{"id":25396,"date":"2013-03-25T10:42:33","date_gmt":"2013-03-25T09:42:33","guid":{"rendered":"https:\/\/blogs.bmj.com\/bmj\/?p=25396"},"modified":"2013-03-25T10:42:33","modified_gmt":"2013-03-25T09:42:33","slug":"richard-lehmans-journal-review-25-march-2013","status":"publish","type":"post","link":"https:\/\/blogs.bmj.com\/bmj\/2013\/03\/25\/richard-lehmans-journal-review-25-march-2013\/","title":{"rendered":"Richard Lehman’s journal review\u201425 March 2013"},"content":{"rendered":"

\"RichardJAMA\u00a0 20 Mar 2013\u00a0 Vol 309<\/strong>
\n1125\u00a0\u00a0\u00a0 Is aliskiren a good drug for heart failure? Despite the negative result of this Novartis-funded trial (ASTRONAUT), I think the answer is probably yes. First of all, let me remind you that aliskiren is a direct renin blocker. In other words, it acts right at the start of the renin-angiotensin- aldosterone cascade. But unfortunately for alis and her sister kirens, these renin blockers have come on the scene too late. We already have perfectly good RAAS inhibitors in the form of ACE inhibitors, ARBs, and aldosterone blockers, and between them they do all that it is possible to do via RAAS inhibition in heart failure: which, by the way, is not much, since typical NNTs lie over 30. Now imagine a world where renin blockers were first on the scene, and we selected patients for heart failure trials on the basis of BNP rather than ejection fraction; then this trial<\/a> would probably have been a resounding success. Because the ASTRONAUT groups were not well matched: the patients put on aliskiren had a mean NT-BNP of 4239 pg\/ml compared with 2718 pg\/ml in the placebo group: in other words, they were experiencing considerably worse ventricular strain. Yet they still had better outcomes than the less ill controls, albeit not to the point of statistical significance. If you removed all the ACE inhibitors, ARBs, and the amazing amount of mineralocorticoid blockade (57%) from these patients, there would probably have been a very significant benefit in mortality and readmission from aliskiren. But life is unfair, and Novartis may just have to face the fact that Alice has come too late to lead them into Wonderland: though a trial in heart failure with preserved systolic ejection fraction, but without diabetes, might be interesting.
\n<\/p>\n

1136\u00a0\u00a0 Having a stroke when you are young (under 50) increases your risk of dying<\/a> over the next 20 years by 3-4 times. Which is sad, but hardly unexpected.<\/p>\n

1146\u00a0\u00a0 The UK and the US health systems each have their idiocies, and these are shared in various fascinating ways. One common theme is that you can easily identify \u201cnon-emergency cases\u201d and then penalise patients or doctors according to how many of these undeserving individuals attend the emergency department. This study from a New York City Emergency Department<\/a> shows that quite a few of these \u201cnon-emergencies\u201d\u2014meaning cases registered on arrival as suitable for non-urgent primary care instead\u2014turn out to be real emergencies requiring immediate care or hospitalisation. Now here in the UK, we have this system called 111\u2026 but I won\u2019t torment you by trying to describe this ultimate refinement of stupidity.<\/p>\n

NEJM\u00a0 21 Mar 2013\u00a0 Vol 368<\/strong>
\n1083\u00a0\u00a0 I love to read about medical progress, which makes me a sucker for giving innovative treatments the benefit of the doubt. About 15 years ago I was really intrigued to learn that quite a few ischaemic strokes were likely to be paradoxical\u2014and that you could actually demonstrate shift of clot from the right to the left heart via a patent foramen ovale. In fact I was about a century late, because this mechanism had been proposed in the 1890s. But although in those days they were very good at performing autopsies, they didn\u2019t have transoesophageal ultrasound to look for functional right-to-left shift. The excellent editorial \u201cStill no Closure on the Question of PFO Closure<\/a>\u201d puts this into perspective: \u201cIn approximately 30% of young survivors of stroke, no clear cause is identified despite a thorough evaluation. Patent foramen ovale is found on transesophageal echocardiography in about half of these patients, as compared with approximately 25% of the general population. Clinicians, then, often assume that the patent foramen ovale was the cause of the stroke, although it may be incidental in some patients.\u201d<\/p>\n

