CARDIOVASCULAR HORIZON SCANNING Volume 3 Issue 1
Is estimating lifetime cardiovascular risk useful?
Cost-effectiveness of interventions to reduce dietary salt intake
Valvular heart disease: the next cardiac epidemic
Further dissemination
CARDIOVASCULAR HORIZON SCANNING Volume 3 Issue 1
Posted: 14 Jan 2011 08:20 AM PST
Filed under: Cardiovascular diseases, Volume 3 Issue 1
Is estimating lifetime cardiovascular risk useful?
Posted: 12 Jan 2011 05:40 AM PST
Source: BMJ, 2010, 342 (7788) p. 62-63
Follow this link for the abstract
Date of publication: January 2011
Publication type: Editorial
In a nutshell: The QRISK lifetime cardiovascular risk model originates from the QResearch database, which has generated the world’s largest cardiovascular risk prediction cohort study, involvingmore than three million people between the ages of 30 and 84. The new QRISK lifetime risk calculator, which is similar to the heart age forecast tool, incorporates both short and longer term risk in one simple display and has important advantages over separate 10 year and lifetime cardiovascular risk calculators.
Length of publication: 2 pages
Some important notes: You will need an NHS Athens username and password to access this article. Please contact your local NHS library if you cannot access the full text. Follow this link to find your local NHS library.Filed under: Cardiovascular diseases, Volume 3 Issue 1 Tagged: risk prediction tools
Cost-effectiveness of interventions to reduce dietary salt intake
Posted: 12 Jan 2011 03:19 AM PST
Source: Heart, 2010, 96 (23) p. 1920-1925
Follow this link for the abstract
Date of publication: December 2010
Publication type: Press release
In a nutshell: This study found that dietary advice targeting individuals is not cost-effective under any of the modelled scenarios, even if directed at those with highest blood pressure risk. Although the current programme that relies on voluntary action by the food industry is cost-effective, the population health benefits could be 20 times greater with government legislation on moderate salt limits in processed foods.
Length of publication: 6 pages
Some important notes: You will need an NHS Athens username and password to access this article. Please contact your local NHS library if you cannot access the full text. Follow this link to find your local NHS library.Filed under: Cardiovascular diseases, Volume 3 Issue 1 Tagged: nutritional advice
Valvular heart disease: the next cardiac epidemic
Posted: 11 Jan 2011 09:05 AM PST
Source: Heart, 2011, 97 (2) p. 91-93
Follow this link for the abstract
Date of publication: January 2011
Publication type: Press release
In a nutshell: With an ageing population, a rise in the number of patients with more advanced valvular heart disease, requiring valve replacement, is anticipated.
Length of publication: 3 pages
Some important notes: You will need an NHS Athens username and password to access this article. Please contact your local NHS library if you cannot access the full text. Follow this link to find your local NHS library.
Showing posts with label cardiovascular risk. Show all posts
Showing posts with label cardiovascular risk. Show all posts
Monday, 17 January 2011
Wednesday, 20 October 2010
JOURNAL SNIPPETS
JAMA 13 Oct 2010 Vol 304
1559 Cardiac surgery was once considered too bloody even to contemplate: now it is commonplace. But there is still no agreement in practice about how much blood should be transfused following heart surgery - rates of transfusion vary between 8% and 93% in similar units across the USA (p.1586). The Brazilian TRAC trial randomised heart surgery patients to be transfused to achieve a target haemoglobin level of 10.5 g/dl in one group and 9.1 in the other. Outcomes were identical. An accompanying editorial is entitled "Blood Transfusion as a Quality Indicator in Cardiac Surgery." Enough said.
http://jama.ama-assn.org/cgi/content/abstract/304/14/1568http://jama.ama-assn.org/cgi/content/abstract/304/14/1559
Lancet 16 Oct 2010 Vol 376
1303 A nice clear NHS-based study shows that the results of renal transplantation are equally good from kidneys donated after cardiac death as from those donated after brain death. The most important factor is not the mode of death but the cold ischaemia time.
http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(10)60827-6/abstract
Arch Intern Med 11 Oct 2010 Vol 170
1622 A decade ago, much hope centred on the fact that levels of homocysteine correlate well with cardiovascular risk, and so it followed (we thought) that using B vitamins to lower homocysteine was bound to be a simple and effective way to reduce the population risk. One person talked to years ago about possible primary care studies was Robert Clarke, now principal author of this meta-analysis of 8 big randomised trials. Every trial succeeded in lowering Hcy but utterly failed to make any impact on cardiovascular outcomes, cancer, or all-cause mortality. You can't push some risk curves the other way by known interventions - as we've also found with a wide range of blood sugar.
http://archinte.ama-assn.org/cgi/content/abstract/170/18/1622
1559 Cardiac surgery was once considered too bloody even to contemplate: now it is commonplace. But there is still no agreement in practice about how much blood should be transfused following heart surgery - rates of transfusion vary between 8% and 93% in similar units across the USA (p.1586). The Brazilian TRAC trial randomised heart surgery patients to be transfused to achieve a target haemoglobin level of 10.5 g/dl in one group and 9.1 in the other. Outcomes were identical. An accompanying editorial is entitled "Blood Transfusion as a Quality Indicator in Cardiac Surgery." Enough said.
http://jama.ama-assn.org/cgi/content/abstract/304/14/1568http://jama.ama-assn.org/cgi/content/abstract/304/14/1559
Lancet 16 Oct 2010 Vol 376
1303 A nice clear NHS-based study shows that the results of renal transplantation are equally good from kidneys donated after cardiac death as from those donated after brain death. The most important factor is not the mode of death but the cold ischaemia time.
http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(10)60827-6/abstract
Arch Intern Med 11 Oct 2010 Vol 170
1622 A decade ago, much hope centred on the fact that levels of homocysteine correlate well with cardiovascular risk, and so it followed (we thought) that using B vitamins to lower homocysteine was bound to be a simple and effective way to reduce the population risk. One person talked to years ago about possible primary care studies was Robert Clarke, now principal author of this meta-analysis of 8 big randomised trials. Every trial succeeded in lowering Hcy but utterly failed to make any impact on cardiovascular outcomes, cancer, or all-cause mortality. You can't push some risk curves the other way by known interventions - as we've also found with a wide range of blood sugar.
http://archinte.ama-assn.org/cgi/content/abstract/170/18/1622
Friday, 6 August 2010
CARDIOVASCULAR DISEASE
Cardiovascular disease
Effect of smoking cessation advice on cardiovascular disease Centre for Reviews and Dissemination
Quantitative effects on cardiovascular risk factors and coronary heart disease risk of replacing partially hydrogenated vegetable oils with other fats and oils Centre for Reviews and Dissemination
Effect of smoking cessation advice on cardiovascular disease Centre for Reviews and Dissemination
Quantitative effects on cardiovascular risk factors and coronary heart disease risk of replacing partially hydrogenated vegetable oils with other fats and oils Centre for Reviews and Dissemination
Wednesday, 23 June 2010
SNIPPETS FROM JOURNAL WATCH
Lancet 19 Jun 2010 Vol 375
2161 Golly - here's something you don't often see in The Lancet: a trial puffing a new drug for angina which costs about £20 per year. Nor is it subsidised and ghost-written by the drug's manufacturers, who have probably long ago lost interest in it. Because the drug is our old friend allopurinol, at 600mg daily, used to improve exercise tolerance in ischaemic heart disease as opposed to preventing gout. It's a very small short-term trial, but there seems to be no reason not to give the drug a go - and quite a few reasons to believe that it may be a good thing for the strained myocardium (see editorial on p.2126).
http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(10)60391-1/abstract
JAMA 9 Jun 2010 Vol 303
2280 "Does This Patient Have a Haemorrhagic Stroke?" asks the latest in The Rational Clinical Examination Series. "How should I know, I haven't seen the scan" might be the usual answer, and it also turns out to be the correct one. Features like coma, headache, neck stiffness and high blood pressure all make haemorrhage a bit more likely, but the only way to know with sufficient certainty is by putting the patient through a CT scanner, preferably within the window for thrombolysis if the stroke turns out to be ischaemic. This is confirmed by 19 prospectively studies, meticulously analysed here.
http://jama.ama-assn.org/cgi/content/abstract/303/22/2280
NEJM 10 Jun 2010 Vol 362
2155 This study is based on the Kaiser Permanente insured population of California and it tells a pretty amazing tale - ST elevation myocardial infarction has fallen by 62% in the last decade. Interestingly the incidence of non-ST elevation MI went up between 2002 and 2004 as troponin assays became widely adopted as the diagnostic gold standard, but even taking this into account, the incidence of any MI has gone down by a third. During this time, Californians became a bit fatter, did slightly more exercise, were banned from smoking in public places, and were prescribed more statins, beta-blockers and ACE inhibitors. We are not told if they drank more of their sometimes passable wines.
http://content.nejm.org/cgi/content/abstract/362/23/2155
Lancet 12 Jun 2010 Vol 375
2073 From the point of view of someone fixated on the cardiovascular system, the body consists of a central pump supplying blood to various tufts - lung-tufts to oxygenate it, gut-tufts to feed it and kidney tufts to get rid of waste products, and so on. I can see that for some the kidney is an interesting organ, but it's essentially a dangling footnote to the business of assessing cardiovascular risk, and delicious when prepared correctly. Now assessing risk (or prognosis) is itself of little importance unless you can use it to guide interventions to reduce risk. All of which makes it very frustrating to wade through a paper like this which pools data from 14 studies (over 100 000 individuals) to derive risk tables for all-cause and cardiovascular mortality graded by eGFR and albuminuria, independently of blood pressure, cholesterol and smoking. There seems to be a definite association which, surprisingly, is slightly U-shaped when you combine the two factors. So was QOF right to make us identify and check out everyone with an eGFR under 60? That's another question entirely, which depends on how much these factors contribute to total CV risk, and what we can do about it.
http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(10)60674-5/abstract
JAMA 2 Jun 2010 Vol 303
2141 Acute heart failure is regarded by most members of the public as synonymous with death, and indeed a proportion of patients admitted to hospital with HF do die within 30 days, but this stands at barely more than one in ten, and has hardly changed between 1993 and 2006, dropping from 12.8% to 10.7%. During that time, nearly 7 million Americans covered by Medicare have been to hospital with acute HF, and very little else has changed either: they get discharged a bit sooner, and readmitted slightly more often. A huge, meticulous, well-described outcomes study of this kind inevitably has one looking for Harlan Krumholz; yes, there he is.
