The latest statistics regarding the use of pacemakers and implantable cardiac devices in Europe was presented on Sunday 21 June, at EUROPACE 2009, the meeting of the European Heart Rhythm Association (EHRA)1 which takes place in Berlin, Germany from 21 to 24 June.
"One of the roles of a European Association like the European Heart Rhythm Association (EHRA), a registered branch of the European Society of Cardiology (ESC), is to promote equal access to therapy for all patients across Europe. To do so, the first step is to compile data on the current situation in various ESC membership countries, compare them, and propose actions to move towards harmonization. The current leadership of EHRA agreed on the importance of obtaining as much current information as possible concerning the situation of the practice of electrophysiology in Europe" stressed Wolpert.
Under the leadership of Professors Christian Wolpert from Germany, Panos Vardas from Greece and Josep Brugada from Spain, a group worked to collect the most recent figures. To ensure up to date data, Presidents of the different Working Groups and National Societies were contacted and asked not only to provide data, but also to verify and authorize all the information that became available through various sources.
Wolpert declared that this data is also the point of comparison for the future: " By knowing where we are today, we will be able to benchmark in the future and see how diverse countries evolve. This means that this book must be an ongoing process, with updated information, new and additional data, and the inclusion of information from those countries that have not yet been able to collect and transmit their records."
Explaining the data, Prof Wolpert highlighted certain trends, such as the fact that "more and more, cardiologists represent the majority of implanters while surgeons are decreasingly active in these procedures."
There is a disparate coverage of diseases and treatments within the European Union and the European Society of Cardiology member countries outside of the EU. Some of the countries have no reimbursement e.g. for ICD or pacemaker therapy and the penetration of catheter ablation of atrial fibrillation is very different. Data shows big differences across ESC member countries in:
•Guideline implementation.
•The number of trained physicians and specialised centres
•The number of implantations which seems to depend not only on reimbursement and financial resources, but also to be a function of the number of centres and physicians dedicated to electrophysiology and implantation of devices.
•The numbers of ICD implanting centres range from less than 1 to 6.87 per million citizens.
•Pacemaker therapy is performed in the range of 88 to a maximum of around 1200/ million inhabitants.
•ICD implant rates including CRT-D devices range from approx. 2.5 to 354 per million inhabitants. The data shows an increase for a subset of 16 western and northern European countries around 15% from 2006 to 2007.
•Regarding a potentially different medical consensus in specific countries the use of biventricular pacemakers vs. biventricular ICDs shows a 8:1 ratio at the highest down to 1:1.2 ratio as the lowest.
•In the field of invasive electrophysiology and catheter ablation for supraventricular and ventricular arrhythmias the number of centres available is variable ranging from less than 0.2 to more than 3 centres/ million. The total number of catheter ablations is increasing and reaches a maximum of more than 200/ million in approx. half of the countries. However, there is a strong discrepancy comparing all 35 countries, displaying a wide range from less than 20 to more than 450/ million.
•The same is true for catheter ablation of atrial fibrillation which varies tremendously, linked to reimbursement policies but also to different approaches in the various EP societies.
"As an example, Germany, hosting the EUROPACE meeting this year, has one of the highest implant rates for ICD's in Europe with a total of 1037 centres which implant pacemakers; 200 centres implanting CRT resynchronisation devices and a total of 360 ICD implanting institutions" highlights Prof Wolpert.
"Within the Non-EU ESC member countries, there has been a steady increase of therapy availability and disease coverage, however, there are still many countries that struggle with reimbursement, trained personnel and technical support, which requires a strong effort and leaves much space for improvement. It is the task and the intention of EHRA to support any initiative to improve steadily the situation for these countries in order to reduce the disparities".
Source-Eurekalert
23.6.09
18.6.09
Protecting Kidney Function During Heart Failure
• Mayo Clinic cardiology researchers have found a peptide that helps preserve and improve kidney function during heart failure, without affecting blood pressure. Earlier variations of this peptide caused blood pressure to drop limiting the potential benefits to the kidneys. The findings appear in the current Proceedings of the National Academy of Sciences.
"Heart failure itself and some of the approaches used to treat it can have detrimental effects on the kidneys," says Mayo cardiologist and lead researcher Robert Simari, M.D. "Our hope is that this compound will help protect kidney function while you're being treated, and possibly shorten your hospital stay and keep you out of the hospital."
