- Email: [email protected]
P4-114
S256 a clear endpoint makes such procedures difficult. We report a case of sinus node modification using cryoenergy as an alternative ablation method. A 51 year old woman with IST was referred for sinus node modification. A steerable 20 pole “halo” catheter was positioned in the right atrium with the proximal poles in the high right atrium (RA) near the junction with the superior vena cava, the middle poles along the lateral RA wall, and the distal poles traversing the cavotricuspid isthmus and proximal coronary sinus. During infusion of isoproterenol the sinus cycle length was 530 ms. A 9F 8 mm tip cryoablation catheter (FreezorTM Max, CryoCath Technologies) was advanced from the right femoral vein into the RA and positioned with the distal bipole near the earliest atrial activation site near halo bipole 9. Pacing from this site did not result in diaphragmatic capture. Cryoablation at -85o C for 15 seconds caused marked slowing of sinus cycle length to 800 ms with a shift in earliest activity to halo bipole 7. After 60 seconds of ablation at this site sinus arrest appeared with emergence of a junctional rhythm. Cryoablation was immediately halted, after which sinus rhythm at a cycle length of 450 ms returned. A full 4 minute cryoablation lesion was then delivered to the same site. Again sinus arrest occurred during the lesion After this lesion sinus rhythm returned but with a sinus cycle length on isoproterenol of 600 ms. During 12 months of follow-up the patient has been free of palpitations. A follow-up Holter monitor has shown sinus rhythm with an average rate of 70 beats per minute, a peak rate of 120 beats per minute and a minimum of 50 beats per minute. Since the sinus node is an epicardial structure, sinus arrest during cryoablation in the high RA suggests a transmural cryolesion. The marked sinus slowing and sinus arrest that occurs during such lesions may provide a useful endpoint to guide sinus node modification procedures in patients with IST. P4-112 SUCCESSFUL ABLATION OF A CONCEALED PARAHISIAN ACCESSORY PATHWAY USING REMOTE CONTROL MAGNETIC NAVIGATION FOLLOWING FAILURE OF CONVENTIONAL METHODS Darryl R. Davis, MD, David H. Birnie, MD, Anthony S. Tang, MD, Rafeeq Samie, MD, Najib Al-Rawahi, MD, Martin S. Green, MD and Michael H. Gollob, MD. University of Ottawa Heart Institute, Ottawa, Ontario, Canada and University of Ottawa Heart Institute, Ottawa, Ontario, Canada. Ablation of parahisian accessory pathways (AP) using RF energy may pose a high risk for heart block. We report the case of a concealed parahisian AP that had failed three prior attempts to ablate using conventional methods. Case History: A 47 yo female with frequent narrow complex tachycardia demonstrated easily inducible atrioventricular reentry tachycardia (AVRT) utilizing a parahisian AP. Ablation using a conventional catheter and RF energy resulted in transient AV block. Retrograde conduction via the AP and inducible AVRT persisted. The patient returned for repeat ablation on two occasions using cryotherapy. Both attempts were acutely successful beyond a 30 min post-ablation wait period; however, she experienced recurrence of tachycardia within 2 weeks on each occasion. She returned for a 4th ablation using remote magnetic navigation. Methods and Results: A 4mm tip magnetic ablation catheter was used in addition to standard diagnostic catheters. Mapping was performed via remote control navigation using a motor drive (Stereotaxis, Inc.) for catheter movements as guided by operator-directed magnetic vectors generated by two external magnets. RF energy (temp-control mode, 47°C, max 40W, 60s) was delivered during sinus rhythm at the site of earliest atrial activation during ventricular pacing, anatomically in the mid-high septal region. Following ablation, VA conduction was absent. Transient AV block did not occur and post-ablation conduction intervals were unchanged compared to baseline. The patient has remained asymptomatic during follow-up (4 mo). Conclusions: This is the first report of successful remote magnetic catheter ablation of a concealed parahisian AP. Magnetic catheter stability during RF application likely contributed to the success of this procedure and may have minimized the risk of AV block.
