WOMEN, HEARTS & DIABETES

Arch Intern Med 14 Sep 2009 Vol 169
1484 If you are going to use thrombolysis for occlusive stroke, the sooner you do it the better: if this sounds obvious now, consider how unobvious it sounded ten years ago, or even five to most people in the street. The number needed to treat is still very high, and if this German cluster-randomised trial of a public awareness campaign had used a hard end-point, like overall reduction of disability or death from stroke, it would have had a zero result. Instead, it yielded a 27% increase in women with stroke reaching hospital within three hours. I think that we can conclude that personal letters with bookmarks and stickers are not a cost-effective basis for a stroke awareness campaign.
http://archinte.ama-assn.org/cgi/content/abstract/169/16/1484

Ann Intern Med 15 Sep 2009 Vol 151
386 When reading papers with the words “net value of health care” in the title, it is always worth remembering that the best way to ensure value in health care is to ensure a swift death for everyone who is not working, especially the elderly. However, this Mayo Clinic study of the net value of health care for patients with type 2 diabetes, 1997 to 2005, is somewhat less drastic in its approach, and bases its figures on the reduction in spending on coronary heart disease in the UKPDS tight control cohort. These were patients in their early fifties with new-onset diabetes, so they don’t actually tell us anything about the economics of treating people with type 2 diabetes in the age beyond retirement. Just as well, really. http://www.annals.org/cgi/content/abstract/151/6/386
394 The thing that goaded me into writing an editorial on tight control of glucose in longstanding type 2 diabetics last March was the silence of diabetologists following the ADVANCE and ACCORD studies in June the previous year, plus the VADT study which told the same story and was published in January 2009. These were prospective randomised trials designed to answer much the same question, and they all gave the same answer: intensive glucose control in established type 2 diabetes does not reduce overall cardiovascular mortality and increases the risk of severe hypoglycaemia. Since then a number of meta-analyses have appeared, this being the latest. These include long-term observational data from UKPDS, which was not designed to answer this question; The Lancet , one also included data from a wildly irrelevant study, and there is a further one waiting in the wings on the Diabetologia website. As a study in the sociology and psychology of medical practice, this is quite interesting and a little dispiriting, but as far as treating patients goes, the message could not be simpler. For type 2 diabetics a few years into the disease process, there is no point aiming for an HbA1c under 7.5%. There is a tendency to fewer non-fatal CV events and perhaps some renal protection for a tiny number, but overall it makes no difference and causes hypoglycaemic episodes, which can cause brain damage. Cognitive impairment should be an end-point in future studies.
http://www.annals.org/cgi/content/abstract/151/6/394

BMJ 5 Sep 2009 Vol 339
And now to the vexed question of which drugs should be used for type 2 diabetes, where nothing quite works out as it should. For example, the thiazolidinediones as a group have a favourable effect on HbA1c , on lipids and on measures of insulin resistance. Rosiglitazone has a greater effect on peroxisome proliferators activated receptors (PPARs) than pioglitazone and by rights it should be the better drug. Both cause an equal amount of peripheral oedema. But in fact pioglitazone causes less heart failure than rosiglitazone and a big Canadian cohort study has a better mortality record as well. Yet the accompanying editorial sounds a note of caution about the data we have at present, and warns us against too much enthusiasm for any of the newer incretin pathway drugs too. The fact is that in diabetic therapeutics, as in most of medicine, you just can’t tell what is going to happen until enough of it has happened.
http://www.bmj.com/cgi/content/abstract/339/aug18_2/b2942

JAMA 2 Sep 2009 Vol 302
947 Funny how medical terms change meaning: to an old pedant like me, acute coronary syndromes mean any acute syndromes caused by the coronary arteries, including myocardial infarction and sudden death, but it seems that JAMA readers automatically assume that it only means coronary syndromes without ST elevation. With these latter syndromes there is still room for debate about the relative merits of immediate versus delayed intervention, the key question in this multicentre French trial. Patients with non-ST elevation ACS were randomised to get their angiographic intervention either immediately (mean 70 minutes) or on the next working day (mean 21 hours) and the outcome was myocardial infarction measured by troponin 1. There was no difference between groups in this important short-term outcome.
http://jama.ama-assn.org/cgi/content/abstract/302/9/947

NEJM 3 Sep 2009 Vol 361
980 A Dutch study shows that patients undergoing vascular surgery do better if they take a perioperative high dose statin. The rate of myocardial infarction and cardiovascular death within 28 days was halved with fluvastatin 80mg. More evidence that the protective effect of statins is not mediated through long-term effects on lipids.
http://content.nejm.org/cgi/content/abstract/361/10/980
990 I have previously described coronary artery calcium screening as the payment of large sums to receive high doses of ionising radiation in return for an increase in anxiety. This article on its place in cardiovascular prevention strategies reaches much the same conclusion, but I’m sure this will do nothing to dent its popularity with the rich worried well.
http://content.nejm.org/cgi/content/extract/361/10/990