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Circulation: Arrhythmia and Electrophysiology On the Beat - Circulation: Arrhythmia and Electrophysiology July 2018 Issue

Circulation: Arrhythmia and Electrophysiology July 2018 Issue

07/15/19 • 15 min

Circulation: Arrhythmia and Electrophysiology On the Beat

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

In our first paper, Moo-Nyun Jin, Tae-Hoon Kim, and associates examined the 1-year serial changes in cognitive function, with or without atrial fibrillation catheter ablation. They used the Montreal cognitive assessment score in 308 patients undergoing atrial fibrillation ablation, the ablation group and 50 atrial fibrillation patients on medical therapy who met the same indication for atrial fibrillation ablation, the control group at baseline three months and 12 months. Cognitive impairment was defined as a published cutoff score of less than 23 points. Pre-ablation cognitive impairment was a detected in 18.5%. The Montreal cognitive assessment score significantly improved one year after radio frequency ablation. In both the overall ablation group, 24.9 to 26.4 p less than 0.001, and the propensity matched ablation group 25.4 to 26.5, but not in the control group. 25.4 to 24.8 p equals 0.012. Pre-ablation cognitive pyramid odds ratio 13.7, was independently associated with an improvement in one-year post ablation cognitive function.

In our next paper, Zian Tseng, James Salazar and associates studied World Health Organization defined sudden cardiac deaths autopsied in the POstmortem Systemic InvesTigation of sudden cardiac death, the POST SCD study to determine whether premortem characteristics could identify autopsy defined sudden arrhythmic death among presumed sudden cardiac deaths. They prospectively identified 615 World Health Organization defined sudden cardiac deaths, of which 144 were witnessed. Autopsy defined sudden arrhythmic death had no extra cardiac or acute heart failure cause of death. Of the 615 presumed sudden critic deaths, 348 or 57% were autopsy defined, sudden arrhythmic deaths. For witness cases, using an emergency medical system model area under the receiver operator curve 0.75, included presenting rhythm of ventricular tech or cardiac fibrillation, pulseless electrical activity, while the comprehensive model, adding medical record data and depression, area under the curve 0.78. If only VTVF witness cases, 48 of those were classified as sudden arrhythmic death. The sensitivity was 0.46, and specificity 0.90.

For unwitnessed cases, the emergency medical system model, area under the curve 0.68, included black race, male sex, age, time since last seen normal, while the comprehensive, area into the curve 0.75, added the use of beta blockers, antidepressants, QT prolonging drugs, opiates, illicit drugs and dyslipidemia. If only unwitnessed cases, less than one hour, n equals 59, were classified as sudden arrhythmic deaths, the sensitivities were 0.18, and specificity was 0.95. The authors concluded that models could identify pre-mortem characteristics to better specify autopsy defined sudden arrhythmic deaths, among presumed sudden cardiac arrests. The authors suggest that the World Health Organization definition can be improved by restricting witnessed sudden cardiac deaths to ventricular tachycardia fibrillation or non-pulseless electrical activity rhythms in unwitnessed cases to less than one hour since last normal, at a cost of sensitivity.

In our next paper, Rafael Jaimes III and associates performed optical mapping of trends, membrane, voltage and pacing studies on isolated Langendorff-perfused rat hearts to assess the cardiac electrophysiology after mono-2-ethylhexyl phthalate, a phthalate with documented exposure in intensive care patients. The authors found that a 30-minute exposure to mono-2-ethylhexyl phthalate increased the atrioventricular node effector in period 147 milliseconds compared to 170 milliseconds in controls and increased the ventricular effective refractory periods of 117 milliseconds compared to 77.5 milliseconds in controls. Optical mapping revealed prolonged action potential duration at slower pacing cycle lengths. Mono-2-ethylhexyl phthalate exposure also slowed epicardial conduction velocity, 25 centimeters per second compared to 60 centimeters per second in controls. The authors concluded that acute mono-2-ethylhexyl phthalate exposure, at clinically relevant doses, has a significant effect on cardiac electrophysiology in the intact heart. Heightened clinical exposure to plasticized medical products may have cardiac safety implications and lead to cardiac arrhythmias.

In our next paper, Stephan Willems and associates report the use of a novel, non-contact imaging and mapping system that uses ultrasound to reconstruct atrial chamber anatomy and measure timing and density of dipolar, ionic activation or charge density across the myocardium to guide ablation of atrial arrhythmias. They conducted a prospective non-randomized study, the UNCOVER AF trial which was conducted at 13 centers across Europe and Canada. In 127 pati...

