Implantable loop recorder (ILR) insertion has historically been performed in a surgical environment such as the electrophysiology (EP) lab. The newest generation loop recorder (Medtronic Reveal LINQ™, Minneapolis, MN, USA) is injectable with potential for implantation in a non‐EP lab setting by advanced practice providers (APPs) facilitating improved workflow and resource utilization. We report the safety and efficacy of injectable ILR placement in the ambulatory care setting by APPs.

Background: Temporary pacemakers (TP) allow short-term ventricular pacing but can be unstable and become ineffective during extended use. Semi-permanent pacemakers (SPP) are active fixation leads connected to an externalized pacemaker generator and may provide a more stable pacing platform. The

Conduction Properties of the Annular Isthmus. Introduction: A functional region of slow conduction located in the inferior right atrium has been postulated to be critical to the induction and maintenance of typical human atrial flutter. We reexamined the potential role of functional conduction delay in the annular isthmus between the tricuspid valve and the inferior vena cava; it is within this region that such delays have been postulated to occur, and where interruption of conduction by radiofrequency energy application has been shown to eliminate typical flutter. Methods and Results: Thirty patients with type I atrial flutter (30 counterclockwise, 14 clockwise) were studied. Counterclockwise and clockwise isthmus activation times adjacent and parallel to the tricuspid valve were measured during three conditions: (1) atrial pacing in sinus rhythm, (2) atrial flutter, and (3) entrainment of atrial flutter. During pacing in sinus rhythm at progressively shorter cycle lengths, both counterclockwise and clockwise isthmus activation times remained unchanged; decremental conduction prior to flutter induction or loss of capture was not observed. Counterclockwise isthmus activation time did not significantly differ during flutter (68 ± 23 msec), inferolateral tricuspid annulus pacing (71 ± 23 msec), or entrainment of flutter (72 ± 23 msec). Similarly, clockwise isthmus activation times did not significantly differ between flutter (65 ± 22 msec), proximal coronary sinus pacing (73 ± 21 msec), or entrainment of flutter (64 ± 15 msec). Conclusion: Decremental conduction is not characteristic of activation through the isthmus when activation is assessed parallel and adjacent to the tricuspid annulus. Functional slowing or conduction delay does not develop in this region during typical atrial flutter.

Limited data suggest that adenosine termination of atrial tachycardia is uncommon. To investigate further the effect of adenosine on atrial tachycardia, adenosine (6–12 mg) was administered during sustained atrial tachycardia in 17 patients. All patients underwent electrophysiological study to exclude other mechanisms of supraventricular tachycardia. Mean patient age was 51 ± 20 years (range 18–82 years). Seven patients had no structural heart disease. The mean atrial tachycardia cycle length was 390 ± 80 msecs (range 260–580). Sustained atrial tachycardia was induced with atrial extrastimuli in 8 patients, and was either incessant at baseline or developed spontaneously during isoproterenol infusion in 9 patients. Adenosine terminated atrial tachycardia in 3 patients (18%), transiently suppressed atrial tachycardia in 4 patients (23%), and produced AV block without affecting tachycardia cycle length in the remaining 10 patients. Adenosine sensitivity was observed in 3 of 8 patients with tachycardias initiated and terminated by atrial extrastimuli, and in 4 of 9 patients with spontaneous, but not inducible tachycardias including 3 of 4 patients with isoproterenol facilitated tachycardias. Of multiple clinical and electrophysiological variables examined as potential predictors of adenosine sensitivity, only isoproterenol facilitation of spontaneous or inducible sustained tachycardia predicted adenosine sensitivity (P = 0.02). These observations suggest that adenosine‐sensitive atrial tachycardia may be more common than previously recognized. Adenosine sensitivity does not appear to be specific for tachycardia mechanism and cannot be predicted by response to pacing. Atrial tachycardias dependent on β‐adrenergic stimulation are most likely to be terminated by adenosine.

