Asirvatham, Samuel J

AbstractIn pacemaker‐dependent patients with a newly implanted cardiac device, acute lead dislodgement constitutes one of the most common causes of loss of capture and ventricular asystole. In a biventricular system, it would be expected that such a potentially catastrophic event would be prevented with back‐up right ventricular pacing unless both leads dislodge.

Abstract Aims Current electrophysiology signal recording and mapping systems have limited dynamic range (DR) and bandwidth, which causes loss of valuable information during acquisition of cardiac signals. We evaluated a novel advanced signal processing platform with the objective to obtain and assess additional information of clinical importance. Methods and results Over 10 canines, we compared intracardiac recordings within all cardiac chambers, in various rhythms, in pacing and during radiofrequency (RF) ablation across two platforms; a conventional system and the PURE EP™ [(PEP); Bio Sig Technologies, Inc., Los Angeles, CA, USA]. Recording cardiac signals with varying amplitudes were consistently and reproducibly observed, without loss of detail or introduction of artefact. Further the amplitude of current of injury (COI) on the unipolar signals correlated with the instantaneous contact force (CF) recorded on the sensing catheter in all the animals (r2 = 0.94 in ventricle). The maximum change in the unipolar COI correlated with the change in local electrogram amplitude during non-irrigated RF ablation (r2 = 0.61 in atrium). Reduction in artefact attributable to pacing (20 sites) and noise during ablation (48 sites) was present on the PEP system. Within the PEP system, simultaneous display of identical signals, filtered differently, aided the visualization of discrete conduction tissue signals. Conclusion Compared to current system, the PEP system provided incremental information including identifying conduction tissue signals, estimates of CF and a surrogate for lesion formation. This novel signal processing platform with increased DR and minimal front-end filtering may be useful in clinical practice.

AbstractBackgroundMagnetic resonance imaging (MRI) in patients with legacy cardiovascular implantable electronic devices (CIEDs) in situ is likely underutilized. We hypothesized the clinical benefit of MRI would outweigh the risks in legacy CIED patients.MethodsThis is a single‐center retrospective study that evaluated and classified the utility of MRI using a prospectively maintained database. The outcomes were classified as aiding in diagnosis, treatment, or both for the patients attributable to the MRI. We then assessed the incidence of adverse effects (AE) when the MRI was performed.ResultsIn 668, MRIs performed on 479 patients, only 13 (1.9%) MRIs did not aid in the diagnosis or treatment of the patient. Power‐on reset events without clinical sequelae in three scans (0.45%) were the only AE. The probability of an adverse event happening without any benefit from the MRI scan was 1.1 × 10−4. A maximum benefit in diagnosis using MRI was obtained in ruling out space‐occupying lesions (121/185 scans, 65.4%). Scans performed in patients for elucidating answers to queries in treatment were most frequently done for disease staging at long term follow‐up (167/470 scans, 35.5%). Conservative treatment (184/470 scans, 39%) followed by medication changes (153/470 scans, 28.7%) were the most common treatment decisions made.ConclusionsThe utility of MRI in patients with non‐MRI‐conditional CIEDs far outweighs the risk of adverse events when imaging is done in the context of a multidisciplinary program that oversees patient safety.

Background Intracerebral hemorrhage (ICH) risk is higher in elderly patients with atrial fibrillation on antithrombotic therapy as well as those with cerebral amyloid angiopathy (CAA). We investigated if mortality among patients with atrial fibrillation on antithrombotic therapy presenting with non‐traumatic ICH was influenced by underlying CAA. Methods and Results We used the Rochester Epidemiology Project to identify 6045 patients with atrial fibrillation aged >55 years on anticoagulation or antiplatelet therapy from 1995 to 2016. Seventy‐four patients in this cohort presented with non‐traumatic ICH. Medical records including imaging data were reviewed to identify those with CAA and record baseline variables and outcomes of interest; 38 of our 74 patients (51.4%) (mean age 81.5 years) met Modified Boston Criteria for possible or probable CAA. Twenty‐six of 74 patients (35%) died during the first 30 days while 56 of the 74 (76%) patients died by 10 years follow‐up after index ICH. Overall mortality was not significantly different between the CAA and non‐CAA groups at any point of time during follow‐up ( P =0.89) even amongst patients restarted on anticoagulation +/− antiplatelet (n=19) ( P =0.46) or those patients restarted only on antiplatelet therapy (n=22) ( P =0.66). Three of the 41 patients who restarted on antithrombotic therapy had a recurrent ICH; these 3 patients met criteria for possible or probable CAA. Conclusions Although more than half of our patients with atrial fibrillation on antithrombotic therapy and non‐traumatic ICH met Modified Boston Criteria for CAA, CAA did not significantly influence the high mortality seen in this cohort.