http://jama.ama-assn.org/cgi/content/abstract/303/21/2141
2148 The heart failure figures are rather disappointing, whichever way you spin them; but one definite way to reduce HF is to save myocardium by timely reperfusion therapy for acute myocardial infarction. We know this from many interventional trials, of course, but given the immense organisational effort that has gone into providing access to immediate percutaneous intervention for MI, it is nice to have observational evidence from a large population too. Voici QuÃÆ'Ã" '©bec. In 2006-7, nearly 80% of quÃÆ'Ã" '©bÃÆ'Ã" '©cois with ST elevation MI received PCI, but in 68% of cases this occurred after more than 90 minutes. If you look at a map of Canada, you will see why: the province is more than twice the size of France and stretches up and beyond the Arctic Circle. Of those who received thrombolysis, 54% got it later than the ideal 30 minutes. The mortality figures following the two modes of treatment are remarkably similar, but outcomes such as recurrent MI and the need for bypass grafting favour PCI. By contrast, the treatment within the ideal window halves your chance of death within 30 days.
http://jama.ama-assn.org/cgi/content/abstract/303/21/2148
BMJ 5 Jun 2010 Vol 340
1231 The star of this week's BMJ is Julia Hippisley-Cox, professor of primary care in Nottingham, who has used the EMIS database of British general practices to derive an improved cardiovascular risk score (QRISK) and has also (see below) worked out from it what the true risks and benefits of statins are in UK primary care. We are lucky to have such studies to refine our practice, since they apply directly to the population we treat. As she has been working on the two versions of QRISK, Gary Collins and Doug Altman have been dogging her footsteps, and here they publish an independent and external validation of QRISK2. Use it with confidence in British general practice - you won't get a better Good Housekeeping Seal of Approval than this.
http://www.bmj.com/cgi/content/full/340/may13_2/c2442
1233 Allan Struthers has done much of the basic work on BNP and the renin-angiotensin pathway. The end product of this pathway is aldosterone, and the Dundee-led RALES trial published in 1999 showed that by blocking it with spironolactone in patients with chronic heart failure, you could improve outcomes even if they were on other RAS-inhibiting treatments. So off I went and gave some to a few of my HF patients, noting that the RALES trial encountered few problems with hyperkalaemia. I duly checked the electrolytes of one patient a couple of weeks later and sent him straight to hospital with a potassium of 6.8. This alarming event proved to be common enough in Canada, too, according to a paper which appeared in the New England Journal in 2004. But here Allan Struthers et al rebut their critics with data from Tayside, proving that your canny Scots GP can use sprironolactone with perfect safety, laddie, aye perfect safety. As the great poet of the Tay might have put it :Physicians of England and Canada kill their patients with hyperkalaemia; But by the banks of the silvery Tay our doctors behave much more seemlier. W. McGonagall op posth.
http://www.bmj.com/cgi/content/full/340/may18_2/c1768
2161 Golly - here's something you don't often see in The Lancet: a trial puffing a new drug for angina which costs about £20 per year. Nor is it subsidised and ghost-written by the drug's manufacturers, who have probably long ago lost interest in it. Because the drug is our old friend allopurinol, at 600mg daily, used to improve exercise tolerance in ischaemic heart disease as opposed to preventing gout. It's a very small short-term trial, but there seems to be no reason not to give the drug a go - and quite a few reasons to believe that it may be a good thing for the strained myocardium (see editorial on p.2126).
http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(10)60391-1/abstract
JAMA 9 Jun 2010 Vol 303
2280 "Does This Patient Have a Haemorrhagic Stroke?" asks the latest in The Rational Clinical Examination Series. "How should I know, I haven't seen the scan" might be the usual answer, and it also turns out to be the correct one. Features like coma, headache, neck stiffness and high blood pressure all make haemorrhage a bit more likely, but the only way to know with sufficient certainty is by putting the patient through a CT scanner, preferably within the window for thrombolysis if the stroke turns out to be ischaemic. This is confirmed by 19 prospectively studies, meticulously analysed here.
http://jama.ama-assn.org/cgi/content/abstract/303/22/2280
NEJM 10 Jun 2010 Vol 362
2155 This study is based on the Kaiser Permanente insured population of California and it tells a pretty amazing tale - ST elevation myocardial infarction has fallen by 62% in the last decade. Interestingly the incidence of non-ST elevation MI went up between 2002 and 2004 as troponin assays became widely adopted as the diagnostic gold standard, but even taking this into account, the incidence of any MI has gone down by a third. During this time, Californians became a bit fatter, did slightly more exercise, were banned from smoking in public places, and were prescribed more statins, beta-blockers and ACE inhibitors. We are not told if they drank more of their sometimes passable wines.
http://content.nejm.org/cgi/content/abstract/362/23/2155
Lancet 12 Jun 2010 Vol 375
2073 From the point of view of someone fixated on the cardiovascular system, the body consists of a central pump supplying blood to various tufts - lung-tufts to oxygenate it, gut-tufts to feed it and kidney tufts to get rid of waste products, and so on. I can see that for some the kidney is an interesting organ, but it's essentially a dangling footnote to the business of assessing cardiovascular risk, and delicious when prepared correctly. Now assessing risk (or prognosis) is itself of little importance unless you can use it to guide interventions to reduce risk. All of which makes it very frustrating to wade through a paper like this which pools data from 14 studies (over 100 000 individuals) to derive risk tables for all-cause and cardiovascular mortality graded by eGFR and albuminuria, independently of blood pressure, cholesterol and smoking. There seems to be a definite association which, surprisingly, is slightly U-shaped when you combine the two factors. So was QOF right to make us identify and check out everyone with an eGFR under 60? That's another question entirely, which depends on how much these factors contribute to total CV risk, and what we can do about it.
http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(10)60674-5/abstract
JAMA 2 Jun 2010 Vol 303
2141 Acute heart failure is regarded by most members of the public as synonymous with death, and indeed a proportion of patients admitted to hospital with HF do die within 30 days, but this stands at barely more than one in ten, and has hardly changed between 1993 and 2006, dropping from 12.8% to 10.7%. During that time, nearly 7 million Americans covered by Medicare have been to hospital with acute HF, and very little else has changed either: they get discharged a bit sooner, and readmitted slightly more often. A huge, meticulous, well-described outcomes study of this kind inevitably has one looking for Harlan Krumholz; yes, there he is.
http://jama.ama-assn.org/cgi/content/abstract/303/21/2141
2148 The heart failure figures are rather disappointing, whichever way you spin them; but one definite way to reduce HF is to save myocardium by timely reperfusion therapy for acute myocardial infarction. We know this from many interventional trials, of course, but given the immense organisational effort that has gone into providing access to immediate percutaneous intervention for MI, it is nice to have observational evidence from a large population too. Voici QuÃÆ'Ã" '©bec. In 2006-7, nearly 80% of quÃÆ'Ã" '©bÃÆ'Ã" '©cois with ST elevation MI received PCI, but in 68% of cases this occurred after more than 90 minutes. If you look at a map of Canada, you will see why: the province is more than twice the size of France and stretches up and beyond the Arctic Circle. Of those who received thrombolysis, 54% got it later than the ideal 30 minutes. The mortality figures following the two modes of treatment are remarkably similar, but outcomes such as recurrent MI and the need for bypass grafting favour PCI. By contrast, the treatment within the ideal window halves your chance of death within 30 days.
http://jama.ama-assn.org/cgi/content/abstract/303/21/2148
BMJ 5 Jun 2010 Vol 340
1231 The star of this week's BMJ is Julia Hippisley-Cox, professor of primary care in Nottingham, who has used the EMIS database of British general practices to derive an improved cardiovascular risk score (QRISK) and has also (see below) worked out from it what the true risks and benefits of statins are in UK primary care. We are lucky to have such studies to refine our practice, since they apply directly to the population we treat. As she has been working on the two versions of QRISK, Gary Collins and Doug Altman have been dogging her footsteps, and here they publish an independent and external validation of QRISK2. Use it with confidence in British general practice - you won't get a better Good Housekeeping Seal of Approval than this.
http://www.bmj.com/cgi/content/full/340/may13_2/c2442
1233 Allan Struthers has done much of the basic work on BNP and the renin-angiotensin pathway. The end product of this pathway is aldosterone, and the Dundee-led RALES trial published in 1999 showed that by blocking it with spironolactone in patients with chronic heart failure, you could improve outcomes even if they were on other RAS-inhibiting treatments. So off I went and gave some to a few of my HF patients, noting that the RALES trial encountered few problems with hyperkalaemia. I duly checked the electrolytes of one patient a couple of weeks later and sent him straight to hospital with a potassium of 6.8. This alarming event proved to be common enough in Canada, too, according to a paper which appeared in the New England Journal in 2004. But here Allan Struthers et al rebut their critics with data from Tayside, proving that your canny Scots GP can use sprironolactone with perfect safety, laddie, aye perfect safety. As the great poet of the Tay might have put it :Physicians of England and Canada kill their patients with hyperkalaemia; But by the banks of the silvery Tay our doctors behave much more seemlier. W. McGonagall op posth.
http://www.bmj.com/cgi/content/full/340/may18_2/c1768
Wednesday, 21 April 2010
ETHNICITY and CARDIOVASCULAR ISSUES
Cardiovascular Diseases:
Ethnic differences in cardiovascular risk
Produced by general practitioners for the British Heart Foundation, this fact file explores the ethnic differences in cardiovascular risk in the UK.
Ethnicity and coronary heart disease: making sense of risk and improving care
This is number 16 in the Race Equality Foundation’s “Better Health Briefing” series.
Ethnic differences in cardiovascular risk
Produced by general practitioners for the British Heart Foundation, this fact file explores the ethnic differences in cardiovascular risk in the UK.
Ethnicity and coronary heart disease: making sense of risk and improving care
This is number 16 in the Race Equality Foundation’s “Better Health Briefing” series.
