Tilt was used physiologically, 1930s–1970s, becoming a clinical diagnostic test for syncope in 1980s. Tilt has been criticized recently for failing to discriminate between reflex and more sinister syncope. Studies on possible benefit of pacing for older reflex syncope patients (2012–2014) yielded unexpected results. Patients with electrocardiogram implantable loop recorder (ILR) documented asystole and negative tilt, despite history strongly suggestive of reflex syncope, did well with pacing having syncope recurrence similar to that in paced His-Purkinje disease, while those with identical ILR findings and positive tilt did little better than those without pacing. These findings prompted explanation. The hypothesis hinged on tilt revealing a hypotensive/vasodepressor tendency rather than defining vasovagal syncope. Support was drawn from literature demonstrating good test sensitivity and specificity but no clinical value in arrhythmic, unexplained, or structural cardiovascular disease syncope. Further, in carotid sinus syndrome, another reflex syncope, the same pattern of disappointing pacing results was seen when tilt was positive but lack of syncope when tilt was negative. Thus, rethinking tilt testing is required to portray it in reflex, arrhythmic, unexplained, and cardiovascular syncope as having value in demonstrating risk of recurrence rather than being diagnostic. Its value in diagnosis of orthostatic hypotension (immediate/delayed), psychogenic pseudosyncope, and postural orthostatic tachycardia remains important and unchanged. The hypothesis has additional implications for management of hypertensive patients with syncope where medication may exacerbate symptoms requiring reduction/discontinuation. Tilt testing has greater value now than that claimed at its 1986 introduction.

Sudden cardiac death (SCD) is the leading cause of cardiovascular mortality and a major international health problem, with an estimated 3.7 million deaths occurring annually, accounting for approximately 15%–20% of all deaths worldwide. The implantable cardiac defibrillator (ICD) is an effective treatment of SCD and has had a major impact on outcomes. However, this therapy has been largely used in patients with left ventricular dysfunction. A changing epidemiology of SCD with fewer patients having marked reductions in left ventricular ejection fraction (LVEF) has renewed the focus on identifying other high risk populations. This article summarizes the current understanding of the diverse clinical, genetic, racial, electrocardiographic and imaging techniques available to detect patients most at risk. Despite many identified risk factors, no single predictor has been shown to have sufficient predictive value to be used to guide preventative therapy and reduce mortality. More recent effort has been directed towards combining markers to define a risk profile for identifying high risk cohorts.

In recent years, silent atrial fibrillation (AF) has acquired broad interest in the neurologic and cardiovascular communities. Silent AF has been associated with similar morbidity and mortality as symptomatic AF and with similar rates of silent embolic events. In current clinical practice, AF remains mostly underdiagnosed, and 25% of patients with AF-associated cardioembolic stroke have not been previously diagnosed with AF. Silent AF detection methods include pulse palpation, ambulatory external electrocardiographic recordings, insertable cardiac monitors, and previously implanted cardiac devices with atrial lead. The increased interest is being directed toward detection of silent AF. Whether this will imply better outcomes for patients remains to be demonstrated.

Background: Elective direct current cardioversion (DCCV) has traditionally been performed by physicians in the United States. A few recent reports from the United Kingdom suggested that a specialist nurse-led service for elective DCCV of persistent atrial fibrillation was feasible. This practice has not been reported in the United States previously. Several years ago, we introduced a program where specially trained advanced practice providers (APPs) (physician assistants and nurse practitioners) assisted by an anesthesiology team, performed elective DCCV in patients with atrial fibrillation and atrial flutter, without direct cardiologist supervision. Methods: Upon receiving approval from the Institutional Review Board, we conducted a retrospective analysis of 447 consecutive DCCVs electively performed by APPs, for atrial fibrillation or atrial flutter, at Regions Hospital between 12/2006 and 10/2010. Transient deep sedation was administered by an anesthesiology team. The cohort was evaluated for procedural success and safety. Results: The procedural success rate was 92% (412/447). The incidence of procedural related adverse events, requiring immediate intervention, was 0.2% (1/447). This patient required emergent temporary pacing catheter insertion followed by a permanent pacemaker implantation at a later date. There were no other procedure-related complications and no thromboembolic events. A comparison with fifty elective cardioversions performed by cardiologists during the same period found no statistical difference in procedural success rates or complications. Conclusion: Under deep sedation administered by anesthesiology service, elective DCCV of atrial fibrillation and atrial flutter performed by well-trained APPs, without direct cardiologist supervision, is feasible and does not compromise patient safety.

