Premature Ventricular Contractions Causing Sinus Arrhythmia and Alternating P-R Prolongation

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/73731/1/j.1540-8167.2007.01020.x.pd

A Wide Complex Tachycardia: What is the Mechanism?

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/73868/1/j.1540-8167.2007.01000.x.pd

1:1 AV Tachycardia: What is the Mechanism?

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/73730/1/j.1540-8159.2009.02516.x.pd

Electromagnetic Interference in an Implantable Loop Recorder Caused by a Portable Digital Media Player

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/75458/1/j.1540-8159.2008.01188.x.pd

Effect of Catheter Ablation on Progression of Paroxysmal Atrial Fibrillation

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/90181/1/j.1540-8167.2011.02137.x.pd

Utility of Atrial and Ventricular Cycle Length Variability in Determining the Mechanism of Paroxysmal Supraventricular Tachycardia

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/72411/1/j.1540-8167.2007.00860.x.pd

Atrioventricular conduction in patients undergoing pacemaker implant following self‐expandable transcatheter aortic valve replacement

BackgroundHeart block requiring a pacemaker is common after self‐expandable transcatheter aortic valve replacement (SE‐TAVR); however, conduction abnormalities may improve over time. Optimal device management in these patients is unknown.ObjectiveTo evaluate the long‐term, natural history of conduction disturbances in patients undergoing pacemaker implantation following SE‐TAVR.MethodsAll patients who underwent new cardiac implantable electronic device (CIED) implantation at Michigan Medicine following SE‐TAVR placement between January 1, 2012 and September 25, 2017 were identified. Electrocardiogram and device interrogation data were examined during follow‐up to identify patients with recovery of conduction. Logistic regression analysis was used to compare clinical and procedural variables to predict conduction recovery.ResultsFollowing SE‐TAVR, 17.5% of patients underwent device placement for new atrioventricular (AV) block. Among 40 patients with an average follow‐up time of 17.1 ± 8.1 months, 20 (50%) patients had durable recovery of AV conduction. Among 20 patients without long‐term recovery, four (20%) had transient recovery. The time to transient conduction recovery was 2.2 ± 0.2 months with repeat loss of conduction at 8.2 ± 0.9 months. On multivariate analysis, larger aortic annular size (odds ratio: 0.53 [0.28–0.86]/mm, P = 0.02) predicted lack of conduction recovery.ConclusionsHalf of the patients undergoing CIED placement for heart block following SE‐TAVR recovered AV conduction within several months and maintained this over an extended follow‐up period. Some patients demonstrated transient recovery of conduction before recurrence of conduction loss. Larger aortic annulus diameter was negatively associated with conduction recovery.Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/150495/1/pace13694_am.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/150495/2/pace13694.pd

Mapping and Ablation of Frequent Post-Infarction Premature Ventricular Complexes

Mapping of Post-Infarction PVCs .  Introduction: Premature ventricular complexes (PVCs) occur frequently in patients with heart disease. The sites of origin of PVCs in patients with prior myocardial infarction and the response to catheter ablation have not been systematically assessed. Methods and Results: In 28 consecutive patients (24 men, age 60 ± 10, ejection fraction [EF] 0.37 ± 0.14) with remote myocardial infarction referred for catheter ablation of symptomatic refractory PVCs, the PVCs were mapped by activation mapping or pace mapping using an irrigated-tip catheter in conjunction with an electroanatomic mapping system. The site of origin (SOO) was classified as being within low-voltage (scar) tissue (amplitude ≤1.5 mV) or tissue with preserved voltage (>1.5 mV). The SOO was confined to endocardial scar tissue in 24/28 patients (86%). The SOO was outside of scar in 3 patients and could not be identified in 1 patient. At the SOO, local endocardial activation preceded the PVC by 46 ± 19 ms, and the electrogram amplitude during sinus rhythm was 0.48 ± 0.34 mV. The PVCs were effectively ablated in 25/28 patients (89%), resulting in a decrease in PVC burden on a 24-hour Holter monitor from 15.6 ± 12.3% to 2.4 ± 4.2% (P < 0.001). The SOO most often was confined to scar tissue located in the left ventricular septum and the papillary muscles. Conclusion: Similar to post-infarction ventricular tachycardia, PVCs after remote myocardial infarction most often originate within scar tissue. Catheter ablation of these PVCs has a high-success rate. (J Cardiovasc Electrophysiol, Vol. 21, pp. 1002-1008, September 2010)Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/79266/1/j.1540-8167.2010.01771.x.pd