This new peptide (a unique link of amino acids) has been tested in the laboratory and in animal models and is expected to move into clinical trials next year.
"One of the biggest additional concerns for patients with heart failure is the health of their kidneys," says Dr. Simari. "The extreme case is that it can lead to the kidneys shutting down completely." Nearly 5 million Americans are living with heart failure, a condition where the heart can't pump enough blood to meet the body's needs. Symptoms include shortness of breath, exercise intolerance and fluid retention. All can occur when heart function is impaired.
Seven Years of Research
The mapping of the human genome (2000-2003) revealed a gene that produces a protein called BNP (B-type natriuretic peptide). BNP was not only useful in diagnosing heart problems, it also proved therapeutic in treating heart failure. Unfortunately, says Dr. Simari, it had limited use because many heart failure patients experience low blood pressure and BNP lowered it further.
The Mayo investigators discovered an alternative splicing (AS) of BNP in messenger RNA (produced by the same gene). When they shortened the amino acid sequence of ASBNP for testing, they found that it had the same therapeutic benefits as BNP, but without the side effects to blood pressure. Positive impacts include increasing the kidney filtration rate, suppressing harmful protein production, and keeping water and salt flowing from the body. Potentially, this new drug would be given by IV to patients who are being treated in the hospital.
"There's an important reduction of kidney function every time one of these acute heart failure episodes happens," says Dr. Simari. "And by stopping one or more of those decrements, we hope there will be an overall improvement in long-term maintenance of kidney function."
Others on the team include Shuchong Pan, M.D., Ph.D., Horng Chen, M.D., Guido Boerrigter, M.D., Candace Lee, Laurel Kleppe, Amir Lerman, M.D., Margaret Redfield, M.D., John Burnett, Jr., M.D., all from Mayo Clinic, and Deborah Dickey, Ph.D., Jennifer Hall, Ph.D., and Lincoln Potter, Ph.D., all from the University of Minnesota. The research was funded by Mayo Clinic, the National Institutes of Health, and Anexon, Inc.
Mayo Clinic and five of the investigators associated with this research have a financial interest in the technology studied in the research. In accordance with the Bayh-Dole Act, that technology has been licensed to Anexon. Mayo Clinic and Drs. R. Simari and Dr. S. Pan have received royalties from the licensing of that technology of greater than the federal threshold for significant financial interest. Drs. J.Burnett, M.Redfield and H.Chen have received royalties less than the federal threshold for significant financial interest. In addition, Mayo Clinic holds an equity position in Anexon.
Source
Mayo Clinic
"Heart failure itself and some of the approaches used to treat it can have detrimental effects on the kidneys," says Mayo cardiologist and lead researcher Robert Simari, M.D. "Our hope is that this compound will help protect kidney function while you're being treated, and possibly shorten your hospital stay and keep you out of the hospital."
This new peptide (a unique link of amino acids) has been tested in the laboratory and in animal models and is expected to move into clinical trials next year.
"One of the biggest additional concerns for patients with heart failure is the health of their kidneys," says Dr. Simari. "The extreme case is that it can lead to the kidneys shutting down completely." Nearly 5 million Americans are living with heart failure, a condition where the heart can't pump enough blood to meet the body's needs. Symptoms include shortness of breath, exercise intolerance and fluid retention. All can occur when heart function is impaired.
Seven Years of Research
The mapping of the human genome (2000-2003) revealed a gene that produces a protein called BNP (B-type natriuretic peptide). BNP was not only useful in diagnosing heart problems, it also proved therapeutic in treating heart failure. Unfortunately, says Dr. Simari, it had limited use because many heart failure patients experience low blood pressure and BNP lowered it further.
The Mayo investigators discovered an alternative splicing (AS) of BNP in messenger RNA (produced by the same gene). When they shortened the amino acid sequence of ASBNP for testing, they found that it had the same therapeutic benefits as BNP, but without the side effects to blood pressure. Positive impacts include increasing the kidney filtration rate, suppressing harmful protein production, and keeping water and salt flowing from the body. Potentially, this new drug would be given by IV to patients who are being treated in the hospital.
"There's an important reduction of kidney function every time one of these acute heart failure episodes happens," says Dr. Simari. "And by stopping one or more of those decrements, we hope there will be an overall improvement in long-term maintenance of kidney function."
