Search

In light of the adverse prognosis related to severe mitral regurgitation, heart failure, or sudden cardiac death in a subset of patients with mitral valve prolapse (MVP), identifying those at higher risk is key. For the first time in decades, researchers have the means to rapidly advance discovery in the field of MVP thanks to state-of-the-art imaging techniques, novel omics methodologies, and the potential for large-scale collaborations using web-based platforms. The National Heart, Lung, and Blood Institute recently initiated a webinar-based workshop to identify contemporary research opportunities in the treatment of MVP. This report summarizes 3 specific areas in the treatment of MVP that were the focus of the workshop: 1) improving management of degenerative mitral regurgitation and associated left ventricular systolic dysfunction; 2) preventing sudden cardiac death in MVP; and 3) understanding the mechanisms and progression of MVP through genetic studies and small and large animal models, with the potential of developing medical therapies., Competing Interests: Funding Support and Author Disclosures Dr Delling is supported by the UCSF Resource Allocation Program 7501268 and by National Institutes of Health (NIH) research grant R01HL153447. Dr Noseworthy has received research funding from the NIH, including the National Heart, Lung, and Blood Institute (R21AG 62580-1, R01HL 131535-4, R01HL 143070-2), the National Institute on Aging (R01AG 062436-1), Agency for Healthcare Research and Quality (R01HS 25402-3), Food and Drug Administration (FD 06292), and the American Heart Association (18SFRN34230146; has filed patents related to the application of artificial intelligence to the ECG for diagnosis and risk stratification and has licensed several A-ECG algorithms to Anumana; is involved in potential equity/royalty relationship with AliveCor; is a study investigator in an ablation trial sponsored by Medtronic; and has served on an expert advisory panel for OptumLabs. Dr Adams’s institution, the Icahn School of Medicine at Mount Sinai, receives royalties for mitral and tricuspid valve repair prostheses related to his intellectual property from Edwards Lifesciences and Medtronic. Dr Borger’s institution receives speakers’ honoraria and/or consulting fees on his behalf from Edwards Lifesciences, Medtronic, Abbott, and CryoLife. Dr Elmariah has received research funding from the NIH (R01HL 151838) and the American Heart Association (19TPA34910170); has received research grants from Edwards Lifesciences, Medtronic, and Abbott Vascular; and is a consultant for Edwards Lifesciences. Dr Gerstenfeld has received lecture honoraria from Medtronic, Boston Scientific, and Abbott; has received research funding from, is on the scientific advisory board, and has received compensation from Biosense Webster; is on the scientific advisory board for and is PI of a clinical ablation trial sponsored by Farapulse; and is on the Data and Safety Monitoring Board for trials sponsored by Thermedical Inc and Abbott. Dr Norris has received research funding from the NIH (HL131546, GM103444, HL149696, HL122906), and the American Heart Association (19TPA34850095, 20SRG35540029, 19TPA34900016, 17CSA33590067). Dr Padala is supported by the National Heart, Lung, and Blood Institute (R01HL135145, R01HL140325, R01HL133667, R01HL144714, R01HL135505) and by the National Institute of Biomedical Imaging and Bioengineering (R01EB031101); has significant stock ownership and a role as a director in Nyra Medical; and has received consulting fees from Heart Repair Technologies Inc in the last 12 months. Dr Weinsaft is supported by NIH research grants R01HL128278 and R01HL151686. Dr Enriquez-Sarano has served as a consultant for Edwards, Cryolife, ChemImage, and HighLife. Dr Levine is supported by NIH research grants R01HL128099 and R01HL141917, American Heart Association 963793/Levine/2022, and funding of the Ellison Foundation. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose., (Copyright © 2022 The Authors. Published by Elsevier Inc. All rights reserved.)

