P1-74
1
D-HBP P-HBP RVAP Base vs. D-HBP Base vs. P-HBP Base vs. RVAP Baseline After pacing Baseline After pacing Baseline After pacing p P p QRS ms 90 12 92 14 88 15 129 22 89 13 156 18 NS 0.05 0.05 Intra-LVd ms 27 10 24 12 34 15 43 11 30 12 54 23 NS NS 0.05 Yu index ms 14 7 13 10 13 6 17 8 14 7 23 11 NS NS 0.05 EML ms 164 25 176 32 171 35 225 41 167 30 227 43 NS 0.05 0.05 P1-74 EVALUATION OF LEFT VENTRICLE PRESSURE DERIVATIVE ENHANCED BY MULTI SITE PACING IN PATIENTS WITH HEART FAILURE Keiji Inoue, MD, Naoto Inoue, MD, Hiroshi Fujita, MD, Tetsuya Tanaka, MD, Akiko Matsuo, MD, Yoshiharu Nishibori, MD, Kenji Suzuki, MD, Norikazu Takechi, MD and Yumi Otsuki, MD. Kyoto 2nd Red Cross Hospital, Kyoto, Japan. Background: One of the essential point of cardiac resynchronization therapy is improvement of left ventricle (LV) pressure derivative (dP/dt). However, evaluation of dP/dt augmented by pacing multi site is not well-established. We assessed the LV pressure derivative maximum (LVdP/dt) and minimum (LV-dP/dt) under various pacing modes includ- ing biventricular pacing, right ventricle (RV) bifocal pacing and trisite stimulation in heart failure cases. Methods: Thirty cardiac failure patients were studied by cardiac catheteriza- tion. LVdP/dt and LV-dP/dt were measured during atrial pacing as control atrial-ventricular sequential stimulation at a rate of 80 beats/min. Atrial-ven- tricular delay was fixed at 100 msec. The measurements of dP/dt during atrial-ventricular sequential stimulation at same rate were made under the following stimulation mode: RV apex, RV outflow, LV lateral, RV bifocal (RV apex RV outflow), biventricular1 (RV apex LV lateral), biventricu- lar2 (RV outflow LV lateral), trisite (RV apex RV outflow LV lateral). Results: The average of baseline LVdP/dt and LVdP/dt were 748mmHg/sec and 781mmHg/sec. RV apex pacing decreased LVdP/dt by 25% significantly(p0.05). LVdP/dt during RV outflow pacing showed no change compared with control. LV lateral, RV bifocal, biven- tricular1, biventricular2 and trisite pacing increased LVdP/dt by 32%, 24%, 35%, 36% and 34%, respectively (p0.05). Biventricular1, biven- tricular2 and trisite pacing increased absolute value of LV-dP/dt by 20%, 19% and 27%, respectively (p0.05) while other pacing mode decreased these data. Trisite pacing increased absolute value of LV-dP/dt more than biventricular pacing. There was no remarkable difference of data between biventricular1 pacing and biventricular2 acing. Conclusions: RV apex stimulation impaired LV function, whereas RV outflow pacing preserved LV function. RV bifocal pacing provided a modest but favorable effect. LV lateral, biventricular and trisite pacing showed better performance in systolic phase than the control equally. Trisite pacing demonstrated additional effect on diastolic function. P1-75 CARDIAC RESYNCHRONISATION AS A RESCUE THERAPY IN UNSTABLE OVERT HEART FAILURE DEPENDENT OF INTRAVENOUS VASOPRESSIVE AGENTS Paul Milliez, MD, PhD, Olivier Thomas, MD, Abdeddayem Haggui, MD, Alexandre Mebazaa, MD, PhD, Patrick Schurando, MD, Fabrice Extramiana, MD, PhD, Philippe Beaufils, MD and Antoine Leenhardt, MD. Lariboisie `re University Hospital, Paris, France and Ambroise Pare Clinic, Neuilly sur Seine, France. Introduction: Cardiac resynchronisation therapy (CRT) is a validated treatment for overt heart failure (HF) in class III-IV of the NYHA patients despite an optimal medical therapy. CRT has demonstrated a significant reduction of overall mortality, hospitalisations for heart failure and a deep improvement of various functional parameters. We aimed to assess in patients with unstable overt heart failure on vasopressive agents the ben- eficial effects of CRT. Methods and Paients: Among 188 implanted patients within 4 years with a CRT device (22 with an ICD-CRT), 14 has been carried out in unstable overt HF despite vasopressive agents (dobutamine or adrenaline or both). All procedures were performed under local anesthesia and with constant arterial monitoring under the