Routine venography should be performed before the device upgrade. Clinicians should not be unconcerned because of the lack of symptoms following lead-related venous occlusion. Knowledge of collateral anatomy is essential for future interventional plans. The venous pathway's return to the right atrium may entail risks to patient outcomes.

Ventricular sensing relies on the analysis of a local intracardiac electrogram in reference to the QRS on the surface electrocardiogram. If both signals do not coincide in time, there is a delay in sensing intrinsic ventricular activity. We evaluated possible differences in the electrical delay between the mid-septum and apex as determined by the right ventricular (RV) lead position using a pacing system analyzer (PSA) during conventional pacemaker implantation. Patients without significant heart disease and intrinsic atrioventricular conduction underwent their first Medtronic (Minneapolis, MN, USA) or Abbott (Chicago, IL, USA) dual-chamber pacemaker implantation with the RV lead first positioned at the apex and then subsequently at the mid-septum. Real-time ventricular sensing data were obtained through PSA to determine the electrical delay Q-VS value as the time difference between the QRS and the released RV-sensed event marker "VS." Among 212 patients, 139 had narrow QRS and 73 had complete right bundle branch block (RBBB). Overall, both narrow QRS and RBBB patients exhibited shorter Q-VS lengths at the mid-septum compared to the apex (50.4 ± 24.2 ms and 66.7 ± 32.3 ms vs. 63.9 ± 27.6 ms and 71.7 ± 32.2 ms; P < .0001 and P < .001, respectively). The Q-VS in patients with Abbott devices was significantly shorter compared to that in patients with Medtronic devices at both the mid-septum and the apex in both patient groups (P < .0001). In conclusion, RV lead positioning at the mid-septum is associated with a shorter electrical delay compared to positioning at the apex in both narrow QRS and RBBB patients.

Abstract Background Pacemaker implantation involves intraoperative testing of ventricular sensing using a device called a pacing system analyzer (PSA). The value obtained is expected to correspond to those taken by the pacemaker after its implantation. This study determined the latency period for sensing intracardiac electrogram (EGM) by the right ventricular (RV) lead. Methods Patients without significant heart disease and underlying intrinsic atrioventricular (AV) conduction underwent Medtronic or Abbott dual‐chamber pacemaker implantation with the RV lead positioned on the mid‐septum. Real‐time sensing data were obtained through PSA and after pacemaker implantation to evaluate latency as the time interval Q‐VS between the onset of QRS on surface electrocardiogram and the sensed EGM by the RV lead. Results Of 157 patients, 105 had narrow QRS (<120 ms) and 52 had wide QRS of complete right bundle branch block (RBBB). Both narrow‐QRS and RBBB patients had longer sensing latency through PSA (50.9 ± 24.2 and 67.8 ± 32.9 ms, respectively) than through pacemaker (18.2 ± 12.8 and 31.2 ± 14.8 ms, respectively, both p < 0.001). RBBB patients had longer sensing latency compared with narrow QRS patients, either through PSA or through pacemaker (p < 0.001). The sensing latency of Medtronic recipients was longer than those of Abbott in narrow‐QRS (p < 0.05), but not in RBBB. Conclusion We demonstrated longer RV lead sensing latency (1) through PSA than through pacemaker, (2) in RBBB than in narrow‐QRS, and (3) in Medtronic pacemakers compared with Abbott pacemakers. Knowledge of sensing latency helps the optimization of the AV delay.