So there\u2019s really no way to find out if PFO closure works better than standard medical therapy without doing a randomised trial, and even this won\u2019t tell you whether any given individual will benefit. This first trial<\/a> was designed 14 years ago to try out the Amplatzer PFO Occluder (St. Jude Medical) versus antiplatelet or anticoagulant treatment. After a mean patient follow-up of 4 years, the triallists conclude: \u201cClosure of a patent foramen ovale for secondary prevention of cryptogenic embolism did not result in a significant reduction in the risk of recurrent embolic events or death as compared with medical therapy.\u201d In fact they are quite harsh on themselves, because the device was observed to reduce strokes and TIAs by a third, but was inadequately powered to reach statistical significance.<\/p>\n

1092\u00a0\u00a0 And now, oddly enough, we get the results from another St Jude-funded trial of the same device in a similar but larger group of patients<\/a>. Again, there were fewer events in the PFO closure group\u2014this time fewer than half\u2014but the authors seem reluctant to trumpet the fact. \u201cIn the primary intention-to-treat analysis, there was no significant benefit associated with closure of a patent foramen ovale in adults who had had a cryptogenic ischemic stroke. However, closure was superior to medical therapy alone in the prespecified per-protocol and as-treated analyses, with a low rate of associated risks.\u201d This is all very admirable, but it makes you wonder what is going on. Is this the NEJM<\/em> responding to criticism that it lets industry get away with too much sales pitching in its abstracts? Or is this industry itself indulging in what you might call \u201creverse marketing\u201d\u2014being so modest in its claims that people will rally to the defence of the product? Either way, I\u2019m sure it won\u2019t affect NEJM<\/em> sales of reprints to St Jude.<\/p>\n

1111\u00a0\u00a0\u00a0 Less than a century ago, the mosquitoes of Northern Europe (and America all the way up to the Great Lakes) used to carry malaria parasites, but they gave up by about 1940. The mosquitoes of hotter countries are another matter. The amazing plasmodia of malaria still multiply within their intestines and spread therefrom to the juicy blood and liver of humans, especially in Africa and India. They have had a million years or more to perfect their evasion of our immune system, but you\u2019d still think that by now we\u2019d have been able to produce a vaccine to kill them. The vaccine called RTS,S\/AS01E was trialled in babies and toddlers in Kilfili, Kenya a few years ago: here are the four year follow up data<\/a>. It was a success: in total, 65 cases were averted per 100 vaccinated children. It was a failure: efficacy declined over time and with increasing malaria exposure, with an estimate over four years of 16.8%. Plasmodium falciparum<\/em> is a horribly elusive enemy, and a weapon of mass destruction. I get angry reading about it.<\/p>\n

Lancet\u00a0 23 Mar 2013\u00a0 Vol 381<\/strong>
\n997\u00a0\u00a0 The old Australian joke runs: \u201cHow can you tell if a flight has arrived from the UK?\u201d \u201cIt\u2019s when they switch the engines off but the whining gets louder.\u201d Dozens of distinguished Poms here join with a few foreigners to whine about how very bad British health outcomes are, compared with most other comparable countries, in a lengthy article with pages of intricate charts<\/a>. You\u2019ve already read about these in the newspapers, so I won\u2019t go into detail; though I could easily do, because a febrile illness means that I am reduced to reading this stuff instead of meeting people I had been looking forward to for months. And actually, I don\u2019t know what the fuss is about. For an overcrowded island with a broken economy, growing social inequality, vile weather, and decades of inadequate health spending, we\u2019re actually doing quite well. And anyway, isn\u2019t a life expectancy of 80 about right?\u2014certainly if you have to spend 80 of them in Britain.<\/p>\n