supervision of an anesthesiologist. Patients were predominantly male (12/14) with a mean age of 69 15 yrs, with ischemic cardiomyopathy in 5 and non-ischemic in 9 with mean LVEF of 20 10%. Dependence to vasopressive agents was defined as the inability to stop or reduce the drugs without occurrence of hypotension, oligoanuria (20ml per hour), and hypoxemia. Results: All patients underwent successful implantation. There were no complications related to the procedure. All patients were subsequently monitored during 72 hours in intensive care unit. All vasopressive agents were withdrawn within 72 hours. One patient with a CRT died 24 hour after the procedure from a ventricular tachyarrhythmia. During the mean follow-up of 3 years (6 months to 4 years), one patient died of HF. Hence, 12 from 14 patients (85%) were alive with improvement of their NYHA class (at least 1 class) and LVEF (mean of 5%). Conclusion: This preliminary study shows that CRT is a feasible, safe and reliable option as a rescue therapy in the setting of an unstable overt HF. CRT could be considered as an additional therapy in patients in end-stage HF ineligible for ventricular assist devices. P1-76 PACING-INDUCED DYSSYNCHRONY PRECONDITIONS RABBIT MYOCARDIUM AGAINST ISCHEMIA/REPERFUSION INJURY Ward Y. R. Vanagt, MD, Richard N. M. Cornelussen, PhD, Erik Blaauw, MS, Tammo Delhaas, MD, PhD and Frits W. Prinzen, PhD. Maastricht University, Maastricht, The Netherlands. Background: Because increased mechanical load induces preconditioning (PC) and dyssynchrony increases loading in late-activated regions we investigated whether dyssynchrony induced by ventricular pacing (VP) at normal heart rate leads to cardioprotection. Methods: Isolated working rabbit hearts were subjected to 35 min global ischemia and 2h of reperfusion, while keeping preload and afterload con- stant. Seven hearts underwent VPPC (3 periods of 5 min VP at the posterior left ventricular (LV) wall), 7 hearts underwent ischemic preconditioning (IPC, 3 periods of 5 min global ischemia) and 9 hearts served as control (C). LV pressure and sonomicrometry were used to assess hemodynamics and segment work (SW) in anterior and posterior LV myocardium. Myo- cardial release of lactate, phosphorylation of ERK and expression of proBNP mRNA were determined to gain insight in the molecular processes involved in VPPC. * p0.05. Results: Infarct size (TTC staining) was 18.313.0% in group C, and was uniformly reduced in the VPPC and IPC groups (1.80.8%*, and 3.53.1%*, respectively, N.S. between VPPC and IPC). During LV pacing (VPPC group) SW increased to 335207%* in anterior and decreased to negative values (2363%*) in posterior myocardium. LV pacing did not significantly affect lactate release and coronary flow. Immediately after the 3rd LV pacing cycle (VPPC3) ERK phosphory- lation was increased in anterior LV myocardium. Ten min later, proBNP mRNA expression was increased 3-4 fold in both anterior and posterior myocardium (Figure). Conclusion: Intermittent dyssynchrony is equally cardioprotective as “classical” IPC. Dyssynchrony-induced protection is not induced by isch- emia but may be mediated by stretch-induced ERK phosphorylation and proBNP mRNA upregulation. S132 Heart Rhythm, Vol 3, No 5, May Supplement 2006
Transcript of P1-74
D-HBP P-HBP RVAP
Basevs.D-HBP
Basevs. P-HBP
Basevs.RVAP
BaselineAfterpacing Baseline
Afterpacing Baseline
Afterpacing p P p
QRSms
90 � 12 92 � 14 88 � 15 129 � 22 89 � 13 156 � 18 NS �0.05 �0.05
Intra-LVdms
27 � 10 24 � 12 34 � 15 43 � 11 30 � 12 54 � 23 NS NS �0.05
Yuindexms
14 � 7 13 � 10 13 � 6 17 � 8 14 � 7 23 � 11 NS NS �0.05
EMLms
164 � 25 176 � 32 171 � 35 225 � 41 167 � 30 227 � 43 NS �0.05 �0.05
P1-74
EVALUATION OF LEFT VENTRICLE PRESSURE DERIVATIVEENHANCED BY MULTI SITE PACING IN PATIENTS WITHHEART FAILUREKeiji Inoue, MD, Naoto Inoue, MD, Hiroshi Fujita, MD,Tetsuya Tanaka, MD, Akiko Matsuo, MD, Yoshiharu Nishibori,MD, Kenji Suzuki, MD, Norikazu Takechi, MD and YumiOtsuki, MD. Kyoto 2nd Red Cross Hospital, Kyoto, Japan.