Tuesday, 6 April 2010
DIABETES RISK
Intensive Systolic Blood Pressure Control May Not Reduce Mortality in Patients with Diabetes
Current guidelines from the American Diabetes Association (ADA) and other organizations recommend a blood pressure target < 130/80 mm Hg for patients with diabetes (Diabetes Care 2010 Jan;33 Suppl 1:S11). To date, there has been little experimental data to guide blood pressure target recommendations, but a new trial directly compared 2 different blood pressure goals. The Action to Control Cardiovascular Risk in Diabetes blood pressure trial (ACCORD BP) compared intensive systolic blood pressure control (target < 120 mm Hg) vs. standard control (target < 140 mm Hg) in 4,733 patients. While the trial did not stipulate specific antihypertensive regimens, patients in both groups were required to receive a drug class associated with reduction in cardiovascular events in patients with diabetes (ACE inhibitors, angiotensin receptor blockers, beta blockers, calcium channel blockers, or diuretics). They could also receive other medications as necessary. Mean systolic blood pressure at 1 year was 119.3 mm Hg for the intensive group and 133.5 mm Hg for the standard group. Intensive control was not associated with a reduction in either cardiovascular mortality or myocardial infarction, but it was associated with a reduced risk of stroke (level 2 [mid-level] evidence). During a mean follow-up of 4.7 years, cardiovascular mortality was 2.5% in each group. There were no significant differences in all-cause mortality (6.3% vs. 6.1%), nonfatal myocardial infarction (5.3% vs. 6.2%), or heart failure (3.5% vs. 3.8%). Stroke occurred in 1.7% of the intensive group compared to 2.6% of the standard group (p = 0.01, NNT 84). However, the risk of serious adverse events from treatment was increased for the intensive group (3.3% vs. 1.3%, p < 0.001, NNH 50). Adverse events reported included hypotension, syncope, bradycardia or other arrhythmia, hyperkalemia, angioedema, and renal failure (N Engl J Med 2010 Mar 14 early online).
Current guidelines from the American Diabetes Association (ADA) and other organizations recommend a blood pressure target < 130/80 mm Hg for patients with diabetes (Diabetes Care 2010 Jan;33 Suppl 1:S11). To date, there has been little experimental data to guide blood pressure target recommendations, but a new trial directly compared 2 different blood pressure goals. The Action to Control Cardiovascular Risk in Diabetes blood pressure trial (ACCORD BP) compared intensive systolic blood pressure control (target < 120 mm Hg) vs. standard control (target < 140 mm Hg) in 4,733 patients. While the trial did not stipulate specific antihypertensive regimens, patients in both groups were required to receive a drug class associated with reduction in cardiovascular events in patients with diabetes (ACE inhibitors, angiotensin receptor blockers, beta blockers, calcium channel blockers, or diuretics). They could also receive other medications as necessary. Mean systolic blood pressure at 1 year was 119.3 mm Hg for the intensive group and 133.5 mm Hg for the standard group. Intensive control was not associated with a reduction in either cardiovascular mortality or myocardial infarction, but it was associated with a reduced risk of stroke (level 2 [mid-level] evidence). During a mean follow-up of 4.7 years, cardiovascular mortality was 2.5% in each group. There were no significant differences in all-cause mortality (6.3% vs. 6.1%), nonfatal myocardial infarction (5.3% vs. 6.2%), or heart failure (3.5% vs. 3.8%). Stroke occurred in 1.7% of the intensive group compared to 2.6% of the standard group (p = 0.01, NNT 84). However, the risk of serious adverse events from treatment was increased for the intensive group (3.3% vs. 1.3%, p < 0.001, NNH 50). Adverse events reported included hypotension, syncope, bradycardia or other arrhythmia, hyperkalemia, angioedema, and renal failure (N Engl J Med 2010 Mar 14 early online).
Monday, 1 February 2010
SNIPPETS FROM JOURNALS
JAMA 27 Jan 2010 Vol 303
333 Paroxysmal atrial fibrillation can vary from a minor nuisance to a cause of intermittent angina and heart failure. This trial shows that catheter radiofrequency ablation is markedly effective in the first nine months for patients whose paroxysmal AF fails to respond to antiarrhythmic drugs. That said, they still carried on with these drugs (excepting amiodarone) and anticoagulation or antiplatelet therapy according to current guidelines. A particular joy for methodologists was the use in this trial of Bayesian boundaries to determine interim analysis times. Put like that, it instantly sounds boring, but honestly it isn't.
http://jama.ama-assn.org/cgi/content/abstract/303/4/333
BMJ 30 Jan 2010 Vol 340
249 Cardiac rehabilitation is now routinely recommended to everyone who survives a heart attack, but 60% don't turn up. From a large number of trials, reviewed in this paper, we know that it is equally effective when given at home. But this does mean that the rehab team has to be flexible, proactive and adequately staffed. Don't hold your breath as the recession cuts start to bite.
http://www.bmj.com/cgi/content/full/340/jan19_4/b5631
252 I suspect it's going to be increasingly common for anaesthetists to insist on patients having non-invasive cardiac stress testing before elective major non-cardiac surgery, and this large Canadian observational study lends some support to this policy - but only for people with known cardiovascular risk factors. I searched in vain for the Web Table A which might have gone some way to explaining the mechanism by which pre-op stress testing actually harmed some low risk patients - the text speculates that it might have been by foisting beta-blockers on them. Anyway, for those with 1-6 risk factors, there is a measurable mortality benefit, even though very few of them actually require an invasive cardiac procedure.
http://www.bmj.com/cgi/content/full/340/jan28_3/b5526
Arch Intern Med 25 Jan 2010 Vol 170
126 DASH it! As you read this paper showing that a low-fat, low salt diet really does bring down blood pressure by as much as a powerful antihypertensive drug - up to 16/10 mm Hg. That's when it's combined with a weight losing regime over 4 months. It would be very hard to maintain that over a longer period so let's settle for 11/7.5 as in the DASH alone group. http://archinte.ama-assn.org/cgi/content/abstract/170/2/126
136 But hang on - here is the opposite message. A diet of unlimited meat and a lot of fat (the low-carbohydrate ketogenic diet) achieved a much better BP reduction than a low-fat diet in this next study - 6/4.5 vs 4.5/O. Moreover the second group had help from orlistat. Both groups lost weight equally. The undoubted benefits of the DASH diet do not seem to derive from fat restriction. In fact they can probably be matched by a wide variety of less puritanical diets.
http://archinte.ama-assn.org/cgi/content/abstract/170/2/136
JAMA 20 Jan 2010 Vol 303
250 Snip, snip. You are a few seconds nearer to death. Your telomeres are shortening. Quick, grab some smoked salmon. "Among this cohort of patients with coronary heart disease, there was an inverse relationship between baseline blood levels of omega-3 fatty acids and the rate of telomere shortening over 5 years." If you can't get hold of oily fish, a good alternative source of omega-3 fatty acids is snake oil. Helps your telomeres. Live Longer With Snake Oil - it's official.
http://jama.ama-assn.org/cgi/content/abstract/303/3/250
NEJM 21 Jan 2010 Vol 362
217 The heart and lungs share a space in the thoracic cavity. When one gets bigger, the other gets squashed. This elementary fact is nicely illustrated by a study of 2816 people aged 45 to 84 without gross cardiovascular or lung disease. The more evidence of emphysema on lung CT scanning, the smaller the capacity of the left ventricle when filling. This means that the ejection fraction was not impaired but cardiac output was. This is nothing to do with cor pulmonale, mainly a problem of the right ventricle, or myocardial ischaemia, though in advanced COPD these may also play a part. O that cardiologists would remember that the chest contains lungs. It's difficult enough to get them to remember that the heart has two ventricles and a phase called diastole.
http://content.nejm.org/cgi/content/abstract/362/3/217
228 Which brings us nicely on to the topic of systolic heart failure, as reviewed here by John McMurray. Whenattending heart failure conferences there were ribs about trialling yet another drug on recumbent male patients aged 60 with reduced ejection fractions in hospital beds. It isn't the best way of informing us how to treat 75 year olds in the community with multiple morbidities including cardiac impairment. Still, we have to pick up what clues we can from what studies there are, though it would be a mistake to call this evidence-based medicine. It is called general practice, and it can be quite hard. Here are some of the easier bits for those who need an update.
http://content.nejm.org/cgi/content/extract/362/3/228
239 "The primary care physician remains the principal provider and care coordinator for patients with Williams-Beuren syndrome." Your practice may well contain such an individual, if your list is over 10,000. But you probably know this as Williams' syndrome without the Beuren - a microdeletion at chromosome 7 causing a characteristic facial appearance, hypercalcaemia, growth failure, heart abnormalities and learning difficulties. If you are a primary care physician who is the principal care provider for this person, you are not going to find a better review than this , so if you work in SWEssex you can have access to this via Athens
http://content.nejm.org/cgi/content/extract/362/3/239
Lancet 23 Jan 2010 Vol 375
283 Plato held that each earthly object was an imperfect approximation to an ideal object. Clopidogrel is your typical earthly product: expensive and disappointing, as it does nothing for about 30% of people who take it. Ticagrelor on the other hand sounds like the Platonic ideal for platelet inhibition - it works for everybody as it is not a pro-drug, but it is reversible and therefore should cause fewer bleeds. But how all the things of earth disappoint. The most striking thing about the PLATO trial is that ticagrelor is nowhere near 30% better than clopidogrel. This massive study in 13,408 people about to undergo invasive treatment for acute coronary syndromes showed a tiny difference in the composite end-point of death, myocardial infarction or stroke - 9.0% v 10.7% in favour of ticagrelor. There was no difference in bleeds. http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(09)62191-7/abstract
Ann Intern Med 19 Jan 2010 Vol 152
69 Here's a study from the USA which examines three strategies for the primary prevention of coronary artery disease using statins. Two are based on measurement of LDL-cholesterol ("treat to target") and the other is based on total estimated 5-year coronary risk ("tailored treatment"). "We assumed that LDL cholesterol reduction is a statin's sole mechanism of action and that change in total LDL cholesterol is a perfect indicator of the amount of risk reduction that a patient receives from a statin, thereby conceding the 2 most important assumptions underlying the treat-to-target approach. We realize that the first assumption is controversial and that the second assumption is untrue (LDL cholesterol determinations have substantial measurement error)." Neatly put. This is a modelling exercise set by Harlan Krumholz for his scholars and they do it beautifully: the most effective way to use these drugs is to give simvastatin 40mg to everyone with a 5-15% CAD risk and 40mg atorvastatin to everyone with a risk above that - and never mind the LDL-C.