Others on the team include Shuchong Pan, M.D., Ph.D., Horng Chen, M.D., Guido Boerrigter, M.D., Candace Lee, Laurel Kleppe, Amir Lerman, M.D., Margaret Redfield, M.D., John Burnett, Jr., M.D., all from Mayo Clinic, and Deborah Dickey, Ph.D., Jennifer Hall, Ph.D., and Lincoln Potter, Ph.D., all from the University of Minnesota. The research was funded by Mayo Clinic, the National Institutes of Health, and Anexon, Inc.
Mayo Clinic and five of the investigators associated with this research have a financial interest in the technology studied in the research. In accordance with the Bayh-Dole Act, that technology has been licensed to Anexon. Mayo Clinic and Drs. R. Simari and Dr. S. Pan have received royalties from the licensing of that technology of greater than the federal threshold for significant financial interest. Drs. J.Burnett, M.Redfield and H.Chen have received royalties less than the federal threshold for significant financial interest. In addition, Mayo Clinic holds an equity position in Anexon.
Source
Mayo Clinic
2.1.09
CAFE-LLA: Statin Therapy Does Not Influence Central Aortic Pressure or Hemodynamics
December 31, 2008 (Leicester, United Kingdom) — The use of statin therapy in hypertensive patients has no impact on central aortic pressures, pulse-wave augmentation, the augmentation index, pressure amplification, or any other central hemodynamic parameter [1].
These are the findings of the Conduit Artery Function Evaluation-Lipid-Lowering Arm (CAFE-LLA) study, a large-scale, placebo-controlled substudy of the Anglo-Scandinavian Cardiac Outcomes Trial-Lipid Lowering Arm (ASCOT-LLA) designed to prospectively evaluate the effect of statin therapy on the relationship between brachial and central aortic pressures.
Publishing their findings online December 22, 2008 in Circulation, lead investigator Dr Bryan Williams (University of Leicester, UK) and colleagues state that the "favorable effects of statins in cardiovascular outcomes in hypertensive patients are via mechanisms that are independent of important effects on large-artery function and central pressure."
Looking at Large-Artery Function in ASCOT
Because statins reduce the risk of cardiovascular events in individuals with hypertension, there has been interest in the hypothesis that the lipid-lowering drugs modulate large-artery function and central aortic pressures independent of cholesterol lowering. With this in mind, the researchers assessed the effects of atorvastatin 10 mg daily in 891 patients enrolled in ASCOT-LLA.
Patients were, on average, 63 years old and enrolled in ASCOT if they had untreated hypertension or treated hypertension >140/90 mm Hg and three cardiovascular risk factors but no history of coronary heart disease. To be eligible for ASCOT-LLA, patients had to have total cholesterol concentrations <250 mg/dL and be untreated with any lipid-lowering medication.
After six months, treatment with atorvastatin reduced LDL cholesterol by 32 mg/dL and total cholesterol by 35 mg/dL from baseline, a relative reduction of approximately 33% and 25%, respectively, compared with placebo.
Despite the reductions in LDL- and total-cholesterol levels, atorvastatin did not have any effect on central aortic blood pressure or various hemodynamic measurements. Time-averaged brachial blood pressure was similar in the placebo and atorvastatin-treatment arms, as was the change in aortic-pulse pressure. The augmentation index and heart rate were also unaltered with statin therapy compared with placebo.
"The results of CAFE-LLA are unequivocal," write Williams and colleagues. The clinical-outcome benefits of atorvastatin in treated hypertensive patients are not mediated by direct effects on central aortic pressure and hemodynamics, they write.
Too Little, Too Late, and Too Short
In an editorial accompanying the published study [2], Drs Michel Safar, Athanase Protogerou, and Jacque Blacher (Hotel-Dieu Centre de Diagnostique et Thérapeutique, Paris, France) suggest that the results of the study are surprising, "because arterial stiffening and atherosclerosis, although different diseases, have overlapping processes due to common cardiovascular risk factors and complications."
The editorialists note that several studies have shown, although the results are not entirely consistent, that statins have a beneficial effect on central aortic stiffness, possibly because of pleiotropic effects on atherosclerotic plaques, such as improved endothelial function and increased nitric-oxide bioavailability. The negative results of CAFE-LLA might be partly attributed to a lack of power to evaluate hemodynamic outcomes, but for the most part, they say the findings are a case of "too little, too late, too short."