Future CardiologyVol. 17, No. 7 Clinical SnapshotVentricular activation during transcutaneous and transvenous pacingFani Zagkli, Christina Jachrista, Panagiotis Chronopoulos & John ChiladakisFani ZagkliDepartment of Cardiology, University Hospital of Patras, Rion, Greece, Christina JachristaDepartment of Cardiology, University Hospital of Patras, Rion, Greece, Panagiotis ChronopoulosDepartment of Cardiology, University Hospital of Patras, Rion, Greece & John Chiladakis *Author for correspondence: Tel.: +30 2610 99071; E-mail Address: chil@otenet.grhttps://orcid.org/0000-0002-5930-5226Department of Cardiology, University Hospital of Patras, Rion, GreecePublished Online:14 Apr 2021https://doi.org/10.2217/fca-2020-0209AboutSectionsView ArticleView Full TextPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareShare onFacebookTwitterLinkedInReddit View articleKeywords: cardiac imagingcardiopulmonary resuscitationelectroanatomic mappingpacingReferences1. Neumar RW, Otto CW, Link MS et al. Part 8: adult advanced cardiovascular life support: 2010 AHA guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. Circulation 122(3 Suppl. 18), 729–767 (2010).Crossref, Medline, Google Scholar2. Kusumoto FM, Schoenfeld MH, Barrett C et al. 2018 ACC/AHA/HRS guideline on the evaluation and management of patients with bradycardia and cardiac conduction delay. Circulation 140(8), e382–e482 (2019).Medline, Google Scholar3. Zagkli F, Georgakopoulou A, Chiladakis J. The electrocardiogram of ventricular capture during transcutaneous cardiac pacing. J. Electrocardiol. 58, 119–124 (2020).Crossref, Medline, Google ScholarFiguresReferencesRelatedDetailsCited ByClinical Snapshot: viewing the future in Future CardiologyJulia Titova & Laura Dormer14 April 2021 | Future Cardiology, Vol. 17, No. 7 Vol. 17, No. 7 Follow us on social media for the latest updates Metrics Downloaded 41 times History Received 28 November 2020 Accepted 26 February 2021 Published online 14 April 2021 Published in print October 2021 Information© 2021 Future Medicine LtdKeywordscardiac imagingcardiopulmonary resuscitationelectroanatomic mappingpacingFinancial & competing interests disclosureThe authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.No writing assistance was utilized in the production of this manuscript.Informed consent disclosureThe authors state that they have obtained verbal and written informed consent from the patient/patients for the inclusion of their medical and treatment history within this clinical snapshot.PDF download

Ιn a 76-year old man with a dual-chamber ICD implanted five years ago, dizzy spells and significant bradycardia on Holter were not initially recognized as inhibition of bradycardia pacing, due to oversensing. Hospital admission was deemed necessary only after repetitive ICD shocks attributed to right ventricular pace-sense lead fracture. The need to ensure adequate ICD antibradycardia backup pacing in pacing-dependent patients when deleterious sensing errors occur, cannot be overemphasized.

The authors declare that there are no conflict of interests.

BACKGROUND:The electrocardiographic (ECG) effects of transcutaneous cardiac pacing (TCP) on ventricular repolarization have not been studied in detail. This study evaluated the influence of TCP on ventricular repolarization. The results were compared with those obtained by conventional transvenous right ventricular pacing (TVP). METHODS:Sixty-two patients with spontaneous bradycardia and standard indication for pacemaker or implantable cardioverter-defibrillator implantation were enrolled. Patients were divided into two groups based on the presence or not of structural heart disease (SHD). Surface 12-lead ECG characteristics of ventricular depolarization (QRS complex) and repolarization (QT and JT intervals, Tpeak to Tend interval [TpTe], QT dispersion [QTd], TpTe dispersion [TpTe-d], and TpTe/QT ratio) were recorded at baseline before device implantation (45 ± 5 beats/min) and were compared with corresponding data during short periods of TCP and TVP at a similar increased heart rate (81 ± 6 beats/min). RESULTS:Both TCP and TVP compared with baseline measures significantly increased the QRS complex and the QTc/JTc intervals regardless of SHD status (P < .001), and QTc-d and TpTe particularly in the patients without SHD (P < .05). TCP caused greater QRS prolongation than TVP in patients without SHD (P < .05), but it was associated with lower TpTe and TpTe/QT in patients without SHD as well as lower QTc-d in patients with SHD (P < .05). CONCLUSION:TCP produces greater lengthening of ventricular repolarization than TVP, but lesser increase of ECG markers of ventricular dispersion of repolarization.

Clinical manifestation of late onset recurrent monomorphic ventricular tachycardia (VT) in patients with normal left ventricular ejection fraction may elude diagnosis despite elaborate testing. This report describes a 67-year-old woman with structurally normal heart who presented with recurrent VT in the absence of predisposing factors. Repeated extensive diagnostic testing, including magnetic resonance imaging and coronary angiography, did not disclose any abnormality. An implantable cardioverter-defibrillator was placed following noninducibility of the third episode of VT at electrophysiological study. Patient's 12-lead electrocardiogram in normal sinus rhythm revealed permanent QRS fragmentation as well as T-wave inversions as the only warning features that heralded the impending appearance of recurrent VTs over the course of 5 years follow-up.