Purposes: There are few vector-based electrocardiogram (ECG) algorithms to differentiate ventricular tachycardia (VT) and premature ventricular complexes (PVCs) originating from the septum (SP) or free wall (FW) in the right ventricular outflow tract (RVOT). Methods: One hundred and twenty-one patients (mean age 41 ± 13 years; 62% female) underwent mapping and ablation of symptomatic PVC or VT with left bundle branch block morphology. Inferior axis and precordial lead transition zone ≥V3 on the ECG were analyzed retrospectively. Ablation was highly successful on the 95 SP patients and among 26 cases in the FW group. The ECG morphology of VT/PVC was analyzed to derive a novel algorithm to localize VT origin within the RVOT. A VT/PVC QRS axis ≥90° or an R wave amplitude ratios ≥1 in leads II and III predicted a septal origin. If neither of these characteristics were present, the following criteria were each given a score of 1: VT/PVC QRS axis <85;°, leads II and III R wave amplitude ratio <0;.88, QRS duration in lead III ≥155 ms, and QRS duration ≥155 ms in lead aVL. A cumulative score of ≥2 predicted an FW origin whereas a total score of <2; predicted an SP origin. A prospective analysis in 99 patients was used to confirm the significance of the algorithm. Results: Retrospective analysis showed that the new algorithm predicted an SP origin with an overall sensitivity, specificity, and positive predictive values of 95.2%, 88%, and 96.3%, respectively. Prospective analysis showed that the new algorithm predicted RVOT-SP origin with a sensitivity, specificity, and positive predictive values of 97.5%, 88.9%, and 97.5%, respectively. Conclusion: The new vector-based ECG algorithm can differentiate septal from FW sites of origin in the RVOT with a high sensitivity, specificity, and positive predictive values.

Background: Entirely leadless pacemakers (LPMs) address limitations of conventional pacemakers that include complications related to the pacing leads, their connections, and pacemaker pockets. The aim of this study was to describe early implantation experience and clinical efficacy of LPM. Methods: A total of eight patients received an LPM (Micra™ Transcatheter Pacing System, Medtronic plc, Minneapolis, MN, USA). LPM was transvenously deployed using a 23 F sheath, and actively fixed by 4 nitinol tines. Results: On average, the patients were 74.3 ± 8.1 years, and 50% were female. All had indications for a ventricular demand (VVI) pacemaker, and ejection fraction was 66.4% ±7.4%. Except for one patient, all were implanted from the right femoral vein. The LPM was deployed either at the right ventricular apex (63%) or at the septum (37%). At implantation, pacing threshold at 0.24 ms was 0.69 ± 0.35 V, and R wave was 8.1 ± 2.9 mV. Successful pacing sites were reached at a median of 1 attempt (range 1–3), and the mean procedure and fluoroscopic times were 74 ± 19 min and 11.0 ± 5.8 min, respectively. 50% were on uninterrupted anticoagulation, and there were no acute complications including groin hematoma. Both pacing threshold and R wave improved at 1 month compared to acute implant value (0.46 ± 0.11 V and 14.5 ± 5.6 mV, respectively, P< 0.05 compared with implant). Between 1 and 3 months follow-up, there was no change in pacing or sensing threshold. The average percentage of ventricular pacing was 65% ± 26%. The intracardiac accelerometer was activated in 3/8 patients, and the satisfactory rate response profile during activity of daily living was achieved. Battery longevity was estimated to be more than 8 years in all patients. Conclusion This study documents excellent implantation success of the Micra™ LPM with stable pacing and sensing and satisfactory rate response profile.