COMMENTARY

John Mandrola's Top 10 (er, 11) Cardiology Stories of 2013

John M. Mandrola, MD

Disclosures

December 20, 2013

In This Article

JNC-8, Obesity and AF, and NOACs

4. High Blood Pressure Guidelines

I often tell this story to patients: When I was a younger doctor, I would take my 94-year-old grandfather around to see the best doctors in town. We both held to the fantasy that doctors could "fix" him. Mostly he had age-related problems. He did, however, own one shining beacon of good health: He had perfect blood pressure, without medication. My message to patients is that my grandfather lived to 94 because of those BP readings.

What I learned from my grandfather's case, which has now been borne out in the new JNC 8 guidelines,[3] is that it matters how one achieves good blood pressure. The new guidelines, chaired by a family medicine professor (how cool is that?), continues to disrupt the concept that more drug treatment leads to better outcomes.

It is indeed striking what can be found when one looks carefully and systematically at absolute benefits of treatments from randomized clinical trials. Truthfully, did you know that there was essentially no evidence that treating mild high blood pressure in patients younger than 60 improves outcomes? I didn't.

Here the affect heuristic looms large. I find great pleasure in the idea that the medical establishment is now poised to embrace common sense. Namely, that modifying a single risk factor with a chemical that surely has multiple system-wide effects does not necessarily improve outcomes.

5. In Electrophysiology, Treat the Underlying Cause of AF

There are a few landmark studies I keep around the exam room for show-and-tell. 2013 brought another keeper. Dr. Prashanthan Sanders and colleagues (from Adelaide, Australia) are authors of the study with most impact in all of cardiology in 2013.[4]

Here is the story: Atrial fibrillation is increasing exponentially. Electrophysiologists see patients at the end of the disease spectrum. Rate control, rhythm control, and anticoagulation are each important treatment strategies, but they don't address the root cause of AF. In previous work in animal models, this group of researchers showed that obesity increases the susceptibility to AF.

The hypothesis was that weight loss (and aggressive attention to other cardiometabolic risk factors) would reduce AF burden. They randomly assigned patients on their waiting list for AF ablation to 2 groups: (1) a physician-led aggressive program that targeted primarily weight loss, but also hypertension, sleep apnea, glucose control, and alcohol reduction; or (2) standard care with lifestyle counseling.

The findings were striking. Compared with the group of patients receiving standard care, patients in the physician-directed program lost weight, reported less AF symptoms, and had fewer AF episodes recorded. Most impressive were the structural effects noted on echocardiograms. Patients in the intervention group had regression of left ventricular hypertrophy and reduction in left atrial size.

Though this is a small trial, it is practice-changing for cardiology. It shows that treating modifiable risk factors remodels the heart and in so doing reduces the burden of AF. In an interview in JAMA, Dr. Sanders says aggressive risk factor treatment should be a standard of care. I agree. Right now, AF ablation is too often thought of in terms of a supraventricular tachycardia ablation -- a fix for a fluke of nature. It's not that way. In the majority of AF cases, the same excesses that cause atherosclerosis also cause AF. Rather than make 50 burns in the atria, it makes much more sense to address the root cause.

NOACs

6. Novel Anticoagulants Face Value-Based Headwinds

Tell me you haven't been in this situation: You are making rounds on a patient with newly diagnosed AF, admitted the night before. She has multiple risk factors for stroke. Her heart rate has been controlled and her symptoms improved. There are now 2 choices for anticoagulation: (1) Start warfarin, and while waiting for an adequate INR, cover with IV-heparin (days in hospital) or low-molecular-weight heparin (teaching- and dollar-intensive); or (2) Begin a novel oral anticoagulant (NOAC) and discharge the patient that day. It's so much easier to use NOAC drugs.

But then what happens when the "starter" kits run out and the patient faces a massive bill at the pharmacy, or her third-party payer denies payment? Now our patient has a problem. She is in AF and has risk factors for stroke. A gap in anticoagulation is not desirable.

At the heart of this issue is the value and superiority of NOAC drugs compared with warfarin. At the 2013 American Heart Association Sessions, the ENGAGE-AF trial showed that the newest NOAC drug, edoxaban, compared favorably to warfarin.[5] All 4 clinical trials of NOAC drugs vs warfarin looked strikingly similar -- namely, that in absolute benefits (stroke reduction) and harm (bleeding), NOAC drugs and warfarin performed similarly, within 1% of each other. In the cost-conscious, evidence-based climate of 2013, NOAC drugs are increasingly recognized as overvalued. Warfarin, with all its imperfections, remains steady.

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