November 24th, 2014

Selections from Richard Lehman’s Literature Review: November 24th

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

JAMA 19 November 2014 Vol 312

Percutaneous Left Atrial Appendage Closure vs. Warfarin for AF (pg. 1988): And now we must turn to the left atrial appendage. As its name suggests, this is a bulge in the left atrium, somewhat fancifully described as “wind-sock shaped.” In non-valvular atrial fibrillation, this is the main site where clot forms. So if you close off the appendage, then you might be able to prevent stroke in AF without the need for anticoagulation. And according to the PROTECT-AF trial, this is indeed the case: “After 3.8 years of follow-up among patients with nonvalvular AF at elevated risk for stroke, percutaneous LAA closure met criteria for both noninferiority and superiority, compared with warfarin, for preventing the combined outcome of stroke, systemic embolism, and cardiovascular death, as well as superiority for cardiovascular and all-cause mortality.” Once we have better long term data, this could change the routine management of AF.

Association of Inpatient vs. Outpatient Onset of STEMI with Treatment and Clinical Outcomes (pg. 1999): If you have a heart attack in hospital, you are less likely to receive invasive treatment and much more likely to die. This finding emerges from a study of outcomes in 303 hospitals in California, and you can guess at some of the reasons why this should be so. The 5% of myocardial infarction patients who have their event in hospital are older and iller than those who are brought in by ambulance; and those whose MIs are immediately fatal in hospital are going to be counted in the figures, unlike patients who drop dead from heart attacks outside hospital.

Association Between Use of β-Blockers and Outcomes in Patients with HF and Preserved EF (pg. 2008): As you should know by now (since I mention it so frequently), half of old people with the syndrome of heart failure do not have a reduced systolic ejection fraction. The treatments that have some effect on people with impaired systolic function have no effect on them, at least in terms of hospital admission and survival. But a Swedish registry study suggests a possible benefit from β-blockade: “In patients with HFPEF, use of β-blockers was associated with lower all cause mortality but not with combined all cause mortality or heart failure hospitalization. B-blockers in HFPEF should be examined in a large randomized clinical trial.” But why? In these patients, whose mean starting age was 76, the difference in five year survival between those taking β-blockers or not was 45% vs 42%. This just scrapes into apparent statistical significance, provided you don’t round up 0.996 to 1 (hazard ratio [HR], 0.93; 95% CI, 0.86-0.996; P = .04). But consider that this is an observational study, not a randomised trial: people who are able to tolerate β-blockers are not the same as those who cannot; and no amount of propensity scoring can make them so, or balance the groups to a CI of 0.004. And then consider what you would want if you were 76 and had a stiff old heart that was beginning to cause you breathlessness and oedema. Would you want to take an extra pill a day, which might conceivably give you a 3% better chance of living out another five years, at the likely cost of more breathlessness and greater tiredness? My guess (confirmed by several studies) is that you would want something to make you feel better, even at the risk of shortening your remaining life. The drugs that need to be trialled in these patients might be β-adrenergic stimulants, not blockers.

Fixed-Dose Combination Therapy (Polypill) for the Prevention of CVD (pg. 2030): And now think about another therapeutic issue: dosing the entire population so that the herd, on average, can live a few weeks longer. How does individual choice fit in? What number needed to treat are you striving for, and what harms should individuals be asked to trade with it? Not that most real people make their choices this way, but never mind. I am talking, of course, about the polypill. I will just leave you with this summary of the evidence: “Polypills are associated with greater reductions in systolic blood pressure and total cholesterol compared with usual care, placebo, or active comparators, but also with a 19% higher risk of any adverse event. Due to limited power from available evidence, the association of polypills with all cause mortality or fatal and nonfatal CVD events is uncertain.”

Ann Intern Med 18 November 2014 Vol 161

Relation of NSAIDs to Serious Bleeding and Thromboembolism Risk in Patients With AF Receiving Antithrombotic Therapy (pg. 690): I do wish there was a journal series that would remind working doctors—especially in primary care—of the risks they run of poisoning patients with common drugs. I was no saint in this respect myself, but after this week I cannot do any more harm as I shan’t be treating patients. What’s the harm of a bit of ibuprofen in someone with atrial fibrillation? A study of 150 900 Danish patients with AF gives us the answer. “Use of NSAIDs was associated with increased absolute risks for serious bleeding and thromboembolism across all antithrombotic regimens and NSAID types.” By using NSAIDs in these patients (and even more in those with heart failure) you are negating the effects of all the protective treatment they are taking.

Lancet 22 November 2014 Vol 384

Unfractionated Heparin vs. Bivalirudin in Primary PCI (HEAT-PPCI) (pg. 1849): Last week I shrugged my shoulders as I told you about the latest meta-analysis of anticoagulant regimens for use during percutaneous coronary intervention (The BMJ): “In patients undergoing primary PCI, unfractionated heparin plus GpIIb/IIIa inhibitor and LMWH plus GpIIb/IIIa inhibitor were most efficacious, with the lowest rate of major adverse cardiovascular events, whereas bivalirudin was safest, with the lowest bleeding.” I remarked that these meta-analyses change with each new piece of evidence, and this week’s print Lancet illustrates the point. The HEAT-PPCI trial concludes: “Compared with bivalirudin, heparin reduces the incidence of major adverse ischaemic events in the setting of PPCI, with no increase in bleeding complications. Systematic use of heparin rather than bivalirudin would reduce drug costs substantially.” OK, so bivalirudin may not be the safest, with the lowest rate of bleeding. Can a mere Toyota owner dispute the findings of a study, which had among its sponsors The Bentley Drivers Club (UK)?

The BMJ 22 November 2014 Vol 349

Decision-Making Tools for Statins:  Margaret McCartney’s excellent column this week has the title “We lack the tools to help patients decide about statins.” It’s true that we lack the ideal tool, but there are several which, with suitable tweaking, could be used in real life primary care. The first and most comprehensive is Victor Montori’s from the Mayo clinic.

A single page tool that is easy to use and which incorporates a wide range of risk reducing options has been developed by James McCormack.

The most recent, which compares statins directly with dietary modification and activity, is the Option Grid, which I helped to develop.

Soon there will be a package directly developed by NICE. But what we really need is a two click tool that allows GPs to instantly calculate the figures for individual people, based on their health record, and print off a personalised decision aid that makes sense to users at all levels of education. Long term risk reduction is a matter for shared decision making, not for pronouncements by experts who never see patients.

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