Atrial Fibrillation: How Bad Can It Be?
Disclaimer: The views and opinions expressed herein are those of the author(s) and do not necessarily reflect the official policy or position of Consultant360 or HMP Global, their employees, and affiliates. Any content provided by our bloggers or authors are of their opinion and are not intended to malign any religion, ethnic group, club, association, organization, company, individual, or anyone or anything.
Alvin B. Lin, MD, FAAFP
Associate Professor of Family and Community Medicine, University of Nevada School of Medicine
Adjunct Professor of Family Medicine and Geriatrics, Touro University Nevada College of Medicine
Advisory Medical Director, Infinity Hospice Care
Medical Director, Lions HealthFirst Foundation
Dr. Lin maintains a small private practice in Las Vegas, NV. The posts represent the views of Dr. Lin, and in no way are to be construed as representative of the above listed organizations. Dr. Lin blogs about current medical literature and news at http://alvinblin.blogspot.com/.
True story: During my 50-year-old patient's recent annual physical, I noted an irregularly irregular rhythm to his heart beat. He denied any recent alcohol (binge) as well as caffeine or stimulant consumption. No palpitations or heart racing/skipping beats. No dizziness or lightheadedness. His thyroid panel, drawn prior to his visit with me, was stone cold normal. He was due to follow up with his cardiologist regarding high cholesterol and hypertension (basic stuff we family docs are well trained to treat) so I just suggested that he point this out to the cardiologist. A few weeks later, he reported back to me that he'd been started on Multaq, an antiarrhythmic, because he had an irregular rhythm. He didn't recall any discussion of the diagnosis, rate control (presumably because he was not tachycardic) or stroke prevention, much less review of calculated stroke risk versus bleeding risk. Boy, was I miffed!
So let's step back a bit. The American College of Chest Physicians (ACCP) promulgated their 9th guidelines on Antithrombotic Therapy and Prevention of Thrombosis last month. In addition to setting standard of care for deep venous thrombosis and pulmonary embolism, this evidence-based guideline also focuses quite a bit of time on atrial fibrillation, since this abnormal heart rhythm increases one's risk for stroke. But with judicious antithrombotic therapy in those at greatest risk, one can mitigate the potential for loss of function.
But who's at risk? That's where the CHADS2 calculator comes in—that's the one specified by the ACCP. Of course, there's also a newer version, known as CHA2DS2-VASc. Both are easy to use. Just plug in your numbers and it spits out your risk of stroke. But don't forget the other side of the equation, major bleeding risk. That's where HAS-BLED comes in. Again, just plug in your numbers and it spits out your risk of bleeding. And take your meds if your risk for stroke is greater than your risk for bleeding.
Simple, right? Well, no, at least not as of last week when Canadian authors reported that atrial fibrillation is linked to cognitive & function decline, regardless of clinical stroke. They arrived at their conclusion by reassessing the data from 2 randomized double-blind placebo-controlled trials (ONTARGET & TRANSCEND) originally designed to look at the effect of ARB +/- ACE inhibitor on heart disease. There were 31,546 participants in these trials, average age 66.5 years old, mean baseline Mini-Mental Status Examination score of 27.7 (out of maximum 30; a higher score is better). Of these, 1016 had baseline atrial fibrillation while the condition developed in 2052 more. From this comparison, everything else being equal, atrial fibrillation was associated with an increase risk of new dementia, loss of independence from loss ability to perform activities of daily living, and institutionalization, regardless of stroke status and antihypertensive regimen.
While ONTARGET and TRANSCEND are both randomized controlled studies designed to demonstrate cause and effect, re-analysis of the data (after completion of the trial) in a fashion for which the original studies were not designed make this study more of a hypothesis generating one, as opposed to demonstrating cause and effect. And while there was not solution or therapy mentioned, I can't help but feel that microembolic phenomena led to repeated microischemic events or infarcts, which over time led to loss of cognitive function and functional decline. The point of this diatribe is that we may want to consider antithrombotic therapy sooner in our otherwise intact patients.