Dec 16, 2020
Paul J. 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, David Okada and associates assess the ability of a novel machine learning approach for quantifying 3D spatial complexity of gray scale patterns on late gadolinium-enhanced cardiac magnetic resonance images to predict ventricular arrhythmias in patients with ischemic cardiomyopathy.
They examined 122 consecutive ischemic cardiomyopathy patients with left ventricular ejection fraction of 35%, without prior history of reentrant ventricular arrhythmias. These patients underwent late gadolinium-enhanced cardiac magnetic resonance imaging. From raw gray scale data, the authors generated graphs encoding the 3D geometry of the left ventricle. They then assess the global regularity of signal intensity patterns using Fourier-like analysis and generated a substrate spatial complexity profile for each patient. A machine learning statistical algorithm was employed to discern which substrate spatial complexity profiles correlated with ventricular arrhythmic events. That is appropriate ICD firings and arrhythmic sudden cardiac death.
At five years of follow-up from the statistical machine learning results, a complexity score ranging from zero to one was calculated for each patient that was tested using multivariate Cox regression models. At five years of follow-up, 40 patients had ventricular arrhythmia events. The machine learning algorithm classified with overall 81% accuracy and correctly classified 86% of those without ventricular arrhythmia. Overall negative predictive value was 91%. Average complexity score was significantly higher in patients with ventricular arrhythmia events versus those without P<0.0001, and was independently associated with ventricular arrhythmia events in a multivariate model hazard ratio, 1.5 P=0.002.
In our next paper, Henry Chubb and associates examine the outcomes of cardiac resynchronization therapy studies in pediatric and or congenital heart disease patients using a propensity score match analysis. They examined 63 matched CRT control pairs. Heart transplant or death occurred in 12 subjects or 19% or 37 controls or 59% with a median follow-up of 2.7 years. Cardiac resynchronization therapy was associated with markedly reduced risk of heart transplant or death. Hazard ratio is 0.24 P<0.001. There were no CRT procedural mortality, and there was one systemic infection at 54 months post-implant.
In our next paper Pachon-M and associates examined whether AF nest ablation eliminates the atropine response and decreases RR variability suggesting that they're related to vagal innervation. The authors perform prospective control longitudinal randomized study enrolling 62 patients in two groups, AF nest group that is 32 patients with functional or reflex Bradyarrhythmias or vagal AF treated with AF Nest ablation and a control group, 30 patients with anomalous bundles, ventricular prematures, atrial flutter, AV nodal reentry and atrial tachycardias who were treated with a conventional ablation approach.
In the AF nest group, ablation was delivered at the AF nest detected by fragmentation or fractionation of the endocardial electrograms and by 3D anatomical location of the ganglionated plexus. Vagal response was evaluated before, during and post ablation by five seconds non-contact vagal stimulation at the jugular foramen through the internal jugular veins, analyzing 15 seconds mean heart rate, longest RR pauses and AV block. A pre-ablation non-contact vagal stimulation due sinus pauses, asystole, and transient AV block in both groups showing a strong vagal response.
Post-ablation non-contact vagal stimulation in the AF nest showed complete abolishment of the cardiac vagal response in all cases, P<0.0001, demonstrating robust vagal denervation. However, in the control group, vagal response remained practically unchanged post-ablation showing that non AF nest ablation promotes no significant denervation.
In our next paper, Domingo Uceda and Xiang-Yang Zhu and associates examined whether progressive increases in pericardial fat volume and inflammation, prospectively dampens the heart rate variability in hypercholesterolemic pigs. The author studied wild type or PCSK9 gain-of-function Ossabaw mini-pigs in-vivo before and after three and six months of a normal diet. Four in the wild type group and six in the PKSK9 group. Or high-fat diet, wild type three, in PCSK9, six.
At diet completion, they found that the hypercholesterolemic PCSK9 had significantly depressed heart rate variability, and both high fat diet groups had higher sympathovagal balance compared to the normal diet. P<0.05 versus baseline. Pericardial fat volumes, LDL concentrations correlated inversely with heart rate variability and directly with sympathovagal balance. While a sympathovagal balance correlated directly with plasma norepinephrine. Pericardial fat TNF alpha expression was upregulated in the PKSK9 animals, co-localized with nerve fibers and correlated inversely with root mean square of deviation and pNN50. These findings are consistent with an association between pericardial fat accumulation and alterations in heart rate variability and the autonomic nervous system.