http://www.annals.org/content/152/2/69.abstract
78 By and large it doesn't matter what you give patients to reduce their blood pressure so long as it works and they keep taking it. However, you may wish to bear in mind that exclusive treatment with calcium channel blockers may carry a higher risk of atrial fibrillation than beta-blockers and ACE inhibitors.
http://www.annals.org/content/152/2/78.abstract
333 Paroxysmal atrial fibrillation can vary from a minor nuisance to a cause of intermittent angina and heart failure. This trial shows that catheter radiofrequency ablation is markedly effective in the first nine months for patients whose paroxysmal AF fails to respond to antiarrhythmic drugs. That said, they still carried on with these drugs (excepting amiodarone) and anticoagulation or antiplatelet therapy according to current guidelines. A particular joy for methodologists was the use in this trial of Bayesian boundaries to determine interim analysis times. Put like that, it instantly sounds boring, but honestly it isn't.
http://jama.ama-assn.org/cgi/content/abstract/303/4/333
BMJ 30 Jan 2010 Vol 340
249 Cardiac rehabilitation is now routinely recommended to everyone who survives a heart attack, but 60% don't turn up. From a large number of trials, reviewed in this paper, we know that it is equally effective when given at home. But this does mean that the rehab team has to be flexible, proactive and adequately staffed. Don't hold your breath as the recession cuts start to bite.
http://www.bmj.com/cgi/content/full/340/jan19_4/b5631
252 I suspect it's going to be increasingly common for anaesthetists to insist on patients having non-invasive cardiac stress testing before elective major non-cardiac surgery, and this large Canadian observational study lends some support to this policy - but only for people with known cardiovascular risk factors. I searched in vain for the Web Table A which might have gone some way to explaining the mechanism by which pre-op stress testing actually harmed some low risk patients - the text speculates that it might have been by foisting beta-blockers on them. Anyway, for those with 1-6 risk factors, there is a measurable mortality benefit, even though very few of them actually require an invasive cardiac procedure.
http://www.bmj.com/cgi/content/full/340/jan28_3/b5526
Arch Intern Med 25 Jan 2010 Vol 170
126 DASH it! As you read this paper showing that a low-fat, low salt diet really does bring down blood pressure by as much as a powerful antihypertensive drug - up to 16/10 mm Hg. That's when it's combined with a weight losing regime over 4 months. It would be very hard to maintain that over a longer period so let's settle for 11/7.5 as in the DASH alone group. http://archinte.ama-assn.org/cgi/content/abstract/170/2/126
136 But hang on - here is the opposite message. A diet of unlimited meat and a lot of fat (the low-carbohydrate ketogenic diet) achieved a much better BP reduction than a low-fat diet in this next study - 6/4.5 vs 4.5/O. Moreover the second group had help from orlistat. Both groups lost weight equally. The undoubted benefits of the DASH diet do not seem to derive from fat restriction. In fact they can probably be matched by a wide variety of less puritanical diets.
http://archinte.ama-assn.org/cgi/content/abstract/170/2/136
JAMA 20 Jan 2010 Vol 303
250 Snip, snip. You are a few seconds nearer to death. Your telomeres are shortening. Quick, grab some smoked salmon. "Among this cohort of patients with coronary heart disease, there was an inverse relationship between baseline blood levels of omega-3 fatty acids and the rate of telomere shortening over 5 years." If you can't get hold of oily fish, a good alternative source of omega-3 fatty acids is snake oil. Helps your telomeres. Live Longer With Snake Oil - it's official.
http://jama.ama-assn.org/cgi/content/abstract/303/3/250
NEJM 21 Jan 2010 Vol 362
217 The heart and lungs share a space in the thoracic cavity. When one gets bigger, the other gets squashed. This elementary fact is nicely illustrated by a study of 2816 people aged 45 to 84 without gross cardiovascular or lung disease. The more evidence of emphysema on lung CT scanning, the smaller the capacity of the left ventricle when filling. This means that the ejection fraction was not impaired but cardiac output was. This is nothing to do with cor pulmonale, mainly a problem of the right ventricle, or myocardial ischaemia, though in advanced COPD these may also play a part. O that cardiologists would remember that the chest contains lungs. It's difficult enough to get them to remember that the heart has two ventricles and a phase called diastole.
http://content.nejm.org/cgi/content/abstract/362/3/217
228 Which brings us nicely on to the topic of systolic heart failure, as reviewed here by John McMurray. Whenattending heart failure conferences there were ribs about trialling yet another drug on recumbent male patients aged 60 with reduced ejection fractions in hospital beds. It isn't the best way of informing us how to treat 75 year olds in the community with multiple morbidities including cardiac impairment. Still, we have to pick up what clues we can from what studies there are, though it would be a mistake to call this evidence-based medicine. It is called general practice, and it can be quite hard. Here are some of the easier bits for those who need an update.
http://content.nejm.org/cgi/content/extract/362/3/228
239 "The primary care physician remains the principal provider and care coordinator for patients with Williams-Beuren syndrome." Your practice may well contain such an individual, if your list is over 10,000. But you probably know this as Williams' syndrome without the Beuren - a microdeletion at chromosome 7 causing a characteristic facial appearance, hypercalcaemia, growth failure, heart abnormalities and learning difficulties. If you are a primary care physician who is the principal care provider for this person, you are not going to find a better review than this , so if you work in SWEssex you can have access to this via Athens
http://content.nejm.org/cgi/content/extract/362/3/239
Lancet 23 Jan 2010 Vol 375
283 Plato held that each earthly object was an imperfect approximation to an ideal object. Clopidogrel is your typical earthly product: expensive and disappointing, as it does nothing for about 30% of people who take it. Ticagrelor on the other hand sounds like the Platonic ideal for platelet inhibition - it works for everybody as it is not a pro-drug, but it is reversible and therefore should cause fewer bleeds. But how all the things of earth disappoint. The most striking thing about the PLATO trial is that ticagrelor is nowhere near 30% better than clopidogrel. This massive study in 13,408 people about to undergo invasive treatment for acute coronary syndromes showed a tiny difference in the composite end-point of death, myocardial infarction or stroke - 9.0% v 10.7% in favour of ticagrelor. There was no difference in bleeds. http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(09)62191-7/abstract
Ann Intern Med 19 Jan 2010 Vol 152
69 Here's a study from the USA which examines three strategies for the primary prevention of coronary artery disease using statins. Two are based on measurement of LDL-cholesterol ("treat to target") and the other is based on total estimated 5-year coronary risk ("tailored treatment"). "We assumed that LDL cholesterol reduction is a statin's sole mechanism of action and that change in total LDL cholesterol is a perfect indicator of the amount of risk reduction that a patient receives from a statin, thereby conceding the 2 most important assumptions underlying the treat-to-target approach. We realize that the first assumption is controversial and that the second assumption is untrue (LDL cholesterol determinations have substantial measurement error)." Neatly put. This is a modelling exercise set by Harlan Krumholz for his scholars and they do it beautifully: the most effective way to use these drugs is to give simvastatin 40mg to everyone with a 5-15% CAD risk and 40mg atorvastatin to everyone with a risk above that - and never mind the LDL-C.
http://www.annals.org/content/152/2/69.abstract
78 By and large it doesn't matter what you give patients to reduce their blood pressure so long as it works and they keep taking it. However, you may wish to bear in mind that exclusive treatment with calcium channel blockers may carry a higher risk of atrial fibrillation than beta-blockers and ACE inhibitors.
http://www.annals.org/content/152/2/78.abstract
Thursday, 21 January 2010
CARDIO ARTICLES
Arch Intern Med 11 Jan 2010 Vol 170
27 Are you bored with guidelines? Fed up with arguments about cardiovascular risk assessment? Then brighten your day with this paper about 27 cardiovascular risk assessment guidelines. They are all different - grossly or subtly - proving that whenever you get a roomful of doctors discussing the same evidence, they will never arrive at the same answer. http://archinte.ama-assn.org/cgi/content/abstract/170/1/27
JAMA 6 Jan 2010 Vol 303
54 Many readers may not be cardiologists or hospital doctors, and I guess quite a few of you didn't know what NSTEMI stands for until about 8 years ago. Troponins only came in around then too, and they are vital to distinguish whether unstable angina is or is not associated with myocardial damage. Immediate angiography is also a relative novelty in the UK. Yet now every second hospital discharge summary now seems to read c/o chest pain NSTEMI troponin 2.1 PCI stents to LAD, Cx, please continue clopidogrel for 12 months. Here is a case study of a 43 year old American man which takes you through the modern management of NSTEMI in full wearisome detail.
http://jama.ama-assn.org/cgi/content/short/303/1/54?home
Lancet 9 Jan 2010 Vol 375
132 C-reactive protein was first described over 70 years ago, and we use it as a "something's wrong" test all the time, instead of or alongside ESR. It isn't actually all that much use, and patients often end up being told "Your blood test tells me you are ill, which I already knew, but it doesn't tell me what's wrong, so I want to repeat it." How many non-sequiturs can you squeeze into a sentence? And yet we all do it, taking obscure comfort later in the fact that 26 has fallen to 13. It's the same if you try to use it as a marker for cardiovascular risk. This immensely painstaking individual participant meta-analysis shows that even minor elevations of CRP are associated with increased risk for coronary heart disease; also for stroke; also for vascular death; also for non-vascular death; also for several cancers; also for lung disease. Elevated CRP is vaguely bad news: a Completely Random Predictor.
http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(09)61717-7/abstract
27 Are you bored with guidelines? Fed up with arguments about cardiovascular risk assessment? Then brighten your day with this paper about 27 cardiovascular risk assessment guidelines. They are all different - grossly or subtly - proving that whenever you get a roomful of doctors discussing the same evidence, they will never arrive at the same answer. http://archinte.ama-assn.org/cgi/content/abstract/170/1/27
JAMA 6 Jan 2010 Vol 303
54 Many readers may not be cardiologists or hospital doctors, and I guess quite a few of you didn't know what NSTEMI stands for until about 8 years ago. Troponins only came in around then too, and they are vital to distinguish whether unstable angina is or is not associated with myocardial damage. Immediate angiography is also a relative novelty in the UK. Yet now every second hospital discharge summary now seems to read c/o chest pain NSTEMI troponin 2.1 PCI stents to LAD, Cx, please continue clopidogrel for 12 months. Here is a case study of a 43 year old American man which takes you through the modern management of NSTEMI in full wearisome detail.
http://jama.ama-assn.org/cgi/content/short/303/1/54?home
Lancet 9 Jan 2010 Vol 375
132 C-reactive protein was first described over 70 years ago, and we use it as a "something's wrong" test all the time, instead of or alongside ESR. It isn't actually all that much use, and patients often end up being told "Your blood test tells me you are ill, which I already knew, but it doesn't tell me what's wrong, so I want to repeat it." How many non-sequiturs can you squeeze into a sentence? And yet we all do it, taking obscure comfort later in the fact that 26 has fallen to 13. It's the same if you try to use it as a marker for cardiovascular risk. This immensely painstaking individual participant meta-analysis shows that even minor elevations of CRP are associated with increased risk for coronary heart disease; also for stroke; also for vascular death; also for non-vascular death; also for several cancers; also for lung disease. Elevated CRP is vaguely bad news: a Completely Random Predictor.
http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(09)61717-7/abstract
Wednesday, 6 January 2010
CARDIOVASCULAR OUTCOMES
Cardiovascular outcomes and mortality in patients using clopidogrel with a PPI: more data
10 December 2009
A large observational study finds no conclusive evidence for a clinically relevant drug interaction between clopidogrel and PPIs in elderly patients after percutaneous coronary intervention or hospitalisation for acute coronary syndrome.