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

In our first paper, Moo-Nyun Jin, Tae-Hoon Kim, and associates examined the 1-year serial changes in cognitive function, with or without atrial fibrillation catheter ablation. They used the Montreal cognitive assessment score in 308 patients undergoing atrial fibrillation ablation, the ablation group and 50 atrial fibrillation patients on medical therapy who met the same indication for atrial fibrillation ablation, the control group at baseline three months and 12 months. Cognitive impairment was defined as a published cutoff score of less than 23 points. Pre-ablation cognitive impairment was a detected in 18.5%. The Montreal cognitive assessment score significantly improved one year after radio frequency ablation. In both the overall ablation group, 24.9 to 26.4 p less than 0.001, and the propensity matched ablation group 25.4 to 26.5, but not in the control group. 25.4 to 24.8 p equals 0.012. Pre-ablation cognitive pyramid odds ratio 13.7, was independently associated with an improvement in one-year post ablation cognitive function.

In our next paper, Zian Tseng, James Salazar and associates studied World Health Organization defined sudden cardiac deaths autopsied in the POstmortem Systemic InvesTigation of sudden cardiac death, the POST SCD study to determine whether premortem characteristics could identify autopsy defined sudden arrhythmic death among presumed sudden cardiac deaths. They prospectively identified 615 World Health Organization defined sudden cardiac deaths, of which 144 were witnessed. Autopsy defined sudden arrhythmic death had no extra cardiac or acute heart failure cause of death. Of the 615 presumed sudden critic deaths, 348 or 57% were autopsy defined, sudden arrhythmic deaths. For witness cases, using an emergency medical system model area under the receiver operator curve 0.75, included presenting rhythm of ventricular tech or cardiac fibrillation, pulseless electrical activity, while the comprehensive model, adding medical record data and depression, area under the curve 0.78. If only VTVF witness cases, 48 of those were classified as sudden arrhythmic death. The sensitivity was 0.46, and specificity 0.90.

For unwitnessed cases, the emergency medical system model, area under the curve 0.68, included black race, male sex, age, time since last seen normal, while the comprehensive, area into the curve 0.75, added the use of beta blockers, antidepressants, QT prolonging drugs, opiates, illicit drugs and dyslipidemia. If only unwitnessed cases, less than one hour, n equals 59, were classified as sudden arrhythmic deaths, the sensitivities were 0.18, and specificity was 0.95. The authors concluded that models could identify pre-mortem characteristics to better specify autopsy defined sudden arrhythmic deaths, among presumed sudden cardiac arrests. The authors suggest that the World Health Organization definition can be improved by restricting witnessed sudden cardiac deaths to ventricular tachycardia fibrillation or non-pulseless electrical activity rhythms in unwitnessed cases to less than one hour since last normal, at a cost of sensitivity.

In our next paper, Rafael Jaimes III and associates performed optical mapping of trends, membrane, voltage and pacing studies on isolated Langendorff-perfused rat hearts to assess the cardiac electrophysiology after mono-2-ethylhexyl phthalate, a phthalate with documented exposure in intensive care patients. The authors found that a 30-minute exposure to mono-2-ethylhexyl phthalate increased the atrioventricular node effector in period 147 milliseconds compared to 170 milliseconds in controls and increased the ventricular effective refractory periods of 117 milliseconds compared to 77.5 milliseconds in controls. Optical mapping revealed prolonged action potential duration at slower pacing cycle lengths. Mono-2-ethylhexyl phthalate exposure also slowed epicardial conduction velocity, 25 centimeters per second compared to 60 centimeters per second in controls. The authors concluded that acute mono-2-ethylhexyl phthalate exposure, at clinically relevant doses, has a significant effect on cardiac electrophysiology in the intact heart. Heightened clinical exposure to plasticized medical products may have cardiac safety implications and lead to cardiac arrhythmias.

In our next paper, Stephan Willems and associates report the use of a novel, non-contact imaging and mapping system that uses ultrasound to reconstruct atrial chamber anatomy and measure timing and density of dipolar, ionic activation or charge density across the myocardium to guide ablation of atrial arrhythmias. They conducted a prospective non-randomized study, the UNCOVER AF trial which was conducted at 13 centers across Europe and Canada. In 127 pati...

