Circulation: Arrhythmia and Electrophysiology September 2018 Issue


Manage episode 217041532 series 1452724
By Discovered by Player FM and our community — copyright is owned by the publisher, not Player FM, and audio streamed directly from their servers.

Dr Paul Wang: Welcome to the monthly podcast On The Beat, where Circulation: Arrhythmia and Electrophysiology. I'm Doctor Paul Wang, editor in chief, with some of the key highlights from this month's issue.

In our first paper, Parikshit Sharma and associates reported on the use of permanent his bundle pacing to improve hemodynamics in 39 patients with right bundle branch block. His bundle pacing was successfully performed in 37, or 95 percent of the patients, and resulted in narrowing of the QRS complex from 158 milliseconds to 127 milliseconds. P = 0.0001. An increase in left ventricular ejection fraction from 31 percent to 39 percent. P = 0.004, an improvement in the New York Heart Association functional class from 2.8 to 2.0 P = 0.0001. This work suggests that his bundle pacing maybe helpful in right bundle branch block patients with left ventricular dysfunction.

In our next paper, Philippe Debruyne and associates added to our understanding of using catheter ablation to modulate the autonomic nervous system in patients with neurally mediated syncope, signs of no dysfunction and functional AV block. Prior reports of autonomic modulation using catheter ablation have required extensive ablation in both atria. In this article, the authors report a significant 95% reduction in syncope at six months as a result of targeted ablation in the right atrium alone, focusing on partial ablation of the interior right ganglionated plexus. Ablation is quite limited, taking a mean of seven minutes and creating a mean surface area of 11 millimeters squared. This technique has promise as a possible treatment for avoiding a need of pacemaker implantation in some patients.

In our next paper, Shankar Baskar and associates examined the characteristics and outcomes of pediatric patients receiving implantable cardioverter defibrillators and compared them to their adult counterparts. They examined ICD recipients in the NCDRICD registry from 2010 to 2016. There were 562,209 total ICD implants, including 3461 pediatric patients. Of the pediatric patients, 60 percent of implants were for primary prevention with non-ischemic cardiomyopathy being present in 60 percent of the patients, the most common underlying disease. Over time, there is an increasing trend of both primary and secondary prevention ICD implantations, P less than 0.05. Compared to adults, pediatric patients were likely to have structural heart disease, hypertrophic cardiomyopathy, ion channelopathy, and to receive a single chamber device. All P less than 0.001. There is no difference in in-hospital complications between the adult and the pediatric cohorts, 2.4 percent versus 2.6 percent. However, among pediatric patients, lower weight, Ebstein's anomaly, worse New York Heart Association class dual chamber and resynchronization defibrillator were associated with greater risk of complications. Although, re-intervention for generator replacement or upgrade was more common in adults, the time to re-intervention was shorter in the pediatric cohort.

In our next paper, Ahmed Hussein and associates examine the effect of using ablation index guiding ablation in 40 patients with persistent HO fibrillation on the rate of pulmonary vein reconnection. Pulmonary vein reconnection was seen as a mandatory repeat electro-physiologic study in 22 percent of patients, effecting seven percent of pulmonary veins. Ablation on the intravenous cryna was required in 44 percent of patients to achieve durable pulmonary vein isolation. Atrial tachyarrhythmia occurrence was documented in eight to 20 percent of patients, only one of whom had pulmonary vein reconnection at repeat study. At 12 months, 30 out of 40, or 95 percent of patients, were in sinus rhythm, with four or 10 percent of patients having starting antiarrhythmic drugs. Higher body mass index and excessive alcohol consumption were the only significant factors associated with atrial tachyarrhythmia occurrence.

In our next paper, Atsushi Hirayama and associates examined whether acute exasperation of chronic obstructive pulmonary disease increases the risk of repeated atrial fibrillation related health care utilization. They examine 944 patients who are hospitalized for acute exasperation of chronic obstructive pulmonary disease and had emergency department visit or hospitalization for atrial fibrillation during a 450 day period. Compared to the reference period, the rate of atrial fibrillation related emergency department visits or hospitalizations significantly increased in the first 90 days after acute exasperation of chronic obstructive pulmonary disease. 7.3 versus 14.1 per one hundred person months, resulting in a risk ratio of 1.93.

