A novel signaling pathway plays a significant role in the production of aldosterone, a hormone that promotes heart failure after a myocardial infarction, according to a study conducted by Thomas Jefferson University researchers.
The findings, which will be published online this week in Proceedings of the National Academy of Sciences, show that aldosterone production is mediated by a protein called beta-arrestin-1. Beta-arrestin-1 binds to angiotensin II receptors when they are activated by angiotensin II.
Aldosterone is secreted by the adrenal cortex. Its levels are elevated in chronic heart failure, and its presence contributes to morbidity and mortality of the disease. It contributes to heart failure progression and diminished cardiac function after myocardial infarction.
The production of aldosterone was previously thought to be solely the result of the activation of G-proteins, which are also activated when angiotensin II binds to its receptors, according to Anastasios Lymperopoulos, Ph.D., a Post-Doctoral Research Fellow in the Center for Translational Medicine and the George Zallie and Family Laboratory for Cardiovascular Gene Therapy at Jefferson Medical College of Thomas Jefferson University.
"The bottom line is that in order to effectively suppress aldosterone production, you need to inhibit beta-arrestin-1 in addition to inhibiting G-proteins," said Dr. Lymperopoulos, who is the lead author of the study.
All the drugs currently available for suppression of aldosterone by angiotensin II primarily target G-protein signaling pathways. However, Walter Koch, Ph.D., the W.W. Smith Professor of Medicine and the Director of the Center for Translational Medicine and the George Zallie and Family Laboratory for Cardiovascular Gene Therapy, said that these data clearly show that beta-arrestin1 plays a more significant role in aldosterone secretion than G-proteins.
"Aldosterone secretion is dependent on beta-arrestin-1," Dr. Koch said. "It may not be independent of G-proteins, but beta-arrestin-1 is definitely the critical player. The goal should be to find a new antagonist that can block beta-arrestin-1 and G-protein activation equally well. Doing so would lead to lower aldosterone levels at its source and alleviate negative remodeling processes in the injured heart."
Thomas Jefferson University
211 S 9th St., Ste. 310
Philadelphia
PA 19107-5506
United States
tju
четверг, 5 мая 2011 г.
вторник, 3 мая 2011 г.
Diabetes Patients At Higher Risk Of Developing Atrial Fibrillation - Risk Increases With Diabetes Duration
Patients with diabetes have a 40% higher risk of developing atrial fibrillation, compared to people who do not have diabetes, according to a study published in the Journal of General Internal Medicine. The study was carried out by Dr. Sarcha Dublin and team of Group Health Research Institute. The scientists also found that atrial fibrillation risk is greater the longer people have diabetes, and the less controlled their blood sugar is.
As the American population continues ageing and gaining weight, diabetes is becoming more prevalent.
For three years, Dr. Dublin and her colleagues tracked more than 1,400 Group Health patients who had newly recognized atrial fibrillation. They compared these cases with more than 2,200 controls. The controls were matched to the cases by age, sex, year, and whether they were treated for high blood pressure; but unlike the cases, they had no atrial fibrillation.
This was the first study to examine the relationship between atrial fibrillation and the duration of patients' diabetes and their blood sugar levels. Unlike most previous studies, this one also adjusted for patients' weight, which is important because both diabetes and atrial fibrillation are more common in heavier people. The study found that:
Patients with diabetes were 40% more likely to be diagnosed with atrial fibrillation than other people.
The risk of atrial fibrillation rose by 3% for each additional year that patients had diabetes.
For patients with high blood sugar (glycosylated hemoglobin, also known as HBA1c more than 9 percent), the risk of atrial fibrillation was twice that for people without diabetes.
But patients with well-controlled diabetes (HBA1c 7 percent or less) were about equally likely to have atrial fibrillation as people without diabetes.
Dr. Dublin said "When a patient with diabetes has symptoms like heart palpitations, clinicians should have a higher level of suspicion that the reason could be atrial fibrillation. This heart rhythm disturbance is important to diagnose, because it can be treated with medications like warfarin that can prevent many of the strokes that the atrial fibrillation would otherwise cause."
It is hard to establish which comes first - diabetes or atrial fibrillation - with this kind of case-control study, unlike a randomized trial, Dr. Dublin said. "But our finding that the risk of atrial fibrillation is higher with longer time since patients started medications for diabetes, and with higher blood glucose levels, is strongly suggestive that diabetes can cause atrial fibrillation." She used time since starting diabetes medication as a measure of how long patients had the disease.
The study was funded through a Veterans' Affairs Health Services Research & Development fellowship and a Paul Beeson Career Development Award from the National Institute on Aging. The Beeson Award is also supported in part by the American Federation for Aging Research, the Hartford Foundation, the Atlantic Philanthropies and the Starr Foundation. The National Heart, Lung, and Blood Institute funds the Heart and Vascular Health Study, which collects data on Group Health patients newly diagnosed with atrial fibrillation and other cardiovascular conditions. The study of atrial fibrillation, led by Dr. Dublin's co-author Dr. Susan Heckbert, aims to find new factors that raise the risk of developing this quivering of the heart's upper chambers (atria).
