Preliminary Evaluation of a Dual Chamber Pacemaker with Bradycardia Diagnostic Functions (original) (raw)

Course of Symptoms and Spontaneous ECG in Pacemaker Patients: A 5-Year Follow-up Study

Pacing and Clinical Electrophysiology, 1988

LANGENFELD, H,, ET AL.: Course of symptoms and spontaneous ECG in pacemaker patients: A 5-year follow-up study. We investigated the course of symptoms and the spontaneous ECG retrospectiveiy in 308 patients who had received a pacemaker because of a trio ventricuJar (AV) block fn = 115), sick sinus syndrome fSSS, n = 107), bradyarrhythmic atriai jibriJiation fbradyarrhythmia, n = 51). carotid sinus syndrome (CSS, n = 16), complete bi/ascicuiar block associated with 1st degree AV block (n = 13) and with other indications fn = 6). The mean impiantation time was 63 months. The c\ir\ica\ state of 93% of all patients improved after pacemaker implantation; their symptoms decreased markedly. Persisting syncopy in some patients with SSS, however, supports a restricted implantation policy. We rarely saw improved AV conduction in patients with AV block fn%). Furthermore, in patients with SSS, afriaJ /ibriliotion occmed significantly more often (35 %) than in those with AV block (17 %; P < 0.01). Only 3% of patients with SSS developed 2nd and 3rd degree AV block within the observation period. In all patients with Initial bi/ascicular block and additional 1st degree AV block, pacing prevented further syncopaJ attacks; four of them showed 3rd degree AV block at control, indicating that pacemaker impiantation is mandatory in symptomatic patients with bifascicular disease and 1st degree AV block. (PACE, Vol. 11, December 1988) folow-up, pacemaker patients, symptoms, spontaneous ECC Address for reprints: Heiner Langenfeld. MD

Implications of mechanism of bradycardia on response to pacing in patients with unexplained syncope

Europace, 2007

Asystole &amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;gt;3 s or sinus bradycardia with a ventricular rate &amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt;40 in association with complete heart block or sinus node dysfunction are considered to be Class 1 indications for permanent cardiac pacing. Nevertheless, these phenomena may be observed in symptomatic patients with neurocardiogenic syncope, who may not respond to pacing therapy. We hypothesized that the pattern of spontaneous bradycardia in symptomatic patients would distinguish patients with sinus node dysfunction or conduction system disease who would benefit from pacing from patients with neurally-mediated syncope who would derive lesser benefit. Patients with symptomatic spontaneous bradycardia during long-term monitoring for unexplained syncope who underwent pacemaker implantation were classified according to the ISSUE classification system and followed for recurrent syncope. Follow-up included review of medical records, pacemaker clinic visits, and telephone interviews. Loop recorder tracings were reviewed to identify characteristics potentially predicting a favourable response to pacing. Thirty-three patients (21 male; age, 70 +/- 14) were followed for 3.56 +/- 1.71 years. Six patients had a recurrence of syncope during the follow-up. All patients with recurrent syncope despite pacing demonstrated a Type 1A (n = 5) or 1B (n = 1) pattern with gradual onset of bradycardia at baseline, suggesting a neurocardiogenic mechanism. There was no difference in the severity of bradycardia or duration of asystole in baseline loop recorded events in responding and non-responding patients. Multivariate analysis using stepwise logistic regression revealed that the ISSUE classification and the absence of structural heart disease were the only independent predictors of treatment failure of cardiac pacing in patients with spontaneous symptomatic bradycardia. Patients with syncope associated with abrupt bradycardia displayed a better response to cardiac pacing therapy than those with gradual onset bradycardia.

Cardiac Pacing for Bradycardia Support: Evidence-based Approach to Pacemaker Selection and Programming

Current treatment options in cardiovascular medicine, 2004

The vast majority of pacemakers implanted in the United States for the treatment of symptomatic bradycardia are dual-chamber systems with a complex array of functions, such as rate responsiveness, dynamic atrioventricular delay, and automatic mode switching. Basic hemodynamic studies have convincingly demonstrated the superiority of maintaining atrioventricular synchrony. However, clinical trials have failed to demonstrate the impressive results expected based on physiologic data. The most recent randomized clinical trials have demonstrated that dual-chamber devices, when compared with single-chamber ventricular pacing, do not prevent mortality or stroke, and lead to an unexpectedly small reduction in heart failure hospitalizations. Although improvements in quality of life have not been consistently found when comparing ventricular-based versus atrial-based pacing, a reduction in the incidence of newly diagnosed atrial fibrillation in dual chamber-paced patients has been reported by...

