The missing link: Unlocking the power of cardiac rhythm monitoring device based QT interval detection.

BACKGROUND: The QT interval is of high clinical value as QT prolongation can lead to Torsades de Pointes (TdP) and sudden cardiac death. Insertable cardiac monitors (ICMs) have the capability of detecting both absolute and relative changes in QT interval. In order to determine feasibility for long-term ICM based QT detection, we developed and validated an algorithm for continuous long-term QT monitoring in patients with ICM. METHODS: The QT detection algorithm, intended for use in ICMs, is designed to detect T-waves and determine the beat-to-beat QT and QTc intervals. The algorithm was developed and validated using real-world ICM data. The performance of the algorithm was evaluated by comparing the algorithm detected QT interval with the manually annotated QT interval using Pearson's correlation coefficient and Bland Altman plot. RESULTS: The QT detection algorithm was developed using 144 ICM ECG episodes from 46 patients and obtained a Pearson's coefficient of 0.89. The validation data set consisted of 136 ICM recorded ECG segments from 76 patients with unexplained syncope and 104 ICM recorded nightly ECG segments from 10 patients with diabetes and Long QT syndrome. The QT estimated by the algorithm was highly correlated with the truth data with a Pearson's coefficient of 0.93 (p < .001), with the mean difference between annotated and algorithm computed QT intervals of -7 ms. CONCLUSIONS: Long-term monitoring of QT intervals using ICM is feasible. Proof of concept development and validation of an ICM QT algorithm reveals a high degree of accuracy between algorithm and manually derived QT intervals.

Cardiac implantable electronic device placement following alcohol septal ablation for hypertrophic cardiomyopathy in the United States.

BACKGROUND: Cardiac implantable electronic devices (CIED) are sometimes required after alcohol septal ablation (ASA) for hypertrophic cardiomyopathy (HCM). The primary objectives of this study were to characterize the incidence, timing, and predictors of CIED placement after ASA for HCM. METHODS: Patients were identified from the 2010-2015 Nationwide Readmissions Databases. Incidence, timing and independent predictors of CIED placement, as well as 30-day readmission rates were examined. RESULTS: There were 1296 patients (national estimate = 2864) with HCM who underwent ASA. CIED were implanted in 322 (25% overall; 14% permanent pacemaker, 11% implantable cardioverter defibrillator) during the index hospitalization. Of these, 21%, 23%, 21%, and 18% occurred on postprocedure day 0, 1, 2, and 3, respectively. Only 17 (1.3%) patients underwent CIED implantation between discharge and 30-day follow up. Independent predictors of index hospitalization CIED implantation included older age, diabetes, heart failure, nonelective index hospital admission and hospitalization at a privately owned hospital. Nonelective 30-day readmission rates among those who did and did not undergo CIED placement during their index hospitalization, were 6.8% and 7.9%, respectively (p = .53); median time to readmission was also similar between groups. CONCLUSIONS: One in four HCM patients undergoing ASA underwent CIED implantation during their index hospitalization; nearly 2/3rd during the first 48 h postprocedure. Private hospital ownership independently predicted CIED placement. More data are needed to better understand the unexpectedly high rates of CIED placement, earlier than anticipated timing of implantation and differential rates by hospital ownership.

Sudden death in a patient with long QT syndrome presenting with an epileptic phenotype.

Patients with epilepsy suffer from a higher mortality rate than the general population, a portion of which is not due to epilepsy itself or comorbid conditions. Sudden unexpected death in epilepsy (SUDEP) is a common but poorly understood cause of death in patients with intractable epilepsy and often afflicts younger patients. The pathophysiology of SUDEP is poorly defined but does not appear to be related to prolonged seizure activity or resultant injury. Interestingly, a subset of patients with confirmed long QT syndrome (LQTS) present with a seizure phenotype and may have concurrent epilepsy. In this case, we present a patient who initially presented with a seizure phenotype. Further workup captured PMVT on an outpatient event monitor, and the patient was subsequently diagnosed with LQTS1. A substantial number of patients with LQTS initially present with a seizure phenotype. These patients may represent a subset of SUDEP cases resulting from ventricular arrhythmias. Appropriate suspicion for ventricular arrhythmias is necessary for proper arrhythmia evaluation and management in patients presenting with epilepsy.