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undefined - Circulation: Arrhythmia and Electrophysiology June 2019 Issue

Circulation: Arrhythmia and Electrophysiology June 2019 Issue

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...

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undefined - Circulation: Arrhythmia and Electrophysiology August 2019 Issue

Circulation: Arrhythmia and Electrophysiology August 2019 Issue

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

In our first paper, Mark McCauley, Flavia Vitale and associates report that carbon nanotube fibers may improve impaired myocardial conduction. In three sheep, radiofrequency ablation was used to create epicardial conduction delay. In addition, in a rodent model, carbon nanotube fibers were sewn across the atrial ventricular junction. They demonstrated acute ventricular preexcitation, but in chronic studies at four weeks, atrial pacing was required for resumption of AV conduction. Carbon nanotube fibers are conductive, biocompatible with no gross or histopathological evidence of toxicity.

In our next paper, Koichiro Ejima and associates compared outcomes of circumferential pulmonary vein isolation for atrial fibrillation ablation randomized to contact force monitoring or unipolar signal modification in 136 patients with paroxysmal atrial fibrillation. In the unipolar signal modification-guided group, each radiofrequency application was delivered until the development of completely positive unipolar electrograms. In the contact force monitoring-guided group, a contact force of 20 grams, ranged 10 to 30 grams, and a minimum force time integral of 400 gram seconds were the targets for each radiofrequency application. The freedom from atrial tachyarrhythmia recurrence at 12 months was 85% in the unipolar signal modification-guided group and 70% in the contact force monitoring-guided group, P equals 0.031. The radiofrequency time for pulmonary vein isolation was shorter in the unipolar signal modification-guided group than contact force monitoring-guided group, but was not statistically significant, P equals 0.077. The incidence of time-dependent in ATP-provoked early electrical reconnections between the left atrium and pulmonary veins, procedural time, fluoroscopic time, and average force-time integral did not significantly differ between the two groups.

In our next paper, Vishal Luther and associates tested whether ripple mapping is superior to conventional annotation-based local activation time mapping for atrial tachycardia diagnosis. Patients with atrial tachycardia were randomized, either ripple mapping or local activation time mapping. The primary endpoint was atrial tachycardia termination with delivery of the planned ablation lesion set. The inability to terminate atrial tachycardia with the first lesion set, the use of more than one entrainment maneuver, or the need to cross over to the other mapping arm were defined as failure to achieve the primary endpoint. The primary endpoint occurred in 38 of 42 patients or 90% in the ripple mapping group, and 29 of 41 patients, 71%, in the local activation time mapping group, P equals 0.45. The primary endpoint was achieved without any entrainment in 31 out of 42 patients or 74% with ripple mapping, and 18 out of 41 patients or 44% with local activation time mapping, P equals 0.01. Of those patients who failed to achieve the primary endpoint, atrial tachycardia termination was achieved in 9 out of 12 patients or 75% in the local activation time mapping group following crossover to ripple mapping with entrainment, but zero out of four patients, 0%, in ripple mapping group crossing over to local activation time mapping with entrainment, P equals 0.04.

In our next paper, Franziska Fochler and associates examined whether anatomical targeting of late gadolinium enhancement MRI-detected gaps and superficial atrial scar is feasible and effective to treat recurrent atrial arrhythmias post-atrial fibrillation ablation. The authors studied 102 patients who underwent initial atrial fibrillation ablation and repeat ablation for recurrent atrial arrhythmias within one-year. 46 patients or 45% with atrial fibrillation recurrence were assigned to group one and underwent fibrosis homogenization as the second procedure. 56 patients or 55% with atrial tachycardia recurrence were assigned to group two and underwent late gadolinium enhancement MRI detected scar-based dechanneling. Both groups underwent re-isolation of pulmonary veins, if necessary.

In the first 25 patients from group two, the atrial tachycardia was electroanatomically mapped and a critical isthmus was defined. It was found that those isthmi were located in the regions with non-transmural scarring detected by late gadolinium enhancement MRI. In the last 31 patients from group 2, an empirical late gadolinium enhancement MRI-based dechanneling was performed solely based on late gadolinium enhancement MRI results. During one-year follow-up after the second ablation, 67% of patients group one and 64% of patients group two were free from occurrence. In group two, 64% in the electroanatomic-guided and 65% in the late gadolinium enhancement MRI dechanneling group were free from ...

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