An electrographic AV optimization for the maximum integrative atrioventricular and ventricular resynchronization in CRT

Background Atrioventricular (AV) delay could affect AV and ventricular synchrony in cardiac resynchronization therapy (CRT). Strategies to optimize AV delay according to optimal AV synchrony (AVopt-AV) or ventricular synchrony (AVopt-V) would potentially be discordant. This study aimed to explore a new AV delay optimization algorithm guided by electrograms to obtain the maximum integrative effects of AV and ventricular resynchronization (opt-AV). Methods Forty-nine patients with CRT were enrolled. AVopt-AV was measured through the Ritter method. AVopt-V was obtained by yielding the narrowest QRS. The opt-AV was considered to be AVopt-AV or AVopt-V when their difference was < 20 ms, and to be the AV delay with the maximal aortic velocity–time integral between AVopt-AV and AVopt-V when their difference was > 20 ms. Results The results showed that sensing/pacing AVopt-AV (SAVopt-AV/PAVopt-AV) were correlated with atrial activation time (Pend-As/Pend-Ap) (P < 0.05). Sensing/pacing AVopt-V (SAVopt-V/PAVopt-V) was correlated with the intrinsic AV conduction time (As-Vs/Ap-Vs) (P < 0.01). The percentages of patients with more than 20 ms differences between SAVopt-AV/PAVopt-AV and SAVopt-V/PAVopt-V were 62.9% and 57.1%, respectively. Among them, opt-AV was linearly correlated with SAVopt-AV/PAVopt-AV and SAVopt-V/PAVopt-V. The sensing opt-AV (opt-SAV) = 0.1 × SAVopt-AV + 0.4 × SAVopt-V + 70 ms (R2 = 0.665, P < 0.01) and the pacing opt-AV (opt-PAV) = 0.25 × PAVopt-AV + 0.5 × PAVopt-V + 30 ms (R2 = 0.560, P < 0.01). Conclusion The SAVopt-AV/PAVopt-AV and SAVopt-V/PAVopt-V were correlated with the atrial activation time and the intrinsic AV conduction interval respectively. Almost half of the patients had a > 20 ms difference between SAVopt-AV/PAVopt-AV and SAVopt-V/PAVopt-V. The opt-AV could be estimated based on electrogram parameters.

A method for accurately and dynamically optimising pacemaker atrio-ventricular delay timing using implantable physiological biomarkers

Funding Acknowledgements Type of funding sources: Other. Main funding source(s): BRAVO trial: BHF SP/10/002/28189, FS/10/038, FS/11/92/29122, FS/13/44/30291) National Institute for Health Research Imperial Biomedical Research Centre. HOPE-HF trial: British Heart Foundation (CS/15/3/31405, FS/13/44/30291, FS/15/53/31615, FS/14/27/30752, FS/10/038). Introduction The optimal atrioventricular (AV) delay for implantable cardiac devices can be derived by echocardiography or beat-by-beat blood pressure measurements. However, both of these approaches are labour intensive and neither could be incorporated into an implantable cardiac device for frequent repeated optimisations. Laser Doppler perfusion monitoring (LDPM) measures blood flow through tissue. LDPM has been miniaturised ready to be incorporated into future implantable cardiac devices. Purpose We studied if LDPM is a clinically reliable alternative method to blood-pressure measurements to determine optimal AV delay. Methods Data from 58 patients undergoing 94 clinical AVD optimisations using LDPM and simultaneous non-invasive beat-by-beat blood pressure was obtained. The optimal AV delay for each method and for each optimisation was determined using a curve of haemodynamic response to switching from AAI (reference state) to DDD (test state) at a series of AV delays (40, 80, 120, 160, 200, 240 ms). We then compared the derived optimal AV delays between the two measurement approaches. We also assessed the impact of the paced heart-rate on agreement between laser Doppler and Blood-Pressure derived optimal AV delays. Results The AV delay derived using LDPM was not clinically significant different from that derived by blood pressure changes. The median difference was -9ms (IQR -26 to 7, p = 0.05). Variability between the two methods was low (median absolute deviation 17ms). Optimisations performed at higher heart-rates resulted in a non-significant smaller difference between the LDPM and blood-pressure derived AV delays (median absolute deviation 12 vs 22 ms, p = 0.11). Conclusions Optimal AVDs derived from non-invasive blood-pressure or laser Doppler perfusion methods are clinically equivalent. The addition of laser Doppler to future implantable cardiac devices may enable devices to dynamically and reliably optimise AV delays. Abstract Figure 1

An electrographic AV optimization for the maximum integrative atrioventricular and ventricular resynchronization in CRT