In our next paper, Namsik Yoon and associates examined the mechanisms underlying the electrocardiographic and arrhythmic manifestation of experimental models of early repolarization syndrome and the ameliorative effects of radio-frequency ablation. The authors recorded axis potentials, bi-polar electrograms, and transmural pseudo electrocardiograms for coronary perfused canine left ventricular wedge preparations in 11 animals.

The ITO agonist, NS5806, the calcium channel blocker Verapamil and acetylcholine were used to pharmacologically mimic the effects of genetic defects associated with early repolarization syndrome. The provocative agents induce prominent j waves in the ECG secondary to the accentuation of the action potential notch in the epicardium but not the endocardium. Bipolar recordings displayed low voltage fractionated potential in the epicardium due to temporal and spatial variability and appearance of the action potential dome conceal the phase two reentry develop when the axon potential dome was lost at some epicardial sites but not others. Appearing in the bipolar electrogram, is discrete high frequency spikes. Successful propagation of the concealed phase two reentered beat precipitated ventricular tachycardia or ventricular fibrillation. Radiofrequency ablation of epicardium destroyed the cell displaying abnormal repolarization and thus suppressed the j waves and the development of ventricular tachycardia and ventricular fibrillation in six out of six preparations.

Stavros Stavrakis and associates described ten patients out of 843 patients, or 1.2 percent with AV nodal reentry tachycardia who required ablation of the basal inferolateral left atria, during stable antegrade slow, retrograde fast, AV nodal reentry tachycardia, a single late atrial extra stimulus was delivered at the inferolateral left atria, near the mitral annulus. All patients had failed ablation in the inferior triangle of Koch, and or roof of the coronary sinus. In all ten patients, a late atrial extra stimulus advanced the his bundle potential by at least ten milliseconds and reset the tachycardia. Ablation at that site, eliminates slow pathway conduction and terminated the tachycardia. Ablation was successful at the site of the latest atrial extra stimulus delivered 49 milliseconds after the onset of this his bundle potential. In their series, no recurrent tachycardia was noted at one year follow up.

In our final paper, Justine Bhar-Amato and Malcolm Finlay and associates examine the hypothesis that increased cholinergic tone exerts its pro-rhythmic effects in Brugada Syndrome through increasing dispersion of transmural repolarization in patients with spontaneous and drug induced Brugada Syndrome. Using a recording array in the right ventricular outflow tract and a micro-catheter in the great cardiac vein to record intracardial and epicardial signals, the authors constructed S1S2 restitution curves from the right ventricular apex at baseline and after edrophonium challenge.

The authors studied eight Brugada Syndrome patients and compared them to eight control patients with super ventricular tachycardia. Electrophysiological studies in controls demonstrated shorter endocardial than epicardial right ventricular activation times, mean difference 26 milliseconds. In contrast, Brugada Syndrome patients showed longer endocardial than epicardial activation times, mean difference -15 milliseconds. Brugada Syndrome patients significantly larger transmural gradient in their activation recovery intervals, mean intervals 20.5 versus 3.5 milliseconds, with longer endocardial than epicardial activation recovery intervals. Edrophonium challenge increased the gradients in both controls to a mean of 16 milliseconds. In Brugada Syndrome, to 29.7 milliseconds. However, these changes were attributed to epicardial activation recovery, interval prolongation in control patients. In endocardial activation recovery interval prolongation in Brugada Syndrome patients. Dynamic changes in repolarization gradients were also observed across the right ventricular wall in Brugada Syndrome patients.

That's it for this month. We hope that you'll find the journal to be the go to place for everyone interest in the field. See you next time.

21 episodes available. A new episode about every 31 days averaging 33 mins duration .