For example, the 10-mg statin dose used in CAFE-LLA might be too low. Although the dose was chosen because baseline cholesterol levels were only modestly elevated, previous studies have shown reductions of aortic stiffness with higher doses of statins, up to 80 mg of atorvastatin. Regarding too late, vascular damage might have already been established in these patients, given that their age was 63 years upon study entry. And finally, too short, in that longer follow-up is needed to observe significant pressure-independent effects on central hemodynamics.
In their paper, Williams and colleagues echo many of these possible explanations in reconciling the differences between large-artery function, hemodynamics, and plasma cholesterol reductions.
Although CAFE-LLA was not powered to assess statin-mediated differences in central pressures and hemodynamics relative to clinical outcomes, the researchers note that atorvastatin in ASCOT-LLA was associated with significant reductions in cardiovascular events compared with placebo.
Williams B, Lacy PS, Cruickshank JK, et al. Impact of statin therapy on central aortic pressures and hemodynamics. Circulation 2009; 119:53-61. Abstract
Safar ME, Protogerou AD, Blacher J. Statins, central blood pressure, and blood pressure amplification. Circulation 2009; 119:9-12. Abstract
The complete contents of Heartwire, a professional news service of WebMD, can be found at www.theheart.org, a Web site for cardiovascular healthcare professionals.
Source: Heartwire/Medscape
These are the findings of the Conduit Artery Function Evaluation-Lipid-Lowering Arm (CAFE-LLA) study, a large-scale, placebo-controlled substudy of the Anglo-Scandinavian Cardiac Outcomes Trial-Lipid Lowering Arm (ASCOT-LLA) designed to prospectively evaluate the effect of statin therapy on the relationship between brachial and central aortic pressures.
Publishing their findings online December 22, 2008 in Circulation, lead investigator Dr Bryan Williams (University of Leicester, UK) and colleagues state that the "favorable effects of statins in cardiovascular outcomes in hypertensive patients are via mechanisms that are independent of important effects on large-artery function and central pressure."
Looking at Large-Artery Function in ASCOT
Because statins reduce the risk of cardiovascular events in individuals with hypertension, there has been interest in the hypothesis that the lipid-lowering drugs modulate large-artery function and central aortic pressures independent of cholesterol lowering. With this in mind, the researchers assessed the effects of atorvastatin 10 mg daily in 891 patients enrolled in ASCOT-LLA.
Patients were, on average, 63 years old and enrolled in ASCOT if they had untreated hypertension or treated hypertension >140/90 mm Hg and three cardiovascular risk factors but no history of coronary heart disease. To be eligible for ASCOT-LLA, patients had to have total cholesterol concentrations <250 mg/dL and be untreated with any lipid-lowering medication.
After six months, treatment with atorvastatin reduced LDL cholesterol by 32 mg/dL and total cholesterol by 35 mg/dL from baseline, a relative reduction of approximately 33% and 25%, respectively, compared with placebo.
Despite the reductions in LDL- and total-cholesterol levels, atorvastatin did not have any effect on central aortic blood pressure or various hemodynamic measurements. Time-averaged brachial blood pressure was similar in the placebo and atorvastatin-treatment arms, as was the change in aortic-pulse pressure. The augmentation index and heart rate were also unaltered with statin therapy compared with placebo.
"The results of CAFE-LLA are unequivocal," write Williams and colleagues. The clinical-outcome benefits of atorvastatin in treated hypertensive patients are not mediated by direct effects on central aortic pressure and hemodynamics, they write.
Too Little, Too Late, and Too Short
In an editorial accompanying the published study [2], Drs Michel Safar, Athanase Protogerou, and Jacque Blacher (Hotel-Dieu Centre de Diagnostique et Thérapeutique, Paris, France) suggest that the results of the study are surprising, "because arterial stiffening and atherosclerosis, although different diseases, have overlapping processes due to common cardiovascular risk factors and complications."