Level of evidence:
Level 2 (limited quality patient-oriented evidence) according to the SORT criteria.
Action
This study adds to the evidence regarding the clinical significance of the interaction between clopidogrel and proton pump inhibitors (PPIs), but by itself should not change practice.
Healthcare professionals should continue to follow the existing advice from the MHRA, relating to the co-prescribing of a PPI with clopidogrel. This states:
The need for PPI therapy in patients who are also taking clopidogrel should be reviewed at their next appointment: avoid concomitant use of these medicines unless considered essential
Prescribe PPIs in line with their licensed indications where possible
Check whether patients who are taking clopidogrel are buying over-the-counter omeprazole and consider whether another gastrointestinal therapy would be more suitable.
No doubt European and UK regulatory authorities are examining this recent data and considering it alongside the rest of the evidence on this topic. Given the interest in this topic, if there are further developments we will produce another MeReC Stop Press or Rapid Review.
What is the background to this?
As reviewed in MeReC Extra 41, a CHMP review in May 2009 concluded that data supports a possible clinically significant interaction between clopidogrel and PPIs, that makes clopidogrel less effective. The CHMP recommended that product information for clopidogrel should be amended to discourage concomitant use of a PPI and clopidogrel unless considered absolutely necessary; hence, the MHRA advice given above.
The present study provides information obtained from three large cohorts (one in Canada, two in the US), on the risk of cardiovascular outcomes and mortality associated with the prescribing of clopidogrel and a PPI to elderly patients after percutaneous coronary intervention (PCI) or hospitalisation for acute coronary syndrome (ACS).
What does this study claim?
This study of 18,565 users of clopidogrel aged 65 years or older identified that 2.6% of those people who were initiated on clopidogrel with a PPI were hospitalised for myocardial infarction [MI], 1.5% died, and 3.4% underwent revascularisation. This compared with 2.1%, 0.9%, and 3.1%, respectively, for clopidogrel-users who were non-users of a PPI. The difference in the primary end point of MI or death was not statistically significantly different (adjusted rate-ratio [RR] 1.22; 95% confidence interval [CI] 0.99 to 1.51).
How does this relate to other studies?
The evidence for a clinically relevant drug interaction of clopidogrel and PPIs comes largely from observational studies (see the July Drug Safety Update). We previously blogged an analysis of two subsequent studies which found that, although PPIs attenuated the in-vitro antiplatelet effects of clopidogrel and prasugrel, the combination was not associated with an increased risk of adverse cardiovascular outcomes. These findings were consistent regardless of which PPI was used, or whether an H2-receptor antagonist was used.
Recently, the FDA has issued a Public Health Advisory that ‘new data’ has shown that when clopidogrel and omeprazole are taken together, the effectiveness of clopidogrel is reduced, and advises patients taking clopidogrel and omeprazole to consult their healthcare provider. The data on which this advisory is based comes from pharmacokinetic studies demonstrating reductions in the blood level of clopidogrel’s active metabolite when clopidogrel was taken with omeprazole, regardless of whether the omeprazole was taken at the same or different time of day. Some limited further information is provided for healthcare professionals. This states that the FDA are aware there are studies, such as the COGENT study (as yet unpublished) that might provide information about the effect of this interaction on clinical outcomes. However, the FDA considered that the applicability of data from this study is limited because of the study design and follow-up.
So what?
Despite the pharmacokinetic evidence of an interaction between clopidogrel and omeprazole, as recently reported by the FDA Public Health Advisory, not all studies measuring clinical outcomes have been able to demonstrate that PPIs significantly reduce the clinical effect of clopidogrel. This has resulted in some US cardiologists questioning the recommendations made by the FDA in response to the pharmacokinetic data.
In the present observational study, which used both traditional and advanced techniques to account for confounders, a higher proportion of patients suffered cardiovascular events or death if taking a PPI in addition to clopidogrel compared with clopidogrel alone. However, the difference was not statistically significant at the normally accepted probability level of 95%. The study did not rule out the possibility, taking 95% confidence intervals into account for the primary endpoint, that there could be as much as a 51% greater relative risk, as opposed to only as little as a 1% decreased relative risk, of patients who took a PPI and clopidogrel suffering a cardiovascular event or death compared with those taking clopidogrel alone. This would seem somewhat at odds with the authors’ concluding statement that the risk, if it exists, is “unlikely to exceed a 20% risk increase”.
This study by itself is inconclusive, but it does provide useful additional data that needs to be considered alongside that of other studies to assess the clinical significance of the clopidogrel/PPI interaction.
Study details
Rassen JA, et al. Cardiovascular outcomes and mortality in patients using clopidogrel with proton pump inhibitors after percutaneous coronary intervention or acute coronary syndrome. Circulation 2009;120:2322–29
Design
Observational study of three cohorts (Pennsylvania and New Jersey, US; British Columbia , Canada) identified from health insurance programs.
Patients
Patients (n=18,565) aged 65 years or older prescribed clopidogrel initially who underwent PCI or were hospitalised for ACS between 2001 and 2005.
Intervention and comparison
Rate ratios [RR] compared the incidence of the study outcomes among clopidogrel users who also used PPIs and those that were non-users of PPIs. Multivariate adjusted RRs were estimated by Cox proportional-hazards regression for each cohort and for the pooled cohorts. Patients were followed up for a median of 29 to 30 days among the PPI users and non-users (maximum 180 days).
Outcomes and results
On a pooled basis, 2.6% of those people who were initiated on clopidogrel with a PPI were hospitalised for MI compared with 2.1% for non-users; figures for death and revascularisation were 1.5% vs. 0.9% and 3.4% vs. 3.1%, respectively. The propensity score-adjusted RR for the primary endpoint of hospitalisation for MI or death was 1.22; 95%CI 0.99 to 1.51). There were also no significant differences between PPI users and non-users for the pooled cohort with respect to death (RR 1.20 [95%CI 0.84 to 1.70]) or revascularisation (RR 0.97 [95%CI 0.79 to 1.21]).
Sponsorship
The trial was publicly funded.
10 December 2009
A large observational study finds no conclusive evidence for a clinically relevant drug interaction between clopidogrel and PPIs in elderly patients after percutaneous coronary intervention or hospitalisation for acute coronary syndrome.
Level of evidence:
Level 2 (limited quality patient-oriented evidence) according to the SORT criteria.
Action
This study adds to the evidence regarding the clinical significance of the interaction between clopidogrel and proton pump inhibitors (PPIs), but by itself should not change practice.
Healthcare professionals should continue to follow the existing advice from the MHRA, relating to the co-prescribing of a PPI with clopidogrel. This states:
The need for PPI therapy in patients who are also taking clopidogrel should be reviewed at their next appointment: avoid concomitant use of these medicines unless considered essential
Prescribe PPIs in line with their licensed indications where possible
Check whether patients who are taking clopidogrel are buying over-the-counter omeprazole and consider whether another gastrointestinal therapy would be more suitable.
No doubt European and UK regulatory authorities are examining this recent data and considering it alongside the rest of the evidence on this topic. Given the interest in this topic, if there are further developments we will produce another MeReC Stop Press or Rapid Review.
What is the background to this?
As reviewed in MeReC Extra 41, a CHMP review in May 2009 concluded that data supports a possible clinically significant interaction between clopidogrel and PPIs, that makes clopidogrel less effective. The CHMP recommended that product information for clopidogrel should be amended to discourage concomitant use of a PPI and clopidogrel unless considered absolutely necessary; hence, the MHRA advice given above.
The present study provides information obtained from three large cohorts (one in Canada, two in the US), on the risk of cardiovascular outcomes and mortality associated with the prescribing of clopidogrel and a PPI to elderly patients after percutaneous coronary intervention (PCI) or hospitalisation for acute coronary syndrome (ACS).
What does this study claim?
This study of 18,565 users of clopidogrel aged 65 years or older identified that 2.6% of those people who were initiated on clopidogrel with a PPI were hospitalised for myocardial infarction [MI], 1.5% died, and 3.4% underwent revascularisation. This compared with 2.1%, 0.9%, and 3.1%, respectively, for clopidogrel-users who were non-users of a PPI. The difference in the primary end point of MI or death was not statistically significantly different (adjusted rate-ratio [RR] 1.22; 95% confidence interval [CI] 0.99 to 1.51).
How does this relate to other studies?
The evidence for a clinically relevant drug interaction of clopidogrel and PPIs comes largely from observational studies (see the July Drug Safety Update). We previously blogged an analysis of two subsequent studies which found that, although PPIs attenuated the in-vitro antiplatelet effects of clopidogrel and prasugrel, the combination was not associated with an increased risk of adverse cardiovascular outcomes. These findings were consistent regardless of which PPI was used, or whether an H2-receptor antagonist was used.
