ARTICLES

New comments from Journal Watch by Richard Lehman
JAMA 21 Oct 2009 Vol 302
1651 This morning I bought a 2kg turbot and I am in a good mood. Turbot is a fish containing huge amounts of omega-3 fatty acids and is the sort that Bertie Wooster recommended to Jeeves for the good of his brain, since it has long been recognised that these fishy acids are concentrated in cerebral synapses. The study here looks at whether adding omega 3 supplements improves the action of setraline in depressed patients with coronary heart disease. The preparation used seemed to have no effect over 10 weeks. Come over to our place for a dish of turbot and a glass or two of Mersault and I bet you’ll notice an immediate difference.
http://jama.ama-assn.org/cgi/content/abstract/302/15/1651

1658 The history of heart failure research over the last 30 years is largely the history of blocking various stages of the renin-angiotensin-aldosterone pathway in patients with a reduced systolic ejection fraction. We have now reached the stage of being able to block everything in the pathway, from renin at the start to aldosterone at the finish. Historically it went the other way, because I was using spironolactone (with furosemide) for most ward patients with heart failure as a houseman in the mid 1970s, whereas ACE inhibitors and angiotensin receptor blockers came much later, and direct renin antagonists last of all. Despite an enormous number of randomised controlled trials of these agents in systolic heart failure, the evidence base for their rational deployment remains a mess. We do know from several trials that aldosterone blockade with spironolactone or eplerenone can improve symptoms and outcomes in patients with systolic HF who are already taking blockers of the earlier stages in the pathway. This study looks at whether they are being used appropriately in a group of American hospitals taking part in a HF Quality Improvement programme. You’d think that such participation would have an enormous Hawthorne effect, raising standards of treatment without further intervention, but not so: two thirds of HF patients admitted to these hospitals leave without an aldosterone antagonist. Think about this when you next see someone with worsening heart failure. And above all, think about why their HF has got worse.
http://jama.ama-assn.org/cgi/content/abstract/302/15/1658

1666 Being a twin in Sweden means that your lifetime medical history will be closely watched, even if you and your sibling popped out as long ago as 1914. There were in fact 31 936 twins born in Sweden between 1914 and 1944, should this question ever arise in a pub quiz. Following their fate allows us all sorts of insights into common associations – such as the unexpected one between cardiovascular diseases and hip fracture. Just having ischaemic heart disease doubles your risk of a hip fracture: having heart failure doubles it again, and having a stroke brings an even higher risk. Various explanations come to mind, but the question which intrigues me most is whether these Nordic twins may suffer both cardiovascular disease and fractures because they are short of vitamin D.
http://jama.ama-assn.org/cgi/content/abstract/302/15/1666

1698 One subject I did make an attempt to look at in greater depth earlier this year was the issue of cardiovascular outcomes in type 2 diabetes trials. Worms crawled out of every can, and they continue to emerge, as in this brief piece about variations in event rates. These vary fourfold between ostensibly comparable diabetic populations recruited to key studies. Why? It’s your turn to chase that worm; I’ve done my bit, and I’m tired.
http://jama.ama-assn.org/cgi/content/abstract/302/15/1685