About 1 in 100 people - and nearly 9 in 100 people over age 80 - have atrial fibrillation, according to Dr. Heckbert, a professor of epidemiology and scientific investigator in the Cardiovascular Health Research Unit at the University of Washington (UW) and an affiliate investigator at Group Health Research Institute. In many cases, atrial fibrillation has no symptoms, and it is not necessarily life threatening. But it can cause palpitations, fainting, fatigue, or congestive heart failure. Atrial fibrillation can also make blood pool - and sometimes clot - in the atria. When parts of clots break off and leave the atria, they can lead to embolic strokes, as happens in more than 70,000 Americans a year.
Other co-authors were Group Health Research Institute Senior Investigator Bruce M. Psaty, MD, PhD, who co-directs the UW's Cardiovascular Health Research Unit; and Nicole L. Glazer, PhD, Thomas Lumley, PhD, Kerri L. Wiggins, MS, RD, of the UW; Nicholas L. Smith, PhD, of the UW and Veterans Affairs Puget Sound Health Care System; and Richard L. Page, MD, of the University of Wisconsin School of Medicine and Public Health in Madison.
"Diabetes Mellitus, Glycemic Control, and Risk of Atrial Fibrillation"
Sascha Dublin, Nicole L. Glazer, Nicholas L. Smith, Bruce M. Psaty, Thomas Lumley, Kerri L. Wiggins, Richard L. Page and Susan R. Heckbert
Journal of General Internal Medicine
DOI: 10.1007/s11606-010-1340-y
View abstract online
View drug information on Warfarin Sodium tablets.
As the American population continues ageing and gaining weight, diabetes is becoming more prevalent.
For three years, Dr. Dublin and her colleagues tracked more than 1,400 Group Health patients who had newly recognized atrial fibrillation. They compared these cases with more than 2,200 controls. The controls were matched to the cases by age, sex, year, and whether they were treated for high blood pressure; but unlike the cases, they had no atrial fibrillation.
This was the first study to examine the relationship between atrial fibrillation and the duration of patients' diabetes and their blood sugar levels. Unlike most previous studies, this one also adjusted for patients' weight, which is important because both diabetes and atrial fibrillation are more common in heavier people. The study found that:
Patients with diabetes were 40% more likely to be diagnosed with atrial fibrillation than other people.
The risk of atrial fibrillation rose by 3% for each additional year that patients had diabetes.
For patients with high blood sugar (glycosylated hemoglobin, also known as HBA1c more than 9 percent), the risk of atrial fibrillation was twice that for people without diabetes.
But patients with well-controlled diabetes (HBA1c 7 percent or less) were about equally likely to have atrial fibrillation as people without diabetes.
Dr. Dublin said "When a patient with diabetes has symptoms like heart palpitations, clinicians should have a higher level of suspicion that the reason could be atrial fibrillation. This heart rhythm disturbance is important to diagnose, because it can be treated with medications like warfarin that can prevent many of the strokes that the atrial fibrillation would otherwise cause."
It is hard to establish which comes first - diabetes or atrial fibrillation - with this kind of case-control study, unlike a randomized trial, Dr. Dublin said. "But our finding that the risk of atrial fibrillation is higher with longer time since patients started medications for diabetes, and with higher blood glucose levels, is strongly suggestive that diabetes can cause atrial fibrillation." She used time since starting diabetes medication as a measure of how long patients had the disease.
The study was funded through a Veterans' Affairs Health Services Research & Development fellowship and a Paul Beeson Career Development Award from the National Institute on Aging. The Beeson Award is also supported in part by the American Federation for Aging Research, the Hartford Foundation, the Atlantic Philanthropies and the Starr Foundation. The National Heart, Lung, and Blood Institute funds the Heart and Vascular Health Study, which collects data on Group Health patients newly diagnosed with atrial fibrillation and other cardiovascular conditions. The study of atrial fibrillation, led by Dr. Dublin's co-author Dr. Susan Heckbert, aims to find new factors that raise the risk of developing this quivering of the heart's upper chambers (atria).
About 1 in 100 people - and nearly 9 in 100 people over age 80 - have atrial fibrillation, according to Dr. Heckbert, a professor of epidemiology and scientific investigator in the Cardiovascular Health Research Unit at the University of Washington (UW) and an affiliate investigator at Group Health Research Institute. In many cases, atrial fibrillation has no symptoms, and it is not necessarily life threatening. But it can cause palpitations, fainting, fatigue, or congestive heart failure. Atrial fibrillation can also make blood pool - and sometimes clot - in the atria. When parts of clots break off and leave the atria, they can lead to embolic strokes, as happens in more than 70,000 Americans a year.
