CardioExchange Archive

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 March 26th

JAMA  21 Mar 2012  Vol 307

Epinephrine in ED Response to Cardiac Arrest (pg. 1161): When in Japan, do not attempt to drop down dead. In 800 fire stations around the Islands of the Sun, teams of emergency medical service personnel stand ready to rush out and perform resuscitation for out-of-hospital cardiac arrest, which cannot be discontinued until an ambulance arrives and you are taken to hospital, barely alive or truly dead. This non-randomized study of Japanese CPR shows that if the emergency team used epinephrine (adrenalin), your chance of having spontaneous circulation when you arrived in hospital would be 18.5%, and if they did not, it would be 5.7%. On the other hand, your chance of being alive at one month without major neurological impairment would be 1.4% if you had been given epinephrine, and 2.2% if you had not. So I think we can conclude that epinephrine should not be given during CPR. Next we need to find out whether out-of-hospital CPR should be given at all, since there is no firm evidence one way or the other.

NEJM  22 Mar 2012  Vol 366

A Thrombolytic Twice as Effective as Alteplase? (pg. 1099): The first trials of thrombolysis for stroke were carried out twenty years ago, but treatment with alteplase still occupies a marginal place in the everyday management of acute ischaemic stroke, despite efforts to encourage its use within the small window of benefit. But what if there were a thrombolytic agent that was nearly twice as good? This publicly funded Antipodean study compared two doses of tenecteplase with a standard dose of alteplase with just 25 carefully selected patients in each group. The higher dose of tenecteplase definitely produced the best results (72% v 40% disability-free at 90 days), but we need a bigger trial.

Phase I Study of Monoclonal Antibodies for Reducing LDL-C (pg. 1108): When monoclonal antibodies were first produced, nearly 40 years ago, we were told to expect lots of magic bullets for a wide array of hitherto untreatable diseases. My whole working lifetime has passed by in those decades, and only a handful of my patients ever received treatment with a monoclonal antibody, usually with broad and unpredictable effects. High low-density lipoprotein cholesterol is a common biochemical finding, whether due to heritable causes or not. It is certainly associated with worse cardiovascular outcomes. So what might happen if we give people with raised LDL-C a monoclonal antibody to the enzyme which promotes LDL-C production? This enzyme is called proprotein convertase subtilisin/kexin 9 [PCSK9], but I don’t expect you to remember that. And the monoclonal antibody to PCSK9 is designated as REGN727/SAR236553 (REGN727), and I don’t expect you to remember that either. In fact I don’t expect you to remember anything about this study at all, except that the stuff reduced LDL-C levels in a few healthy volunteers and a few subjects with familial and non-familial hypercholesterolaemia, and did them no immediate harm. Or good. Now just keep this in the back of your mind, for the ten years of phase 2 and 3 trials that it will need to see if it’s safe and if it reduces events.