Occasional patients have excessive defibrillation energy requirements despite appropriate transvenous defibrillation lead position and modification of defibrillation waveform and configuration. Preliminary data suggest that use of subcutaneous defibrillation electrode arrays with nonthoracotomy systems is associated with a substantial reduction in defibrillation threshold. The current operative approach to subcutaneous lead array implantation involves the use of a separate left chest incision. We present two cases in which implantation of a subcutaneous lead array in combination with a transvenous defibrillation electrode was performed via a single infraclavicular incision and associated with a reduction in defibrillation threshold. Such an approach simplifies implantation and avoids the potential morbidity of the additional incision required of a left lateral chest approach.

Pacing and Clinical ElectrophysiologyVolume 17, Issue 4 p. 637-664 The Clinical Significance of Nonsustained Ventricular Tachycardia: Current Perspectives CHARLES KINDER, CHARLES KINDER Electrophysiology Laboratory, Loyola University Medical Center, Maywood, IllinoisSearch for more papers by this authorPAUL TAMBURRO, PAUL TAMBURRO Electrophysiology Laboratory, Loyola University Medical Center, Maywood, IllinoisSearch for more papers by this authorDOUGLAS KOPP, DOUGLAS KOPP Electrophysiology Laboratory, Loyola University Medical Center, Maywood, IllinoisSearch for more papers by this authorJOHN KALL, JOHN KALL Electrophysiology Laboratory, Loyola University Medical Center, Maywood, IllinoisSearch for more papers by this authorBRIAN OLSHANSKY, BRIAN OLSHANSKY Electrophysiology Laboratory, Loyola University Medical Center, Maywood, IllinoisSearch for more papers by this authorDAVID WILBER, Corresponding Author DAVID WILBER Electrophysiology Laboratory, Loyola University Medical Center, Maywood, IllinoisAddress for reprints: David Wilber, M.D., Director, Cardiac Electrophysiology, Loyola University Medical Center, 2160 S. First Ave., Rm. 1847 Russo, Maywood, IL 60153–5500. Fax: (708) 216-6829.Search for more papers by this author CHARLES KINDER, CHARLES KINDER Electrophysiology Laboratory, Loyola University Medical Center, Maywood, IllinoisSearch for more papers by this authorPAUL TAMBURRO, PAUL TAMBURRO Electrophysiology Laboratory, Loyola University Medical Center, Maywood, IllinoisSearch for more papers by this authorDOUGLAS KOPP, DOUGLAS KOPP Electrophysiology Laboratory, Loyola University Medical Center, Maywood, IllinoisSearch for more papers by this authorJOHN KALL, JOHN KALL Electrophysiology Laboratory, Loyola University Medical Center, Maywood, IllinoisSearch for more papers by this authorBRIAN OLSHANSKY, BRIAN OLSHANSKY Electrophysiology Laboratory, Loyola University Medical Center, Maywood, IllinoisSearch for more papers by this authorDAVID WILBER, Corresponding Author DAVID WILBER Electrophysiology Laboratory, Loyola University Medical Center, Maywood, IllinoisAddress for reprints: David Wilber, M.D., Director, Cardiac Electrophysiology, Loyola University Medical Center, 2160 S. First Ave., Rm. 1847 Russo, Maywood, IL 60153–5500. Fax: (708) 216-6829.Search for more papers by this author First published: April 1994 https://doi.org/10.1111/j.1540-8159.1994.tb02400.xCitations: 16AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat Citing Literature Volume17, Issue4April 1994Pages 637-664 RelatedInformation

