Live Blog—Boston AF symposium
January 12, 2012
Guest post by Dr. John Mandrola
I’ve never tried this before: giving some brief snips of an AF symposium, on the fly.
Maybe doing so will help me remember. My comments are in italics.
Little proofreads—consider these quick notes.
First talk: Dr Jalife. Molecular mechanisms AF:
Think fibrosis, or the infiltration of scar tissue within the muscle of the heart. This is bad because it disrupts the normal propagation of electricity. The cells that make the scar are called Fibroblasts. I learned about them the first semester of med school; who knew they would be so involved as the root cause of my profession.
To quote Dr Jalife, a very famous researcher…“To prevent AF…start early!” Treat similarly to CHF [congestive heart failure] and atherosclerosis.”
This makes sense.
Dr Stanley Nattel: Obesity and sleep apnea. (OSA = Obstructive Sleep Apnea). Mechanisms in the generation of AF.
Dr Nattel presented data from rats. He compared sleep apnea models in obese vs. lean rats.
OSA increases AF inducibility, especially in obese rats.
Why? Because the disordered breathing in OSA causes acute LA [left atrial] dilation and the effect was greater in obese rats, though still present in lean rats.
“CPAP [continuous positive airway pressure] applied early may prevent acute effects of repeated episodes, as long as it is started early.”
Early intervention again. Ask about sleep disorders. Sleep, the third prong of good health–the other two of course, exercise and nutrition.
Dr Patrick Ellinor: Genetics of AF. How will GWAS (Genome wide association studies) findings apply to clinical practice? GWAS uses an entire population to look for genetic variants.
Background: Parental history doubles AF risk. Any first degree relative with AF increases risk by 40%. Risk of inheritance higher with early onset of AF. Old data here.
Variants on chromosome 4 increases AF risk. But the odds ratios are not high enough to be useful. “Right now, taking a history in the office yields better predicative value than any gene test,” Dr Ellinor adds.
Why the interest in genetics and AF then?
Dr Ellinor says, “Discovery tool…Science takes time.”
Interesting topic—AF is definitely clustered in certain phenotypes and is markedly decreased is some populations, African-Americans for example have less AF than northern Europeans???
Dr Charlie Antzelevitch — New directions in AF drug therapy.
Atrial-selective K-blockers thought to be good place to look for new drugs, but thus far, these drugs have not worked.
What about atrial-selective Na [sodium] channel inhibition?
Vernakalent: Maybe +
Wenxin Keli: Chinese herb with significant electrical effects on the atria, but not so much in the ventricle, intriguing. Stay tuned.
Combinations of drugs: amiodarone and ranolazine. Effective, but scary.
Dronedarone and ranolazine. Not too bad. But again, a scary combination.
I may be wrong, but the future of drug therapy for AF seems limited. Heck, you know how I feel about treating heart disease: drugs are always second or third choices. The chinese herb is worth a Google search, if nothing else, for curiosity.
Final talk of the morning session:
Dr. Jalife: Best basic science papers in 2011.
Circ [Circulation] research 2011 108: 164 — AF induces myocardial fibrosis–role of angiotensin 2. Losartan, a commonly used blood pressure medicine may help reduce fibrosis. Again, hope if one starts early.
Circ 2011 124 1212– Defects in ankyrin-based membrane proteins… Important in AF susceptibility. This protein plays a role in AF. Sorry. This was over my head.
Circ cardiovascular Genet 2011 4: 269 On genetics, the role of a funny-sounding gene PITX2. I have little to translate on this one as well. Basic science is tough for regular doctors.
Dr. Mandrola is a cardiac electrophysiologist who blogs at Dr. John M