The editorialists note that several studies have shown, although the results are not entirely consistent, that statins have a beneficial effect on central aortic stiffness, possibly because of pleiotropic effects on atherosclerotic plaques, such as improved endothelial function and increased nitric-oxide bioavailability. The negative results of CAFE-LLA might be partly attributed to a lack of power to evaluate hemodynamic outcomes, but for the most part, they say the findings are a case of "too little, too late, too short."
For example, the 10-mg statin dose used in CAFE-LLA might be too low. Although the dose was chosen because baseline cholesterol levels were only modestly elevated, previous studies have shown reductions of aortic stiffness with higher doses of statins, up to 80 mg of atorvastatin. Regarding too late, vascular damage might have already been established in these patients, given that their age was 63 years upon study entry. And finally, too short, in that longer follow-up is needed to observe significant pressure-independent effects on central hemodynamics.
In their paper, Williams and colleagues echo many of these possible explanations in reconciling the differences between large-artery function, hemodynamics, and plasma cholesterol reductions.
Although CAFE-LLA was not powered to assess statin-mediated differences in central pressures and hemodynamics relative to clinical outcomes, the researchers note that atorvastatin in ASCOT-LLA was associated with significant reductions in cardiovascular events compared with placebo.
Williams B, Lacy PS, Cruickshank JK, et al. Impact of statin therapy on central aortic pressures and hemodynamics. Circulation 2009; 119:53-61. Abstract
Safar ME, Protogerou AD, Blacher J. Statins, central blood pressure, and blood pressure amplification. Circulation 2009; 119:9-12. Abstract
The complete contents of Heartwire, a professional news service of WebMD, can be found at www.theheart.org, a Web site for cardiovascular healthcare professionals.
Source: Heartwire/Medscape
24.9.08
Sucking Out a Coronary Thrombus Before Stenting Seems Worthwhile
Previous work in The Netherlands has shown that percutaneous coronary intervention (PCI) can induce embolization of atherothrombotic material with resulting impaired myocardial reperfusion, and that thrombus aspiration before stenting can prevent this effect.
In this study, reported in The Lancet in 2008,[1] 12 investigators analyzed, by intention to treat, cardiac death or nonfatal myocardial reinfarction after 1 year in 1060 randomized patients.
In the group treated by conventional PCI, 6.7% suffered cardiac death vs only 3.6% in the thrombus aspiration group; the data for cardiac death or nonfatal reinfarction after 1 year were 5.6% vs 9.9%.
The intuitively sensible action of aspirating thrombus in acute myocardial infarction prior to stenting is supported by data.
This article is selected from Medscape Best Evidence. Dr George Lundberg.
In this study, reported in The Lancet in 2008,[1] 12 investigators analyzed, by intention to treat, cardiac death or nonfatal myocardial reinfarction after 1 year in 1060 randomized patients.
In the group treated by conventional PCI, 6.7% suffered cardiac death vs only 3.6% in the thrombus aspiration group; the data for cardiac death or nonfatal reinfarction after 1 year were 5.6% vs 9.9%.
The intuitively sensible action of aspirating thrombus in acute myocardial infarction prior to stenting is supported by data.
This article is selected from Medscape Best Evidence. Dr George Lundberg.
29.8.08
In-Stent Restenosis Best Corrected With Drug-Eluting Stent
NEW YORK (Reuters Health) Aug 21
- The risk of restenosis is significantly lower when revascularization is achieved with a paclitaxel-eluting stent than by vascular brachytherapy for a bare metal stent in-stent restenosis, according to the 2-year findings of the TAXUS V-ISR multicenter trial.
Dr. Stephen G. Ellis of the Cleveland Clinic in Ohio and colleagues prospectively randomized 396 patients with a bare metal stent restenosis to receive either a Taxus stent or vascular brachytherapy treatment.
Ischemia-driven target lesion revascularization was required less frequently with the paclitaxel-eluting stent than with vascular brachytherapy, with revascularization rates of 5.3% and 10.3% at 9 to 24 months, respectively, the investigators report in the July issue of the European Heart Journal.
At 24 months, ischemia-driven target lesion revascularization was significantly reduced with paclitaxel-eluting stent, with a rate of 10.1% compared with 21.6% for vascular brachytherapy.
There were no significant differences in death, myocardial infarction, or target vessel thrombosis between the two groups after 1 or 2 years.
In an editorial, Dr. Debabrata Mukherjee of the University of Kentucky at Lexington notes that the era of bare metal stent is waning again, while the use of drug-eluting stents is once again becoming the preferred option for in-stent restenosis.