1021\u00a0\u00a0 This report about a new tuberculosis vaccine<\/a> reads a bit like the NEJM<\/em> report on the malaria vaccine. It may be a step forward, but it\u2019s really hard to tell. The vaccine in question contains modified Vaccinia Ankara virus expressing antigen 85A (MVA85A), and was designed to enhance the protective efficacy of BCG given to infants in areas of high TB prevalence. It \u201cwas well tolerated and induced modest cell-mediated immune responses\u201d but it didn\u2019t protect the kids from getting clinical TB. The editorial nonetheless describes it as \u201ca major event for new TB vaccines.\u201d Go there if you want more detail: I got lost.<\/p>\n

BMJ\u00a0\u00a0 23 Mar 2013\u00a0 Vol 346<\/strong>
\nI don\u2019t generally comment on politics in these reviews, but the best pieces in this week\u2019s BMJ<\/em> are the superb editorial on the soon-to-disappear NHS by Fiona Godlee, \u201cSleepwalking into the market,<\/a>\u201d and Martin McKee\u2019s summary of how we came to the to the point where \u201cEngland\u2019s healthcare now lies in the hands of lawyers.<\/a>\u201d These are the competition lawyers who will feast on the ambiguities of the revised regulations that come into force on 1st April. Don\u2019t worry folks: there\u2019s nothing you can do about this. No normal human being could actually make sense of the NHS Act, and no Clinical Commissioning Group can fight these corporate lawyers. No political party that you voted for ever promised you anything like this. You are powerless. They would like you to know that.<\/p>\n

It\u2019s a wonder that any Australian truck driver, with no company but the local radio station and a dangling nylon kangaroo, can cover the 3000 kilometres across the Australian desert without an accident caused by tiredness. Their secret is caffeine. At least, that is what this case-control study would have you believe<\/a>. 43% of Australian truckies reported taking caffeine-containing substances expressly to stay awake, and they had a 63% reduced likelihood of crashing. It should be made compulsory.<\/p>\n

In a well-written analysis<\/a>, the NICE \u201ctraffic light\u201d clinical decision rule for serious bacterial infection in children comes under scrutiny from Australian academics. Between 2004 and 2006, they collected a cohort of over 15,000 children presenting with fever at the Children\u2019s Hospital at Westmead. The predictive characteristics of any diagnostic or triage tool depend on the population seen, of course, and I don\u2019t know how closely these kids resemble the ones I see in British out-of-hours primary care, but I imagine they are very similar. And the NICE traffic lights don\u2019t do all that well, either for sensitivity (catching all serious infections) or specificity (bundling up minor with major illness). Adding a urine dipstick test helped, though an eye-watering 45.2% of these children underwent direct bladder sampling with an in-out catheter. My conclusion is that the NICE traffic lights are a NICE start, but there is something we are missing here\u2014and what is the magic ingredient that would give us a better tool? Is it the test of time? Clinical and parental gut feeling? Do we just have to accept that the price we have to pay for maintaining our amazingly low death rates is a degree of over-caution?<\/p>\n

JAMA\u00a0 Intern Med\u00a0 11 Mar 2013\u00a0 Vol 173<\/strong>
\n345\u00a0\u00a0\u00a0 Here\u2019s an intriguing paper<\/a> which takes us into a future where patient care will be much more interactive. It\u2019s called \u201cParticipatory Surveillance of Hypoglycemia
\nand Harms in an Online Social Network:\u201d what you don\u2019t learn from the title, or even the abstract, is that most of the participants had type 1 diabetes and the few that had type 2 were almost all taking insulin. And because the respondents were self-selected, the actual numerical data have no absolute meaning, but they tell a very clear story: \u201cOf 613 respondents (24.3% of app users), 49.1% reported more than 4 episodes of \u201cgoing low\u201d in the past 2 weeks and 29.2% reported 1 or more severe low in the past year; 16.6% reported both more than 4 recent low episodes and 1 or more severe event in the past year. Harms were common, including daily debilitating worry (45.8%), vehicle crash or injury (15.0%), and withdrawal from exercise, driving, leaving home, and having sex (54.0%, 37.4%, 24.8%, and 22.7%, respectively).\u201d We are entering a world where it will be impossible to hide from what individual patients experience, and this is the best hope for medicine.<\/p>\n

