Showing posts with label hormone replacement therapy. Show all posts
Showing posts with label hormone replacement therapy. Show all posts

Tuesday, 2 March 2010

SNIPPETS FROM JOURNALS

The following are all from www.cebm.net

Lancet 27 Feb 2010 Vol 375
727 Not long ago, someone had a myocardial infarction on a transatlantic flight. So what does a professor of surgery do under these circumstances? Possibly take an aspirin and pray a good deal. He should have squeezed his arm repeatedly for periods of five minutes or so at a pressure above systolic. Believe it or not, this simple manoeuvre can reduce the area of myocardial damage, as proved in this Danish trial where patients with presumptive MI were randomised to have the squeezing done (or not done) by a sphygmomanometer in the ambulance conveying them to hospital. This is known as ischaemic preconditioning, though in such circumstances it should perhaps be known as simultaneous ischaemic conditioning. There were no hard end-points in this trial but a convincing reduction in damage on myocardial perfusion imaging at 30 days. More trials are needed, but meantime there seems no possible reason not to give it a try.
http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(09)62001-8/abstract

752 This is a rather rambling 10-page review of dilated cardiomyopathy. The Panel of Mechanisms covers just about everything except interference by aliens, and there's a panel of gene loci too, but no panel of relative frequencies and prognoses for each aetiology. There is no mention of spontaneous recovery, which can't be rare if it has been seen twice.
http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(09)62023-7/abstract

763 Say you had stable coronary artery disease: would you want an angiogram? And if the cardiologist saw a stenosis, would you want a stent put in? A year or two ago, these questions would have seemed like no-brainers, but then along came COURAGE and BARI-2D showing that medical treatment is as good as percutaneous intervention. Do you truly and deeply believe this, though? See how you feel when you read this review by two Swiss and an American cardiologist. It presents enough evidence to allow a tailored approach, and says that it "proposes a treatment algorithm that is applicable to daily clinical practice." The word "algorithm" is to be avoided, but people who use it generally refer to a flow chart, but there isn't one. http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(10)60168-7/abstract

BMJ 27 Feb 2010 Vol 340
459 A useful systematic review compares the results of carotid endarterectomy vs. carotid stenting in 11 randomised trials. On the face of it, endarterectomy wins, because the risk of periprocedural stroke is less; in the longer term there is little difference. Techniques and experience increase all the time - it may happen that the guy who puts in stents near you does that better than the guy who scrapes arteries. So more studies are justified and the matter is not quite settled yet.
http://www.bmj.com/cgi/content/full/340/feb12_1/c467

JAMA 17 Feb 2010 Vol 303
631 The Women's Genome Health Study is a prospective cohort of 19,313 women followed up for a median of 12.3 years, during which they experienced 777 cardiovascular events. In these women, 101 single nucleotide polymorphisms were added with one or two other genomic factors to create a genetic risk score. Surely this would usher in a new era of refined cardiovascular risk prediction? Well, actually it showed no significant association with the incidence of total cardiovascular disease: a simple family history alone was more predictive. On the other hand, there is so much anonymized data about the participants that you could probably find out the full disease status of any individual if you could identify their genome from some other source. This is discussed in a fascinating commentary on p.659. Genomic studies seem almost disconcertingly useless at the population level, but if you know 35,000 gene variants in a single individual, you can measure their left ventricular mass more accurately than if you had an echocardiogram.
http://jama.ama-assn.org/cgi/content/abstract/303/7/631

NEJM 18 Feb 2010 Vol 362
590 Some people like to see evidence from randomised controlled trials with hard end-points before a computer prediction that a certain intervention will reduce new cases of CHD in America by up to 120,000 annually, stroke by up to 66,000, and death by up to 92,000. The editorial on p. 650 suggests a saving in health costs of $10-24 billion. Aha, we save health costs by keeping older people alive longer, do we? Apart from that basic point, there is also the problem that the evidence for salt reduction is - as far as I can tell - nowhere near as strong as the computer model in this economic simulation suggests. The evidence we have is about a surrogate marker - blood pressure - which can be reduced slightly by the sort of salt reductions proposed here and already in force in the UK for prepared foods. On the balance of probabilities, I'm happy to support salt reduction, as I am carbon emission reduction; but that doesn't mean swallowing every extrapolation that zealots come up with. A paper like this doesn't really belong in the world's leading medical journal.
http://content.nejm.org/cgi/content/abstract/362/7/590

Ann Intern Med 16 Feb 2010 Vol 152
211 The Women's Health Initiative trial was an RCT of hormone replacement therapy which brought about a volte-face in clinical practice but which is described as "far from impeccable" in a letter in this week's BMJ (p.382). Peccability is openly confessed in this Lenten analysis of the effect of continuous combined HRT on coronary heart disease. They more or less admit to residual confounding and small subgroup sizes. The bottom line message is that continuous HRT may confer added risk of CHD in the first years, then decreased risk after 6 years. Which is not quite what we were all initially led to believe.
http://www.annals.org/content/152/4/211.abstract

218 Initiated permanent anticoagulation for severe recurrent superficial thrombophlebitis with the reluctant concurrence of the local haematologist. Such events are benign and self-limiting and do not herald serious thromboembolism, but this French study casts doubts on that. In fact 25% of subjects with superficial phlebitis of 5cm or more had or went on to develop deep vein thrombosis in this series of 844 consecutive cases in a specialist referral centre. We need some primary care studies, quite urgently.
http://www.annals.org/content/152/4/218.abstract