Article preview from Start-Up - May, 2013
Topera Medical questions the assumptions underlying current therapies for atrial fibrillation. Sanjiv Narayan, MD, PhD, the electrophysiologist who founded Topera, has developed a means of identifying focal sources of aberrant electrical activity called rotors, and in late breaking clinical trials at the 2013 annual meeting of the Heart Rhythm Society, was able to show a definitive link between their ablation and treatment success.
At HRS, Topera Topples Conventional Wisdom About Atrial Fibrillation
Article preview from Start-Up - May, 2013
Atrial fibrillation has always been frustratingly resistant to a cure. Even among the so-called easiest groups of patients, those with paroxysmal atrial fibrillation (which is intermittent and terminates on its own), conventional ablation procedures using radiofrequency or some other energy modality to scar the heart and isolate the instigating electrical impulses (or triggers) provide long-term freedom from AF only 50% of the time. The search for better efficacy is compelling because patients that suffer from atrial fibrillation have a five to seven-fold increased risk for stroke.
While much of the cardiology industry has tried to improve the results by incrementally improving the therapies, Topera Medical Inc. challenges the assumptions upon which therapy has been based. Back in 2011, Topera’s scientific founder, electrophysiologist Sanjiv Narayan, MD, PhD, of the department of medicine at the University of California, San Diego, and the Veterans Affairs Medical Center in San Diego was a lone voice at the Heart Rhythm Society’s (HRS) 32nd annual scientific sessions. At the time, Narayan presented study results that concluded that there were previously theorized but never before seen sources of AF that drive and sustain arrhythmias. At this year’s annual meeting Narayan was flanked by a chorus of electrophysiology professionals carrying the same tune.
Atrial fibrillation is typically treated based on an anatomical, rather than a physiologic treatment strategy. That is, physicians have isolated the pulmonary vein, or targeted the roof of the left atrium as a treatment strategy, without truly identifying the source of the aberrant electrical signals. For whatever reason, those anatomical strategies resulted in lackluster efficacy for patients with paroxysmal atrial fibrillation even after retreatments, and very little efficacy for the harder-to-treat persistent AF patients further along in the course of their disease. Topera has apparently revealed the reason.
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