Circulation: Arrhythmia and Electrophysiology June 2019 Issue

Circulation: Arrhythmia and Electrophysiology On the Beat

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

In our first paper, Jeremy Wasserlauf and associates compare the accuracy of an atrial fibrillation sensing smartwatch with simultaneous recordings from an insertable cardiac monitor.

The authors use smart rhythm 2.0, a convolutional neuro-network, trained on anonymized data of heart rate, activity level and EKGs from 7500 AliveCor users.

The network was validated on data collected in 24 patients with insertable cardiac monitor, and a history of paroxysmal atrial fibrillation who simultaneously wore the atrial fibrillation sensing smart watch with smart rhythm 0.1 software.

The primary outcome was sensitivity of the atrial fibrillation sensing smart watch for atrial fibrillation episodes of greater than equal to one hour. Secondary end points include sensitivity of atrial fibrillation sensing smart watch for detection of atrial fibrillation by subject and sensitivity for total duration across all subjects.

Subjects with greater than 50% false positive atrial fibrillation episodes on insertable cardiac monitor were excluded.

The authors analyzed 31,349 hours meaning 11.3 hours per day of simultaneous atrial fibrillation sensing smart watch and insertable cardiac monitor recordings in 24 patients. Insertable cardiac monitor detected 82 episodes of atrial fibrillation of one hour duration or greater while the atrial fibrillation sensing smartwatch was worn. With a total duration of 1,127 hours.

Of these, the smart rhythm 2.0 neural network detected 80 episodes. Episode sensitivity 97.5% with total duration 1,101 hours. Duration sensitivity 97.7%.

Three of the 18 subjects with atrial fibrillation of one hour or greater had atrial fibrillation only when the watch was not being worn. Patient sensitivity 83.3% or 100% during the time worn. Positive predictive value for atrial fibrillation episodes was 39.9%.

The authors concluded that an atrial fibrillation sensing smartwatch is highly sensitive to detection of atrial fibrillation and assessment of atrial fibrillation duration in an ambulatory population when compared to insertable cardiac monitor.

In our next paper, Liliana Tavares and associates examine the autonomic nervous system response to apnea in its mechanistic connection to atrial fibrillation. They study the effects of ablation of cardiac sensory neurons with resiniferatoxin, a neurotoxic transient receptor potential vanilloid one agonist.

In a canine model, apnea was induced by stopping ventilation until oxygen saturation decreased in 90%. Nerve recordings from bilateral vagal nerves left stellate ganglion and anterior right ganglion plexi were obtained before and during apnea, before and after resiniferatoxin injection in the anterior white ganglion plexi in seven animals.

Each refractory period and atrial fibrillation inducibility upon single extra stimulation was assessed before and during apnea, before and after intrapericardial resiniferatoxin administration in nine animals.

The authors found that apnea increased anterior wide ganglion plexi activity followed by cluster crescendo vagal bursts synchronized with heart rate and blood pressure oscillation.

Upon further oxygen desaturation, a tonic increase in left stellate ganglion activity in blood pressure oscillations ensued. Apnea induced atrial effective refractory shortening from 110 to 90 milliseconds, P less than 0.001 and atrial fibrillation induction in nine animals vs. zero out of nine at baseline.

After resiniferatoxin administration increases in ganglion plexi and left stellate ganglion activity, and blood pressure during apnea were abolished, in addition, the atrial effector refractory period increased to 127 milliseconds, P=0.0001 and atrial fibrillation was not induced.

Vagal bursts remain unchanged. Ganglion plexi cells showed cytoplasmic microvacuolation and apoptosis. The authors concluded that apnea increased ganglion plexi activity followed by vagal bursts and tonic left stellate ganglion firing. Resiniferatoxin decreases sympathetic and ganglion plexi nerve activity, abolishes apnea's electrophysiotic response and atrial fibrillation inducibility indicating that sensory neurons play a role in apnea induced atrial fibrillation.

In our next paper, Thomas Pambrun and associates examined whether using unipolar signal modification as a local end point would improve the safety and efficacy of high-power ablation during pulmonary vein isolation. They studied four swine and 100 consecutive patients referred for pulmonary vein isolation with the first 50 patients in a control group using 25 to 30 watts and the last 50 patients in a study group with 40 to 50 watts.