AbstractObjectiveThis study sought to determine if single‐chamber operation and/or loss of rate response (RR) during elective replacement indicator (ERI) in patients with dual‐chamber pacemakers lead to increased symptom burden, healthcare utilization, and atrial fibrillation (AF).BackgroundDual‐chamber pacemakers often change from dual‐ to single‐chamber pacing mode and/or lose RR functionality at ERI to preserve battery. Single‐chamber pacing increases the incidence of heart failure, AF, and pacemaker syndrome suggesting these changes may be deleterious.MethodsA retrospective analysis of 700 patients was completed. Three comparisons were analyzed: Comparison 1: mode change and RR loss versus no change; Comparison 2: RR loss only versus no change; Comparison 3: mode change only versus no change (in patients with no RR programmed at baseline).ResultsIn Comparison 1, 121 (46%) patients with setting changes experienced symptoms (most often dyspnea and fatigue/exercise intolerance) versus 3 (4%) without setting changes (p < .0001). Similar results were noted in Comparisons 2 and 3 (p = .0016 and p = .0001, respectively). In Comparison 1, patients with setting change sought provider contact more than patients without setting changes (p = .0001). A significant difference was not noted in Comparison 2 or 3. Overall 14 (2%) patients were hospitalized, all of whom had setting changes.ConclusionsSetting changes at ERI including a change from dual‐ to single‐chamber pacing and/or loss of RR results in a significantly increased symptom burden and increased healthcare utilization.

Abstract The primary goal of the initial ECG evaluation of every wide complex tachycardia is to determine whether the tachyarrhythmia has a ventricular or supraventricular origin. The answer to this question drives immediate patient care decisions, ensuing clinical workup, and long‐term management strategies. Thus, the importance of arriving at the correct diagnosis cannot be understated and has naturally spurred rigorous research, which has brought forth an ever‐expanding abundance of manually applied and automated methods to differentiate wide complex tachycardias. In this review, we provide an in‐depth analysis of traditional and more contemporary methods to differentiate ventricular tachycardia and supraventricular wide complex tachycardia. In doing so, we: (1) review hallmark wide complex tachycardia differentiation criteria, (2) examine the conceptual and structural design of standard wide complex tachycardia differentiation methods, (3) discuss practical limitations of manually applied ECG interpretation approaches, and (4) highlight recently formulated methods designed to differentiate ventricular tachycardia and supraventricular wide complex tachycardia automatically.

Objective Previous studies have postulated a causal role of patent foramen ovale (PFO) in the aetiology of embolic stroke in the general population. We hypothesised that the presence of concomitant PFO and atrial fibrillation (AF) will add incremental risk of ischaemic stroke to that linked to AF alone. Methods We analysed data on 3069 consecutive patients (mean age 69.4±12.2 years; 67.1% men) undergoing transoesophageal echocardiography-guided electrical cardioversion (ECV) for AF between May 2000 and March 2012. PFO was identified by colour Doppler and agitated saline contrast study. All patients were followed up after ECV for first documentation of ischaemic stroke. Outcomes were compared using Cox regression models. Results The prevalence of PFO was 20.0% and the shunt direction was left-to-right in the majority of patients (71.4%). Patients with PFO had a higher frequency of obstructive sleep apnoea (21.7% vs 17.1%, p=0.01) and higher mean peak left atrial appendage emptying velocity (38.3±21.8 vs 36.1±20.4 cm/s; p=0.04) compared with those without PFO. Otherwise, baseline characteristics were similar between groups. During a mean follow-up period of 7.3±4.6 years, 214 patients (7.0%) had ischaemic stroke. Multivariable analysis showed no significant association between PFO and ischaemic stroke (HR, 0.82 (95% CI 0.57 to 1.18)). PFO shunt direction was strongly associated with stroke: HR, 1.91 (95% CI 1.16 to 3.16) for right-to-left shunt and HR, 0.58 (95% CI 0.36 to 0.93) for left-to-right shunt. Conclusions The presence of concurrent PFO in this largely anticoagulated group of patients with AF was not associated with increased risk of ischaemic stroke.

