Karthik Viswanathan

Rapid Device-Detected Nonsustained Ventricular Tachycardia in the Risk Stratification of Hypertrophic Cardiomyopathy.

Nonsustained ventricular tachycardia (NSVT) detected by ambulatory Holter (Holter NSVT) is a major risk factor for sudden cardiac death in hypertrophic cardiomyopathy (HCM). We hypothesized that the prognostic utility of Holter NSVT in HCM would improve with prolonged monitoring and a higher heart rate cut‐off for detection.

Implantable Defibrillator Timing Windows When Coincidence Can Be Confusing

We present the case of a 68-year-old man with dilated cardiomyopathy who had an implantable cardioverter defibrillator implanted for primary prevention (Unify Assura with a Durata 7122Q ventricular lead, St. Jude Medical). The device was programmed DDDR 60–110 beats per minute and Table shows more specific programming parameters. View this table: Table. Programming Parameters for Bradycardia and Tachycardia Therapies From the Patient’s Defibrillator See Editor’s Perspective by Asirvatham and Stevenson Six months after implantation, routine device interrogation revealed many asymptomatic episodes logged as nonsustained lead noise (NSLN). The electrograms from one of these episodes are shown in Figure 1A. What is the differential diagnosis? Figure 1. A , A stored electrogram from the patients implantable cardioverter defibrillator that was classified as nonsustained right ventricular lead noise. Respective electrograms and marker channels are labeled and are consistent for each panel. Numbered arrows indicate key points in the tracing for discussion. Intervals annotated with a (−) on the ventricular marker channel indicate that the current interval is within the tachycardia zone, however, the interval average (average of the current interval and the previous 3 intervals) is not. These beats do not count toward tachycardia detection. B , Electrograms in sinus rhythm for comparison. C and D , Tachycardias recorded on different occasions. AP indicates atrial pace; F, beat in the ventricular fibrillation zone; NSLN, nonsustained lead noise; SIR, sensor-indicated rate; VP, ventricular pace; VS, ventricular sense; and VSP, ventricular safety pace. A rhythm strip showing sinus rhythm is shown for comparison in Figure 1B and similar episodes of tachycardia are shown in Figure 1C and 1D from subsequent interrogation. These subsequent figures assist in clarifying the rhythm diagnosis; however, further questions arise as to the behavior of …

Automated Quantification of Low-Amplitude Abnormal QRS Peaks From High-Resolution ECG Recordings Predicts Arrhythmic Events in Patients With Cardiomyopathy

Background— Cardiomyopathy patients are at risk of sudden death, typically from scar-related abnormalities of electrical activation that promote ventricular tachyarrhythmias. Abnormal intra-QRS peaks may provide a measure of altered activation. We hypothesized that quantification of such QRS peaks (QRSp) in high-resolution ECGs would predict arrhythmic events in implantable cardioverter–defibrillator (ICD)–eligible cardiomyopathy patients. Methods and Results— Ninety-nine patients with ischemic or non-ischemic dilated cardiomyopathy undergoing prophylactic ICD implantation were prospectively enrolled (age 62±11 years, left ventricular ejection fraction 27±7%). High-resolution (1024 Hz) digital 12-lead ECGs were recorded during intrinsic rhythm. QRSp was quantified for each precordial lead as the total number of low-amplitude deflections that deviated from their respective naive QRS template. The primary end point of arrhythmic events was defined as appropriate ICD therapy or sustained ventricular tachyarrhythmias. After a median follow-up of 24 (15–43) months, 20 (20%) patients had arrhythmic events. Both QRSp and QRS duration were greater in those with arrhythmic events (both P<0.001) and this was consistent for QRSp for both cardiomyopathy types. In a multivariable Cox regression model that included age, left ventricular ejection fraction, QRS duration, and QRSp, only QRSp was an independent predictor of arrhythmic events (hazard ratio, 2.1; P<0.001). Receiver operating characteristic analysis revealed that a QRSp ≥2.25 identified arrhythmic events with greater sensitivity (100% versus 70%, P<0.05) and negative predictive value (100% versus 89%, P<0.05) than QRS duration ≥120 ms. Conclusions— QRSp measured from high-resolution digital 12-lead ECGs independently predicts ventricular tachyarrhythmias in ICD-eligible cardiomyopathy patients. This novel QRS morphology index has the potential to improve sudden death risk stratification and patient selection for prophylactic ICD therapy.

An unusual course of a pacemaker lead in congenitally corrected transposition of the great arteries.

A 56-year-old female with congenitally corrected transposition of the great arteries (ccTGA), mechanical systemic atrio-ventricular valve, dual chamber pacemaker for complete heart block and severe subaortic (morphological right) ventricular dysfunction was referred for upgrade to a biventricular pacemaker. She also had multiple nonfunctioning pacemaker leads from previous procedures. Her current functioning transvenous pacemaker system (implanted via the right subclavian vein ten years ago) included an active

Serendipitous induction of ventricular tachycardia during pace-mapping: Should we ablate?

Case presentation A 63-year-old man with ischemic cardiomyopathy, severely impaired left ventricular systolic function, and an implantable defibrillator presented with multiple episodes of protracted slow ventricular tachycardia (VT). He was brought to the electrophysiology laboratory for catheter ablation. Initial programmed stimulation induced VT at 154 bpm that was associated with hemodynamic instability necessitating cardioversion. Subsequently, a substrate-based mapping approach was undertaken with pacing from the right ventricle (RV) at 50 bpm. An electroanatomic voltage map (using CARTO-3 mapping system, Biosense Webster, Diamond Bar, CA) was created with tagging of late potentials/late abnormal ventricular activity along with pace-mapping where appropriate. Figure 1A shows the intracardiac electrogram (IEGM) seen during mapping within the scar in the mid-anterior wall of the left ventricle and with RV pacing. Figure 1B shows the IEGMs and surface QRS morphology during pace-mapping from the ablation catheter at 600 ms at this site. Figure 2A shows the last 3 beats of pacing from the ablation catheter and onset of VT immediately after pacing. Radiofrequency ablation was then performed at 50 W (NaviStar catheter, Biosense Webster) at this site. Figure 2B shows the response after 15 seconds of ablation. Based on these observations, what is the mechanism of initiation of VT? Crucially, where is this site in relation to the VT circuit, and is this an optimal site for ablation? Finally, was VT initiated during or after pacing?