Hemodynamic effects of left atrial appendage occlusion.

BACKGROUND: Percutaneous left atrial appendage occlusion (LAAO) devices have emerged as alternatives to anticoagulation for embolic stroke prevention in patients with non-valvular atrial fibrillation (NVAF). The left atrial appendage is known to produce vasoactive neuroendocrine hormones involved in cardiovascular homeostasis. The hemodynamic impact of LAA occlusion on cardiac function remains poorly characterized. METHODS: This is a single-center, retrospective study of sixty-seven consecutive patients who received LAAO utilizing the WATCHMAN device from May 2017 to June 2019. All patients received a comprehensive 2D transthoracic echocardiogram (TTE) prior to the procedure and a post-procedural TTE. 2D echocardiographic pre-/post-procedural measurements including left ventricular ejection fraction, tricuspid regurgitation, estimated pulmonary artery pressure, diastolic parameters, and left atrial and right ventricular strain were statistically analyzed using the paired t-test. RESULTS: Seventy percent of study patients were male with an overall mean age of 73.0 ± 9.0 years. Analysis of post-procedural LAAO revealed statistically significant improvement in left ventricular ejection fraction (52.4 ± 12.6 vs. 56.7 ± 12.7, p < 0.001), an increase in mitral E/e' (14.1 ± 6.5 vs. 18.3 ± 10.8, p < 0.001), and a decrease right ventricular global longitudinal strain (RVGLS) (- 17.5 ± 4.6 vs. - 19.6 ± 5.7, p = 0.027) as compared to pre-procedural TTE. Peak left atrial longitudinal strain (PALS) improved post-LAAO (20.6 ± 12.2 to 22.9 ± 12.9, p = 0.040) with adjustment for cardiac arrhythmias. Post-LAAO, heart failure hospitalizations occurred in 23.9% of patients. CONCLUSIONS: Percutaneous LAAO results in real-time atrial and ventricular hemodynamic changes as assessed by echocardiographic evaluation of LV filling pressures (E/e'), PALS, RVGLS, and LVEF.

Incidence and Predictors of New-Onset Atrial Fibrillation After Transcatheter Edge-to-Edge Repair of the Mitral Valve (from the Nationwide Readmissions Database).

Patients who underwent transcatheter edge-to-edge repair (TEER) for mitral regurgitation with atrial fibrillation (AF) at baseline have higher mortality than those without AF. Data on new-onset AF (NOAF) after TEER are limited. Using the 2016 to 2018 Nationwide Readmissions Database, we identified a cohort of patients who underwent TEER and classified them into 3 groups based on AF presence during the study period. The primary end point was the incidence and timing of NOAF up to 6 months after TEER. Logistic regression modeling identified independent predictors of NOAF at readmission. Of the 6,861patients that underwent TEER, 4,134 (59.9%) had AF at baseline, and 239 (3.5%) developed NOAF. Median time-to-NOAF admission was 47 days (interquartile range 16 to 113), and 37% of patients with NOAF presented within 30 days after TEER. Patients with NOAF experienced costlier and longer index-TEER hospitalization and had more co-morbidities. Chronic kidney disease (odds ratio [OR] 1.51, 95% confidence interval [CI] 1.03 to 2.20), fluid and electrolyte disorders (OR 1.59, 95% CI 1.01 to 2.52), and heart failure (OR 1.86, 95% CI 1.01 to 3.44) were identified as independent predictors of NOAF. Hypertensive complications and heart failure were the leading causes of readmission. In conclusion, those patients that developed NOAF after TEER tended to be an overall sicker group at baseline compared with the remainder of the study cohort. These data, obtained from a nationally representative cohort, highlight a particular group of patients subject to developing NOAF and their association with increased rehospitalization in the post-TEER setting. Predictors of NOAF can be screened for during TEER workup to identify patients at increased risk.