Other co-authors were Group Health Research Institute Senior Investigator Bruce M. Psaty, MD, PhD, who co-directs the UW's Cardiovascular Health Research Unit; and Nicole L. Glazer, PhD, Thomas Lumley, PhD, Kerri L. Wiggins, MS, RD, of the UW; Nicholas L. Smith, PhD, of the UW and Veterans Affairs Puget Sound Health Care System; and Richard L. Page, MD, of the University of Wisconsin School of Medicine and Public Health in Madison.
"Diabetes Mellitus, Glycemic Control, and Risk of Atrial Fibrillation"
Sascha Dublin, Nicole L. Glazer, Nicholas L. Smith, Bruce M. Psaty, Thomas Lumley, Kerri L. Wiggins, Richard L. Page and Susan R. Heckbert
Journal of General Internal Medicine
DOI: 10.1007/s11606-010-1340-y
View abstract online
View drug information on Warfarin Sodium tablets.
Successful Treatment For Acute Heart Failure Remains Elusive
In recent years, cardiologists have begun to view acute heart failure syndrome (AHFS) as a distinct condition, not merely a part of the chronic heart failure continuum. However, there is not yet a consensus on a definition, epidemiology, appropriate therapy and directions for future research for acute heart failure syndrome, says a Special Report published in today's Circulation journal. The report is the result of the First and Second International Workshops on Acute Heart Failure Syndrome that took place in May 2004 and April 2005.
"Although we've accomplished much in the management of chronic heart failure, the absence of evidence-based clinical practice guidelines for acute heart failure syndrome is striking," says the report's lead author, Mihai Gheorghiade, MD, associate chief, Division of Cardiology at the Bluhm Cardiovascular Institute of Northwestern Memorial Hospital. "I liken the current state of our understanding of acute heart failure to cardiologists understanding of heart attacks before 1980," says Dr. Gheorghiade. "Until then, we thought the clot was the result of the heart attack, not the cause, and so the clot was not being treated. In 2005, we're just at the point of looking for the 'clot' in acute heart failure - what causes it and how can we best treat it?"
Heart failure is the inability of the heart to supply adequate blood flow and therefore oxygen to peripheral tissues and organs and leads to over one million hospitalizations each year in the United States. "We've been successful in finding ways to treat chronic heart failure," says Dr. Gheorghiade. "And, on the surface it looks like we're successful at treating ACHF. Patients are treated, feel better and are discharged. The problem is that within 90 days of discharge, nearly 10 percent of patients die and about 30 percent are readmitted."
Traditionally, cardiologists have treated chronic heart failure and acute heart failure in the same fashion, says Dr. Gheorghiade. "Acute heart failure does not equal chronic heart failure. What's good for one may not be good for the other. For the last two years, every clinical trial with acute heart failure patients has been unsuccessful in improving mortality," says Dr. Gheorghiade.
The report calls for a systematic research efforts on the clinical application and translation of promising basic science results and a focus on the choice of appropriate management strategies, including minimizing the use of drugs with adverse effects and development and validation of known prognostic markers to guide AHFS interventions.
The report also states that a significant number of AHFS patients are not being evaluated for potential beneficial surgical procedures that include myocardial revascularization, LV reconstruction, mitral valve surgery, or cardiac transplantation.
The workshops were attended by a selected group of physician scientists, epidemiologists, clinicians, regulatory and government funding agencies, and industry representatives from North and South America and Europe.
About Northwestern Memorial Hospital Northwestern Memorial Hospital is one of the country's premier academic medical centers and is the primary teaching hospital of Northwestern University's Feinberg School of Medicine. Northwestern Memorial and its Prentice Women's Hospital and Stone Institute of Psychiatry have 744 beds and more than 1,200 affiliated physicians and 5,000 employees. Providing state-of-the-art care, Northwestern Memorial is recognized for its outstanding clinical and surgical advancements in such areas as cardiothoracic and vascular care, gastroenterology, neurology and neurosurgery, oncology, organ and bone marrow transplantation, and women's health.
Northwestern Memorial received the prestigious 2005 National Quality Health Care Award and is listed in eight specialties in this year's US News & World Report's issue of "America's Best Hospitals." The hospital is also cited as one of the "100 Best Companies for Working Mothers" by Working Mother magazine for the past 5 years and has been chosen by Chicagoans for a decade as their "most preferred hospital" in National Research Corporation's annual survey.
Amanda Widtfeldt
awidtfelnmh
Northwestern Memorial Hospital
nmh
"Although we've accomplished much in the management of chronic heart failure, the absence of evidence-based clinical practice guidelines for acute heart failure syndrome is striking," says the report's lead author, Mihai Gheorghiade, MD, associate chief, Division of Cardiology at the Bluhm Cardiovascular Institute of Northwestern Memorial Hospital. "I liken the current state of our understanding of acute heart failure to cardiologists understanding of heart attacks before 1980," says Dr. Gheorghiade. "Until then, we thought the clot was the result of the heart attack, not the cause, and so the clot was not being treated. In 2005, we're just at the point of looking for the 'clot' in acute heart failure - what causes it and how can we best treat it?"