In 2007, the use of drug-eluting stents dropped because of concerns with restenosis. "We have more objective data now to support the use of drug-eluting stents. The key is the use of aspirin and clopidogrel, with their use extended for 1 year," Dr. Mukherjee commented in an interview with Reuters Health.
"The bottom line is that at this point in time, drug-eluting stents implantation (for in-stent restenosis) is best," Dr. Mukherjee asserted. "There are some exceptions, such as diffuse stenosis of the proximal (left anterior descending artery), when bypass surgery would be a better option."
"Still, about one third of patients in the US receive a bare metal stent," Dr. Mukherjee cautioned. "That's a significant population; it's about 100,000 people."
Eur Heart J 2008;29:1595-1596,1625-1634.
--------------------------------------------------------------------------------
Reuters Health Information 2008. © 2008 Reuters Ltd.
- The risk of restenosis is significantly lower when revascularization is achieved with a paclitaxel-eluting stent than by vascular brachytherapy for a bare metal stent in-stent restenosis, according to the 2-year findings of the TAXUS V-ISR multicenter trial.
Dr. Stephen G. Ellis of the Cleveland Clinic in Ohio and colleagues prospectively randomized 396 patients with a bare metal stent restenosis to receive either a Taxus stent or vascular brachytherapy treatment.
Ischemia-driven target lesion revascularization was required less frequently with the paclitaxel-eluting stent than with vascular brachytherapy, with revascularization rates of 5.3% and 10.3% at 9 to 24 months, respectively, the investigators report in the July issue of the European Heart Journal.
At 24 months, ischemia-driven target lesion revascularization was significantly reduced with paclitaxel-eluting stent, with a rate of 10.1% compared with 21.6% for vascular brachytherapy.
There were no significant differences in death, myocardial infarction, or target vessel thrombosis between the two groups after 1 or 2 years.
In an editorial, Dr. Debabrata Mukherjee of the University of Kentucky at Lexington notes that the era of bare metal stent is waning again, while the use of drug-eluting stents is once again becoming the preferred option for in-stent restenosis.
In 2007, the use of drug-eluting stents dropped because of concerns with restenosis. "We have more objective data now to support the use of drug-eluting stents. The key is the use of aspirin and clopidogrel, with their use extended for 1 year," Dr. Mukherjee commented in an interview with Reuters Health.
"The bottom line is that at this point in time, drug-eluting stents implantation (for in-stent restenosis) is best," Dr. Mukherjee asserted. "There are some exceptions, such as diffuse stenosis of the proximal (left anterior descending artery), when bypass surgery would be a better option."
"Still, about one third of patients in the US receive a bare metal stent," Dr. Mukherjee cautioned. "That's a significant population; it's about 100,000 people."
Eur Heart J 2008;29:1595-1596,1625-1634.
--------------------------------------------------------------------------------
Reuters Health Information 2008. © 2008 Reuters Ltd.
12.6.08
The benefits of thrombus aspiration after heart attack
SummaryBackground
Percutaneous coronary intervention (PCI) for ST-elevation myocardial infarction can be complicated by spontaneous or angioplasty-induced embolisation of atherothrombotic material. Distal blockage induces microvascular obstruction and can result in less than optimum reperfusion of viable myocardium. The Thrombus Aspiration during Percutaneous coronary intervention in Acute myocardial infarction Study (TAPAS) found that thrombus aspiration resulted in improved myocardial reperfusion compared with conventional PCI, but whether this benefit improves clinical outcome is unknown. We aimed to investigate whether the early efficacy of thrombus aspiration seen in TAPAS translated into clinical benefit after 1 year.
Methods
Patients with ST-elevation myocardial infarction enrolled at the University Medical Centre Groningen were randomly assigned in a 1:1 ratio to either thrombus aspiration or conventional treatment, before undergoing initial coronary angiography. Exclusion criteria were rescue PCI after thrombolysis and known existence of a concomitant disease with life expectancy less than 6 months. Of the 1071 patients enrolled between January, 2005, and December, 2006, vital status at or beyond 1 year after randomisation was available for 1060 (99%). The primary endpoint was cardiac death or non-fatal reinfarction after 1 year, and analysis was by intention to treat. The TAPAS trial is registered with Current Controlled Trials number ISRCTN16716833.
