CardioExchange Archive

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  2 Jan 2014  Vol 370

Stenting and Medical Therapy for Atherosclerotic Renal-Artery Stenosis (pg. 13): There’s scale in the pipes: call for Mr Stent the plumber. This has proved an enormously appealing idea for patients and plumbers over the last two decades, and Messrs Stent and Sons now have an annual turnover of billions. Pushing mesh into arteries is a rite of passage in many specialties, and even patients often talk of their stents with a kind of pride. A shame that most of them do nothing at all, even in coronary arteries. In renal arteries they may be universally pointless, according to this large publicly funded American trial. ” We randomly assigned 947 participants who had atherosclerotic renal-artery stenosis and either systolic hypertension while taking two or more antihypertensive drugs or chronic kidney disease to medical therapy plus renal-artery stenting or medical therapy alone. Renal-artery stenting did not confer a significant benefit with respect to the prevention of clinical events when added to comprehensive, multifactorial medical therapy in people with atherosclerotic renal-artery stenosis and hypertension or chronic kidney disease.”

Mitral-Valve Repair vs. Replacement for Severe Ischemic Mitral Regurgitation (pg. 23): If you suffer major ischaemic damage to your left ventricle, it is quite likely to fibrose and remodel itself in such a way as to distort the mitral valve and cause what is known as “functional” mitral regurgitation. This is associated with a substantial increase in the risk of progressive heart failure and death, and it affects a lot of people—probably over two million in the US alone. The leaflets of the mitral valve remain healthy, but their alignment is wrong, so if surgical treatment is attempted, it is usually in the form of mitral valve repair rather than replacement. But that may not be as good in the long term as replacing the valve, according to the authors of a trial which randomly assigned 251 patients with severe ischemic mitral regurgitation to undergo either mitral valve repair or chordal-sparing replacement. In the short term, clinical outcomes are identical, but in the long term, valve replacement is likely to prove more durable.

Unexpected Abrupt Increase in Left Ventricular Assist Device Thrombosis (pg. 33): Left ventricular assist devices have become popular in America, where a brand leader is HeartMate II, a small axial-flow device made by Thoratec. Unfortunately there seems to have been an epidemic of pump-related thrombosis in these devices associated with high morbidity and mortality, which began abruptly in March 2011. It shows no sign of stopping.

JAMA  1 Jan 2014  Vol 311

Effect of Prehospital Induction of Mild Hypothermia on Survival and Neurological Status Among Adults With Cardiac Arrest (pg. 45): Another trial shows that cooling people down on the way to hospital following cardiac arrest in the community makes no difference to outcomes.

Mechanical Chest Compressions and Simultaneous Defibrillation vs. Conventional CPR in Out-of-Hospital Cardiac Arrest (pg. 53): Nor does mechanically assisted cardiopulmonary resuscitation for out-of-hospital cardiac arrest make any difference to short term survival or long-term neurological outcomes.

Transendocardial Mesenchymal Stem Cells and Mononuclear Bone Marrow Cells for Ischemic Cardiomyopathy (pg. 62): And for a final bit of dèja vu to start the new year, here is yet another trial showing that you can safely put transendocardial stem cells with autologous mesenchymal stem cells (MSCs) and bone marrow mononuclear cells (BMCs) into patients with ischaemic cardiomyopathy. What happens thereafter is anybody’s guess. Wake me up when there are some meaningful results.

BMJ   4 Jan 2014  Vol 348

Two Large Systematic Reviews of Coronary Stents: When I first started writing these reviews in 1998, coronary artery stents were quite a new thing: there were even radioactive stents on the market, but they didn’t last long when it was found that they caused arterial wall fibrosis. So how did they get on the market in the first place? Simply because regulatory control of medical device marketing was farcically lax then, and it hasn’t changed much since. I’ve recently heard a medical device manufacturer say quite openly that products simply can’t be subjected to lifetime safety testing because their business cycle simply couldn’t be run that way. New must always be pushed as better, until someone comes along and proves otherwise, at which point you take stock of the profits and move on.

This is not just the industry position: it also just about sums up the regulatory position for anything from absorbent dressings to left ventricular assist devices. This week’s BMJ has two large systematic reviews of coronary stents: one is a comprehensive network meta-analysis comparing durable polymer stents with biodegradable stents, and the other is “mixed treatment comparison meta-analysis” which also includes bare metal stents. Confused already? This is not entirely accidental: it is in the interests of device manufacturers to sow confusion as they go along. And since they pay for nearly all the trials, they can choose their case-mix and their comparators. What they will never tell you is what happens years down the line.

I genuinely admire these gigantic efforts: the first paper looks at data from 60 trials and the second looks at 126. What really puzzles me is that they both combine results from trials in acute coronary syndromes, for which there is a good evidence for PCI including stenting, and trials in stable coronary disease, where stenting is grossly overused and problems of case-mix become insuperable. Both articles plump for certain products as the safest, but I simply don’t believe that you can do that given the nature, duration, and quality of the data available.

Effect of β Blockers on Mortality after MI in adults with COPD: Atenolol was the wonder drug of the mid1980s, if your memory goes back that far. Even humble young GPs such as myself got word of ISIS-1 and duly prescribed it for all our post infarct patients, unless they have something called asthma. This was the era when there was much confusion between “asthma,” “chronic bronchitis,” and the new kid on the block, “chronic obstructive airways disease,” which shortly after morphed into COPD. Here is a study of British primary and secondary care databases which shows that only 39% of patients with COPD are prescribed a beta-blocker after MI in hospital, and that those who do receive one are twice as likely to be alive at three years. This is dire. Practice changed in the USA from 2001 onwards, after a paper in JACC by Krumholz and colleagues, and now 90% of COPD patients there receive beta-blockers after MI. It’s crazy that the message still hasn’t got through in Britain.

Role of Diuretics, β Blockers, and Statins in Increasing the Risk of Diabetes in Patients with Impaired Glucose Tolerance: Three classes of cardioprotective drugs have come under a cloud for inducing “diabetes:” β-blockers, thiazides, and statins. The NAVIGATOR study was a study of the effect of nateglinide and valsartan on 9306 subjects with impaired glucose tolerance, who were prescribed other drugs at the discretion of their doctors. So they form a high risk cohort for observing the effects of other medications as well as the effects of those they were randomised to receive as part of the trial. I am uneasy about the biases that creep in here, but let that be. “New diabetes” was a fasting glucose of 7mmol/L or above. Beta-blockers did not increase its occurrence but “diuretics” (presumably mostly thiazides) and statins did, by about a third. To discuss the relevance or otherwise of this would take too long here, so if you are interested I will point you to my recent exchange of views with a young American diabetologist on CardioExchange.