Management of Tachyarrhythmias with Dual-Chamber Pacemakers

Pace-pacing and Clinical Electrophysiology, 1983

Des stimulaleurs multiprogrammables AV séquentiels de type “double-demande” (DVI, MN) ont été implantés chez 23 patienls porteurs ?anomalies variées de tachycardies supraventriculaires. De plus, des stimuloteurs AV séquenfiels à paire “nonobligée” (DVI, MN e(DDD, M) ont été utilisés pour le traitement de lachyarhythmies ventriculaires. Nous avons observé que ľexpérience avec ee type de stimulateur multiprogrammable est favorable chez les patients sans fibrillation auriculaire chronique, qui ont besoin ?un stimutafeur et qui nécéssitent un froilement anti-tachycardique. Ľévolution des stimulateurs du type DDD contribuera sans doute à un traitement encore plus éfficace.Multi-programmable dual-demand AV sequential (DVI, MN) pacemakers were implanted in twenty-three potients (in one of them a DVI, MN unit was used as a VVI, MN with the aid of an atrial plug) with suproventricular tachycardias after electrophysiological studies revealed a great voriety of AV reentry circuits. The latter included tachycardios involving accessory pathways of the Kent type, manifest or concealed Wolff-Parkinson-White syndromes, nodo-ventricular (Mahaim) tracts, “enhanced” AV node for extra AV nodal) pothwaysand dual AV pathways. In addition, multiprogrammable “non-committed” AV sequential (DVI, MN and DDD, M) pacemakers were permanently implonted to treat different forms of ventricular tachyarrhythmias that included: torsode de pointes in the Romano-Ward syndrome and Chagas' cardiomyopathy, ventricular tachycordia which is bradycardia-dependent (in Chagas' cardiomyopathy) and reciprocal beats indueed by, and producing severe hemodynamic derangements in a patient with a conventional VVI unit. With smallsize multiprogrammable units, arrhythmias may be treated by changing parameters non-invasively. By temporary inhibition, one may analyze the underlying rhythm and pacemaker dependency. In potients without chronic atrial flutterJfibrillation who require pacing and possibly tachyarrhythmia control, our experience with multiprogrammable “non-committed” AV sequential pacing has been very satisfactory. The evolution toward newer pacing modes which provide atrial sensing and trackmg (DDD), and thus preserve AV synchrony over a wider range of atrial rates, may contribute even further to successful patient management. This may be applicable to pediatric patients as well.

Is the diagnostic function of pacemakers a reliable source of information about ventricular arrhythmias

Abstract Background: The aim of this study was to evaluate the reliability of pacemaker diagnostic function in diagnosing ventricular arrhythmias. Methods: We compared the occurrence of ventricular ectopic beats in 51 simultaneous 24-hour electrocardiogram (ECG) recordings and pacemaker event counters printouts. The diagnostic function of a pacemaker allowed also for a qualitative assessment in 38 patients. In these cases, the occurrence of complex forms of ventricular arrhythmias was cross-checked for accelerated ventricular rhythms together with ventricular tachycardia, and triplets and couplets. The detection of at least one type of complex ventricular form of arrhythmia, diagnosed by both methods, was considered as an agreement between the methods. Results: The results of ventricular ectopic beat counts differed significantly between the methods. In three (6%) patients, the results were consistent; in 20 (39%) the pacemaker underestimated results; in 28 (55%) they were overestimated. When more liberal criteria of agreement were applied, clinically significant differences were observed in 24 (47%) patients; in seven (29%) patients the count made by the pacemaker was lowered; and in 17 (71%) it was overestimated. Ventricular tachycardias were recorded in 24-hour ECG in eight patients. In three, they were identified by the pacemaker diagnostic function. In five, the pacemaker did not recognize tachycardia (because of its frequency being below 120/min). In nine, tachycardia was recognized falsely. The sensitivity in ventricular tachycardia diagnosis by pacemaker diagnostic function was 38%, specificity — 70%, the value of a positive result — 25%, negative — 81%. Conclusions: The evaluation of ventricular arrhythmias by pacemaker cannot serve as the only reliable diagnostic method of arrhythmias. The presence of a large number of sequences that may correspond to ventricular arrhythmia or failure to sense, should result in verification via 24-hour ECG monitoring. (Cardiol J 2010; 17, 5: 495–502)