Heart failure is the inability of the heart to supply adequate blood flow and therefore oxygen to peripheral tissues and organs and leads to over one million hospitalizations each year in the United States. "We've been successful in finding ways to treat chronic heart failure," says Dr. Gheorghiade. "And, on the surface it looks like we're successful at treating ACHF. Patients are treated, feel better and are discharged. The problem is that within 90 days of discharge, nearly 10 percent of patients die and about 30 percent are readmitted."
Traditionally, cardiologists have treated chronic heart failure and acute heart failure in the same fashion, says Dr. Gheorghiade. "Acute heart failure does not equal chronic heart failure. What's good for one may not be good for the other. For the last two years, every clinical trial with acute heart failure patients has been unsuccessful in improving mortality," says Dr. Gheorghiade.
The report calls for a systematic research efforts on the clinical application and translation of promising basic science results and a focus on the choice of appropriate management strategies, including minimizing the use of drugs with adverse effects and development and validation of known prognostic markers to guide AHFS interventions.
The report also states that a significant number of AHFS patients are not being evaluated for potential beneficial surgical procedures that include myocardial revascularization, LV reconstruction, mitral valve surgery, or cardiac transplantation.
The workshops were attended by a selected group of physician scientists, epidemiologists, clinicians, regulatory and government funding agencies, and industry representatives from North and South America and Europe.
About Northwestern Memorial Hospital Northwestern Memorial Hospital is one of the country's premier academic medical centers and is the primary teaching hospital of Northwestern University's Feinberg School of Medicine. Northwestern Memorial and its Prentice Women's Hospital and Stone Institute of Psychiatry have 744 beds and more than 1,200 affiliated physicians and 5,000 employees. Providing state-of-the-art care, Northwestern Memorial is recognized for its outstanding clinical and surgical advancements in such areas as cardiothoracic and vascular care, gastroenterology, neurology and neurosurgery, oncology, organ and bone marrow transplantation, and women's health.
Northwestern Memorial received the prestigious 2005 National Quality Health Care Award and is listed in eight specialties in this year's US News & World Report's issue of "America's Best Hospitals." The hospital is also cited as one of the "100 Best Companies for Working Mothers" by Working Mother magazine for the past 5 years and has been chosen by Chicagoans for a decade as their "most preferred hospital" in National Research Corporation's annual survey.
Amanda Widtfeldt
awidtfelnmh
Northwestern Memorial Hospital
nmh
Community Pharmacy Can Deliver Vascular Risk Assessment
Commenting on the Department of Health's announcement on the new national
vascular risk screening programme, Sue Sharpe, CEO, PSNC said:
"We are very pleased that the government is committed to developing
community pharmacy's role in tackling vascular disease.
Pharmacies can play an important role in reducing the impact of vascular
disease, by looking at risk factors, and advising on the measures that can be
taken to reduce the risk of development of the condition.
We can use the network of pharmacies and their easy accessibility to provide
this support to people in locations and at times that are convenient to them."
PSNC identified vascular risk screening as a target service for community
pharmacy provision two years ago and has been lobbying the Department of
Health and other key influencers to ensure inclusion of pharmacy within
government plans. A draft Enhanced service specification has been developed
and was submitted to the Department of Health for consideration last year.
Notes
1. The Pharmaceutical Services Negotiating Committee (PSNC) is the body that
represents community pharmacy on NHS matters and seeks to secure the
best possible NHS services provided by pharmacy contractors in England and
Wales.
Pharmaceutical Services Negotiating Committee
vascular risk screening programme, Sue Sharpe, CEO, PSNC said:
"We are very pleased that the government is committed to developing
community pharmacy's role in tackling vascular disease.
Pharmacies can play an important role in reducing the impact of vascular
disease, by looking at risk factors, and advising on the measures that can be
taken to reduce the risk of development of the condition.
We can use the network of pharmacies and their easy accessibility to provide
this support to people in locations and at times that are convenient to them."
PSNC identified vascular risk screening as a target service for community
pharmacy provision two years ago and has been lobbying the Department of
Health and other key influencers to ensure inclusion of pharmacy within
government plans. A draft Enhanced service specification has been developed
and was submitted to the Department of Health for consideration last year.
Notes
1. The Pharmaceutical Services Negotiating Committee (PSNC) is the body that
represents community pharmacy on NHS matters and seeks to secure the
best possible NHS services provided by pharmacy contractors in England and
Wales.
Pharmaceutical Services Negotiating Committee
UNC Scientists Discover Gatekeeper Protein In Blood Clotting
New research from the University of North Carolina at Chapel Hill School of Medicine has identified a protein that may control blood clotting by keeping blood platelets from sticking together.