Background: Transcutaneous cardiac pacing (TCP) is deeply entwined with the problem of assessing ventricular capture on the electrocardiogram (ECG). We sought clarification of ventricular capture during TCP. Methods: We studied one hundred and ten patients (75 +/- 12 years) with bradycardia who underwent pacemaker or implantable cardioverter-defibrillator implantation. The cohort was stratified by structural heart disease (SHD) status and presence of narrow or wide QRS during spontaneous heart rhythm. We compared 12 lead ECG data at baseline (48 +/- 7 beats/min) with those of TCP as well as of transvenous pacing (TVP) at a similar increased heart rate (76 +/- 9 beats/min) to ensure constant ventricular capture. The QT interval was corrected for heart rate (QTc) using Bazett's method as well as by the Hodges and Rautaharju's formulae depending on the presence of narrow or wide QRS at baseline. Electromechanical coupling was assessed by noninvasive arterial pressure measurement. Results: TCP (median 80 mA) produced a QRS pattern resembling left bundle branch block. Overall, both TCP and TVP induced significant QRS and QTc prolongations when compared with baseline measures (p < 0.001). TCP created narrower QRS than TVP in those patients with SHD and narrow QRS (p < 0.006). There was no significant QTc duration difference between TCP and TVP. Mean arterial pressure underwent similar significant decrease following either TCP or TVP over baseline (p < 0.001), without difference between the two pacing approaches in any patient group. Conclusion: TCP is associated with similar ECG and hemodynamic responses to those of TVP, regardless of the presence of SHD. (C) 2019 Elsevier Inc. All rights reserved.

Η πρόληψη του αιφνιδίου καρδιακού θανάτου συνιστά πρωταρχικό στόχο της αρρυθμιολογίας μe τους eμφυτeύσιμους καρδιομeτατροπeίς-απινιδωτές να αποτeλούν ακρογωνιαίο λίθο στην προσπάθeια αυτή. Ωστόσο, η διαστρωμάτωση αρρυθμιολογικού κινδύνου στα πλαίσια πρωτογeνούς πρόληψης παραμένeι προβληματική, καθώς βασίζeται eξ ολοκλήρου στο κλάσμα eξωθήσeως της αριστeράς κοιλίας. Μe τον τρόπο αυτό, υφίστανται πeριπτώσeις αφ’ eνός ασθeνών που λαμβάνουν απινιδωτή δίχως να ωφeλούνται, αλλά υποκeίμeνοι σe όλeς τις eπιπλοκές eκ της eμφύτeυσης, αφ’ eτέρου ασθeνών που στeρούνται αυτής της δυνητικά σωτήριας συσκeυής. Μe το παρόν κeίμeνο, eπιχeιρeίται να προταθeί μία eναλλακτική, διαβαθμισμένη και ηλeκτροφυσιολογικά καθοδηγούμeνη προσέγγιση στην διαστρωμάτωση αρρυθμιολογικού κινδύνου ούτως ώστe να eπιτeυχθeί η ορθολογικότeρη και αποτeλeσματικότeρη αξιοποίηση του απινιδωτή ως μέσο πρόληψης αιφνιδίου καρδιακού θανάτου. Eπισημαίνeται ότι δeν eπέχeι θέση κατeυθυντηρίων οδηγιών αλλά αποτeλeί το eπιστέγασμα συζητήσeως και ανταλλαγής απόψeων μeταξύ των μeλών της αρμόδιας ομάδας eργασίας της Eλληνικής Καρδιολογικής Eταιρeίας.

BackgroundThe study was designed to investigate the effect of heart rate and pacing mode on QRS fragmentation (f-QRS). Moreover, the usefulness of f-QRS in distinguishing patients with impaired left ventricular ejection function (EF) and ventricular tachycardia (VT) from patients with normal EF was assessed. MethodsThree hundred and six recipients, with dual-chamber device, with intrinsic narrow or wide QRS complex and preserved atrioventricular conduction were grouped into normal-EF or impaired-EF VT. We analyzed intrinsic narrow f-QRS and wide f-QRS as well as ventricular-paced f-QRS following different heart rates (baseline, 100bpm) and pacing modes. ResultsIn the baseline state, overall, patients with impaired-EF VT (359%), compared to those with normal-EF, had more f-QRS (56% vs 27%, P<.001) and ventricular-paced f-QRS (62% vs 16%, P<.0001). Ventricular pacing conferred both at baseline and at higher heart rate more ventricular-paced f-QRS in patients with impaired-EF VT than in normal-EF (P<.001). Detection of ventricular-paced f-QRS markedly improved overall specificity (84%) and positive predictive value (91%) in identifying patients with impaired-EF VT. ConclusionsIncreased heart rate or/and ventricular pacing uncover QRS fragmentations. Detection of ventricular-paced f-QRS adds value toward noninvasive identification of patients with impaired-EF VT.

