{"id":28380,"date":"2012-04-18T20:18:48","date_gmt":"2012-04-19T00:18:48","guid":{"rendered":"http:\/\/blogs.nejm.org\/cardioexchange\/?post_type=voices&p=28380"},"modified":"2012-04-19T10:59:06","modified_gmt":"2012-04-19T14:59:06","slug":"selections-from-richard-lehmans-literature-review-week-of-april-16th","status":"publish","type":"post","link":"https:\/\/blogs.nejm.org\/cardioexchange\/2012\/04\/18\/selections-from-richard-lehmans-literature-review-week-of-april-16th\/","title":{"rendered":"Selections from Richard Lehman’s Literature Review: Week of April 16th"},"content":{"rendered":"

CardioExchange is pleased to reprint selections from Dr. Richard Lehman\u2019s weekly journal review blog<\/a> at BMJ.com<\/a>. Selected summaries are relevant to our audience, but we encourage members to engage with the entire blog<\/a>.<\/em><\/p>\n

Week of April 16th<\/strong><\/p>\n

JAMA\u00a0 11 April 2012\u00a0 Vol 307<\/strong><\/p>\n

Should This Patient Get Statin Therapy? (pp. 1489 and 1491):<\/strong> The new editor of JAMA<\/em> feels that his worthy journal needs a bit of livening up, and who can disagree? He has borrowed an old idea from the BMJ<\/em>, in the form of head-on For and Against articles. \u201cShould a 55-year-old man who is otherwise well, with systolic blood pressure of 110 mm Hg, total cholesterol of 250 mg\/dL, and no family history of premature CHD be treated with a statin?\u201d This is an awful question for several reasons. It implies that the doctor is the one who should decide, and the \u201cpatient\u201d is the object who should, or should not, \u201cbe treated.\u201d But in what way is this man a patient?\u00a0 Why is he \u201cotherwise\u201d well? Is his illness being 55, having low blood pressure, or having a total cholesterol of 250 mg\/dL? In this exchange of views, three doctors think he should \u201cbe treated\u201d<\/a>, and two doctors (one the editor of Arch Intern Med<\/em>) think he shouldn\u2019t<\/a>. I would argue that it is none of their business: give him the evidence and let him decide.<\/p>\n

Should This Patient Get an ECG? (p. 1497):<\/strong> Gah, this is so boring! <\/a>Are major and minor ECG abnormalities associated with coronary heart disease events? Yes. Does this mean that everybody should have a regular ECG? No. And why? Oh for goodness sake don\u2019t bother me \u2013 just go back to medical school or read Overdiagnosed<\/em>.<\/p>\n

ARBs and HF (p. 1506):<\/strong> Next, a Danish nationwide database study<\/a> looking at everyone over 45 admitted with heart failure for the first time and treated with an angiotensin receptor blocker. Does it make any mortality difference whether they are given candesartan or losartan? No, provided they are given a decent dose (100 mg losartan).<\/p>\n

NEJM\u00a0 12 Apr 2012\u00a0 Vol 366<\/strong><\/p>\n

CCTA in the ED (p. 1393):<\/strong>\u00a0 Coronary computed tomographic angiography (CCTA) is a high-radiation procedure which is very good at ruling out significant coronary artery disease. This important study<\/a> from the Commonwealth of Pennsylvania shows that it can be used in emergency departments to rule out coronary ischaemia as the cause of chest pain in patients with low-moderate probability. That way more patients can go home more quickly. But I can see drawbacks. For a start, CCTA picks up coronary artery disease in 9% of these patients, as opposed to a 3.5% pick-up rate if CCTA is not used. A lot of this will represent overdiagnosis of asymptomatic disease, and may lead to further (radiation- and cost-intensive) investigation. Secondly, the routine use of CCTA to save an average of 6 hours waiting for biochemical tests will drive up costs and increase the \u201cdefensive\u201d use of radiation, meaning that in some instances patients going to different hospitals with recurrent non-cardiac chest pain and getting pretty massive cumulative X ray doses. I think this is a development to be welcomed with caution.<\/p>\n