Uncontrolled interactions between blood platelets such as those that occur during heart attacks and strokes contribute to these leading causes of death nationwide.
The study, which appears in the Jan. 17 edition of the Journal of Cell Biology, indicates that CIB1 binds to and keeps the platelet adhesion receptor GPIIb/IIIa in an inactive state, thus blocking platelet-to-platelet interactions in the blood.
Dr. Weiping Yuan, an assistant professor in UNC's department of pharmacology and the study's lead author, said CIB1's role was as a "gatekeeper" of GPIIb/IIIa activation. "Originally, I was a little surprised. We expected CIB1 itself to activate GPIIb/IIIa, but that is clearly not the case. CIB1 keeps GPIIb/IIIa turned off until it should be activated."
The UNC laboratory of Dr. Leslie V. Parise, professor of pharmacology and the new study's senior author, discovered the protein CIB1 in 1997. It was found inside platelets as a protein that binds to GPIIb/IIIa.
Under normal conditions, GPIIb/IIIa, found on the surface of platelets, remains in a resting, inactive state that allows normal blood flow. However, during clotting, GPIIb/IIIa becomes active, binds platelets to one another and attaches them to the blood vessel wall, thus forming a clot.
GPIIb/IIIa also is the target of several anti-coagulation drug therapies used in the clinic today, but the study suggests that knowledge of how CIB1 functions may lead to new therapeutic approaches.
The report, which used platelet precursor cells, demonstrated that decreasing the amount of CIB1 in these cells makes GPIIb/IIIa more responsive, thus more likely to mediate blood clotting. Increasing the amount of CIB1 prevented GPIIb/IIIa activation.
"Our data suggest that CIB1 may be one of the body's own natural anti-coagulants - as long as CIB1 is bound to GPIIb/IIIa, the platelet stays quiet. However, if a person doesn't have enough CIB1 or their CIB1 isn't functional, then their platelets may have the potential to be hyper-responsive and pathologically predisposed to clotting," Parise said. Additionally, the authors propose that CIB1 maintains the adhesion receptor in its inactive state by preventing the binding of another protein called talin to GPIIb/IIIa, which has been shown in other studies to be an adhesion receptor activator.
"CIB1 and talin compete for binding to the adhesion receptor; therefore, we think that as long as CIB1 is bound to the adhesion receptor, this prevents talin from binding and activating the receptor," said Dr. Tina Leisner, assistant professor of pharmacology and one of the study's primary authors.
The group now plans further study of the molecular mechanisms of the CIB1/GPIIb/IIIa interaction, which could lead to the development of new therapies in the prevention of platelet activation.
Along with Parise, Yuan and Leisner, co-authors on the study include Parise lab members Andrew W. McFadden, Dr. Zhengyan Wang, Shantres Clark, Dr. Christel Boudignon-Proudhon and Dr. Mark K. Larson. Stephen C.-T. Lam of the University of Illinois at Chicago's department of pharmacology also co-authored the study.
This work was supported by grants from the National Institutes of Health.
L.H. Lang
University of North Carolina School of Medicine
Uncontrolled interactions between blood platelets such as those that occur during heart attacks and strokes contribute to these leading causes of death nationwide.
The study, which appears in the Jan. 17 edition of the Journal of Cell Biology, indicates that CIB1 binds to and keeps the platelet adhesion receptor GPIIb/IIIa in an inactive state, thus blocking platelet-to-platelet interactions in the blood.
Dr. Weiping Yuan, an assistant professor in UNC's department of pharmacology and the study's lead author, said CIB1's role was as a "gatekeeper" of GPIIb/IIIa activation. "Originally, I was a little surprised. We expected CIB1 itself to activate GPIIb/IIIa, but that is clearly not the case. CIB1 keeps GPIIb/IIIa turned off until it should be activated."
The UNC laboratory of Dr. Leslie V. Parise, professor of pharmacology and the new study's senior author, discovered the protein CIB1 in 1997. It was found inside platelets as a protein that binds to GPIIb/IIIa.
Under normal conditions, GPIIb/IIIa, found on the surface of platelets, remains in a resting, inactive state that allows normal blood flow. However, during clotting, GPIIb/IIIa becomes active, binds platelets to one another and attaches them to the blood vessel wall, thus forming a clot.
GPIIb/IIIa also is the target of several anti-coagulation drug therapies used in the clinic today, but the study suggests that knowledge of how CIB1 functions may lead to new therapeutic approaches.
The report, which used platelet precursor cells, demonstrated that decreasing the amount of CIB1 in these cells makes GPIIb/IIIa more responsive, thus more likely to mediate blood clotting. Increasing the amount of CIB1 prevented GPIIb/IIIa activation.
"Our data suggest that CIB1 may be one of the body's own natural anti-coagulants - as long as CIB1 is bound to GPIIb/IIIa, the platelet stays quiet. However, if a person doesn't have enough CIB1 or their CIB1 isn't functional, then their platelets may have the potential to be hyper-responsive and pathologically predisposed to clotting," Parise said. Additionally, the authors propose that CIB1 maintains the adhesion receptor in its inactive state by preventing the binding of another protein called talin to GPIIb/IIIa, which has been shown in other studies to be an adhesion receptor activator.
