April 29th, 2013
Selections from Richard Lehman’s Literature Review: April 29th
Richard Lehman, BM, BCh, MRCGP
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.
JAMA 24 Apr 2013 Vol 309
Association of Perioperative β-Blockade with Mortality and CV Morbidity Following Major Noncardiac Surgery (pg. 1704): A great big retrospective study finds that taking a beta-blocker is associated with a small reduction in post-operative mortality and major cardiac events in some subclasses of patient undergoing non-vascular surgery. Alarm bells: how tightly were these groups pre-specified? How watertight was the propensity scoring and matching? The NNT to prevent one post-op death was 241: this could be massaged down by factoring in cardiac risk factors, to about 18 for the highest risk patients—but questions remain. The comparison was not between patients given beta-blockers short term for the peri-surgical period, but with people mostly taking them long-term. And high-risk patients undergoing vascular surgery showed no benefit. It doesn’t really add up: this is why we always need to do prospective randomized trials to decide the merits of treatment, rather than processing big bagfuls of old data.
NEJM 25 Apr 2013 Vol 368
Intestinal Microbial Metabolism of Phosphatidylcholine and CV Risk (pg. 1575): Trimethylamine-N-oxide (TMAO) is the new enemy within. We make it in our bowels, I am sorry to have to report, by microbial metabolism of the choline moiety in dietary phosphatidylcholine (lecithin). The fault lies with our microbiome, because as this study demonstrates, if you kill off the bacterial flora with metronidazole and ciprofloxacin, production of TMAO stops totally. The second part of the study goes on to associate TMAO levels with atherosclerosis, proving to its own satisfaction that if you produce shitloads (I use the word in its technical sense) of TMAO then you get major adverse cardiovascular events, independent of other known risk factors. I am naturally inclined to pooh-pooh this idea, but to do so would involve going into a level of detail that neither you nor I could quite face. There is lecithin in the kinds of food that cardiologists traditionally dislike—eggs, red meat, liver and pork—but there is also plenty in fish and most plants. I have just eaten a bagful of whelks—probably lots of lecithin there too, but you won’t stop me so easily. After all, “Lecithin may help to prevent the buildup of fats in the body and protect against cardiovascular disease by lowering cholesterol,” says the Nutritional Supplements Health Guide website.
Biventricular Pacing for Atrioventricular Block and Systolic Dysfunction (pg. 1585): I keep a safe distance from interventional cardiologists, but hope that when my turn comes they will know what they are doing. If I had systolic heart failure, I would most definitely not want a cardioverter-defibrillator, but if I had atrioventricular block I would want to have whatever kind of pacing gave me the most benefit. In this life-shortening condition, I would place a high value on symptomatic improvement. Unfortunately, this Medtronic-funded trial of right ventricular pacing versus biventricular pacing did not measure quality of life at all: it went for the usual mixture of hard end-points (death, admission for IV treatment) and a surrogate—an end-systolic volume increase of 15%. Biventricular pacing proved superior on those counts, and we also know from other studies that it improves symptoms, so that’s what I’d go for if I had grade 1-3 systolic HF. My aim would be to live better and then die suddenly: so yes to BVP, and no, no, no to that ICD.
JAMA Intern Med 22 Apr 2013 Vol 173
HIV Infection and the Risk for MI (pg. 614): Living with human immunodeficiency virus doubles your chance of having a myocardial infarction, according to this Veteran’s cohort study. It sound like everyone on antiretroviral treatment should be taking a statin.
Dietary and Supplemental Calcium Intake and CV Disease Mortality (pg. 639): The debate about dietary calcium intake and cardiovascular disease continues. This study examines the relation in a whopping cohort of 388 229 men and women aged 50 to 71 years from the National Institutes of Health–AARP Diet and Health Study. The chalk-eating men seem to get more CVD whereas the women don’t.
Bias in Associations of Emerging Biomarkers With CV Disease (pg. 664): There are far too many cardiovascular risk factors. Most of the studies are bad. Even when they are of reasonable quality, they tend to be of doubtful clinical significance. This paper written under the supervision of that invaluable sceptic, John Ioannidis, concludes that “Selective reporting biases may be common in the evidence on emerging cardiovascular biomarkers. Most of the proposed associations of these biomarkers may be inflated.”