AIM We assessed whether antiarrhythmic drug-induced QT interval prolongation affects left ventricular function. METHODS Study population included 54 patients with symptomatic recent onset atrial fibrillation spontaneously cardioverted to sinus rhythm. Electrocardiographic and echocardiographic studies were done before initiating and after achieving drug's steady state. RESULTS Significantly prolonged corrected QT interval (QTc) was noticed following only sotalol and amiodarone. The corrected precontraction time increased after sotalol (p = 0.005) and amiodarone (p = 0.017), not propafenone (p = 0.139). Analysis results between ΔEF and ΔQTc, ΔEF and ΔQTc(p), ΔE/e' and ΔQTc, ΔE/e' and ΔQTc(p) for amiodarone group were (p = 0.66, p = 0.20, p = 0.66, p = 0.33), for sotalol (p = 0.36, p = 0.51, p = 0.44, p = 0.33) and for propafenone (p = 0.38, p = 0.12, p = 0.89, p = 0.61), respectively. CONCLUSION QT interval prolongation following antiarrhythmic therapy does not affect significantly left ventricular function.

Background: We evaluated the effect of heart rate on the intrinsic and the ventricular-paced QRS duration in implanted device recipients with normal or reduced left ventricular ejection fraction (EF).Methods: We studied 239 outpatients with preserved intrinsic ventricular activation and normal (n = 92) or reduced (n = 147) EF who had apical (RVA) or mid-septal (RVS) right ventricular lead position. The QRS duration was measured at baseline and during atrial-based pacing at increased heart rate to ensure intrinsic or ventricular-paced QRS activation.Results: The heart rate increase shortened the intrinsic QRS only in patients with normal EF, and further prolonged the ventricular-paced QRS in patients with reduced EF and either narrow or wide QRS (p < 0.001), irrespective of RVA or RVS pacing (p < 0.01).Conclusion: Heart rate increase is associated with further QRS prolongation in patients with reduced EF, regardless of RVA or RVS pacing site. (C) 2015 Elsevier Inc. All rights reserved.

To the Editor: Despite the best efforts of healthcare providers, guideline-conform treatment failure is expected to occur, particularly in real-world emergency situations [1]. In the case reported here, a 79-year-old man with a history of coronary artery disease and implantation of a cardioverter defibrillator (ICD) presented to the emergency room with recurrent ventricular tachycardia. The junior physician-incharge applied an external biphasic DC shock of 200 J to the patient, holding the paddle in one hand and placing it directly over the ICD (Electronic Supplementary Material Fig. 1)—but without success. Arrhythmic stability was finally achieved by multiple, appropriate ICD shocks and intravenous amiodarone. Subsequent device interrogation and defibrillation testing of the ICD showed no instance of device malfunction. Coronary angiography revealed arteries free of significant stenoses. Strong electromagnetic interference induced by transthoracic DC shocks may cause permanent damage or alter the operation of the implanted device [2]. When attempting external defibrillation, clinicians are advised to place the paddles/pads as far as possible from any pulse generator and to choose biphasic over monophasic shock waveforms. A less deleterious effect might be expected if the orientation of the applied electric field is perpendicular—and not parallel—to the device with its lead(s), whereas if the device is located in the left pectoral region, an anterior– apex paddle position may be also acceptable. With an anterior–posterior electrode orientation and a distance between device and hand-held shock electrode of [8 cm, Manegold et al. [3] did not observe any dysfunction in patients with rightor left-sided implanted pacemakers or ICDs treated with external cardioversion for atrial fibrillation.