Background: One of the essential point of cardiac resynchronizationtherapy is improvement of left ventricle (LV) pressure derivative (dP/dt).However, evaluation of dP/dt augmented by pacing multi site is notwell-established. We assessed the LV pressure derivative maximum(LV�dP/dt) and minimum (LV-dP/dt) under various pacing modes includ-ing biventricular pacing, right ventricle (RV) bifocal pacing and trisitestimulation in heart failure cases.Methods: Thirty cardiac failure patients were studied by cardiac catheteriza-tion. LV�dP/dt and LV-dP/dt were measured during atrial pacing as controlatrial-ventricular sequential stimulation at a rate of 80 beats/min. Atrial-ven-tricular delay was fixed at 100 msec. The measurements of dP/dt duringatrial-ventricular sequential stimulation at same rate were made under thefollowing stimulation mode: RV apex, RV outflow, LV lateral, RV bifocal(RV apex � RV outflow), biventricular1 (RV apex � LV lateral), biventricu-lar2 (RV outflow � LV lateral), trisite (RV apex � RV outflow � LV lateral).Results: The average of baseline LV�dP/dt and LV�dP/dt were748mmHg/sec and �781mmHg/sec. RV apex pacing decreased LV�dP/dtby 25% significantly(p�0.05). LV�dP/dt during RV outflow pacingshowed no change compared with control. LV lateral, RV bifocal, biven-tricular1, biventricular2 and trisite pacing increased LV�dP/dt by 32%,24%, 35%, 36% and 34%, respectively (p�0.05). Biventricular1, biven-tricular2 and trisite pacing increased absolute value of LV-dP/dt by 20%,19% and 27%, respectively (p�0.05) while other pacing mode decreasedthese data. Trisite pacing increased absolute value of LV-dP/dt more thanbiventricular pacing. There was no remarkable difference of data betweenbiventricular1 pacing and biventricular2 acing.Conclusions: RV apex stimulation impaired LV function, whereas RVoutflow pacing preserved LV function. RV bifocal pacing provided amodest but favorable effect. LV lateral, biventricular and trisite pacingshowed better performance in systolic phase than the control equally.Trisite pacing demonstrated additional effect on diastolic function.
P1-75
CARDIAC RESYNCHRONISATION AS A RESCUE THERAPY INUNSTABLE OVERT HEART FAILURE DEPENDENT OFINTRAVENOUS VASOPRESSIVE AGENTSPaul Milliez, MD, PhD, Olivier Thomas, MD, AbdeddayemHaggui, MD, Alexandre Mebazaa, MD, PhD, PatrickSchurando, MD, Fabrice Extramiana, MD, PhD, PhilippeBeaufils, MD and Antoine Leenhardt, MD. LariboisiereUniversity Hospital, Paris, France and Ambroise Pare Clinic,Neuilly sur Seine, France.