Cardiac Resynchronization and Circulating Markers of Sarcoplasmic Reticulum Calcium Handling and Sudden Death Risk.

Cardiac resynchronization therapy (CRT) can improve heart function and decrease arrhythmic events. We tested whether CRT altered circulating markers of calcium handling and sudden death risk. Circulating cardiac sodium channel messenger RNA (mRNA) splicing variants indicate arrhythmic risk, and a reduction in sarco/endoplasmic reticulum calcium adenosine triphosphatase 2a (SERCA2a) is thought to diminish contractility in heart failure. CRT was associated with a decreased proportion of circulating, nonfunctional sodium channels and improved SERCA2a mRNA expression. Patients without CRT did not have improvement in the biomarkers. These changes might explain the lower arrhythmic risk and improved contractility associated with CRT.

Predictors of right ventricular pacing and pacemaker dependence in transcatheter aortic valve replacement patients.

PURPOSE: Transcatheter aortic valve replacement (TAVR) is an increasingly prevalent therapy in patients with severe symptomatic aortic stenosis. Conduction disturbances requiring permanent pacemaker (PPM) implantation are a known complication of TAVR. This study investigated the progression of cardiac conduction disease in the post-TAVR pacemaker population and identified predictors of post-TAVR right ventricular (RV) pacing dependence. METHODS: Prospectively collected echocardiographic, ECG, and PPM interrogation data of 262 consecutive patients who underwent TAVR with placement of a balloon-expandable valve at one institution from March 2012 to October 2016 were analyzed. RESULTS: A total of 25 patients (11.1%) required post-TAVR PPM implantation. Seventeen patients who received PPMs did not require RV pacing at 30 days. Nine of these 17 patients had no RV pacing requirement within 10 days. Pre-existing right bundle branch block (RBBB) (OR 105.4, 4.52-2458.5, p = 0.0002), bifascicular block (OR 12.50, 1.60-97.65, p = 0.02), intra-procedural complete heart block (OR 12.83, 1.26-130.52, p = 0.03), and QRS duration > 120 ms (OR 70.43, 3.23-1535.22, p = 0.0002) on pre-TAVR ECG were associated with RV pacing dependence at 30 days. CONCLUSIONS: Sixty-eight percent of patients meeting post-procedural guideline indications for PPM did not require RV pacing at 30 days. Fifty-two percent of these patients demonstrated recovery of sinus node function or AV conduction within 10 days post-implant. RBBB, intra-procedural complete heart block, bifascicular block, and QRS duration > 120 ms were associated with RV pacing dependence at 30 days. These findings suggest that post-TAVR conduction disturbances may be acutely reversible in a significant proportion of patients receiving PPM within 10-30 days of implant.

Cardiac-specific loss of N-cadherin leads to alteration in connexins with conduction slowing and arrhythmogenesis.

The remodeling of ventricular gap junctions, as defined by changes in size, distribution, or function, is a prominent feature of diseased myocardium. However, the regulation of assembly and maintenance of gap junctions remains poorly understood. To investigate N-cadherin function in the adult myocardium, we used a floxed N-cadherin gene in conjunction with a cardiac-specific tamoxifen-inducible Cre transgene. The mutant animals appeared active and healthy until their sudden death approximately 2 months after deleting N-cadherin from the heart. Electrophysiologic analysis revealed abnormal conduction in the ventricles of mutant animals, including diminished QRS complex amplitude consistent with loss of electrical coupling in the myocardium. A significant decrease in the gap junction proteins, connexin-43 and connexin-40, was observed in N-cadherin-depleted myocytes. Perturbation of connexin function resulted in decreased ventricular conduction velocity, as determined by optical mapping. Our data suggest that perturbation of the N-cadherin/catenin complex in heart disease may be an underlying cause, leading to the establishment of the arrythmogenic substrate by destabilizing gap junctions at the cell surface.

Leadless Cardiac Pacemakers: The Next Evolution in Pacemaker Technology.