Background:Atrioventricular (AV) delay could affect AV and ventricular synchrony in cardiac resynchronization therapy (CRT). Strategies to optimize AV delay according to optimal AV synchrony (AVopt-AV) or ventricular synchrony (AVopt-V) would potentially be in discordant. This study aimed to explore a new AV delay optimization algorithm guided by electrograms to get the maximum integrative effects of AV and ventricular resynchronization (opt-AV).Methods:Forty-nine patients with CRT were enrolled. AVopt-AV was measured through the Ritter method. AVopt-V was obtained by yielding the narrowest QRS. The opt-AV was considered to be AVopt-AV or AVopt-V when their difference was <20ms, and to be the AV delay with the maximal aortic velocity-time integral between AVopt-AV and AVopt-V when their difference was >20ms.Results:The results showed sensing/pacing AVopt-AV (SAVopt-AV/PAVopt-AV) were correlated with atrial activation time (Pend-As/ Pend-Ap)( P＜0.05 ). Sensing/pacing AVopt-V (SAVopt-V/PAVopt-V) were correlated with the intrinsic AV conduction time (As-Vs/Ap-Vs) (P＜0.01). The percentages of patients with more than 20ms differences between SAVopt-AV/PAVopt-AV and SAVopt-V/PAVopt-V were 62.9% and 57.1%, respectively. Among them, the opt-AV were linearly correlated with SAVopt-AV/PAVopt-AV and SAVopt-V/PAVopt-V. The sensing opt-AV (opt-SAV)=0.1×SAVopt-AV+0.4×SAVopt-V+70ms (R2=0.665, P<0.01) and the pacing opt-AV (opt-PAV)=0.25×PAVopt-AV+0.5×PAVopt-V+30ms (R2=0.560, P<0.01).Conclusion:The SAVopt-AV/PAVopt-AV and SAVopt-V/PAVopt-V were correlated with the atrial activation time and the intrinsic AV conduction interval respectively. Almost half of patients had a >20ms difference between SAVopt-AV/PAVopt-AV and SAVopt-V/PAVopt-V. The opt-AV could be estimated based on electrogram parameters.

Improving atrioventricular coupling in heart failure patients with PR prolongation, the ReachPR Trial

Background PR prolongation is associated with poor hemodynamic performance and may contribute to heart failure (HF). There is some evidence that in HF patients, normalization of atrioventricular (AV) coupling can attenuate HF. Purpose To investigate acute hemodynamic effects of restoration of AV coupling by atrio-biventricular (BiV) pacing in patients with HF and PR prolongation, but without evident ventricular dyssynchrony. Methods Nineteen patients underwent BiV pacemaker implantation. An invasive hemodynamic pacing protocol was performed during BiV and right ventricular (RV) pacing with four paced AV delays (100, 75, 50 and 25% of patient's PR interval during baseline AAI pacing). All patients had symptomatic HF, left ventricular ejection fraction (LVEF) &lt;35% and PR interval ≥230 ms, without evident prolonged QRS duration &gt;150 ms or left bundle branch block. Acute hemodynamic response was assessed by invasive left ventricular (LV) stroke work measurements (conductance catheter technique). Results At baseline, PR interval was 255±22 ms, QRS duration 122±19 ms and LVEF 29±6%. Reducing AV delay to 50% of patient's intrinsic PR interval by BiV pacing resulted in a median 25% increase (p&lt;0.05) in LV stroke work relative to baseline (figure, left panel). This increase in LV stroke work was mainly determined by an increase in LV stroke volume (figure, right panel). In contrast to BiV pacing, reducing AV delay by RV pacing did not improve LV stroke work (figure, left panel). Conclusion In patients with HF and PR prolongation, BiV pacing can be used to improve AV coupling that leads to hemodynamic improvement. These results suggest that BiV pacing may also be beneficial in this subset of HF patients that are currently not indicated for CRT. ReachPR Trial Funding Acknowledgement Type of funding source: Private company. Main funding source(s): Abbott funded a part of this study.