Introduction: Cardiac resynchronisation therapy (CRT) is a validatedtreatment for overt heart failure (HF) in class III-IV of the NYHA patientsdespite an optimal medical therapy. CRT has demonstrated a significantreduction of overall mortality, hospitalisations for heart failure and a deepimprovement of various functional parameters. We aimed to assess inpatients with unstable overt heart failure on vasopressive agents the ben-eficial effects of CRT.Methods and Paients: Among 188 implanted patients within 4 years witha CRT device (22 with an ICD-CRT), 14 has been carried out in unstableovert HF despite vasopressive agents (dobutamine or adrenaline or both).All procedures were performed under local anesthesia and with constantarterial monitoring under the supervision of an anesthesiologist. Patientswere predominantly male (12/14) with a mean age of 69 � 15 yrs, withischemic cardiomyopathy in 5 and non-ischemic in 9 with mean LVEF of20 � 10%. Dependence to vasopressive agents was defined as the inabilityto stop or reduce the drugs without occurrence of hypotension, oligoanuria(�20ml per hour), and hypoxemia.Results: All patients underwent successful implantation. There were nocomplications related to the procedure. All patients were subsequentlymonitored during 72 hours in intensive care unit. All vasopressive agentswere withdrawn within 72 hours. One patient with a CRT died 24 hourafter the procedure from a ventricular tachyarrhythmia. During the meanfollow-up of 3 years (6 months to 4 years), one patient died of HF. Hence,12 from 14 patients (85%) were alive with improvement of their NYHAclass (at least 1 class) and LVEF (mean of �5%).Conclusion: This preliminary study shows that CRT is a feasible, safe andreliable option as a rescue therapy in the setting of an unstable overt HF.CRT could be considered as an additional therapy in patients in end-stageHF ineligible for ventricular assist devices.
P1-76
PACING-INDUCED DYSSYNCHRONY PRECONDITIONS RABBITMYOCARDIUM AGAINST ISCHEMIA/REPERFUSION INJURYWard Y. R. Vanagt, MD, Richard N. M. Cornelussen, PhD,Erik Blaauw, MS, Tammo Delhaas, MD, PhD and Frits W.Prinzen, PhD. Maastricht University, Maastricht, TheNetherlands.
Background: Because increased mechanical load induces preconditioning(PC) and dyssynchrony increases loading in late-activated regions weinvestigated whether dyssynchrony induced by ventricular pacing (VP) atnormal heart rate leads to cardioprotection.Methods: Isolated working rabbit hearts were subjected to 35 min globalischemia and 2h of reperfusion, while keeping preload and afterload con-stant. Seven hearts underwent VPPC (3 periods of 5 min VP at the posteriorleft ventricular (LV) wall), 7 hearts underwent ischemic preconditioning(IPC, 3 periods of 5 min global ischemia) and 9 hearts served as control(C). LV pressure and sonomicrometry were used to assess hemodynamicsand segment work (SW) in anterior and posterior LV myocardium. Myo-cardial release of lactate, phosphorylation of ERK and expression ofproBNP mRNA were determined to gain insight in the molecular processesinvolved in VPPC. * � p�0.05.Results: Infarct size (TTC staining) was 18.3�13.0% in group C, andwas uniformly reduced in the VPPC and IPC groups (1.8�0.8%*, and3.5�3.1%*, respectively, N.S. between VPPC and IPC). During LVpacing (VPPC group) SW increased to 335�207%* in anterior anddecreased to negative values (�23�63%*) in posterior myocardium.LV pacing did not significantly affect lactate release and coronary flow.Immediately after the 3rd LV pacing cycle (VPPC3) ERK phosphory-lation was increased in anterior LV myocardium. Ten min later,proBNP mRNA expression was increased 3-4 fold in both anterior andposterior myocardium (Figure).Conclusion: Intermittent dyssynchrony is equally cardioprotective as“classical” IPC. Dyssynchrony-induced protection is not induced by isch-emia but may be mediated by stretch-induced ERK phosphorylation andproBNP mRNA upregulation.
S132 Heart Rhythm, Vol 3, No 5, May Supplement 2006