Ann Intern Med\u00a0 19 Mar 2013\u00a0 Vol 158<\/strong>
\n447\u00a0\u00a0\u00a0 I always bridle when I see articles describing \u201cdiuretics\u201d as a treatment for hypertension. Say thiazides if you mean thiazides. And also specify your thiazide: if in the UK, you probably mean bendroflumethiazide, in Canada you probably mean hydrochlorthiazide, and in the USA and other countries you might perhaps mean chlortalidone. Are they all the same? Irfan Dhalla and colleagues seek to find out<\/a> by looking at the records of people started on chlortalidone at age 66 and over and comparing them with people started on hydrochlorthiazide. In up to five years of follow-up there was no difference in cardiovascular outcomes, but more hypokalaemia in the chlortalidone group. As for good old standard British BFZ, I suspect we just don\u2019t know.<\/p>\n

Plant of the Week: Magnolia campbellii<\/em><\/a><\/strong><\/p>\n

We get through winter by telling ourselves it will all get better by the time that the middle of March arrives: there will be a little heaven of hellebores, daffodils, wood anemones, and the first big flowering magnolias. Well, I saw from a picture that the big magnolias had started flowering in Cornwall three weeks ago: now no doubt they shudder and bend in the wind and sleet, covered in tattered shreds of brown where the great pink and white blossoms had been lured out by a day or two of sunshine.<\/p>\n

But these big Himalayan trees are made to last, and in the warmer, wetter parts of England there are many which have flourished for over a hundred years, despite many horrible winters and dank summers. They can take a bit of rough. Here is Frank Kingdon Ward describing them in their native mountains in March:<\/p>\n

\u201cSuddenly around a corner we come across that first Magnolia in full bloom. It is just below us and we look right into the heart of the tree, spouting with blossom. The sight overwhelms us. After that, we see scores of trees, some glowing with pink, others with ivory-white flowers. From our giddy ledge we look down over the wide waves of the forest beating against the cliff, where the Magnolia blooms toss like white horses, or lie like a fleet of pink water lilies riding at anchor in a green surf.\u201d<\/p>\n

Plant Hunting on the Edge of the World (1930)<\/em><\/p>\n","protected":false},"excerpt":{"rendered":"

JAMA\u00a0 20 Mar 2013\u00a0 Vol 309 1125\u00a0\u00a0\u00a0 Is aliskiren a good drug for heart failure? Despite the negative result of this Novartis-funded trial (ASTRONAUT), I think the answer is probably […]<\/p>\n

More…<\/a><\/p>\n","protected":false},"author":1,"featured_media":38363,"comment_status":"open","ping_status":"closed","sticky":false,"template":"","format":"standard","meta":{"footnotes":""},"categories":[111],"tags":[],"class_list":["post-25396","post","type-post","status-publish","format-standard","has-post-thumbnail","hentry","category-richard-lehmans-weekly-review-of-medical-journals"],"yoast_head":"\nRichard Lehman's journal review\u201425 March 2013 - The BMJ<\/title>\n<meta name=\"robots\" content=\"index, follow, max-snippet:-1, max-image-preview:large, max-video-preview:-1\" \/>\n<link rel=\"canonical\" href=\"https:\/\/blogs.bmj.com\/bmj\/2013\/03\/25\/richard-lehmans-journal-review-25-march-2013\/\" \/>\n<meta property=\"og:locale\" content=\"en_US\" \/>\n<meta property=\"og:type\" content=\"article\" \/>\n<meta property=\"og:title\" content=\"Richard Lehman's journal review\u201425 March 2013 - The BMJ\" \/>\n<meta property=\"og:description\" content=\"JAMA\u00a0 20 Mar 2013\u00a0 Vol 309 1125\u00a0\u00a0\u00a0 Is aliskiren a good drug for heart failure? 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