Pseudoatrial Fibrillation during Pacemaker Interrogation: What is the Mechanism? (original) (raw)
Related papers
Pacing and Clinical Electrophysiology, 2017
We present the case of a 75-year-old patient with a single-chamber St. Jude Medical internal cardioverter defibrillator (ICD; St. Jude Medical, St. Paul, MN, USA) for primary prevention, who was admitted with 39 inappropriate ICD shocks because of atrial fibrillation with rapid ventricular frequention, despite magnet placement. Review of the device manual and literature revealed that apart from different responses to magnet placement programmed for the various manufacturers, the type of magnet and the positioning can be of specific interest. In the case presented, the donut-shaped magnet should have been placed off-center instead of directly over the device. (PACE 2017; 00:1-3) magnet response, ICD shock, implantable defibrillator therapy Case Report A 75-year-old male patient was presented to the emergency department with multiple internal cardioverter defibrillator (ICD) shocks. He received a single-chamber ICD 2 weeks prior (St. Jude Medical Fortify Assura VR1359-40QC, St. Jude Medical, St. Paul, MN, USA) for primary prevention. His medical history consisted of ischemic cardiomyopathy with a left ventricular ejection fraction of 30% and permanent atrial fibrillation (AF) for which he was treated with metoprolol 300 mg/day for rate control. The device was programmed with a monitor zone >160 beats/min, a ventricular tachycardia (VT) zone >190 beats/min with antitachycardia pacing (ATP) and shocks, and a ventricular fibrillation zone >222 beats/min with ATP and shocks. As discriminators, morphology (90% match), sudden onset (onset delta 20 ms), and interval stability (stability delta 40 ms) were programmed, with two out of three discrimination criteria requested to indicate VT. The electrocardiogram at presentation showed AF with a fast ventricular rate of approximately 200 beats/min. Hereby inappropriate therapy was delivered. Attempts to disable ICD therapy by placement of a magnet on the ICD were unsuccessful. In-hospital
Heart Rhythm O2, 2021
BACKGROUND Atrial fibrillation (AF) is the most common sustained arrhythmia in adults. Research suggests that autonomic nervous (ANS) system dysfunction contributes to AF pathophysiology. Animal studies have shown that low-level electromagnetic fields (LL-EMF) are potentially capable of AF suppression. This study evaluated the safety and efficacy of LL-EMF in suppressing AF in humans. OBJECTIVE To investigate the impact of LL-EMF on AF inducibility in humans. METHODS Patients presenting for ablation of paroxysmal AF were randomized to a sham protocol or LL-EMF (3.2 ! 10-8 G at 0.89 Hz) applied via a Helmholtz coil around the head. AF was induced via atrial pacing, and was cardioverted if duration was greater than 15 minutes. The protocol was then run for 60 minutes, followed by reinduction of AF. The primary endpoint was the duration of pacing-induced AF after protocol completion compared between groups. RESULTS Eighteen patients completed the study protocol (n 5 10 sham, n 5 8 LL-EMF). Pacing-induced AF duration in the LL-EMF group was 11.0 6 3.43 minutes shorter than control after protocol completion (CI 3.72-18.28 minutes, P 5 .03). A smaller proportion of LL-EMF patients experienced spontaneous firing initiating an AF episode (0/7 vs 5/6, P 5 .0047). A significantly greater proportion of patients in the control group required direct current cardioversion after 1 hour (0.78 vs 0.13, P 5 .02). CONCLUSION In patients with paroxysmal AF, LL-EMF stimulation results in shorter episodes of pacing-induced AF and a reduced likelihood of spontaneous firing initiating an episode of AF.
Pacemaker Stimulus Alternans: What Is the Mechanism?
Pacing and Clinical Electrophysiology, 2008
A 77-year-old man was admitted due to decompensated heart failure. Eight years prior to this admission, a single-chamber VVI pacemaker (Pikos LP01, Biotronik, Berlin, Germany) and a bipolar lead (TIR 60-BP, Biotronik) had been implanted due to sick sinus syndrome. This device was programmed for unipolar pacing at 70 bpm. The patient had not undergone a pacemaker check-up for several years. An electrocardiogram (ECG) recorded at admission showed no inhibition of pacemaker output by intrinsic QRS complexes, and an apparent pacing rate of 32 bpm, with occasional lack of capture. However, further inspection of the tracing revealed that the pacemaker spikes actually occurred at a rate of 63 bpm, but every second spike was very small and did not cause ventricular capture. Several subsequent longer ECG tracings confirmed this observation. What was the mechanism underlying this ECG pattern?
