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Implantable cardioverter defibrillators (ICDs) prevent sudden cardiac death. However, in patients with terminal illnesses, these devices may disrupt the dying process. This study was undertaken to review our current strategies surrounding device deactivation. A retrospective chart review was performed at Kingston Health Sciences Centre of patients with an ICD who died from 2015 to 2018. Data collected included patient demographics, clinical details surrounding device implantation, patient co-morbidities leading to deactivation, time to deactivation, physical place of deactivation, and device programming information. Ethics approval was obtained from the Queen's University Health Sciences Research Ethics Board. A total of 49 patients were included for analysis. Mean age at the time of death was 77.5 years (range: 57 to 94 years) and 12.2% (6/49) were women. The indications for ICD implantation were primary prevention of sudden cardiac death in 69.4% (34/49) and secondary prevention in 30.6% (15/49). Deactivation as part of end-of-life care was performed in 32.7% of patients (16/49). Deactivations occurred in clinic in 6.1% (3/49) of patients, on hospital inpatient wards in 12.2% (6/49) of patients, and in critical care settings in 14.2% (7/49) of patients. The remaining 67.3% (33/49) of patients died with fully functioning devices in place. The most prevalent terminal diagnoses were metastatic cancer (22.4%) and end-stage congestive heart failure (20.4%). On average, patients had their devices deactivated 13 months (range: 0 to 62 months) after their terminal diagnosis was established. Once a patient was documented as Do Not Resuscitate (DNR), deactivation was discussed and carried out within a mean time of 38 days (range: 0 to 400 days). Seven patients had their device active for more than 1 month after being documented as DNR. Ten patients (20.4%) received ICD shocks after their terminal diagnosis, 9 received shocks in the month before death, and 2 received shocks after formal DNR orders were in place. Approximately one-third of patients with ICDs received deactivation of their cardioversion/defibrillation therapies as part of their end-of-life care plan. A relatively high proportion of patients (20%) received an ICD shock in the last month of life. In conclusion, addressing device programming needs, including deactivation of cardioversion/defibrillation therapies, should be considered in the context of a patient's goals of care in every patient with an ICD who has a co-existing life-limiting diagnosis.

Atrial fibrillation (AF) is a risk factor for ischemic stroke and reported to be associated with severe obstructive sleep apnea (OSA). The aim of this study was to determine the occurrence of newly detected AF in patients with severe OSA and no previous history of AF. Prospective observational study included patients with severe OSA (Apnea-Hypopnea Index [AHI] ≥ 30) and no history of AF. Primary outcome was detection of AF lasting ≥10 seconds. Patients were subjected to 2 24-hour Holter monitors, and if no AF was detected, implanted with a Medtronic Reveal XT implantable loop recorder. Follow-up was done every 6 months for a total of 3years. Implantable loop recorder was explanted if the primary outcome was detected (AF) or the battery was exhausted. Of the 31 patients enrolled, 6 withdrew participation in the study before implantation. Mean age was 57 ± 10years, mean body mass index was 35 ± 6; 52% male patients. Hypertension 56% and coronary artery disease 24%. Mean AHI was 55 ± 18. AF was detected in 5 patients (20%). AF mean duration was 4.8hours (range 20 seconds to 15.3 hours). Mean time to diagnosis was 11 ± 7 months. Male gender was predictive for AF detection (p = 0.04). Continuous positive airway pressure therapy was used by 96% of patients with 68% total adherence. Mean follow-up was 27 months. In conclusion, extended cardiac monitoring of patients with severe OSA may facilitate the identification of newly detected AF.

PurposeAs cardiovascular implantable electronic devices (CIEDs) are increasingly indicated in older patients, and the burden of cancer is rising with the aging population, the management of patients with CIEDs who require radiotherapy (RT) is a timely concern. The objective of the study was to evaluate the management of, and malfunctions in, patients with CIEDs undergoing RT.MethodsA retrospective study of patients with CIEDs receiving RT at Kingston Health Sciences Center from March 2007–April 2018 was conducted. Data on demographics, RT, devices, and management were compared for the primary outcome of device malfunction.ResultsOf the 189 patients with CIEDs receiving a total of 297 courses of RT, 4 patients (2.1%) experienced device malfunctions. Higher beam energy was associated with a malfunction (p < 0.05). Patients with malfunctions received a lower dose of radiation per fraction (267 ± 93 cGy vs. 477 ± 282 cGy; p < 0.05) and were significantly younger (71.4 ± 2.2 years vs. 77.8 ± 9.8 years; p < 0.01) compared to patients without malfunctions.ConclusionRT-induced device malfunctions are rare, but given the potential complications, a better understanding of the potential predictors of malfunction and the development of evidence-based guidelines will help optimize patient safety.