The prognostic significance of a de novo sustained ventricular tachyarrhythmia occurring during a dobutamine infusion is unknown. This study was performed to determine (1) the risk of recurrent ventricular arrhythmia, (2) the safety of future dobutamine infusions, and (3) the role of electrophysiologic testing. The study population consisted of 15 patients, six with coronary artery disease, and nine with idiopathic dilated cardiomyopathy. Mean ejection fraction was 17% +/- 4.1%. The arrhythmia during the infusion was ventricular tachycardia in 13 patients and ventricular fibrillation in two patients and was not associated with preceding hemodynamic instability, electrolyte abnormality, digoxin toxicity, or antiarrhythmic drug therapy. During electrophysiologic testing, 7 of 15 patients had inducible ventricular tachycardia. All patients with inducible ventricular tachycardia were treated with either antiarrhythmic drugs, defibrillators, or ablation. Over a 12.3 +/- 5.2 month follow-up period, all 15 patients received further dobutamine treatment. Seven of 15 (47%) had a recurrent sustained ventricular tachyarrhythmia. Although three of seven recurrences occurred during a dobutamine infusion, all three of these patients had hemodynamically unstable conditions and were receiving high-dose (> 10 micrograms/kg/min) therapy at the time of recurrence. The other four recurrent arrhythmias were not associated with clear precipitating factors. Ejection fraction, origin of left ventricular dysfunction, and inducibility at baseline electrophysiologic testing did not predict arrhythmia recurrence. The de novo occurrence of a sustained ventricular tachyarrhythmia during dobutamine infusion is associated with a significant risk of arrhythmia recurrence (47%), which can occur in the presence or absence of dobutamine therapy.(ABSTRACT TRUNCATED AT 250 WORDS)

Over a 3 year period, 140 patients underwent attempted implanation of an automatic cardioverter/defibrillator using the nonthoracotomy lead (NTL) system. Indications included sustained monomorphic ventricular (VT) (84), nonsustained (VT) with poor ventricular function (7), ventricular fibrillation (VF) (31), VT/VF (16), and familial long QT syndrome (2). A total of 115 males and 25 females comprised the group; mean age was 57 +/- 14 years; 59% had previous coronary bypass and/or valve surgery. Mean left ventricular ejection fraction was 31 +/- 14%, cardiac index was 2.4+/-1 L/m2, and systolic pulmonary artery pressure was 42+/-15 mm Hg. Under general anesthesia the NTL was introduced through the left subclavian vein. The subcutaneous patch and generator were placed posteriorly on the serratus muscle and left upper quadrant, respectively. The length of the procedure was 117 +/- 46 minutes, and the mean number of defibrillation shocks for a successful implant was 9 +/- 4. A total of 110 patients (79%) had successful implantations. Failures were caused by a high defibrillation threshold (27) and the inability to place the right ventricular lead (3). Predictors of failure included preoperative antiarrhythmic drugs and cardiac index less-than-or-equal-to 1.8 +/- 4. Only 3 patients (2.0%) died postoperatively, from heart failure (2) and chronic heart transplant rejection (1). migration or dislodgement (8), infection (1), and hematoma (4). In summary, the NTL system provides an alternative to epicardial systems in patients requiring cardioverter/defibrillator implantation.

Catheter ablation has been used to treat atrioventricular node reentrant and atrioventricular reentrant tachycardias with extremely high success rates. The suitability of catheter ablation for treatment of atrial tachycardia, a much less common type of supraventricular tachycardia, has not been well addressed. Fifteen patients (8 females) ranging from 10 to 83 years (mean 38 +/- 22) were referred for catheter ablation of supraventricular tachycardia. The diagnosis of atrial tachycardia was established by standard electrophysiologic techniques. A combination of activation and pace mapping was used to identify a suitable site for radiofrequency current catheter ablation. Medical therapy was unsuccessful in all but 1 patient. Two patients had surgically corrected congenital heart disease, 2 had coronary artery disease and 1 had dilated cardiomyopathy. Seven patients had depressed left ventricular function. Six patients had incessant tachycardias. Presumed tachycardia mechanism was automatic in 11 patients and reentrant in 4. Mean tachycardia cycle length was 372 +/- 74 ms. Catheter ablation was acutely successful in 12 patients (80%) with application of 11.1 +/- 6.6 lesions at a mean voltage of 60 +/- 9 V. In the other 3 patients, 16 to 38 lesions were applied. At a mean follow-up of 18.5 +/- 6.5 months, 2 patients have had recurrences with different P-wave morphologies and underwent a second successful catheter ablation procedure. An additional 2 patients had recurrences with the same P-wave morphology and 1 underwent a second successful catheter ablation procedure. Thus, radiofrequency ablation can be used in a diverse population of patients with atrial tachycardia with an acute success rate of 80% and a long-term success rate of 73%.