Europace, 2012
Research on paroxysmal atrial fibrillation (AF) assumes that fibrillation induced by rapid pacing adequately reproduces spontaneously occurring paroxysmal AF in humans. We aimed to compare the spectral properties of spontaneous vs. induced AF episodes in paroxysmal AF patients. Methods and results Eighty-five paroxysmal AF patients arriving in sinus rhythm to the electrophysiology laboratory were evaluated prior to ablation. Atrial fibrillation was induced by rapid pacing from the pulmonary vein-left atrial junctions (PV-LAJ), the coronary sinus (CS), or the high right atrium (HRA). Simultaneous recordings were obtained using multipolar catheters. Off-line power spectral analysis of 5 s bipolar electrograms was used to determine dominant frequency (DF) at recording sites with regularity index .0.2. Sixty-eight episodes were analysed for DF. Comparisons were made between spontaneous (n ¼ 23) and induced (n ¼ 45) AF episodes at each recording site. No significant differences were observed between spontaneous and induced AF episodes in HRA (5.18 + 0.69 vs. 5.06 + 0.91 Hz; P ¼ 0.64), CS (5.27 + 0.69 vs. 5.36 + 0.76 Hz; P ¼ 0.69), or LA (5.72 + 0.88 vs. 5.64 + 0.75 Hz; P ¼ 0.7) regardless of pacing site. Consistent with these results, paired analysis in seven patients with both spontaneous and induced AF episodes, showed no regional DFs differences. Moreover, a left-to-right DF gradient was also present in both spontaneous (PV-LAJ 5.71 + 0.81 vs. HRA 5.18 + 0.69 Hz; P ¼ 0.005) and induced (PV-LAJ 5.62 + 0.72 vs. HRA 5.07 + 0.91 Hz; P ¼ 0.002) AF episodes, with no differences between them (P ¼ not specific). Conclusion In patients with paroxysmal AF, high-rate pacing-induced AF adequately mimics spontaneously initiated AF, regardless of induction site.
Pacemaker Stimulation Criticism at ECG
New Concepts in ECG Interpretation, 2018
Cardiac implantable electronic devices' (CIEDs) numbers have grown up worldwide over the last years [1]. At the same time, functions and algorithms' complexity implementation also expanded. It will be therefore more and more frequent for the clinician to deal with pacemaker (PM) ECGs and unusual device behaviors, particularly when they mimic pseudo-malfunctions. In this chapter, we present some examples of challenging electrocardiograms, aiming to show how the clinician, just by analyzing the ECG, could reach or at least suspect the correct diagnosis. 16.1 Case 1 An 82-year-old man with a history of systemic hypertension and previous dual-chamber PM implantation for second-degree atrioventricular (AV) block was referred to our clinic with a suspected PM malfunction. The patient was asymptomatic. ECG is shown in Fig. 16.1a, b.
Magnet Application, a Cause of Persistent Arrhythmias in Physiological Pacemakers. Report of 2 Cases
Pacing and Clinical Electrophysiology, 1982
Magnet application, a cause of persistent arrhythmias in physiological pacemakers. Report of 2 cases. MagenI application during routine pacemaker checkup induced persistent arrhythmias in two patients with physioiogicaJ pacemakers. One patient had received an atrial synchronous ventricuiar demand pacemaker (VDD} because of alternating secondand third-degree atrio-ventricuJar biock. During routine pacemaker follow-up, a magnet was applied over the pulse generator to measure the pacemaker rate. This converted the system to fixed rate ventricular pacing at a rate of 65 bpm which resulted in retrograde atrial activation. When the magnet was removed the retrograde conducted P-waves were sensed by the atrial amplifier and the ventricuiar output was triggered again, causing a re-entry pacemaker tachycardia with a rate of 175 bpm. The tachycardia could be suppressed by applying a magnet once more, but the puise generator had to be programmed in the VVl-mode to prevent induction of the tachycardia again. A second patient had complete atrioventricular block and left heart failure. After three years of ventricular demand pacing, we decided to implant a DDD pacemaker because of persisting left heart failure and poor exercise tolerance. During a routine visit io the pacemaker clinic a magnet was applied over the pulse generator to measure the basic rate. The system was thus converted to fixed rate A-V-sequential pacing fDOOJ which resulted in atrial flutter. When the magnet was removed and the pulse generator returned io its DDD mode, the atrial flutter was partially sensed by the atrial amplifier, resulting in a tachycardia with a variable rate up to 125 bpm. Fortunately we were able to terminate the atrial arrhythmia by applying the magnet again. In this patient fixed rate underdrive pacing stopped the atrial arrhythmia. (PACE, Vol. 5, September-October. 1982} magnet-induced arrhythmias, physiological pacemakers, pacemaker follow-up Application of a magnet over a pulse generator is a generally accepted method of determining pacemaker ftinction. This technique is used at the pacemaker clinic and outside the clinic during transtelephone monitoring. There are few reported cases of arrhythmias caused by magnet application. The purpose of this paper is to report two such cases in which magnet application over a physiological pacemaker induced persistent arrhythmias, Case reports
Circulation, 2006