In our next paper, Konstantinos Aronis and Rheeda Ali and associates examined myocardial conduction velocity and myocardial fibrosis density on late gadolinium enhanced cardiac magnetic resonance imaging in patients with ischemic cardiomyopathy. The author studied six patients with ischemic cardiomyopathy undergoing VT ablation, and five with structurally normal left ventricle serving as controls. All patients underwent late gadolinium enhanced cardiac magnetic resonance, and electroatomic mapping in sinus rhythm. Median conduction velocity in ischemic cardiomyopathy patients and controls was 0.41 meters per second and 0.65 meters per second respectively. In ischemic cardiomyopathy patients conduction velocity in areas with no visible fibrosis was 0.81 meters per second. For each 25% increase in normalized late gadolinium-enhanced intensity conduction velocity decreased by 1.34 fold. Dense scar areas have an average of 1.97 to 2.66 fold slower conduction velocity compared to areas without dense scar. Ablation lesions that terminate at VT were localized in areas of slow conduction on conduction velocity maps. The authors found that conduction velocity is inversely associated with late gadolinium enhanced cardiac magnetic resonance fibrosis density in patients with ischemic cardiomyopathy.
In our next paper, Bence Hegyi and associates examined whether the IKR current or the sodium L-type current play counterbalancing roles in the ventricular action potential. The authors found that a comparable amount of net charge carried by these two currents during the physiological action potential, suggesting that the outward potassium current via IKR and the inward sodium current via the sodium L-type current are in balance during physiological repolarization. These two current integrals in control myocytes were highly correlated, but this close correlation was lost in heart failure myocytes. Pretreatment with E-4031 to block IKR mimicking long QT syndrome 2, or ATX II to impair a sodium channel inactivation mimicking long QT3 prolong the action potential duration. However, using GS-967 to inhibit sodium L-type current sufficiently restored action potential control to control in both cases.
Furthermore, the sodium L-type inhibition significantly reduced the beat to beat and short-term variabilities of action potential duration. Sodium L-type current inhibition also restored action potential duration in repolarization stability in heart failure. Conversely, pretreatment with GS-967 shortened action potential duration mimicking short QT syndrome and E-4031 reverted APD shortening. Furthermore, the amplitude of action potential alternans occurring at high pacing frequency was decreased by sodium L-type inhibition, increased by IKR inhibition and restored by a combination of sodium L-type and IKR inhibitions. The author suggests that targeting these two ionic currents to normalize or balance may have significant therapeutic potential in heart diseases with repolarization abnormalities.
In our next paper, Derek Chew and associates examine the impact of the duration between first diagnosis of atrial fibrillation and ablation or diagnosis to ablation time on AF recurrence following catheter ablation by conducting a systematic review and meta analysis of observational studies. They found six studies that met inclusion criteria with a total of 4,950 participants undergoing atrial fibrillation ablation for symptomatic AF. A shorter diagnosis to ablation time of one year or less was associated with a lower relative risk of AF recurrence compared to diagnose to the ablation time greater than one year. Relative risk 0.73 P<0.001.
The authors concluded that the duration between time to first day of AF and AF ablation is associated with an increased likelihood of atrial fibrillation ablation procedural success.
In a research letter by Kapuaola Gellert and associates, 48 hour continuous ECG was found to have an association between sleep apnea and atrial fibrillation in the community-based population study, the ARIC study.
In a special report, Francesco Notaristefano reported that the risk of device pocket hematoma 10 days after CIED surgery showed an independent association with the type of interventional procedure such as device implementation, odds ratio 3.5, implantable cardioverter defibrillator 4.4, cardiac resynchronization therapy, odds ratio 11.7, and antithrombotic treatment, but not with novel oral anticoagulants.
In an interesting review article Nicholas Tan and associates describe the current and future perspectives of left bundle branch block.
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.
Copyright American Heart Association 2020.