February 21st, 2012

Selections from Richard Lehman’s Weekly Review: Week of February 20th

CardioExchange is pleased to reprint selections from Dr. Richard Lehman’s weekly journal review blog at BMJ.com. Selected summaries are relevant to our audience, but we encourage members to engage with the entire blog.

Week of February 20th

JAMA  15 Feb 2012  Vol 306

Left Ventricular Hypertrophy (page 674): One way in which JAMA lags behind other journals is in flagging up the role of the funder in interventional trials. It would have helped if we were told right at the beginning that Abbott paid for this study of paracalcitol in patients with an estimated glomerular filtration rate of less than 60 and echographic evidence of left ventricular hypertrophy. The title of the paper tells you little about the contents and the whole study (PRIMO) is a wonderful exercise in futility. It is completely free of clinical outcomes – a closed loop of nearly meaningless surrogate end-points relating to cardiac and renal function: and even on this basis it was a dud. Why on earth did JAMA think this worth publishing?

Pollution and MI (page 713): There have been lots of recent studies linking short term air pollution and myocardial infarction and this systematic review and meta-analysis usefully combines the results of 34 of them. Small but statistically significant increases in MI can be traced to atmospheric pollution with carbon monoxide, nitrogen dioxide, sulphur dioxide and particulate matter. Another small item on the list of reasons why we need to end our dependence on carbon-based fuels.

NEJM  16 Feb 2012  Vol 366

Genetics of Cardiomyopathy (page 619): I’ve come across surgeons who were daunted at the size of their patients, but I didn’t realize that genomic scientists could be similarly affected, until I read here that “TTN, the gene encoding the sarcomere protein titin, has been insufficiently analyzed for cardiomyopathy mutations because of its enormous size.” I like the idea of thousands of gene gnomes swarming to tie down the Titin gene, like the famous illustration in Gulliver’s Travels. And this could turn out to be genuinely useful: “TTN truncating mutations are a common cause of dilated cardiomyopathy, occurring in approximately 25% of familial cases of idiopathic dilated cardiomyopathy and in 18% of sporadic cases.” Anything that brings some order and understanding into this perplexing group of disorders must be welcome, even if it takes decades to translate into therapy.

Lancet  18 Feb 2012  Vol 379

A-Fib (page 648): A very nice seminar on atrial fibrillation by Greg Lip and colleagues provides an excellent map of what has become quite a complex subject. Generalists as well as cardiologists will learn a lot from this painstaking account of the latest evidence on the treatment of a highly prevalent condition which most of us encounter at least once a day. As we gain more knowledge, treatment is becoming more patient-focused, and more may sometimes mean less: “Lenient or strict rate control strategies might not provide great differences in outcomes, whereas the availability of non-pharmacological approaches has allowed additional possibilities for the management of atrial fibrillation in patients who are unsuitable or intolerant of pharmacological therapy.”

Arch Intern Med  13 Feb 2012  Vol 172

Aspirin for Primary Prevention (page 209): Last year, Peter Rothwell and colleagues published a celebrated meta-analysis based on individual patient data from randomized controlled trials which showed that daily low-dose aspirin reduces total cancer mortality. This meta-analysis used summary patient data from a somewhat different set of trials and concludes: “Despite important reductions in nonfatal MI, aspirin prophylaxis in people without prior CVD does not lead to reductions in either cardiovascular death or cancer mortality. Because the benefits are further offset by clinically important bleeding events, routine use of aspirin for primary prevention is not warranted and treatment decisions need to be considered on a case-by-case basis.” I wish I could take you through the merits and faults of each analysis, but I am afraid you will have to do this for yourselves. The Invited Commentary by Samia Mora (p.217) provides no help in resolving the clash of conclusions about cancer mortality.

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