Atrial radiofrequency applications were stopped two seconds in the study group and swine or five seconds in the control group after unipolar signal modification. Ventricular radiofrequency applications of 500 joules were performed at the swine epicardium.

The authors found that swine did not show any extracardiac damage related to atrial lesions. At equal energy of 500 joules, 50 watt lesions were deeper, three vs. 2.6 millimeters, P=0.3 and wider, 6.2 vs. five millimeters, P=0.006 and 25 watt lesions.

In a clinical study, there were no complications occurring at either power output. The study group displayed higher first pass pulmonary vein isolation, 92% vs. 73%, P less than 0.001. In addition, the study group had a lower acute pulmonary vein reconnection, 2% vs. 17%, P less than 0.001 as well as reduced procedure time, 73.1 vs. 107.4 minutes and ablation team, 13 vs. 30.3 minutes. Sinus rhythm maintenance at 12 months was similar, 90% and 88%.

The authors concluded that high power pulmonary vein isolation guided by unipolar signal modification safely decreases procedural burden while achieving similar 12-month outcomes.

In our next paper, Toshiaki Sato and associates attempted to identify predictors of low his-bundle pacing threshold. They studied 51 patients, 53% with atrial ventricular block undergoing his-bundle pacing for bradycardia with an intrinsic QRS duration of less than 120 milliseconds.

His-bundle pacing lead positioning was guided by unipolar his-bundle electrograms recorded with an electrophysiology recording system. In total, 153 attempts at anchoring the his-bundle pacing lead were made, of which 45 achieved acceptable his-bundle pacing thresholds, less than or equal to 2.5 volts at one millisecond.

The amplitude of negative deflection in unipolar his-bundle electrograms and the selective his-bundle pacing at fixation where independently associated with achieving a acceptable threshold. A negative amplitude of greater than or equal to 0.06 millivolts in the his-bundle electrograms was determined as the optimal value for identifying acceptable threshold. This deep negative his-bundle electrogram was recorded with a his-bundle pacing threshold of 1.4 volts in 34 attempts, significantly lower than the positive his-bundle electrogram without deep negative deflection, 2.8 volts in 31 trials or greater than five volts in 38 trials.

The permanent his-bundle pacing lead remained with a deep negative, greater than or equal to 0.06 millivolts or positive his-bundle electrogram in 28 or 14 patients respectively and with a positive or negative his-bundle pacing injury current in 19 and 23 patients respectively.

During follow-up, increased his-bundle pacing threshold of greater than one volt was significantly more prevalent in the positive his-bundle electrogram group. The his-bundle pacing threshold of deep negative his-bundle electrogram and his-bundle injury current but not of selective his-bundle pacing group were significantly lower than other sub-groups during follow-up.

In the next paper, Claire Martin and associates examined whether altering activation wavefront affects activation timing and local abnormal ventricular activity characterization in patients with ischemic cardiomyopathy. They use the ultra-high density arrhythmia to generate maps for all stable ventricular tachycardias and with pacing from the atrium, right ventricular apex and left ventricular branch of the coronary sinus.

56 pace maps and 23 ventricular tachycardia circuits were mapped in 22 patients. In 79% of activation maps, there was one or greater lines of block in the pace conduction wavefront with 93% having fixed block and 32% showing functional partial block. Bipolar scar was larger with atrial than right ventricular, 31.7 centimeters squared vs. 27.6 centimeters squared, P = 0.003 or left ventricular pacing, 31.7 centimeters squared vs. 27.0 centimeters squared, P = 0.009.

Local abnormal ventricular activities areas were smaller with atrial than right ventricular pacing, 12.3 centimeters squared vs. 18.4 centimeters squared or left ventricular pacing, 12.3 centimeters squared vs. 17.1 centimeters squared. Local abnormal ventricular activities were larger with wavefront propagation perpendicular vs. parallel to the line of block along isthmus boundaries, 9.3 vs. 13.6 centimeters squared P = 0.01.

All patients had successful tachycardia isthmus ablation in 11 months follow-up, two patients had a recurrence.