Implantable pacemakers stand as a mainstay in our therapeutic arsenal, affording those suffering from advanced cardiac conduction system disease both an improved quality of life and reduced mortality. Annually, over 225,000 new pacemakers are implanted in the United States for bradyarrhythmias and heart block. The first implantable transvenous pacemakers appeared in 1965; they were bulky devices, hobbled by a short battery life, and a single pacing mode. Modern transvenous pacemakers have evolved considerably with significant improvements in battery life, pacing options, and lead technology but are still subject to a spectrum of complications stemming from either the subcutaneous pocket or the leads, including: hematoma, infection, wound dehiscence, pneumothorax, cardiac tamponade, lead dislodgment, upper extremity deep vein thrombosis, lead failure, venous obstruction, tricuspid valve insufficiency, and endocarditis. Single-chamber right ventricular (RV) leadless cardiac pacemakers, a concept from the past, has been revitalized to address these complications. Improvements in battery life, device miniaturization, catheter-based delivery tools, and advanced programming have made leadless cardiac pacemakers a viable option. In this review, we will discuss single-component leadless cardiac pacemaker technology, provide an overview of the two approved devices, and discuss their benefits as well as their limitations. [Full article available at http://rimed.org/rimedicaljournal-2017-11.asp].

Minimally Invasive Closure of the Left Atrial Appendage: A Non-Pharmacologic Approach to Prevention of Stroke in Patients with Atrial Fibrillation.

Atrial Fibrillation's (AF) role in the pathogenesis of thromboembolic stroke has been well established, with estimates from trials of approximately 15-20% of all strokes in the U.S. Research shows more than 90% of atrial thrombi originate from the left atrial appendage (LAA). Traditionally, oral anticoagulants (OACs) have been the keystone of management for AF in reducing the risk of thromboembolic stroke. However, OACs also pose a non-negligible risk of bleeding with between 30-50% of eligible patients not receiving OACs due to absolute contraindications or perceived increased bleeding risk. New technologies aimed at isolating the LAA through ligation, exclusion, or occlusion are attempting to mitigate the embolic risk posed by LAA thrombi while simultaneously reducing the bleeding risk associated with OAC. In this review, we discuss the safety, efficacy, and clinical utility of these technologies as alternatives to OACs. [Full article available at http://rimed.org/rimedicaljournal-2017-05.asp].

Atrial arrhythmias in patients with arrhythmogenic right ventricular cardiomyopathy/dysplasia and ventricular tachycardia.

Information on atrial arrhythmia associated with right ventricular cardiomyopathy/dysplasia (ARVC/D) is limited. In 36 patients with task force criteria for ARVC/D and history of ventricular tachycardia (VT), we confirmed the incidence and type of atrial arrhythmia, onset related to referral for VT ablation, fastest documented ventricular rate, management, and clinical and hemodynamic factors associated with their development. Thirty-six patients (28 men) had a mean age of 47 years (range 17 to 80) and mean follow-up of 56 +/- 44 months. Thirty-five patients (97%) had implantable cardioverter-defibrillator (ICD) devices, 15 with atrial leads. Fifteen of 36 patients (42%) had documented atrial arrhythmias, with atrial flutter (aFL) in 11, atrial fibrillation (AF) in 11 patients, and aFL and AF in 7 patients. Maximum heart rate noted with atrial arrhythmia was 62 to 150 beats/min. In 9 patients, initial atrial arrhythmia preceded or was concurrent with presentation for VT ablation. In the remaining 6 patients, atrial arrhythmia (symptomatic in 4 patients) followed VT presentation. Three of these patients received ICD shock therapy for atrial arrhythmias. Seven of 11 patients with recurrent aFL required aFL ablation, 1 patient underwent His-bundle ablation for AF with rapid rate, and 8 patients required long-term drug therapy for AF control. Atrial arrhythmias were more common in patients with RV enlargement and moderate/severe tricuspid regurgitation. In conclusion, in patients with ARVC/D and VT, atrial arrhythmias are common, frequently necessitate ablative or pharmacologic treatment, and are more common in patients with moderate/severe tricuspid regurgitation and markedly enlarged right ventricle.