Over a 2-year period, 110 patients underwent attempted implantation of an automatic cardioverter-defibrillator using the nonthoracotomy lead system. Indications included sustained monomorphic ventricular (n = 62), nonsustained with poor ventricular function (n = 7), ventricular fibrillation (n = 21), ventricular tachycardia/fibrillation (n = 18), and familial long QT syndrome (n = 2). There were 90 male and 20 female patients. Mean age was 57 +/- 15 years. Sixty percent had previous coronary bypass or valve operations, or both. Mean left ventricular ejection fraction was 30% +/- 14%, cardiac index was 2.4 +/- 0.9 L/m2, and systolic pulmonary artery pressure was 41 +/- 14 mm Hg. Under general anesthesia, the nonthoracotomy lead was introduced through the left subclavian vein. The subcutaneous patch and generator were placed posteriorly on the serratus muscle and left upper quadrant, respectively. The length of the procedure was 116 +/- 44 minutes and the mean number of defibrillation shocks for a successful implant was 8 +/- 4. Eighty-five patients (77%) had successful implantations. Failures were due to high defibrillation threshold (n = 23) and inability to place a right ventricular lead (n = 2). Predictors of failure included preoperative antiarrhythmic drugs and cardiac index of 1.8 +/- 4 L/m2 or less (p = 0.004). Three patients (2.7%) died after the operation of heart failure (n = 2) and chronic heart transplant rejection (n = 1). Complications included lead migration or dislodgment (n = 8), infection (n = 1), and hematoma (n = 3). In summary, the nonthoracotomy lead system may provide an alternative in patients undergoing cardioverter-defibrillator implantation.

Electropbysiology of the Sinus Node. Differentiation of normal from abnormal sinus nodal function is frequently difficult because the electrocardiographic and electrophysiologic presentations of abnormal and normal sinus nodal function are quite diverse. The autonomic nervous system greatly influences sinus nodal function, making this differentiation even more complicated. Data obtained from the recording of sinus nodal electrogram in animals and humans have helped in elucidating changes in automaticity and conduction of the sinus node. In this review, we provide examples of rhythms related to normal and abnormal sinus nodal function. (J Cardiovasc Electrophysiol, Vol. 3, pp. 187–197, April 1992)

HomeCirculationVol. 65, No. 2Esophageal pacing: a diagnostic and therapeutic tool. Free AccessAbstractPDF/EPUBAboutView PDFSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessAbstractPDF/EPUBEsophageal pacing: a diagnostic and therapeutic tool. J J Gallagher, W M Smith, C R Kerr, J Kasell, L Cook, M Reiter, R Sterba and M Harte J J GallagherJ J Gallagher , W M SmithW M Smith , C R KerrC R Kerr , J KasellJ Kasell , L CookL Cook , M ReiterM Reiter , R SterbaR Sterba and M HarteM Harte Originally published1 Feb 1982https://doi.org/10.1161/01.CIR.65.2.336Circulation. 1982;65:336–341 eLetters(0)eLetters should relate to an article recently published in the journal and are not a forum for providing unpublished data. Comments are reviewed for appropriate use of tone and language. Comments are not peer-reviewed. Acceptable comments are posted to the journal website only. Comments are not published in an issue and are not indexed in PubMed. Comments should be no longer than 500 words and will only be posted online. References are limited to 10. Authors of the article cited in the comment will be invited to reply, as appropriate.Comments and feedback on AHA/ASA Scientific Statements and Guidelines should be directed to the AHA/ASA Manuscript Oversight Committee via its Correspondence page.Sign In to Submit a Response to This Article Previous Back to top Next FiguresReferencesRelatedDetailsCited By (2021) The ECG Recording Clinical Electrocardiography, 10.1002/9781119536475.ch6, (56-68), Online publication date: 6-Dec-2021. (2021) Limitations of the Conventional ECG Clinical Electrocardiography, 10.1002/9781119536475.ch25, (552-570), Online publication date: 6-Dec-2021. 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