JAMA 2 Dec 2009 Vol 302
2345 Rarely has an issue of JAMA contained so little worth commenting on. I only point your attention to this article on the assessment of claims of improved prediction beyond the Framingham score because our overlords and paymasters sometimes direct us to use such scores, and perhaps some of you actually do. Personally, I seldom bother. Still less do I care about the veracity of claims that additional factors improve the score: and in fact this paper shows that there is scant evidence that they do. The authors don't enter into the Q-RISK debate arena because that's about a separate issue of generalisability to different populations. The fact is that in the NHS every major cardiac risk factor is subject to its separate irrational dictates. Treat all blood pressure if it is above a certain limit. Treat cholesterol only if it part of a risk score. Treat obesity with interventions which have been shown not to work, but not with bariatric surgery, which does work, and usually cures diabetes to boot. Treat smoking with small supplies of nicotine replacement rather than with drugs that have been shown to work much better. And so on. A percentage point or two in some score is never going to bring reason into this chaos.
http://jama.ama-assn.org/cgi/content/abstract/302/21/2345
NEJM 3 Dec 2009 Vol 361
2241 This week's New England Journal is no diamond mine either, but this study of advanced heart failure treated with a continuous-flow left ventricular assist device may be a pointer for the future. At the moment, if one of your patients with advanced HF becomes pulseless, you can predict with considerable certainty that he is dead. But increasingly you will encounter pulseless HF patients walking around alive, each of them carrying a briefcase. This does not contain native soil to allow daytime rest in a coffin, but heavy duty batteries to keep a continuous-flow pump going in the left ventricle. I know one such patient who had his briefcase pinched, but managed to survive. LVADs are still very expensive and fraught with problems, but this study shows that they do help patients with very poor LV function to live on and that they are much better than pulsatile devices.
http://content.nejm.org/cgi/content/abstract/361/23/2241
2261 Mitral valve prolapse is commoner than you think. If Framingham Offspring data are generalisable, then your personal list of 2,000 patients will include no less than 50 with the condition, and of these about 5-7 will eventually develop significant mitral regurgitation. The traditional cure is mitral valve replacement, but this clinical review cites good evidence that mitral valve repair is a better option. There are nice illustrations, as indeed there are in the LVAD paper. It's all rather awe-inspiring and a definite incentive to become a heart surgeon in your next life.
http://content.nejm.org/cgi/content/extract/361/23/2261
BMJ 5 Dec 2009 Vol 339
I continue to follow the literature about salt and cardiovascular disease with a furrowed brow. This is not quite science as I understand it. The interventional studies are weak. The whole-population observational studies are painstaking but their measurement methods are poor and there is endless room for confounding. Proponents of the salt hypothesis (see editorial) sometimes resort to quasi-religious discourse about WHO targets and the Neolithic diet, i.e. a mixture of authority and ignorance. We might do better to state simply that salt is a modifiable factor which we would probably benefit from modifying, whether the central theory is true or not, since we have no way of knowing. A bit like climate change, which The Lancet discusses this week.
http://www.bmj.com/cgi/content/full/339/nov24_1/b4567
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