AF Symposium 2017
Hypercoagulability May Cause A-Fib, NOACs May Prevent It
Novel oral anticoagulants (NOACs) may both prevent and stop A-Fib, according to a thought-provoking hypothesis by Dr. Ulrich Schotten of the University of Maastricht, Maastricht, The Netherlands.
We know that untreated A-Fib increases the risk of stroke 4-5 times and causes decreased blood flow (ischemia). A-Fib also increases the heart’s tendency for blood to coagulate and form clots (hypercoagulability).
Dr. Schotten presented a different, somewhat contrary, and thought-provoking hypothesis that flips current thinking― that hypercoagulability increases and promotes A-Fib (versus A-Fib increasing hypercoagulability).
Research with mice: Working with specially designed mice with increased thrombin activity (hypercoagulated mice), Dr. Schotten found that these mice had increased atrial fibrosis and A-Fib, that a hypercoagulated state promotes atrial fibrosis and A-Fib. Coagulation factors produce profibrotic and proinflammatory responses which can both induce and maintain A-Fib.
The anticoagulant Nadroparin used primarily in surgery (brand name fraxiparine or fraxodi) was used in these mice to reduce their hypercoagulabity. This inhibited the development of A-Fib in these mice.
Dr. Schotten found that Novel Oral Anticoagulants (NOACs), but not warfarin, inhibit collagen synthesis (atrial fibrosis) by reducing the activity of Protease Activated Receptors (PARs).
What Patients Need to Know
Dr. Schotten’s preliminary research indicates there may be a special benefit to taking NOACs. Not only do they reduce hypercoagulability and thereby work to prevent A-Fib strokes, but they may both prevent and stop A-Fib. This is a ground-breaking hypothesis which may lead to major advances in A-Fib research and treatments.
More About Dr. Ulrich Schotten
See a short video by Dr. Schotten: Digital tools for personalized therapy of cardiac arrhythmia presentation at the European Health Science Match, October 2016. (3:11 min.)