Background: Heart rate variability (HRV) and pulse rate variability are indices of autonomic cardiac modulation. Increased pericardial fat is associated with worse cardiovascular outcomes. We hypothesized that progressive increases in pericardial fat volume and inflammation prospectively dampen HRV in hypercholesterolemic pigs. Methods: WT (wild type) or PCSK9 (proprotein convertase subtilisin-like/kexin type-9) gain-of-function Ossabaw mini-pigs were studied in vivo before and after 3 and 6 months of a normal diet (WT-normal diet, n=4; PCSK9-normal diet, n=6) or high-fat diet (HFD; WT-HFD, n=3; PCSK9-HFD, n=6). The arterial pulse waveform was obtained from an arterial telemetry transmitter to analyze HRV indices, including SD (SD of all pulse-to-pulse intervals over a single 5-minute period), root mean square of successive differences, proportion >50 ms of normal-to-normal R-R intervals, and the calculated ratio of low-to-high frequency distributions (low-frequency power/high-frequency power). Pericardial fat volumes were evaluated using multidetector computed tomography and its inflammation by gene expression of TNF (tumor necrosis factor)-α. Plasma lipid panel and norepinephrine level were also measured. Results: At diet completion, hypercholesterolemic PCSK9-HFD had significantly ( P <0.05 versus baseline) depressed HRV (SD of all pulse-to-pulse intervals over a single 5-minute period, root mean square of successive differences, proportion >50 ms, high-frequency power, low-frequency power), and both HFD groups had higher sympathovagal balance (SD of all pulse-to-pulse intervals over a single 5-minute period/root mean square of successive differences, low-frequency power/high-frequency power) compared with normal diet. Pericardial fat volumes and LDL (low-density lipoprotein) cholesterol concentrations correlated inversely with HRV and directly with sympathovagal balance, while sympathovagal balance correlated directly with plasma norepinephrine. Pericardial fat TNF-α expression was upregulated in PCSK9-HFD, colocalized with nerve fibers, and correlated inversely with root mean square of successive differences and proportion >50 ms. Conclusions: Progressive pericardial fat expansion and inflammation are associated with a fall in HRV in Ossabaw mini-pigs, implying aggravated autonomic imbalance. Hence, pericardial fat accumulation is associated with alterations in HRV and the autonomic nervous system. Visual Overview: A visual overview is available for this article.

Background Patients with Eisenmenger syndrome are known to have a high incidence of sudden cardiac death ( SCD ), yet the underlying causes are not well understood. We sought to define the predictors of SCD in this population. Methods and Results A retrospective analysis of all patients with Eisenmenger syndrome from 2 large tertiary referral centers was performed. ECGs, prolonged ambulatory recordings, echocardiograms, and clinical histories were reviewed; and the cause of death was identified. A total of 246 patients (85 [34.6%] men) with a mean age of 37.3 (±14.2) years were followed up for a median of 7 years. Over the study period, 136 patients died, with 40 experiencing SCD and 74 experiencing cardiac death (sudden and nonsudden). Age, atrial fibrillation, prolonged QRS duration, complete heart block, right atrial enlargement, right bundle branch block, increased right atrial pressure, impaired biventricular function, and the presence of a pacemaker were associated with increased risk of SCD , whereas advanced pulmonary hypertension therapies were protective. Atrial fibrillation (11.45‐fold increased risk; P <0.001) and QRS duration ≥120 ms (2.06‐fold increased risk; P =0.034) remained significant predictors of SCD in the multivariate analysis, whereas advanced pulmonary hypertension therapies were strongly protective against SCD ( P <0.001). Conclusions Atrial arrhythmias, impaired ventricular function, and conduction system disease were associated with increased risk of SCD in this cohort of patients with Eisenmenger syndrome, providing an opportunity for early risk stratification and potential intervention. Clinical heart failure symptoms (New York Heart Association class ≥ II ) were predictive of increased mortality but not of SCD , suggesting a potential arrhythmic cause behind SCD .