Objectives: The aim of the study was to define the epicardial substrate and ablation outcome in patients with left ventricular nonischemic cardiomyopathy (NICM) and suspected epicardial ventricular tachycardia (VT)., Background: Ventricular tachycardia in NICM often originates from the epicardium., Methods: Twenty-two patients with NICM underwent detailed endocardial and epicardial bipolar voltage maps and VT ablation for suspected epicardial VT. Eight patients with normal hearts and idiopathic VT served to define normal epicardial electrograms. Low-voltage regions were also assessed for wide (>80 ms), split, or late electrograms., Results: Normal epicardial bipolar voltage was identified as >1.0 mV on the basis of the reference population. Confluent low-voltage areas were present in 18 epicardial (82%) and 12 endocardial (54%) maps and were typically over basal lateral LV. In the 18 patients with epicardial VT on the basis of activation/pacemapping, the mean epicardial area was greater than the endocardial low-voltage area (55.3 +/- 33.5 cm(2) vs. 22.9 +/- 32.4 cm(2), p < 0.01). Epicardial low-voltage areas showed 49.7% wide (>80 ms), split, and/or late electrograms rarely seen in the reference patients (2.3%). During follow-up of 18 +/- 7 months, ablation resulted in VT elimination in 15 of 21 patients (71%) including 14 of 18 patients (78%) with epicardial VT., Conclusions: In patients with NICM and VT of epicardial origin, the substrate is characterized by areas of basal LV epicardial > endocardial bipolar low voltage. The electrograms in these areas are not only small (<1.0 mV) but wide (>80 ms), split, and/or late, and help identify the substrate targeted for successful ablation., (2009 by the American College of Cardiology Foundation)

Objectives: The purpose of this study was to determine if atrial pacing is effective in reducing postoperative atrial fibrillation (AF)., Background: Atrial fibrillation after coronary artery bypass grafting (CABG) is a common problem for which medical management has been disappointing. Atrial-based pacing has become an attractive nonpharmacologic therapy for the prevention of AF., Methods: Sixty-one post-CABG patients (mean age = 65 years) were randomized to one of three groups: no atrial pacing (NAP), right atrial pacing (RAP) or biatrial pacing (BAP). Each patient had one set of atrial wires attached to both the right and left atria, respectively, at the conclusion of surgery. Patients in the RAP and BAP groups were continuously paced at a rate of 100 pulses per minute for 96 h or until the onset of sustained AF (>10 min). All patients were monitored with Holter monitors or full disclosure telemetry to identify the onset of AF. The primary end point of the study was the first onset of sustained AF., Results: There was no significant difference in the proportion of patients developing AF in the three groups (NAP = 33%; RAP = 29%; BAP = 37%; p > 0.7). However, for the subset of patients on beta-adrenergic blocking agents after CABG, there was a trend toward less AF in the paced groups. There were no serious complications related to pacing, although in three patients the pacemaker appeared to induce AF by pacing during atrial repolarization., Conclusions: Continuous right or biatrial pacing in the postoperative setting is safe and well tolerated. We did not find that post-CABG pacing prevented AF in this pilot study; however, the role of combined pacing and beta-blockade merits further study.

The ability of a catheter with an orthogonal electrode configuration to sense differences in the direction of local atrial endocardial activation was tested in 18 consecutive patients with intact retrograde conduction. In all 18, discrimination of anterograde from retrograde conduction at a single atrial site was examined; in 5 of the 18, multiple sites were examined to determine if the discriminatory ability of the catheter was site dependent. The catheter was specially designed with bipoles in the x, y and z directions. A vector was computed for each electrogram during anterograde and retrograde conduction. Electrogram amplitude along the standard bipole was also compared for anterograde and retrograde conduction. Mean electrogram amplitude for the standard bipole was significantly different for anterograde than for retrograde conduction in 17 of 18 patients (mean +/- SD 4 +/- 1.9 vs. 2.7 +/- 1.3 mV; p less than 0.005), with complete separation of amplitude distributions in 4 patients. The electrogram vector during anterograde conduction was significantly different from that during retrograde conduction in all 18 patients (p less than 0.0001), with complete separation of vector distributions in 14. In some patients with multiple site recordings, the choice of site greatly affected separation based on electrogram amplitude or vector, or both. The orthogonal catheter can be used to sense directional differences in local endocardial activation. The catheter shows promise for discriminating anterograde from retrograde conduction and examining the direction of endocardial activation in the heart during an electrophysiologic examination.