Recently, the FDA has issued a Public Health Advisory that ‘new data’ has shown that when clopidogrel and omeprazole are taken together, the effectiveness of clopidogrel is reduced, and advises patients taking clopidogrel and omeprazole to consult their healthcare provider. The data on which this advisory is based comes from pharmacokinetic studies demonstrating reductions in the blood level of clopidogrel’s active metabolite when clopidogrel was taken with omeprazole, regardless of whether the omeprazole was taken at the same or different time of day. Some limited further information is provided for healthcare professionals. This states that the FDA are aware there are studies, such as the COGENT study (as yet unpublished) that might provide information about the effect of this interaction on clinical outcomes. However, the FDA considered that the applicability of data from this study is limited because of the study design and follow-up.
So what?
Despite the pharmacokinetic evidence of an interaction between clopidogrel and omeprazole, as recently reported by the FDA Public Health Advisory, not all studies measuring clinical outcomes have been able to demonstrate that PPIs significantly reduce the clinical effect of clopidogrel. This has resulted in some US cardiologists questioning the recommendations made by the FDA in response to the pharmacokinetic data.
In the present observational study, which used both traditional and advanced techniques to account for confounders, a higher proportion of patients suffered cardiovascular events or death if taking a PPI in addition to clopidogrel compared with clopidogrel alone. However, the difference was not statistically significant at the normally accepted probability level of 95%. The study did not rule out the possibility, taking 95% confidence intervals into account for the primary endpoint, that there could be as much as a 51% greater relative risk, as opposed to only as little as a 1% decreased relative risk, of patients who took a PPI and clopidogrel suffering a cardiovascular event or death compared with those taking clopidogrel alone. This would seem somewhat at odds with the authors’ concluding statement that the risk, if it exists, is “unlikely to exceed a 20% risk increase”.
This study by itself is inconclusive, but it does provide useful additional data that needs to be considered alongside that of other studies to assess the clinical significance of the clopidogrel/PPI interaction.
Study details
Rassen JA, et al. Cardiovascular outcomes and mortality in patients using clopidogrel with proton pump inhibitors after percutaneous coronary intervention or acute coronary syndrome. Circulation 2009;120:2322–29
Design
Observational study of three cohorts (Pennsylvania and New Jersey, US; British Columbia , Canada) identified from health insurance programs.
Patients
Patients (n=18,565) aged 65 years or older prescribed clopidogrel initially who underwent PCI or were hospitalised for ACS between 2001 and 2005.
Intervention and comparison
Rate ratios [RR] compared the incidence of the study outcomes among clopidogrel users who also used PPIs and those that were non-users of PPIs. Multivariate adjusted RRs were estimated by Cox proportional-hazards regression for each cohort and for the pooled cohorts. Patients were followed up for a median of 29 to 30 days among the PPI users and non-users (maximum 180 days).
Outcomes and results
On a pooled basis, 2.6% of those people who were initiated on clopidogrel with a PPI were hospitalised for MI compared with 2.1% for non-users; figures for death and revascularisation were 1.5% vs. 0.9% and 3.4% vs. 3.1%, respectively. The propensity score-adjusted RR for the primary endpoint of hospitalisation for MI or death was 1.22; 95%CI 0.99 to 1.51). There were also no significant differences between PPI users and non-users for the pooled cohort with respect to death (RR 1.20 [95%CI 0.84 to 1.70]) or revascularisation (RR 0.97 [95%CI 0.79 to 1.21]).
Sponsorship
The trial was publicly funded.
Tuesday, 24 November 2009
CARDIOSNIPS FROM JOURNAL WATCH
JAMA 18 Nov 2009 Vol 302
2135 I like to say nice things about JAMA’s The Rational Clinical Examination series and this latest paper, Does This Patient with Palpitations Have a Cardiac Arrhythmia? maintains its high standards of thoroughness. But is this a real-life question? You feel the pulse and it’s irregular, so you do an ECG. Or you feel the pulse and it isn’t irregular, so you do a 24-hour ECG, or give the patient an event monitor (we have just acquired a nice dinky one). Rationally, the clinical examination is never enough. The one possible exception cited here is a regular rapid-pounding sensation in the neck or visible neck pulsations – this apparently signifies atrioventricular nodal reentry tachycardia. To which I would add syncope on sudden loud noises in a healthy young person, which is likely to be long QT syndrome.
http://jama.ama-assn.org/cgi/content/abstract/302/19/2135
BMJ 21 Nov 2009 Vol 339
1178 Income inequality generates bad health – this might be called the Marmot Effect, not after the personable rodent, but in honour of Michael Marmot, who first demonstrated it in the Whitehall Studies and was improbably knighted by the Major government as a result. There have been lots of subsequent studies all over the world, which are analysed here. They all show the same thing, independently of level of income.
http://www.bmj.com/cgi/content/full/339/nov10_2/b4471
1186 British general practice has led patients a merry old dance in recent years, as we’ve been incentivised to do one thing, then another, then the first thing again. If it’s had any benefit – other than to our personal income – it’s made us look very hard at certain groups of patients, notably those who have had heart disease. The QOF rules for secondary prevention are very clear, which won’t prevent them changing in the near future, when losartan and atorvastatin – which we are currently discouraged from prescribing - come off patent. Patient care plans in this context become largely a matter of rule-book medicine: they work, but soon show a ceiling effect. As you’d expect.
http://www.bmj.com/cgi/content/full/339/oct29_4/b4220
1187 Well-functioning old French people who walk slowly have a markedly increased risk of death from cardiovascular causes. This is illustrated on the front cover of the BMJ by a tortoise, which walks slowly and has a very low risk of death from cardiovascular causes. Still, it’s sweet.
http://www.bmj.com/cgi/content/full/339/nov10_2/b4460
Ann Intern Med 17 Nov 2009 Vol 151
677 All that a hand-held computer can do for me is make me swear. It is impossible to maintain the dignity and authority of age while taking one’s glasses off and squinting uncomprehendingly at an insolent little screen, while some young creature nearby rattles away at her tiny keys and comes up with all the right answers. So I am glad that the editorial which accompanies this study of a computerised handheld decision-support system to improve pulmonary embolism diagnosis sticks up for the superior utility of a proper nineteen-inch screen and a server that can do lots of things in an elegant and leisurely way. In fact the diagnosis of PE is a very good illustration of how a clinical decision rule can be applied, and I’m all for the principle of computers helping us to arrive at Bayesian applications of new diagnostic tests. It’s just those bloody little machines... And people who can use them…http://www.annals.org/content/151/10/677.abstracthttp://www.annals.org/content/151/10/748.extract
687 Many people are not very good at taking their blood pressure medication. In fact writing this has made me scuttle off to take the tiny dose of losartan that may (with a NNT of about 200 in my case) prevent me from having the stroke I might get anyway, or alternatively might never get. BP control is hugely important on a population level (see the Lancet’s piece on China, p.1765), but many people find it difficult to be an obedient member of the herd and take their pills without reminders. This trial shows that two self-management interventions can improve hypertension control: home monitoring and a nurse phone call every 2 months – preferably both.
http://www.annals.org/content/151/10/687.abstracthttp://www.thelancet.com/journals/lancet/article/PIIS0140-6736%2809%2961199-5/abstract
BMJ 14 Nov 2009 Vol 339
1125 Most group analyses of cardiovascular risk conclude that nearly all differences can be explained by known risk factors such as lipids and blood pressure and smoking, but this area–stratified Glasgow study is an exception. However, it did not measure event rates but a popular surrogate measure of atherosclerosis – the common carotid intima-media thickness. Glaswegians in deprived areas develop plaque in their carotids out of all proportion to known cardiovascular risk factors, including “emerging” ones like von Willebrand factor, tissue plasminogen activator antigen and all the rest.
http://www.bmj.com/cgi/content/full/339/oct27_4/b4170
Arch Intern Med 9 Nov 2009 Vol 169
1851 The thiazide diuretics have been around for 50 years, and this article celebrates them, the best of drugs for high blood pressure. They cause hypokalaemia and hyperglycaemia, but no study has ever found these to affect long-term outcomes. They may conserve bone mineral, though this isn’t discussed here. Americans always use hydrochlorthiazide or chlorthalidone: we always use bendroflumethiazide or chlortalidone. God knows why: but just keep using them.
http://archinte.ama-assn.org/cgi/content/abstract/169/20/1851
2135 I like to say nice things about JAMA’s The Rational Clinical Examination series and this latest paper, Does This Patient with Palpitations Have a Cardiac Arrhythmia? maintains its high standards of thoroughness. But is this a real-life question? You feel the pulse and it’s irregular, so you do an ECG. Or you feel the pulse and it isn’t irregular, so you do a 24-hour ECG, or give the patient an event monitor (we have just acquired a nice dinky one). Rationally, the clinical examination is never enough. The one possible exception cited here is a regular rapid-pounding sensation in the neck or visible neck pulsations – this apparently signifies atrioventricular nodal reentry tachycardia. To which I would add syncope on sudden loud noises in a healthy young person, which is likely to be long QT syndrome.
http://jama.ama-assn.org/cgi/content/abstract/302/19/2135
BMJ 21 Nov 2009 Vol 339
1178 Income inequality generates bad health – this might be called the Marmot Effect, not after the personable rodent, but in honour of Michael Marmot, who first demonstrated it in the Whitehall Studies and was improbably knighted by the Major government as a result. There have been lots of subsequent studies all over the world, which are analysed here. They all show the same thing, independently of level of income.
http://www.bmj.com/cgi/content/full/339/nov10_2/b4471
1186 British general practice has led patients a merry old dance in recent years, as we’ve been incentivised to do one thing, then another, then the first thing again. If it’s had any benefit – other than to our personal income – it’s made us look very hard at certain groups of patients, notably those who have had heart disease. The QOF rules for secondary prevention are very clear, which won’t prevent them changing in the near future, when losartan and atorvastatin – which we are currently discouraged from prescribing - come off patent. Patient care plans in this context become largely a matter of rule-book medicine: they work, but soon show a ceiling effect. As you’d expect.
http://www.bmj.com/cgi/content/full/339/oct29_4/b4220
1187 Well-functioning old French people who walk slowly have a markedly increased risk of death from cardiovascular causes. This is illustrated on the front cover of the BMJ by a tortoise, which walks slowly and has a very low risk of death from cardiovascular causes. Still, it’s sweet.