"CIB1 and talin compete for binding to the adhesion receptor; therefore, we think that as long as CIB1 is bound to the adhesion receptor, this prevents talin from binding and activating the receptor," said Dr. Tina Leisner, assistant professor of pharmacology and one of the study's primary authors.
The group now plans further study of the molecular mechanisms of the CIB1/GPIIb/IIIa interaction, which could lead to the development of new therapies in the prevention of platelet activation.
Along with Parise, Yuan and Leisner, co-authors on the study include Parise lab members Andrew W. McFadden, Dr. Zhengyan Wang, Shantres Clark, Dr. Christel Boudignon-Proudhon and Dr. Mark K. Larson. Stephen C.-T. Lam of the University of Illinois at Chicago's department of pharmacology also co-authored the study.
This work was supported by grants from the National Institutes of Health.
L.H. Lang
University of North Carolina School of Medicine
Most Cardiologists Ignore Nutraceutical And OTC Drug Use Among Heart Patients
Half of all patients worldwide, and especially those with chronic illnesses such as cardiovascular disease, use nutraceuticals and over-the-counter (OTC) drugs. However, these patients often do not discuss the use of these agents with their clinicians.
Researchers evaluated cardiologits' attitudes towards and accuracy in identifying their patients' nutraceutical and OTC drug use. A clinical pharmacist observed patient interactions and recorded how the provider inquired about nutraceutical and OTC drug use. When the clinician left the room, the observer asked the patient about nutriceutical and OTC drug use. While the pharmacists identified 54 patients who together were using 86 nutraceuticals and 45 OTC drugs, the providers only identified nutraceutical and OTC use during seven encounters.
According to the researchers, "providers neglect evaluation of these agents because they consider them innocuous; lump them with dietary measures and lifestyle interventions; or consider them to be 'natural' and, therefore, safe and effective."
The researchers conclude that clinicians should use a structured approach for identifying patient use of nutraceuticals and OTC drugs.
News from the Annals of Internal Medicine: July 6, 2010
Researchers evaluated cardiologits' attitudes towards and accuracy in identifying their patients' nutraceutical and OTC drug use. A clinical pharmacist observed patient interactions and recorded how the provider inquired about nutraceutical and OTC drug use. When the clinician left the room, the observer asked the patient about nutriceutical and OTC drug use. While the pharmacists identified 54 patients who together were using 86 nutraceuticals and 45 OTC drugs, the providers only identified nutraceutical and OTC use during seven encounters.
According to the researchers, "providers neglect evaluation of these agents because they consider them innocuous; lump them with dietary measures and lifestyle interventions; or consider them to be 'natural' and, therefore, safe and effective."
The researchers conclude that clinicians should use a structured approach for identifying patient use of nutraceuticals and OTC drugs.
News from the Annals of Internal Medicine: July 6, 2010
Largest Study To Date Finds Drug Eluting Stents And Bare Metal Stents Yield Similarly Low Mortality Rates
A network meta analysis of 38 randomized controlled trials encompassing more than 18,000 patients found that the mortality risks associated with drug eluting stents and bare metal stents are similarly low. This analysis, the largest of its kind to date comparing drug eluting stents (the CYPHER® Sirolimus eluting Coronary Stent and the Taxus Stent) to bare metal stents, appears this week in the medical journal The Lancet.
The analysis also found a substantial reduction in the risk of myocardial infarction (heart attack) and reintervention with the CYPHER® Stent when compared to bare metal stents and the Taxus Stent, and no significant differences in the rates of stent thrombosis (blood clots) between the CYPHER® Stent and bare metal stents. The data from this analysis also identified a significant decrease in the risk of blood clots occurring more than 30 days after stent implantation with the CYPHER® Stent compared to the Taxus Stent.
"This large set of data indicates that the mortality associated with drug eluting stents and bare metal stents is comparable. Recent concerns about increases in mortality associated with drug eluting stents are not supported by thisanalysis assessing long-term outcomes," stated Dr. Christoph Stettler, M.D., from the University of Bern, Switzerland, one of the authors of the study. Dr. Stettler is with the Department of Endocrinology, Diabetes and Clinical Nutrition there.
In addition, the corresponding author, Dr. Peter Juni, M.D., stated that, "These results have also led us to conclude that the CYPHER® Stent is clinically superior to bare metal stents and the Taxus Stent when the safety and effectiveness outcomes in this analysis are taken into account." Dr. Juni is Head of Division, Clinical Epidemiology and Biostatistics, University of Bern in Switzerland.