Vorapraxar for Secondary Prevention (p. 1404):<\/strong> Vorapaxar is a novel antithrombotic agent which works by preventing thrombin binding to platelets, by blocking the protein-activated receptor (PAR-1). To test such agents these days requires enormous trial sizes \u2013 this one <\/a>recruited 26,449 subjects with a history of myocardial infarction, ischaemic stroke or peripheral artery disease to see how well it prevented further events. The prize for Merck would have been a new blockbuster drug for the whole secondary prevention market. But Fate, bleeding Fate, intervened and the trial was halted. There were fewer ischemic events in the group who got vorapaxar rather than a thienopyridine, but more cerebral hemorrhage. Vorapaxar is an interesting drug which may have some kind of future, but blockbuster it is unlikely ever to be.<\/p>\n

Lancet\u00a0 14 April 2012\u00a0 Vol 379<\/strong><\/p>\n

Stent Wars (p. 1393):<\/strong> In 1998, when I first started writing these brief notes on the journals for a few friends and colleagues, I decided that coronary artery stents were an interesting new development that I should tell people about whenever they cropped up in the literature. How dearly I (and you who have followed me) have paid for that decision! Paclitaxel, sirolimus, everolimus, zotarolimus\u2026 I have tried to make them interesting by pretending they were creatures from Star Wars, or minor characters from Antony and Cleopatra, or members of a zany family called Olimus, whose next son will no doubt be called boralotimus. And now it turns out we may have been looking at the wrong thing all along: what matters in the Stent Wars is not the drug these things elute, but the metal they are made of. According to this \u201ccomprehensive network meta-analysis<\/a>\u201d of 49 trials with 50,844 randomly assigned patients, the clear winner is a cobalt-chromium stent which elutes everolimus. For the first time in 14 years, my remarks on stents will actually be read by some interventional cardiologists, thanks to their appearance on the CardioExchange website run by the NEJM<\/em>. OK you guys, start quarreling about this study: the rest of us are off for a nice snooze.<\/p>\n","protected":false},"excerpt":{"rendered":"

This week’s topics include an “awful question” about statin therapy, coronary computed tomographic angiography in the ED, vorapraxar for secondary prevention, and stent wars.<\/p>\n","protected":false},"author":475,"featured_media":0,"comment_status":"open","ping_status":"closed","sticky":false,"template":"","format":"standard","meta":{"footnotes":""},"categories":[1,14,9,7],"tags":[647,501,1216,584,437],"class_list":["post-28380","post","type-post","status-publish","format-standard","hentry","category-general","category-heart-failure","category-interventional-cardiology","category-prevention","tag-arbs","tag-cct","tag-ecg","tag-statins","tag-stents"],"_links":{"self":[{"href":"https:\/\/blogs.nejm.org\/cardioexchange\/wp-json\/wp\/v2\/posts\/28380","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/blogs.nejm.org\/cardioexchange\/wp-json\/wp\/v2\/posts"}],"about":[{"href":"https:\/\/blogs.nejm.org\/cardioexchange\/wp-json\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"https:\/\/blogs.nejm.org\/cardioexchange\/wp-json\/wp\/v2\/users\/475"}],"replies":[{"embeddable":true,"href":"https:\/\/blogs.nejm.org\/cardioexchange\/wp-json\/wp\/v2\/comments?post=28380"}],"version-history":[{"count":0,"href":"https:\/\/blogs.nejm.org\/cardioexchange\/wp-json\/wp\/v2\/posts\/28380\/revisions"}],"wp:attachment":[{"href":"https:\/\/blogs.nejm.org\/cardioexchange\/wp-json\/wp\/v2\/media?parent=28380"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/blogs.nejm.org\/cardioexchange\/wp-json\/wp\/v2\/categories?post=28380"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/blogs.nejm.org\/cardioexchange\/wp-json\/wp\/v2\/tags?post=28380"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}