO, proven by
1998 Nobel Prize winners Furchgott, Ignarro, and Murad to impact
cardiovascular function. Quantitative studies in mouse models showed
animals fed PPIs were more likely than controls to have tense vascular
tissue.
"We found that PPIs interfere with the ability of blood vessels to
relax," said Ghebremariam, a Houston Methodist molecular biologist.
"PPIs have this adverse effect by reducing the ability of human blood
vessels to generate nitric oxide. Nitric oxide generated by the lining
of the vessel is known to relax, and to protect, arteries and veins."
The researchers found PPIs led to an approximately 25 percent increase
in ADMA in mouse and tissue cultures, and reduced the ability of mouse
blood vessels to relax by over 30 percent on average.
Also contributing to this report were Paea LePendu, Ph.D., Jerry Lee,
Daniel Erlanson, Ph.D., and Nigam H. Shah, Ph.D. (Stanford University)
and Anna Slaviero, Ph.D., and James Leiper, Ph.D. (Imperial College
London). Work was funded with grants from the National Institutes of
Health, the American Heart Association, the Stanford SPARK program, and
the Stanford Translational Research and Applied Medicine (TRAM) program.
Circulation is published by the American Heart Association.
The Methodist Hospital recently changed its name to Houston Methodist
Hospital.
To speak with Ghebremariam or Cooke, please contact David Bricker,
Houston Methodist, at 832-667-5811 or dmbricker@tmhs.org
<mailto:dmbricker@tmhs.org>.
Media Contact: David Bricker Houston Methodist 832-667-5811
dmbricker@tmhs.org <mailto:dmbricker@tmhs.org>
SOURCE Houston Methodist
RELATED LINKS
http://www.methodisthealth.com
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