Journal of Cardiovascular ElectrophysiologyVolume 24, Issue 9 p. 1055-1055 EP Image Ischemia-Triggered Pause-Dependent Polymorphous Ventricular Tachycardia Storm Complicating Acute Myocardial Infarction Terminated by Complete Coronary Reperfusion JOHN CHILADAKIS M.D., F.E.S.C., Corresponding Author JOHN CHILADAKIS M.D., F.E.S.C. Cardiology Department, University Hospital of Patra, Rion-Patra, GreeceAddress for correspondence: John Chiladakis, M.D., F.E.S.C., Agias Lavras, Patra 26504, Greece. Fax: +011-30-2610-990-713; E-mail: [email protected]Search for more papers by this authorFANI ZAGKLI M.D., FANI ZAGKLI M.D. Cardiology Department, University Hospital of Patra, Rion-Patra, GreeceSearch for more papers by this authorKONSTANTINOS CHOUCHOULIS M.D., KONSTANTINOS CHOUCHOULIS M.D. Cardiology Department, University Hospital of Patra, Rion-Patra, GreeceSearch for more papers by this authorDIMITRIOS ALEXOPOULOS M.D., F.E.S.C., F.A.C.C., DIMITRIOS ALEXOPOULOS M.D., F.E.S.C., F.A.C.C. Cardiology Department, University Hospital of Patra, Rion-Patra, GreeceSearch for more papers by this author JOHN CHILADAKIS M.D., F.E.S.C., Corresponding Author JOHN CHILADAKIS M.D., F.E.S.C. Cardiology Department, University Hospital of Patra, Rion-Patra, GreeceAddress for correspondence: John Chiladakis, M.D., F.E.S.C., Agias Lavras, Patra 26504, Greece. Fax: +011-30-2610-990-713; E-mail: [email protected]Search for more papers by this authorFANI ZAGKLI M.D., FANI ZAGKLI M.D. Cardiology Department, University Hospital of Patra, Rion-Patra, GreeceSearch for more papers by this authorKONSTANTINOS CHOUCHOULIS M.D., KONSTANTINOS CHOUCHOULIS M.D. Cardiology Department, University Hospital of Patra, Rion-Patra, GreeceSearch for more papers by this authorDIMITRIOS ALEXOPOULOS M.D., F.E.S.C., F.A.C.C., DIMITRIOS ALEXOPOULOS M.D., F.E.S.C., F.A.C.C. Cardiology Department, University Hospital of Patra, Rion-Patra, GreeceSearch for more papers by this author First published: 11 March 2013 https://doi.org/10.1111/jce.12139 J Cardiovasc Electrophysiol, Vol. 24, p. 1055, September 2013. No disclosures. Read the full textAboutPDF 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 onEmailFacebookTwitterLinkedInRedditWechat No abstract is available for this article. Volume24, Issue9September 2013Pages 1055-1055 RelatedInformation

To the Editor: Early and strong platelet inhibition is highly desirable in patients with ST-segment elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PCI). Ticagrelor, which has direct action on the P2Y12 receptor and no need for previous metabolic

Objectives: To determine the optimal method of ventricular repolarization assessment in predicting torsade de pointes (Tdp) in acquired long QT syndrome (LQTS) within the context of the recommended cutoff levels of concern for QT/corrected QT (QTc) interval prolongation. Methods: Twenty-nine patients with LQTS and Tdp (age 66 ± 11 years) and matched controls were studied. Standard 12-lead electrocardiograms were utilized to evaluate ventricular repolarization by using six different QT/JT heart rate correction methods. We compared the distribution of QT/QTc and JT/corrected JT intervals of patients who experienced Tdp with (1) the corresponding intervals in the matched controls and (2) the recommended cutoff levels for QT/JT interval prolongation. Results: Patients with Tdp (23 with narrow QRS, 6 with wide QRS) had longer ventricular repolarization intervals than controls (p < 0.001). For patients with narrow QRS, the QTc interval as determined firstly by the method of Hodges (t = 7.56, c = 0.933, p < 0.001), followed by the Nomogram and Fridericia methods, best discriminated Tdp patients from controls and provided the optimal balance between sensitivity and specificity at all three cutoff levels. For patients with wide QRS, the JT interval or, alternatively, the Hodges method seemed most useful. Conclusions: Assessment of ventricular repolarization by the Hodges, Nomogram and Fridericia methods performs best in identifying subsequent Tdp.

AIMSWe aimed to facilitate the assessment of the QT interval duration during conventional right ventricular pacing (VP) by uncovering relationships with the underlying QT interval during intrinsic atrioventricular conduction (IC).METHODS AND RESULTSThe study patients (n = 122, age 68 ± 11 years) were dual-chamber device recipients with preserved IC and narrow QRS complexes. Patients were classified into either 'normal-QT' (n = 70) or 'prolonged-QT' (n = 52) group. Incremental atrial pacing rates were exercised to record serial QT/JT intervals over 5 min periods in IC mode and then in VP mode. Six different QT correction methods for heart rate were applied to assess the effect (i) of pacing mode (IC vs. VP) and (ii) of heart rate on the derived QT(c)/JT(c) intervals by mixed-effects linear models. Following VP, the uncorrected QT/JT intervals as well as the JTc intervals shortened (P < 0.001), whereas the QTc intervals prolonged (P < 0.001). In both patient groups, the Framingham and Nomogram methods demonstrated the optimal balance to assess QTc, with low heart rate dependence during VP and minimal interaction between pacing mode and heart rate. The Rautaharju formula provided excellent correction for the QT changes induced by VP, but the QTc interval responded differently to rate changes in IC vs. VP mode. Bazett's formula exaggerated QTc/JTc rate dependency during VP.CONCLUSIONThe Framingham and Nomogram correction methods perform most reliably in assessing the underlying QT interval during IC from the ventricular paced QT interval.