http://www.bmj.com/cgi/content/full/339/nov10_2/b4460
Ann Intern Med 17 Nov 2009 Vol 151
677 All that a hand-held computer can do for me is make me swear. It is impossible to maintain the dignity and authority of age while taking one’s glasses off and squinting uncomprehendingly at an insolent little screen, while some young creature nearby rattles away at her tiny keys and comes up with all the right answers. So I am glad that the editorial which accompanies this study of a computerised handheld decision-support system to improve pulmonary embolism diagnosis sticks up for the superior utility of a proper nineteen-inch screen and a server that can do lots of things in an elegant and leisurely way. In fact the diagnosis of PE is a very good illustration of how a clinical decision rule can be applied, and I’m all for the principle of computers helping us to arrive at Bayesian applications of new diagnostic tests. It’s just those bloody little machines... And people who can use them…http://www.annals.org/content/151/10/677.abstracthttp://www.annals.org/content/151/10/748.extract
687 Many people are not very good at taking their blood pressure medication. In fact writing this has made me scuttle off to take the tiny dose of losartan that may (with a NNT of about 200 in my case) prevent me from having the stroke I might get anyway, or alternatively might never get. BP control is hugely important on a population level (see the Lancet’s piece on China, p.1765), but many people find it difficult to be an obedient member of the herd and take their pills without reminders. This trial shows that two self-management interventions can improve hypertension control: home monitoring and a nurse phone call every 2 months – preferably both.
http://www.annals.org/content/151/10/687.abstracthttp://www.thelancet.com/journals/lancet/article/PIIS0140-6736%2809%2961199-5/abstract
BMJ 14 Nov 2009 Vol 339
1125 Most group analyses of cardiovascular risk conclude that nearly all differences can be explained by known risk factors such as lipids and blood pressure and smoking, but this area–stratified Glasgow study is an exception. However, it did not measure event rates but a popular surrogate measure of atherosclerosis – the common carotid intima-media thickness. Glaswegians in deprived areas develop plaque in their carotids out of all proportion to known cardiovascular risk factors, including “emerging” ones like von Willebrand factor, tissue plasminogen activator antigen and all the rest.
http://www.bmj.com/cgi/content/full/339/oct27_4/b4170
Arch Intern Med 9 Nov 2009 Vol 169
1851 The thiazide diuretics have been around for 50 years, and this article celebrates them, the best of drugs for high blood pressure. They cause hypokalaemia and hyperglycaemia, but no study has ever found these to affect long-term outcomes. They may conserve bone mineral, though this isn’t discussed here. Americans always use hydrochlorthiazide or chlorthalidone: we always use bendroflumethiazide or chlortalidone. God knows why: but just keep using them.
http://archinte.ama-assn.org/cgi/content/abstract/169/20/1851
Monday, 23 November 2009
ARTICLE ABSTRACTS
BMJ 14 Nov 2009 Vol 339
1125 Most group analyses of cardiovascular risk conclude that nearly all differences can be explained by known risk factors such as lipids and blood pressure and smoking, but this area–stratified Glasgow study is an exception. However, it did not measure event rates but a popular surrogate measure of atherosclerosis – the common carotid intima-media thickness. Glaswegians in deprived areas develop plaque in their carotids out of all proportion to known cardiovascular risk factors, including “emerging” ones like von Willebrand factor, tissue plasminogen activator antigen and all the rest.
http://www.bmj.com/cgi/content/full/339/oct27_4/b4170
NEJM 5 Nov 2009 Vol 361
1827 Coronary artery bypass grafting has become the commonest surgical operation in the world, we keep being informed, though I bet that isn’t counting circumcision. Still, everyone who isn’t Jewish, Muslim, American or male can still have CABG so it obviously wins on some higher criterion of ubiquity. Eighty percent of it is still performed using a cardiopulmonary bypass pump to help the surgeon by keeping the heart still. These pumps are known to generate debris and causing microemboli, which have been held responsible for the cognitive impairment often seen after open heart procedures. Innovative cardiothoracic surgeons have argued for off-pump CABG and here they show willingness to put their assertions to the test of a randomised trial. As the accompanying editorial (p.1897) notes, this in itself should be seen as an enormous success. As for the result: sorry innovators, off-pump patients fare slightly worse by criteria of graft completion and late patency, and no better in neuropsychological assessments. http://content.nejm.org/cgi/content/abstract/361/19/1827
1125 Most group analyses of cardiovascular risk conclude that nearly all differences can be explained by known risk factors such as lipids and blood pressure and smoking, but this area–stratified Glasgow study is an exception. However, it did not measure event rates but a popular surrogate measure of atherosclerosis – the common carotid intima-media thickness. Glaswegians in deprived areas develop plaque in their carotids out of all proportion to known cardiovascular risk factors, including “emerging” ones like von Willebrand factor, tissue plasminogen activator antigen and all the rest.
http://www.bmj.com/cgi/content/full/339/oct27_4/b4170
NEJM 5 Nov 2009 Vol 361
1827 Coronary artery bypass grafting has become the commonest surgical operation in the world, we keep being informed, though I bet that isn’t counting circumcision. Still, everyone who isn’t Jewish, Muslim, American or male can still have CABG so it obviously wins on some higher criterion of ubiquity. Eighty percent of it is still performed using a cardiopulmonary bypass pump to help the surgeon by keeping the heart still. These pumps are known to generate debris and causing microemboli, which have been held responsible for the cognitive impairment often seen after open heart procedures. Innovative cardiothoracic surgeons have argued for off-pump CABG and here they show willingness to put their assertions to the test of a randomised trial. As the accompanying editorial (p.1897) notes, this in itself should be seen as an enormous success. As for the result: sorry innovators, off-pump patients fare slightly worse by criteria of graft completion and late patency, and no better in neuropsychological assessments. http://content.nejm.org/cgi/content/abstract/361/19/1827
Friday, 25 September 2009
WOMEN, HEARTS & DIABETES
Arch Intern Med 14 Sep 2009 Vol 169
1484 If you are going to use thrombolysis for occlusive stroke, the sooner you do it the better: if this sounds obvious now, consider how unobvious it sounded ten years ago, or even five to most people in the street. The number needed to treat is still very high, and if this German cluster-randomised trial of a public awareness campaign had used a hard end-point, like overall reduction of disability or death from stroke, it would have had a zero result. Instead, it yielded a 27% increase in women with stroke reaching hospital within three hours. I think that we can conclude that personal letters with bookmarks and stickers are not a cost-effective basis for a stroke awareness campaign.
http://archinte.ama-assn.org/cgi/content/abstract/169/16/1484
Ann Intern Med 15 Sep 2009 Vol 151
386 When reading papers with the words “net value of health care” in the title, it is always worth remembering that the best way to ensure value in health care is to ensure a swift death for everyone who is not working, especially the elderly. However, this Mayo Clinic study of the net value of health care for patients with type 2 diabetes, 1997 to 2005, is somewhat less drastic in its approach, and bases its figures on the reduction in spending on coronary heart disease in the UKPDS tight control cohort. These were patients in their early fifties with new-onset diabetes, so they don’t actually tell us anything about the economics of treating people with type 2 diabetes in the age beyond retirement. Just as well, really. http://www.annals.org/cgi/content/abstract/151/6/386
394 The thing that goaded me into writing an editorial on tight control of glucose in longstanding type 2 diabetics last March was the silence of diabetologists following the ADVANCE and ACCORD studies in June the previous year, plus the VADT study which told the same story and was published in January 2009. These were prospective randomised trials designed to answer much the same question, and they all gave the same answer: intensive glucose control in established type 2 diabetes does not reduce overall cardiovascular mortality and increases the risk of severe hypoglycaemia. Since then a number of meta-analyses have appeared, this being the latest. These include long-term observational data from UKPDS, which was not designed to answer this question; The Lancet , one also included data from a wildly irrelevant study, and there is a further one waiting in the wings on the Diabetologia website. As a study in the sociology and psychology of medical practice, this is quite interesting and a little dispiriting, but as far as treating patients goes, the message could not be simpler. For type 2 diabetics a few years into the disease process, there is no point aiming for an HbA1c under 7.5%. There is a tendency to fewer non-fatal CV events and perhaps some renal protection for a tiny number, but overall it makes no difference and causes hypoglycaemic episodes, which can cause brain damage. Cognitive impairment should be an end-point in future studies.
http://www.annals.org/cgi/content/abstract/151/6/394
BMJ 5 Sep 2009 Vol 339
And now to the vexed question of which drugs should be used for type 2 diabetes, where nothing quite works out as it should. For example, the thiazolidinediones as a group have a favourable effect on HbA1c , on lipids and on measures of insulin resistance. Rosiglitazone has a greater effect on peroxisome proliferators activated receptors (PPARs) than pioglitazone and by rights it should be the better drug. Both cause an equal amount of peripheral oedema. But in fact pioglitazone causes less heart failure than rosiglitazone and a big Canadian cohort study has a better mortality record as well. Yet the accompanying editorial sounds a note of caution about the data we have at present, and warns us against too much enthusiasm for any of the newer incretin pathway drugs too. The fact is that in diabetic therapeutics, as in most of medicine, you just can’t tell what is going to happen until enough of it has happened.
http://www.bmj.com/cgi/content/abstract/339/aug18_2/b2942
JAMA 2 Sep 2009 Vol 302
947 Funny how medical terms change meaning: to an old pedant like me, acute coronary syndromes mean any acute syndromes caused by the coronary arteries, including myocardial infarction and sudden death, but it seems that JAMA readers automatically assume that it only means coronary syndromes without ST elevation. With these latter syndromes there is still room for debate about the relative merits of immediate versus delayed intervention, the key question in this multicentre French trial. Patients with non-ST elevation ACS were randomised to get their angiographic intervention either immediately (mean 70 minutes) or on the next working day (mean 21 hours) and the outcome was myocardial infarction measured by troponin 1. There was no difference between groups in this important short-term outcome.
http://jama.ama-assn.org/cgi/content/abstract/302/9/947
NEJM 3 Sep 2009 Vol 361
980 A Dutch study shows that patients undergoing vascular surgery do better if they take a perioperative high dose statin. The rate of myocardial infarction and cardiovascular death within 28 days was halved with fluvastatin 80mg. More evidence that the protective effect of statins is not mediated through long-term effects on lipids.
http://content.nejm.org/cgi/content/abstract/361/10/980
990 I have previously described coronary artery calcium screening as the payment of large sums to receive high doses of ionising radiation in return for an increase in anxiety. This article on its place in cardiovascular prevention strategies reaches much the same conclusion, but I’m sure this will do nothing to dent its popularity with the rich worried well.
