February 3rd, 2014
Selections from Richard Lehman’s Literature Review: February 3rd
CardioExchange is pleased to reprint this selection 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.
NEJM 30 Jan 2014 Vol 370
Proteome-wide Analysis and CXCL4 as a Biomarker in Systemic Sclerosis (pg. 433): The Preacher has an ambivalent relationship to biomarkers. A lot of them are jut vanity and vexation of spirit, but there are one or two—cardiac troponins being a prime example—that are of huge clinical value and redefine an entire condition, albeit at the potential expense of overdiagnosis. Systemic sclerosis is many thousands of times less common than myocardial infarction, but it is a very nasty disease without a diagnostic or prognostic marker. So full marks to the Dutch team who through proteome-wide analysis and validation showed that CXCL4 is the predominant protein secreted by plasmacytoid dendritic cells in systemic sclerosis, both in circulation and in skin. This study shows that careful and arduous science can bring real progress in medicine: “Levels of CXCL4 were elevated in patients with systemic sclerosis and correlated with the presence and progression of complications, such as lung fibrosis and pulmonary arterial hypertension.”
Ann Intern Med 21 Jan 2014 Vol 160
Effectiveness of ICDs for Primary Prevention of Sudden Cardiac Death in Subgroups (pg. 111): I keep mentioning implantable cardioverter defibrillators in these reviews, partly because they keep coming up in the literature, but also because I am worried by them. I will spare you the detail of this systematic review of ICD effectiveness for primary prevention of sudden cardiac death across subgroups by sex, age, New York Heart Association class, left ventricular ejection fraction, heart failure, left bundle branch block, QRS interval, time since myocardial infarction, blood urea nitrogen level, and diabetes: but the bottom line is that for none of these groups taken alone can it be shown that ICDs are of any benefit at all. It is only if you aggregate them that you can show an effect. This tells you two things: that their benefit is very small, and that you cannot predict if implanting an ICD is going to help the patient in front of you. So it seems to me that these devices should be reserved for the tiny minority of patients who have a strong theoretical preference for being kept alive at any cost rather than running a risk of dying suddenly and painlessly.
JAMA Intern Med Jan 2014 Vol 174
Deathbed Shock (pg. 88): At present, more than 100,00 ICDs are fitted to American patients every year. You can read about dying with one in situ in a commentary from JAMA Intern Med.
Interpreting Treatment Effects From Clinical Trials in the Context of Real-World Risk Information: When you start somebody on medication for “hypertension,” do you calculate their overall cardiovascular risk and explain the benefit of treatment in absolute terms such as a number-needed-to treat? Of course not, because even if you wanted to, you wouldn’t be able to find a suitable tool and you might lose QOF points. That’s how good we are at being patient-centred doctors. And if that’s awful, turn to the domain of “chronic kidney disease,” as Ken Covinsky and colleagues do in this analysis. Even if you can extrapolate accurately from the clinical trials to the elderly patient in front of you (which, by the way, you can’t), you would find NNTs in excess of 100 for any treatment you might give them in order to prevent end-stage renal failure, unless they are on the brink of it already. This is where tunnel-vision interpretations of “evidence-based” medicine have got us.
Lancet 1 Feb 2014 Vol 383
DUTCH PEERS (pg. 413): Strictly for Stent War enthusiasts and pharma-watchers only: “Third generation zotarolimus eluting and everolimus eluting stents in all comer patients requiring a percutaneous coronary intervention (DUTCH PEERS): a randomised, single blind, multicentre, non inferiority trial.” “Both stents were similarly efficacious and safe, and provided excellent clinical outcomes, especially in view of the large number of patients who presented with acute myocardial infarctions.” It’s beyond parody. Is this an academic paper or an advertisement? Do I need to tell you that his trial was sponsored by the makers of the two stents?
Association Between Change in Daily Ambulatory Activity and CV Events in People with Impaired Glucose Tolerance: Wanted: a pharma-sponsored trial that doesn’t push a pharmaceutical intervention. Found: an analysis of NAVIGATOR that dwells on the dose related benefits of daily activity in individuals at high cardiovascular risk. Thank you, Novartis. See, I can be nice to a drug company.
Acute MI: A Comparison of Short-Term Survival in National Outcome Registries in Sweden and the U.K.: “We used data from national registries on consecutive patients registered between 2004 and 2010 in all hospitals providing care for acute coronary syndrome in Sweden and the UK. The primary outcome was all cause mortality 30 days after admission.” I really wouldn’t have predicted the result of this comparison: 30-day mortality was 7•6% (95% CI 7•4—7•7) in Sweden and 10•5% (10•4—10•6) in the UK. One factor driving this may be the finding that “in Sweden, compared with the UK, there was earlier and more extensive uptake of primary percutaneous coronary intervention (59% vs 22%) and more frequent use of β blockers at discharge (89% vs 78%).” If a country with such a scattered population as Sweden can achieve such a good rate of primary PCI, what excuse do we have in the UK?