113 Echocardiographic assessment of right ventricular outflow tract obstruction in hypertrophic cardiomyopathy - efficacy of dual chamber pacing in reducing of gradient

Hypertrophy of the right ventricle (RV) in the course of hypertrophic cardiomyopathy (HCM) is found in 30-60% of cases, with the possibility of a right ventricular outflow tract obstruction (RVOTO), obstruction in the apex or the middle part of the right ventricle. A patient, aged 41, admitted due to limitation of exercise tolerance, effort dyspnea, presyncope. In an echocardiogram, interventricular septum (IVS) hypertrophy was observed up to 2.0 cm; normal size of the heart cavities; normal left ventricular systolic function (EF-70%). A color doppler mapping detected the zone of flow acceleraction and turbulent flow in right ventricular outflow tract (RVOT), next a spectral doppler examination showed the RVOT obstruction with a maximal gradient of 64 mmHg. Because of the suboptimal echocardiographic imaging, a heart CT scan was performed, revealing the features of left ventricular hypertrophy, most severe at the base and the medium part of IVS (up to 25 mm). Asymmetric hypertrophy of the middle portion of the right ventricle and right ventricular outflow tract obstruction was also observed. A hemodynamic study confirmed the presence of gradient in RVOT, up to 40 mmHg. Holter electrocardiogram recorded an episode of non-sustained ventricular tachycardia. Taking into account the clinical picture, the family history of the disease, and calculated HCM Risk SCD (7.55%), the decision was made to implant a dual chamber cardioverter defibrillator. The defibrillator electrode was fixed at the apex of the right ventricle. A short AV delay was programmed for prevalent right ventricular stimulation (AV delay 100 ms), resulting in 99.6% ventricular stimulation. The control echocardiogram showed a reduction in the maximum gradient in RVOT to 24 mmHg. In addition, the patient was treated with a beta-blocker. To sum up, in the case of HCM we should always examine the RV with color and spectral doppler to exclude potential narrowing in RV. Constant AV sequential stimulation with a short AV delay is a recognized method that can be considered in symptomatic adult HCM patients with a left ventricular outflow tract obstruction. In the case described here, the above mentioned method proved effective in the significant reduction of the gradient in the right ventricular outflow tract. Abstract 113 Figure. gradient in RVOT

CRT Pacing: Midterm Follow-Up in LV Only Pacing without RV Lead in Patients with Normal AV Conduction

Background: The aim of our study was to assess the real life cardiac resynchronization therapy (CRT) fusion left ventricular (LV) only pacing in patients with normal AV conduction (NAVc) without right ventricular (RV) lead. Methods: Consecutive NAVc patients with CRT indication were implanted with a right atrium RA/LV DDD pacing system. Complete follow-up at 1, 3 and every 6 months thereafter included echocardiography and stress testing. Results: We analysed 55 patients (62 ± 11 years). All patients were responders with significant LV reverse remodelling (LV end-diastolic volume 193.7 ± 81 vs. 243.2 ± 82 mL at baseline, p < 0.002) and increased LV ejection fraction (38 ± 7.9% vs. 27 ± 5.2% at baseline, p < 0.001). Mitral regurgitation decreased in 38 patients (69%). During follow-up (35 ± 18 months), 20 patients (36%) needed reprogramming sensed/paced AV delay or maximum tracking rate (MTR) because of inadequate or lost LV capture at exercise test; personalized programming to achieve up to 100% fusion pacing was used in all patients. One patient developed Mobitz II second degree AV block and triple chamber CRT-P upgrade was performed; defibrillator upgrade was not necessary. Conclusions: LV only pacing CRT-P without RV lead showed a positive outcome in carefully selected patients.

Επίδραση τον συνδυασμού διαφόρων θέσεων βηματοδότησης στη λειτουργικότητα της αριστερής κοιλίας μετά απο οξύ έμφραγμα μυοκαρδίου