http://content.nejm.org/cgi/content/extract/361/10/990
1484 If you are going to use thrombolysis for occlusive stroke, the sooner you do it the better: if this sounds obvious now, consider how unobvious it sounded ten years ago, or even five to most people in the street. The number needed to treat is still very high, and if this German cluster-randomised trial of a public awareness campaign had used a hard end-point, like overall reduction of disability or death from stroke, it would have had a zero result. Instead, it yielded a 27% increase in women with stroke reaching hospital within three hours. I think that we can conclude that personal letters with bookmarks and stickers are not a cost-effective basis for a stroke awareness campaign.
http://archinte.ama-assn.org/cgi/content/abstract/169/16/1484
Ann Intern Med 15 Sep 2009 Vol 151
386 When reading papers with the words “net value of health care” in the title, it is always worth remembering that the best way to ensure value in health care is to ensure a swift death for everyone who is not working, especially the elderly. However, this Mayo Clinic study of the net value of health care for patients with type 2 diabetes, 1997 to 2005, is somewhat less drastic in its approach, and bases its figures on the reduction in spending on coronary heart disease in the UKPDS tight control cohort. These were patients in their early fifties with new-onset diabetes, so they don’t actually tell us anything about the economics of treating people with type 2 diabetes in the age beyond retirement. Just as well, really. http://www.annals.org/cgi/content/abstract/151/6/386
394 The thing that goaded me into writing an editorial on tight control of glucose in longstanding type 2 diabetics last March was the silence of diabetologists following the ADVANCE and ACCORD studies in June the previous year, plus the VADT study which told the same story and was published in January 2009. These were prospective randomised trials designed to answer much the same question, and they all gave the same answer: intensive glucose control in established type 2 diabetes does not reduce overall cardiovascular mortality and increases the risk of severe hypoglycaemia. Since then a number of meta-analyses have appeared, this being the latest. These include long-term observational data from UKPDS, which was not designed to answer this question; The Lancet , one also included data from a wildly irrelevant study, and there is a further one waiting in the wings on the Diabetologia website. As a study in the sociology and psychology of medical practice, this is quite interesting and a little dispiriting, but as far as treating patients goes, the message could not be simpler. For type 2 diabetics a few years into the disease process, there is no point aiming for an HbA1c under 7.5%. There is a tendency to fewer non-fatal CV events and perhaps some renal protection for a tiny number, but overall it makes no difference and causes hypoglycaemic episodes, which can cause brain damage. Cognitive impairment should be an end-point in future studies.
http://www.annals.org/cgi/content/abstract/151/6/394
BMJ 5 Sep 2009 Vol 339
And now to the vexed question of which drugs should be used for type 2 diabetes, where nothing quite works out as it should. For example, the thiazolidinediones as a group have a favourable effect on HbA1c , on lipids and on measures of insulin resistance. Rosiglitazone has a greater effect on peroxisome proliferators activated receptors (PPARs) than pioglitazone and by rights it should be the better drug. Both cause an equal amount of peripheral oedema. But in fact pioglitazone causes less heart failure than rosiglitazone and a big Canadian cohort study has a better mortality record as well. Yet the accompanying editorial sounds a note of caution about the data we have at present, and warns us against too much enthusiasm for any of the newer incretin pathway drugs too. The fact is that in diabetic therapeutics, as in most of medicine, you just can’t tell what is going to happen until enough of it has happened.
http://www.bmj.com/cgi/content/abstract/339/aug18_2/b2942
JAMA 2 Sep 2009 Vol 302
947 Funny how medical terms change meaning: to an old pedant like me, acute coronary syndromes mean any acute syndromes caused by the coronary arteries, including myocardial infarction and sudden death, but it seems that JAMA readers automatically assume that it only means coronary syndromes without ST elevation. With these latter syndromes there is still room for debate about the relative merits of immediate versus delayed intervention, the key question in this multicentre French trial. Patients with non-ST elevation ACS were randomised to get their angiographic intervention either immediately (mean 70 minutes) or on the next working day (mean 21 hours) and the outcome was myocardial infarction measured by troponin 1. There was no difference between groups in this important short-term outcome.
http://jama.ama-assn.org/cgi/content/abstract/302/9/947
NEJM 3 Sep 2009 Vol 361
980 A Dutch study shows that patients undergoing vascular surgery do better if they take a perioperative high dose statin. The rate of myocardial infarction and cardiovascular death within 28 days was halved with fluvastatin 80mg. More evidence that the protective effect of statins is not mediated through long-term effects on lipids.
http://content.nejm.org/cgi/content/abstract/361/10/980
990 I have previously described coronary artery calcium screening as the payment of large sums to receive high doses of ionising radiation in return for an increase in anxiety. This article on its place in cardiovascular prevention strategies reaches much the same conclusion, but I’m sure this will do nothing to dent its popularity with the rich worried well.
http://content.nejm.org/cgi/content/extract/361/10/990
Tuesday, 21 April 2009
Cardiovascular Risk
National Library for Public Health Specialist Library
CVD risk assessment and management: Cardiovascular disease risk assessment and management
CVD risk assessment and management: Cardiovascular disease risk assessment and management
Click here to go to the full text
This record contains the following:
- Clinical summary: Assessing cardiovascular risk
How should I determine whether a person is at high risk of cardiovascular events?
What blood tests are recommended when screening someone for cardiovascular disease risk?
Which calculator should I use to calculate a person's risk of cardiovascular disease?
How should I interpret the calculated cardiovascular risk?
What information and advice should I give a person when their CVD risk is assessed?
Clinical summary: Managing comorbidities to reduce cardiovascular risk
Which conditions need particular management because they are associated with increased risk of cardiovascular disease?
- Clinical summary: Advising on lifestyle to reduce cardiovascular risk
How can I encourage and support a person to adopt a healthy lifestyle?
What should I advise about adopting a cardioprotective diet?
What should I advise about stopping smoking?
What should I advise about physical activity?
What should I advise about alcohol consumption?
What should I advise about losing weight?
Clinical summary: Drug interventions to reduce cardiovascular risk
How should I manage lipids to reduce cardiovascular risk?
How should I manage blood pressure to reduce cardiovascular risk?
How should I prescribe antiplatelet therapy to reduce cardiovascular risk?
What treatment is recommended to reduce the risk of cardiovascular disease after a myocardial infarction?
Publication Date: 01 Dec 2008
Publisher: CKS
Source: Clinical Knowledge Summaries
Keywords
Risk of cardiovascular disease
Topics
Determinants
Individual behaviour
Eating habits
Physical activity
Outcomes
Circulatory diseases
Cardiovascular diseases
Endocrine disorders
Diabetes
Management & interventions
Services
Population based & preventative services
Screening
The following Specialist Libraries also reference this resource
Cardiovascular Diseases
Stroke
Vascular
**********************************************************************************
Consensus on the Management of Cardiovascular Risk in Primary Care : a summary for general practice
Available as a webcast at www.healthcarerepublic.com/webcasts
Wednesday, 4 February 2009
CVD risk assessment and management: Cardiovascular disease risk assessment and management
This record contains the following:
Clinical summary: Assessing cardiovascular risk
How should I determine whether a person is at high risk of cardiovascular events?
What blood tests are recommended when screening someone for cardiovascular disease risk?
Which calculator should I use to calculate a person's risk of cardiovascular disease?
How should I interpret the calculated cardiovascular risk?
What information and advice should I give a person when their CVD risk is assessed?
Clinical summary: Managing comorbidities to reduce cardiovascular risk
Which conditions need particular management because they are associated with increased risk of cardiovascular disease?
Clinical summary: Advising on lifestyle to reduce cardiovascular risk
How can I encourage and support a person to adopt a healthy lifestyle?
What should I advise about adopting a cardioprotective diet?
What should I advise about stopping smoking?
What should I advise about physical activity?
What should I advise about alcohol consumption?
What should I advise about losing weight?
Clinical summary: Drug interventions to reduce cardiovascular risk
How should I manage lipids to reduce cardiovascular risk?
How should I manage blood pressure to reduce cardiovascular risk?
How should I prescribe antiplatelet therapy to reduce cardiovascular risk?
What treatment is recommended to reduce the risk of cardiovascular disease after a myocardial infarction?
Publication Date: 01 Dec 2008
Publisher: CKS
Source: Clinical Knowledge Summaries
Keywords
Risk of cardiovascular disease
Topics
Determinants
Individual behaviour
Eating habits
Physical activity
Outcomes
Circulatory diseases
Cardiovascular diseases
Endocrine disorders
Diabetes
Management & interventions
Services
Population based & preventative services
Screening
The following Specialist Libraries also reference this resource
Cardiovascular Diseases
Stroke
Vascular
Clinical summary: Assessing cardiovascular risk
How should I determine whether a person is at high risk of cardiovascular events?
What blood tests are recommended when screening someone for cardiovascular disease risk?
Which calculator should I use to calculate a person's risk of cardiovascular disease?
How should I interpret the calculated cardiovascular risk?
What information and advice should I give a person when their CVD risk is assessed?
Clinical summary: Managing comorbidities to reduce cardiovascular risk
Which conditions need particular management because they are associated with increased risk of cardiovascular disease?
Clinical summary: Advising on lifestyle to reduce cardiovascular risk
How can I encourage and support a person to adopt a healthy lifestyle?
What should I advise about adopting a cardioprotective diet?
What should I advise about stopping smoking?
What should I advise about physical activity?
What should I advise about alcohol consumption?
What should I advise about losing weight?
Clinical summary: Drug interventions to reduce cardiovascular risk
How should I manage lipids to reduce cardiovascular risk?
How should I manage blood pressure to reduce cardiovascular risk?
How should I prescribe antiplatelet therapy to reduce cardiovascular risk?
What treatment is recommended to reduce the risk of cardiovascular disease after a myocardial infarction?
Publication Date: 01 Dec 2008
Publisher: CKS
Source: Clinical Knowledge Summaries
Keywords
Risk of cardiovascular disease
Topics
Determinants
Individual behaviour
Eating habits
Physical activity
Outcomes
Circulatory diseases
Cardiovascular diseases
Endocrine disorders
Diabetes
Management & interventions
Services
Population based & preventative services
Screening
The following Specialist Libraries also reference this resource
Cardiovascular Diseases
Stroke
Vascular
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