Findings
Cardiac death at 1 year was 3•6% (19 of 535 patients) in the thrombus aspiration group and 6•7% (36 of 536) in the conventional PCI group (hazard ratio [HR] 1•93; 95% CI 1•11–3•37; p=0•020). 1-year cardiac death or non-fatal reinfarction occurred in 5•6% (30 of 535) of patients in the thrombus aspiration group and 9•9% (53 of 536) of patients in the conventional PCI group (HR 1•81; 95% CI 1•16–2•84; p=0•009).
Interpretation
Compared with conventional PCI, thrombus aspiration before stenting of the infarcted artery seems to improve the 1-year clinical outcome after PCI for ST-elevation myocardial infarction.
Funding
Medtronic and the Thorax Centre of the University Medical Centre Groningen.
Affiliations
a. Department of Cardiology, University Medical Centre Groningen, University of Groningen, Netherlands
b. Department of Pathology, University Medical Centre Groningen, University of Groningen, Netherlands
Correspondence to: PJ Vlaar, Department of Cardiology, University Medical Centre Groningen, Thorax Centre, Netherlands
Percutaneous coronary intervention (PCI) for ST-elevation myocardial infarction can be complicated by spontaneous or angioplasty-induced embolisation of atherothrombotic material. Distal blockage induces microvascular obstruction and can result in less than optimum reperfusion of viable myocardium. The Thrombus Aspiration during Percutaneous coronary intervention in Acute myocardial infarction Study (TAPAS) found that thrombus aspiration resulted in improved myocardial reperfusion compared with conventional PCI, but whether this benefit improves clinical outcome is unknown. We aimed to investigate whether the early efficacy of thrombus aspiration seen in TAPAS translated into clinical benefit after 1 year.
Methods
Patients with ST-elevation myocardial infarction enrolled at the University Medical Centre Groningen were randomly assigned in a 1:1 ratio to either thrombus aspiration or conventional treatment, before undergoing initial coronary angiography. Exclusion criteria were rescue PCI after thrombolysis and known existence of a concomitant disease with life expectancy less than 6 months. Of the 1071 patients enrolled between January, 2005, and December, 2006, vital status at or beyond 1 year after randomisation was available for 1060 (99%). The primary endpoint was cardiac death or non-fatal reinfarction after 1 year, and analysis was by intention to treat. The TAPAS trial is registered with Current Controlled Trials number ISRCTN16716833.
Findings
Cardiac death at 1 year was 3•6% (19 of 535 patients) in the thrombus aspiration group and 6•7% (36 of 536) in the conventional PCI group (hazard ratio [HR] 1•93; 95% CI 1•11–3•37; p=0•020). 1-year cardiac death or non-fatal reinfarction occurred in 5•6% (30 of 535) of patients in the thrombus aspiration group and 9•9% (53 of 536) of patients in the conventional PCI group (HR 1•81; 95% CI 1•16–2•84; p=0•009).
Interpretation
Compared with conventional PCI, thrombus aspiration before stenting of the infarcted artery seems to improve the 1-year clinical outcome after PCI for ST-elevation myocardial infarction.
Funding
Medtronic and the Thorax Centre of the University Medical Centre Groningen.
Affiliations
a. Department of Cardiology, University Medical Centre Groningen, University of Groningen, Netherlands
b. Department of Pathology, University Medical Centre Groningen, University of Groningen, Netherlands
Correspondence to: PJ Vlaar, Department of Cardiology, University Medical Centre Groningen, Thorax Centre, Netherlands
26.3.08
More Heparin Recalls in Europe and US
March 25, 2008 (London, UK) – The heparin-contamination saga is continuing, with the latest countries to recall products being France, Italy, and Denmark.
The heparin products recalled in France are medicinal products manufactured by Rotexmedica, the same company that supplied the heparin products recalled previously in Germany. These were recalled in Germany because of an association with an increased rate of adverse events. A spokesperson from the European Medicines Agency (EMEA) told heartwire that no additional adverse reactions had been reported in France, but that Rotexmedica was recalling a limited number of batches "because of a suspicion of the presence of a contaminant."