[...]the regular noise in this case was 8 Hz. [...]we believe that this was the actual cause of the auto-mode switch. [...]12-lead ECG interpretation is important in recognizing possible PPM-related problems. Conflict of interest and disclosure of funding All authors declare that the manuscript, as submitted or its content in another version, is not under consideration for publication elsewhere and will not be submitted elsewhere, until a final decision is made by the editors of the Journal of Arrhythmia.

ATRIAL FIBRILLATION (AF) is the most common sustained dysrhythmia in adults. It is ironic, then, that although mechanisms and effective treatments for most other supraventricular tachyarrhythmias have been discovered, AF remains incompletely understood and poorly treated. Nonetheless, our understanding of the pathophysiology of AF has improved in the last half-century, including some groundbreaking observations made in the last 10 years. Indeed, for some patients, the potential for cure now appears to be available. Because no unifying mechanism of AF has been proven, the aim of this review is to describe some of the common and important concepts behind current mechanistic theories of AF and how they contribute to our clinical understanding of AF.

Atrial fibrillation (AF) is the most common sustained dysrhythmia in adults. It is ironic, then, that although mechanisms and effective treatments for most other supraventricular tachyarrhythmias have been discovered, AF remains incompletely understood and poorly treated. Nonetheless, our understanding of the pathophysiology of AF has improved in the last half-century, including some groundbreaking observations made in the last 10 years. Indeed, for some patients, the potential for cure now appears to be available. Because no unifying mechanism of AF has been proven, the aim of this review is to describe some of the common and important concepts behind current mechanistic theories of AF and how they contribute to our clinical understanding of AF.Atrial fibrillation (AF) is the most common sustained dysrhythmia in adults. It is ironic, then, that although mechanisms and effective treatments for most other supraventricular tachyarrhythmias have been discovered, AF remains incompletely understood and poorly treated. Nonetheless, our understanding of the pathophysiology of AF has improved in the last half-century, including some groundbreaking observations made in the last 10 years. Indeed, for some patients, the potential for cure now appears to be available. Because no unifying mechanism of AF has been proven, the aim of this review is to describe some of the common and important concepts behind current mechanistic theories of AF and how they contribute to our clinical understanding of AF.

In an important study, the inducibility, rate and duration of AF in an animal model were increased when AF was artificially maintained.7 By using a pacemaker capable of delivering 1-second bursts of very rapid stimuli, nonsustained AF lasting only a few seconds could be induced. By repeatedly inducing (and thus maintaining) AF for 24 hours, bursts of induced AF lasted approximately 20 seconds. After 2 weeks of artificially maintained AF, it became sustained. Consistent with a model of functional re-entry, the perpetuation of AF was accompanied by a shortening of the atrial refractory period. The authors concluded that \"AF begets AF\": AF is capable of inducing electrophysiologic changes that promote further AF. These include electrical, contractile and structural changes to the atria that have collectively become known as atrial remodelling. Atrial remodelling, which prepares the atrium for multiple wavelets of functional re-entry, addresses the substrate for AF, but what of the trigger? A landmark paper published in 1998 identified the muscular sleeve of the pulmonary veins as a source of tachyarrhythmias and atrial premature beats that could trigger paroxysms of AF.23 It was later determined that in patients with frequent paroxysms of AF, the muscular sleeve of the pulmonary veins displays electrophysiologic properties (including shorter refractory periods) distinct from those of both the adjacent left atrial muscle and the muscular sleeve of the pulmonary veins in control subjects without AF;24 specialized conduction cells in the pulmonary veins have also been discovered.25 Although atrial tissue and the muscular sleeves of other cardiac veins, including the coronary sinus,26 the vein of Marshall27 and the superior vena cava,28,29 have been implicated as sources of tachyarrhythmias and AF triggering beats, none do so with nearly the frequency of the pulmonary veins. The proposed mechanisms for diese \"focal\" tachyarrhythmias (micro-re-entry v. disorders of impulse formation) are reviewed elsewhere.30 The likelihood that AF will terminate, either spontaneously or as a result of a medical intervention, is inversely related to the duration of the episode. This clinical observation mirrors the experimental adage that \"AF begets AF,\" which is founded in cellular mechanisms of atrial remodelling. Pretreatment with a calcium-channel blocker reduces early recurrences of AF after cardioversion, which emphasizes the remodelling process itself as a novel therapeutic target.35 Because electrical remodelling resolves rather quickly, it cannot explain late recurrences of AF after cardioversion. Furthermore, the frequent association of AF with structural heart disease emphasizes the clinical significance of structural remodelling. Along these lines, use of renin-angiotensin system inhibitors has been associated with a reduction in the incidence of AF among patients with a myocardial infarction or impaired left ventricular systolic function and among patients receiving amiodarone who have undergone elective cardioversion.36-38 Thus, angiotensin receptor blockers and angiotensin-converting-enzyme inhibitors are an attractive therapeutic option for people who have hypertension and AF. The strategy of treating normotensive AF with an angiotensin receptor blocker is currently being tested in a randomized trial (Dr. Stuart Connolly, Professor of Medicine, McMaster University: personal communication, 2004).