In our next paper, Andrew Tseng and Katie Kunze and associates conducted a systematic review and network meta-analysis on the effect of medication device therapies and reduced ejection fraction on all-cause mortality. Randomized control trials published between January 1980 and July 2017 were identified.

The authors found that combination therapy of angiotensin converting enzyme inhibitors or angiotensin receptor blockers with beta blockers alone or in addition to implantable cardioverter defibrillator or cardiac resynchronization therapy with defibrillators demonstrated significant reduction in all cause of mortality when compared to placebo.

By probability rank, implantable cardio defibrillator plus angiotensin receptor blockers plus beta blockers plus mineralocorticoid receptor blockers, implantable cardioverter defibrillators plus angiotensin receptor blockers plus beta blockers and angiotensin receptor-neprilysin inhibitor plus beta blockers and mineralocorticoid receptor antag as combination therapies have the highest probability of being ranked the best treatment. There was no significant difference in the rate of mortality when comparing angiotensin receptor-neprilysin inhibitors plus beta blockers plus mineralocorticoid receptor antagonist to ICD plus optimal pharmacologic combination therapy.

In our next paper, Karl-Heinz Kuck and associates examined repeat ablation in the fire and ice trial, which examined efficacy and safety of pulmonary vein isolation using cryoballoon vs. radio-frequency current ablation in patients with drug refractory symptomatic paroxysmal atrial fibrillation.

Patients with re-ablation procedures during fire and ice were retrospectively consented and rolled at 13 trial centers. 89, 36 cryo-balloon and 53 radio-frequency patients were studied. Paroxysmal atrial fibrillation was the predominant recurring arrhythmia, 69% prior to re-ablation. Re-ablations occurred at the median of 173 and 182 days in the cryoballoon and radio frequency cohorts.

The number of reconnected pulmonary veins was significantly higher in the radio frequency than the cryo-balloon, 2.1 vs. 1.4 P = 0.01, which was significantly driven by more connected left superior pulmonary veins and markedly more reconnected right superior pulmonary veins.

The number of predominantly radio frequency lesions applied during re-ablation was significantly greater in patients originally treated with radio frequency, 3.3 vs. 2.5, P=0.015 with no difference in overall acute success.

After re-ablation, no differences in procedure related rehospitalization or antiarrhythmic drug utilization was observed between cohorts.

In the next paper, Ayelet Shapira-Daniels and Michael Barkagan and associates examined the ability of reducing baseline impedance to improve ventricular ablation success. In 16 patients with ventricular tachycardia or frequent ventricular premature complexes with failed rate of frequency ablation with irrigated catheters, the impedance was modulated by adding or repositioning return patches.

Ablation was repeated at similar location and power settings. The authors studied six patients with idiopathic ventricular premature complexes originated from the left ventricular summit, N=4 or papillary muscles, N=2. Six patients with non-infarct related ventricular tachycardia and four patients with infarc related ventricular tachycardia. Prior unsuccessful radio frequency ablation at critical sites had a number of 10.4 applications, power of 43.3 watts, duration 55.3 seconds and impedance reduction, 14.6 Ohms in low ionic solution was used in 81%.

Modulating the return patches resulted in reduced baseline impedance, 111.7 vs. 34.7 ohms, P less than 0.0001. Increased current output 0.6 vs. 0.56 amps, P also less than 0.0001. And impedance dropped 16.8 ohms.

Repeat ablation at similar locations had successful effect in 12 out of 16 or 75% patients. During a follow-up duration of 13 months, 10 out of 12 or 83% patients remained free of arrhythmia occurrence. The frequency of steam pops was similar between higher and lower baseline impedance settings.

The authors concluded that in patients with deep ventricular substrate, reducing the baseline impedance is a simple, safe and effective technique for increasing the effect of radio frequency ablation.

However, the combination with low ionic solutions may increase the risk for steam pops and neurological events.

Our last paper is a review by Robert Anderson and associates. The authors summarize all of the published 12 lead ECD algorithms used to localize ventricular arrhythmias from the right ventricular and left ventricular outflow tracks.

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

This program is copyright American Heart Association 2019.