In Italy and Denmark, the recall involves a number of batches of heparin active pharmaceutical ingredient (API) made by the Italian company Opocrin. The EMEA spokesperson said he didn't think these batches of heparin API had made their way into the final heparin medicinal products as yet and were being recalled because the presence of a contaminant had been confirmed. He added: "We presume this is the same contaminant as identified in the US, as it has been detected by the same tests as used in the US, but we have no definite confirmation of the identity of the contaminant found in the Opocrin heparin API as yet."
He added that the heparin medicinal products from Rotexmedica and the heparin API from Opocrin had all been manufactured using products sourced originally from China by four Chinese companies. Rotexmedica's heparin products were sourced from Changzhou Qianhong Biopharmaceutical Co Ltd and Yantai Dongcheng Biopharmaceutical Co Ltd, while Opocrin's heparin API had been sourced from Yantai Dongcheng Biopharmaceutical Co Ltd, Shenzen Hepalink Pharmaceutical Co Ltd, and Shanghai No 1 Biochemical Co Ltd. These appear to be different from the Chinese company to which affected heparin in the US has been traced (Changzhou Scientific Protein Labs).
The EMEA spokesperson explained to heartwire that heparin products were regulated by each individual country in Europe. EMEA, being the centralized medical agency, was just providing an information-sharing role on the issue. He added that as there were many companies supplying heparin in Europe, it was not expected that a heparin shortage would occur.
Another US manufacturer affected
Meanwhile, another US heparin manufacturer has recalled some heparin products because of concern about the contaminant. B Braun Medical is recalling 23 lots of heparin after its supplier, Scientific Protein Laboratories, disclosed that one lot of heparin sodium active pharmaceutical ingredient supplied to B Braun may contain the contaminant implicated in the adverse reactions. To date, B Braun has not received any adverse-event reports related to these products, the company said.
The complete contents of Heartwire, a professional news service of WebMD, can be found at www.theheart.org, a Web site for cardiovascular healthcare professionals.
Source: Heartwire
The heparin products recalled in France are medicinal products manufactured by Rotexmedica, the same company that supplied the heparin products recalled previously in Germany. These were recalled in Germany because of an association with an increased rate of adverse events. A spokesperson from the European Medicines Agency (EMEA) told heartwire that no additional adverse reactions had been reported in France, but that Rotexmedica was recalling a limited number of batches "because of a suspicion of the presence of a contaminant."
In Italy and Denmark, the recall involves a number of batches of heparin active pharmaceutical ingredient (API) made by the Italian company Opocrin. The EMEA spokesperson said he didn't think these batches of heparin API had made their way into the final heparin medicinal products as yet and were being recalled because the presence of a contaminant had been confirmed. He added: "We presume this is the same contaminant as identified in the US, as it has been detected by the same tests as used in the US, but we have no definite confirmation of the identity of the contaminant found in the Opocrin heparin API as yet."
He added that the heparin medicinal products from Rotexmedica and the heparin API from Opocrin had all been manufactured using products sourced originally from China by four Chinese companies. Rotexmedica's heparin products were sourced from Changzhou Qianhong Biopharmaceutical Co Ltd and Yantai Dongcheng Biopharmaceutical Co Ltd, while Opocrin's heparin API had been sourced from Yantai Dongcheng Biopharmaceutical Co Ltd, Shenzen Hepalink Pharmaceutical Co Ltd, and Shanghai No 1 Biochemical Co Ltd. These appear to be different from the Chinese company to which affected heparin in the US has been traced (Changzhou Scientific Protein Labs).
The EMEA spokesperson explained to heartwire that heparin products were regulated by each individual country in Europe. EMEA, being the centralized medical agency, was just providing an information-sharing role on the issue. He added that as there were many companies supplying heparin in Europe, it was not expected that a heparin shortage would occur.
Another US manufacturer affected
Meanwhile, another US heparin manufacturer has recalled some heparin products because of concern about the contaminant. B Braun Medical is recalling 23 lots of heparin after its supplier, Scientific Protein Laboratories, disclosed that one lot of heparin sodium active pharmaceutical ingredient supplied to B Braun may contain the contaminant implicated in the adverse reactions. To date, B Braun has not received any adverse-event reports related to these products, the company said.
The complete contents of Heartwire, a professional news service of WebMD, can be found at www.theheart.org, a Web site for cardiovascular healthcare professionals.
Source: Heartwire
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