Εισαγωγή: Τα τελευταία χρόνια η θεραπεία καρδιακού επανασυγχρονισμού, που επιτυγχάνεται με την αμφικοιλιακή βηματοδότηση, αποτελεί σημαντικό κομμάτι της θεραπείας των ασθενών με καρδιακή ανεπάρκεια, προσφέροντας βελτίωση των συμπτωμάτων, μείωση της νοσηρότητας και αύξηση της επιβίωσης. Εντούτοις, υπάρχει αρκετός προβληματισμός αναφορικά με το σημαντικό ποσοστό ασθενών που λαμβάνουν αυτή τη θεραπεία αλλά τελικά δεν ανταποκρίνονται επαρκώς, κυρίως λόγω της ακατάλληλης θέσης βηματοδότησης της αριστερής κοιλίας. Το ερευνητικό ενδιαφέρον, σχετικά με εναλλακτικές θέσεις βηματοδότησης της αριστερής κοιλίας (ΑΚ) που θα μπορούσαν να αυξήσουν την ανταπόκριση στη θεραπεία, είναι αρκετά μεγάλο. Ωστόσο είναι ελάχιστα τα δεδομένα αναφορικά με την επίδραση συνδυασμών διαφόρων θέσεων βηματοδότησης στη λειτουργικότητα της ΑΚ στο άθικτο και στο ισχαιμικό μυοκάρδιο.Σκοπός: Να ερευνηθεί η επίδραση του συνδυασμού διαφόρων θέσεων βηματοδότησης στη λειτουργικότητα της αριστερής κοιλίας στο άθικτο μυοκάρδιο και μετά από πειραματικό οξύ πρόσθιο έμφραγμα του μυοκαρδίου (ΟΕΜ), με απώτερο στόχο την ανεύρεση του βέλτιστου συνδυασμού και θέσης βηματοδότησης.Μέθοδοι: Σε 16 υγιείς χοίρους πραγματοποιήθηκε κολποκοιλιακή επικαρδιακή βηματοδότηση με διάφορους συνδυασμούς θέσεων, πριν και μετά από ΟΕΜ. Οι συνδυασμοί θέσεων που μελετήθηκαν ήταν: 1) ΔΚ+ΑΚ βασικό οπίσθιο 2) ΔΚ+ΑΚ κορυφαίο πλάγιο 3) ΔΚ+ΑΚ βασικό πρόσθιο 4) ΔΚ+ΑΚ βασικό πρόσθιοι βασικό οπίσθιο 5) ΑΚ βασικό πρόσθιο+ΑΚ κορυφαίο πλάγιο 6) ΑΚ βασικό οπίσθιο+ΑΚ κορυφαίο πλάγιο και 7) ΑΚ βασικό οπίσθιο+ΑΚ βασικό πρόσθιο, σε τυχαία σειρά. Η συχνότητα βηματοδότησης ήταν κάθε φορά υψηλότερη κατά 10 παλμούς από την ενδογενή καρδιακή συχνότητα. Κατά τη διάρκεια της κολποκοιλιακής161βηματοδότησης ο χρόνος κολποκοιλιακής καθυστέρησης (AV-delay) ήταν αρκετά βραχύς ώστε η παραγόμενη διέγερση να προέρχεται από το κοιλιακό ηλεκτρόδιο βηματοδότησης. Για την αξιολόγηση της επίδρασης κάθε συνδυασμού βηματοδότησης χρησιμοποιήθηκαν αιμοδυναμικές παράμετροι από κοινού με κλασσικούς και νεότερους υπερηχοκαρδιογραφικές δείκτες. Η μελέτη παραμόρφωσης έγινε με τη χρήση της δύο διαστάσεων υπερηχοκαρδιογραφικής απεικόνισης με την τεχνική Speckle Tracking και του ειδικού λογισμικού EchoPac.Αποτελέσματα: Στο άθικτο μυοκάρδιο, οι περισσότερες μεταβλητές απόδοσης της ΑΚ που μετρήθηκαν, συμπεριλαμβανομένων και των παραμέτρων παραμόρφωσης επηρεάστηκαν δυσμενώς κατά τη διάρκεια της βηματοδότησης (σε όλους τους συνδυασμούς, όλες οι μεταβλητές p<0,05). Ωστόσο μετά από ΟΕΜ, ο συνδυασμός βηματοδότησης του κορυφαίου πλάγιου τοιχώματος της ΑΚ και του βασικού οπισθίου τοιχώματος της ΑΚ φάνηκε να έχει το ευνοϊκότερο αποτέλεσμα στην λειτουργικότητα της ΑΚ, οδηγώντας σε ισοδύναμες αιμοδυναμικές και στροφικές επιδράσεις με τον φλεβοκομβικό ρυθμό (όλες οι μεταβλητές p>0,05).Συμπεράσματα: Στο άθικτο μυοκάρδιο, η λειτουργικότητα της ΑΚ ελαττώνεται σε σύγκριση με τον φλεβοκομβικό ρυθμό, με όλους τους συνδυασμούς θέσεων βηματοδότησης που μελετήθηκαν. Εντούτοις, κατά τη διάρκεια του ΟΕΜ ο συνδυασμός βηματοδότησης του κορυφαίου πλάγιου τοιχώματος της ΑΚ και του βασικού οπισθίου τοιχώματος της ΑΚ φάνηκε να διατηρεί τη λειτουργικότητα της ΑΚ σε επίπεδο παρόμοιο με το φλεβοκομβικό ρυθμό.

Assessment of optimal atrioventricular delay in dual chamber pacing patients with atrioventricular first degree block

Septal pacing in patients with dual chamber pacemakers and atrio-ventricular (AV) conduction malfunction, but without structural heart muscle impairment, is not worse than own AV conduction. Optimized AV delay in patients with first degree AV block and PQ interval &amp;amp;gt; 220 ms may be better than preserving own contraction with pathologic atrio-ventricular delay, leading to asynchrony, ventricle remodeling and relaxation disorders.