Background-This study investigated onset scenarios of atrial fibrillation (AF), the first phase of the Atrial Fibrillation Therapy (AFT) trial, to determine potential arrhythmogenic triggers as targets for atrial pacing algorithms that have been proposed for prevention of AF. Methods and Results-Ninety-eight patients (58 men; age 65Ϯ11 years) with recurrent, symptomatic, drug-refractory AF and a conventional pacemaker indication in 31 of 98 received a dual-chamber pacemaker. Using novel diagnostic pacemaker features AF onset scenarios were prospectively evaluated in 612 AF episodes during a 2-month monitoring period, with atrial pacing limited to 40 bpm. The most common onset scenario was premature atrial complexes (PACs) before AF (48% onsets per patient), followed by bradycardia (33%), sudden onset (17%), and tachycardia (0%). Combinations of onset scenarios were frequent (median 2 different scenarios per patient). A main study finding was the significance of repetitive AF, with 33% of onsets per patient being initiated within 5 minutes of a previous AF episode. Sudden onsets were more frequent among patients with than without repetitive AF (24% versus 0% onsets per patient, Pϭ0.011), whereas the proportion of PACs before AF was not statistically different (50% versus 37%, Pϭ0.52); however, patients with repetitive AF had more PACs per hour (72 versus 29, Pϭ0.023) and a higher number of AF episodes per day (17 versus 0, Pϭ0.001) and were more likely to have at least 1 PAC-related onset (90% versus 53%, PϽ0.0001). Conclusions-Novel diagnostic pacemaker features allowed a detailed individual analysis of rate and rhythm changes before AF and thus uncovered a substantial intraindividual and interindividual variability of AF onset scenarios.
Interaction of pacemakers as generating mechanism of atrial fibrillation
2011 Computing in Cardiology, 2011
We study, if mechanisms for the generation of fibrillation patterns observed recently in studies of the FitzHugh-Nagumo (FHN) model can be seen also in the model of Bueno-Orovio, Cherry and Fenton (BOCF), that has been adapted specifically to the atrial electrophysiology. The mechanisms are associated with the interference of two spatially separated pacemakers that are connected by a small bridge of the conducting tissue. One of the two pacemakers represents the sinus node, while the second one represents a self-excitatory source in the left atrium, as an ectopic focus or microreentrant circuit. In the FHN model, three different types of irregular patterns are observed and which type occurs depends on the frequency ratio of the two pacemakers. However, only one of these types is observed in the BOCF model. Particularly interesting is the fact that the strength of the irregularity is determined by the sinus node frequency. This may be an explanation why AF is typically intermittent at its beginning.
Journal of thoracic disease, 2018
Today's pacemakers and defibrillators include diagnostic tools for detecting and treating cardiac arrhythmias like silent atrial fibrillation as atrial high rate episodes (AHREs). This diagnostic capability is crucial to prevent the potential embolic complications this AHREs are related to. However, sometimes data retrieved from diagnostic counters may be misleading reflecting limitations of detection algorithms, which must follow mathematical rules to classify events on a beat-to-beat basis. The incorporation of stored electrograms has been an important milestone in improving the diagnostic capabilities of these devices confirming the arrhythmia diagnosis.
Cardiac Autonomic Control Mechanisms in Power-Frequency Magnetic Fields: A Multistudy Analysis
Environmental Health Perspectives, 2000
Heart rate vaiability (HRV), a noninvasive indicator of autonomic control of cardiac activity, is predictive of long-term cardiac morbidity and mortality. Epidemiologic research suggests that occupational exposure to power-frequency magnetic fields may be associated with autonomically mediated cardiac mortality. Results from our laboratory studies of humans exposed to 60-Hz magetic fields overnigt,. however, are inconsistent. HRV is altered in some studies but not other. To carify this, the pooled data from seven studies involving 172 men were analyzed to test specific hypotheses concerning this inconsistency. After analysis, we exduded a) measurement drift or instability over time because HRV was stable under sham-exposed conditions across all studies;. b) inadequate statistical power or failure to mantain double-blind controls; c) differences in field intensity (283 vs. 127.3 pT) or exposure pattern (intermittent versus continuous) as main efhcts; or 4) the indusion of individuals sensitive to magnetic field exposure in some studies but not others. Four separate analytic techniques failed to identify a valid subpopulation of sensitive individuals. In some studies, however, hourly blood samples were collected using an indwelling venous catheter. HRV alterations occurred during intermittent exposure in these studies (p < 0.05) but not in similar studies without blood sampling. This result suggests a field interaction with modest arousal or disturbance. Because HRV is tightly coupled to electroencephalographic activity during sleep, these results are physiologically plausible and suggest that HRV alterations during exposure to magnetic fields may occur when accompanied by increases in physiologic arousal, stress, or sleep disturbance.