Symptomatic Bradyarrhythmias in the Adult: Natural History Following Ventricular Pacemaker Implantation

Pacing and Clinical Electrophysiology, 1982

ventricular pacemaker impiantation. The preimplantation arrhythmias, coexistent medical conditions, the causes of death, and survival course are described for 399 patients who received their initial ventricuJar pacemaker impiantation for a bradyarrhythmia (AV block, sinus node disease, and hyper-sensitjVe carotid sinus syndrome] at the (Jniversity of Michigan from 1961 to 1979. Factors which correlated with a poor survival are elucidated. Survival for those with sinus node disease was virtually identi:;al to those with AV block, with only 63% surviving over jive years. Advanced age and congestive heart failure prior to implantation, and underlying ischemic or hypertensive heart disease portended a poorer survival in both groups. Patients with hypersensitive carotid sinus syndrome had a distinctly better prognosis-no deaths occurred until (he eighth year after pacing. Patients with no underlying heart disease and those with valvular disease did remarkably better than those with an ischemic or myopathic etiology. Apparent progression or complications of the underlying heart disease v/as the major cause of mortality. Sudden death, congestive heart failure, myocardial infarction, and major arrhythmias were the causes of death in 48% of those who died. Implications of improved pacing modalities an late complications and death are discussed.

An overview of diagnosis and management of bradycardia

Archives Of Pharmacy Practice, 2021

Background: Bradycardia is a common finding on physical examination in symptomatic and asymptomatic patients. It can be linked to physiological changes as well as the pathological progression of an underlying disease. The symptoms of bradycardia include lightheadedness, syncope, exercise intolerance, or, in some cases, cardiac arrest. A proper history and physical exam focused on the severity assessment of bradycardia and the underlying condition is essential for the management. Objectives: We aimed to review the literature reviewing bradycardia, along with the possible etiologies, clinical features, diagnosis, and management in both the acute setting and definitively. Methodology: PubMed database was used for article selection, and papers were obtained and reviewed. Conclusion: Bradycardia, while is an innocent presentation in most cases, can progress rapidly into cardiac arrest and death. Proper recognition and risk assessment of which patients might develop the severe sequelae of this presentation is essential in the care process of patients. While this subject has been heavily understudying, the only effective treatment for irreversible bradycardia remains permanent pacing of the heart.

Improved method for evaluating ventriculoatrial conduction before implantation of atrial-sensing dual chamber pacemakers

Journal of the American College of Cardiology, 1985

Pacemaker-mediated tachycardia may occur when a spontaneous ventricular premature depolarization is retrogradely conducted to the atrium with a ventriculoatrial (VA) interval that exceeds the atrial refractory period of an atrial-sensing dual chamber pacemaker. Previous methods for evaluating VA conduction have failed to predict clinical occurrences of pacemaker-mediated tachycardia. In this study, maximal VA intervals after ventricular extrastimuli during atrial or atrioventricular (AV) sequential pacing were compared with intervals measured by the standard method of ventricular pacing. VA intervals were 201 :t 53 ms during ventricular pacing and 224 :t 52 ms after ventricular extrastimuli Atrial sensing allows a demand pacemaker to respond to physiologic variations in heart rate (1). Furthermore, coupling ventricular pacing to atrial sensing with an appropriate atrioventricular (AV) delay may prevent symptoms associated with ventricular pacing, collectively described as the "pacemaker syndrome" (2-10). However , coupling of ventricular pacing to atrial depolarization may be hazardous when ventriculoatrial (VA) conduct ion occurs after a ventricular premature depolarization. When a retrograde atrial depolarization is sensed, a VDO or ODD pacer responds with another premature ventricular stimulus and , if retrograde conduction is consistent, " endless loop" or pacemaker-mediated tachycardia occurs (II). Therefore, physiologic pacing is not optimally utilized because the potential for pacemaker-mediated tachycardia is currently unpredict-From the