Funded by the Swiss National Science Foundation, this network meta-analysis was designed to compare the safety and effectiveness of bare metal stents, the CYPHER® Stent and the Taxus Stent in a large patient population to increase the ability to detect and understand low frequency events, such as death and stent thrombosis. It included data up to four years of follow-up. The safety outcomes comprised mortality (death), myocardial infarction and Academic Research Consortium (ARC) definite stent thrombosis. The effectiveness outcome was target lesion revascularization (or the need for a repeat intervention).
The mortality rates were similar for all three stents: hazard ratios (HR) were 1.00 (95 percent credibility interval 0.82 to 1.25) for the CYPHER® Stent versus bare-metal stents, 1.03 (CI 0.84 to 1.22) for the Taxus Stent versus bare-metal stents and 0.96 (CI 0.83 to 1.24) for the CYPHER® Stent vs. the Taxus Stent.
The CYPHER® Stent was associated with the lowest risk of myocardial infarction. The corresponding hazard ratios were 0.81 versus bare-metal stents (CI 0.66 to 0.97, p=0.030) and 0.83 versus the Taxus Stent (CI 0.71-1.00, p=0.045).
The ARC definite stent thrombosis rates between the CYPHER® Stent and bare metal stents were not significantly different over the entire follow-up. However, the risk of late stent thrombosis (occurring more than 30 days after the procedure) was more than twice as likely with the Taxus Stent compared to bare-metal stents (HR 2.11, CI 1.19-4.23, p=0.017). In addition, the study found that a late stent thrombosis event was 46 percent less likely to occur in a patient implanted with the CYPHER® Stent than in a patient who received the Taxus Stent (HR 0.54, CI 0.26-0.98, p=0.041).
While both drug-eluting stents were associated with significantly lower risks of target lesion revascularization compared to bare-metal stents, the CYPHER® Stent reduced the risk substantially further compared to the Taxus Stent. The CYPHER® Stent reduced the risk by 70 percent (HR 0.30, CI 0.24 to 0.37, p=0.0001) and the Taxus Stent by 58 percent (HR 0.42, CI 0.33 to 0.53, p=0.0001) compared to bare-metal stents. When the target lesion revascularization rate for the CYPHER® Stent was compared directly to the rate for the Taxus Stent, a patient implanted with the CYPHER® Stent was found to be 30 percent less likely to need another procedure than a patient treated with the Taxus Stent (HR 0.70, CI 0.56 to 0.84, p=0.0021).This difference is consistent with other meta-analyses of randomized controlled trials directly comparing the two stents.
"This network meta analysis constitutes the largest and most robust set of data published to date in an eminent international peer-reviewed journal assessing the long-term safety and efficacy outcomes of drug-eluting stents," said David E. Kandzari, M.D., F.A.C.C., F.S.C.A.I., Chief Medical Officer, Cordis Corporation. "It significantly enriches the large body of evidence that interventional cardiologists have at their disposal to make the right choice for their patients. These data clearly demonstrate the benefits of drug-eluting stents versus bare metal stents and further provide clarity as to the differences between the CYPHER® Stent and the Taxus Stent."
About the CYPHER® Stent
The CYPHER® Stent has been chosen by cardiologists worldwide to treat approximately three million patients with coronary artery disease. The safety and efficacy of the device is supported by a robust clinical trial program that includes more than 70 studies that examine the performance of the CYPHER® Stent in a broad range of patients.
Developed and manufactured by Cordis Corporation, the CYPHER® Stent is currently available in more than 80 countries and has the broadest clinical experience and longest-term clinical follow-up of any drug-eluting stent. The next version of sirolimus-eluting stent, the CYPHER SELECT™ Sirolimus-eluting Coronary Stent, was launched in Europe, Asia Pacific, Latin America and Canada in 2003. The CYPHER SELECT™ Plus Stent, the third version of a sirolimus-eluting coronary stent, received CE Mark in 2006 and is currently available in many markets outside the United States.
For more complete information on indications, contraindications, warnings and precautions, see the Instructions for Use available at cypherstent.
About Cordis Corporation
Cordis Corporation, a Johnson & Johnson company, is a worldwide leader in the development and manufacture of interventional vascular technology. Through the company's innovation, research and development, Cordis partners with interventional cardiologists worldwide to treat millions of patients who suffer from vascular disease. More information about Cordis Corporation can be found at cordis.
The analysis also found a substantial reduction in the risk of myocardial infarction (heart attack) and reintervention with the CYPHER® Stent when compared to bare metal stents and the Taxus Stent, and no significant differences in the rates of stent thrombosis (blood clots) between the CYPHER® Stent and bare metal stents. The data from this analysis also identified a significant decrease in the risk of blood clots occurring more than 30 days after stent implantation with the CYPHER® Stent compared to the Taxus Stent.
"This large set of data indicates that the mortality associated with drug eluting stents and bare metal stents is comparable. Recent concerns about increases in mortality associated with drug eluting stents are not supported by thisanalysis assessing long-term outcomes," stated Dr. Christoph Stettler, M.D., from the University of Bern, Switzerland, one of the authors of the study. Dr. Stettler is with the Department of Endocrinology, Diabetes and Clinical Nutrition there.
In addition, the corresponding author, Dr. Peter Juni, M.D., stated that, "These results have also led us to conclude that the CYPHER® Stent is clinically superior to bare metal stents and the Taxus Stent when the safety and effectiveness outcomes in this analysis are taken into account." Dr. Juni is Head of Division, Clinical Epidemiology and Biostatistics, University of Bern in Switzerland.
Funded by the Swiss National Science Foundation, this network meta-analysis was designed to compare the safety and effectiveness of bare metal stents, the CYPHER® Stent and the Taxus Stent in a large patient population to increase the ability to detect and understand low frequency events, such as death and stent thrombosis. It included data up to four years of follow-up. The safety outcomes comprised mortality (death), myocardial infarction and Academic Research Consortium (ARC) definite stent thrombosis. The effectiveness outcome was target lesion revascularization (or the need for a repeat intervention).
The mortality rates were similar for all three stents: hazard ratios (HR) were 1.00 (95 percent credibility interval 0.82 to 1.25) for the CYPHER® Stent versus bare-metal stents, 1.03 (CI 0.84 to 1.22) for the Taxus Stent versus bare-metal stents and 0.96 (CI 0.83 to 1.24) for the CYPHER® Stent vs. the Taxus Stent.
The CYPHER® Stent was associated with the lowest risk of myocardial infarction. The corresponding hazard ratios were 0.81 versus bare-metal stents (CI 0.66 to 0.97, p=0.030) and 0.83 versus the Taxus Stent (CI 0.71-1.00, p=0.045).
The ARC definite stent thrombosis rates between the CYPHER® Stent and bare metal stents were not significantly different over the entire follow-up. However, the risk of late stent thrombosis (occurring more than 30 days after the procedure) was more than twice as likely with the Taxus Stent compared to bare-metal stents (HR 2.11, CI 1.19-4.23, p=0.017). In addition, the study found that a late stent thrombosis event was 46 percent less likely to occur in a patient implanted with the CYPHER® Stent than in a patient who received the Taxus Stent (HR 0.54, CI 0.26-0.98, p=0.041).
While both drug-eluting stents were associated with significantly lower risks of target lesion revascularization compared to bare-metal stents, the CYPHER® Stent reduced the risk substantially further compared to the Taxus Stent. The CYPHER® Stent reduced the risk by 70 percent (HR 0.30, CI 0.24 to 0.37, p=0.0001) and the Taxus Stent by 58 percent (HR 0.42, CI 0.33 to 0.53, p=0.0001) compared to bare-metal stents. When the target lesion revascularization rate for the CYPHER® Stent was compared directly to the rate for the Taxus Stent, a patient implanted with the CYPHER® Stent was found to be 30 percent less likely to need another procedure than a patient treated with the Taxus Stent (HR 0.70, CI 0.56 to 0.84, p=0.0021).This difference is consistent with other meta-analyses of randomized controlled trials directly comparing the two stents.
"This network meta analysis constitutes the largest and most robust set of data published to date in an eminent international peer-reviewed journal assessing the long-term safety and efficacy outcomes of drug-eluting stents," said David E. Kandzari, M.D., F.A.C.C., F.S.C.A.I., Chief Medical Officer, Cordis Corporation. "It significantly enriches the large body of evidence that interventional cardiologists have at their disposal to make the right choice for their patients. These data clearly demonstrate the benefits of drug-eluting stents versus bare metal stents and further provide clarity as to the differences between the CYPHER® Stent and the Taxus Stent."
About the CYPHER® Stent
The CYPHER® Stent has been chosen by cardiologists worldwide to treat approximately three million patients with coronary artery disease. The safety and efficacy of the device is supported by a robust clinical trial program that includes more than 70 studies that examine the performance of the CYPHER® Stent in a broad range of patients.
Developed and manufactured by Cordis Corporation, the CYPHER® Stent is currently available in more than 80 countries and has the broadest clinical experience and longest-term clinical follow-up of any drug-eluting stent. The next version of sirolimus-eluting stent, the CYPHER SELECT™ Sirolimus-eluting Coronary Stent, was launched in Europe, Asia Pacific, Latin America and Canada in 2003. The CYPHER SELECT™ Plus Stent, the third version of a sirolimus-eluting coronary stent, received CE Mark in 2006 and is currently available in many markets outside the United States.
For more complete information on indications, contraindications, warnings and precautions, see the Instructions for Use available at cypherstent.
About Cordis Corporation
Cordis Corporation, a Johnson & Johnson company, is a worldwide leader in the development and manufacture of interventional vascular technology. Through the company's innovation, research and development, Cordis partners with interventional cardiologists worldwide to treat millions of patients who suffer from vascular disease. More information about Cordis Corporation can be found at cordis.
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