Heart Rhythm, Vol 3, No 5, May Supplement 2006
P4-113 TWO VENTRICULAR TACHYCARDIAS WHICH SHOWED THE OPPOSITE AXIS SHARED THE CRITICAL ISTHMUS IN A PATIENT WITH DOUBLE OUTLET RIGHT VENTRICLE AFTER RASTELLI PROCEDURE Yoko Hagiwara, MD, Kyoko Soejima, MD, Seiji Takatsuki, MD, Kojiro Tanimoto, MD, Akiko Kase, RN, Kotaro Fukumoto, MD, Masaki Ieda, MD, Toshiaki Sato, MD, Shunichiro Miyoshi, MD, Hideo Mitamura, MD and Satoshi Ogawa, MD. Keio University School of Medicine, Tokyo, Japan and Saiseikai Central Hospital, Tokyo, Japan. A 33-year-old male, s/p Rastelli procedure at the age of 9 y/o for double outlet right ventricle (DORV) was admitted to our hospital due to ventricular tachycardia (VT). The morphology of clinical VT was LBBB, superior axis (CL 410 ms). During the EP study, 2 types of VTs including the clinical VT were induced. VT2 had LBBB with inferior axis (CL 440 ms). Activation mapping was performed both in VT1 and VT2, early-diastolic potential during VT1 and mid-diastolic potential during VT2 were recorded at the same channel in LVOT. Entrainment mapping confirmed the site being the central portion of the isthmus for VT1 and the exit portion of the isthmus for VT2. Interestingly, pace mapping at this site showed the perfect pace matches to VT2 with gradual prolongation of S-QRS interval, and QRS morphology changed to that of VT1. RF application at this site abolished both VT1 and 2. From this observation, this small channel was shared with two types of VTs which had different CL and exits.
P4-114 THE ACTIVATION PATTERN OF THE PREMATURE VENTRICULAR CONTRACTIONS TRIGGERING AN ELECTRICAL
Poster 4 STORM IN A PATIENT WITH REMOTE MYOCARDIAL INFARCTION Kenji Yodogawa, MD, Yasushi Miyauchi, MD, Yoshinori Kobayashi, MD, Koji Katoh, MD, Yuki Iwasaki, MD, Takeshi Yamamoto, MD, Hiroshi Taniguchi, MD, Tsutomu Horie, MD, Yasuhiro Hirasawa, MD, Norishige Morita, MD, Meiso Hayashi, MD, Mitsunori Maruyama, MD, Naoki Satoh, MD, Keiji Tanaka, MD, Takao Katoh, MD and Teruo Takano, MD. Nippon Medical School, Tokyo, Japan. Background: Premature ventricular contractions (PVCs) triggering electrical storms in patients with a myocardial infarction (MI) often originate from the Purkinje network in the ischemic border zone. However, the activation pattern of such PVC has not been reported in detail. Case Report: A 68-year-old male with a remote MI and frequent unifocal PVCs triggering electrical storms underwent an electrophysiologic study. The PVC had a QRS complex with a right bundle branch block and superior axis configuration and a duration of 130msec. The VT was initiated by a PVC couplet, but not single PVCs. The activation pattern of the single PVCs was visualized using an electroanatomical mapping system. A spiky Purkinje potential (PP) that preceded the onset of the QRS could be recorded over a wide area of the MI border zone (0.5-1.5mV) in the anteroseptal to inferior endocardial LV (white tags in panel A). During the PVC, the earliest PP preceded the onset of the QRS complex by 53msec, and rapidly spread to the entire Purkinje network (Panel A). Then the ventricular depolarization involving ⬎85% of the endocardial LV (except for the dense scar in the inferobasal LV) occurred within the first 50 ms of the QRS complex (Panel B). During the second PVC that initiated the VT, the PP-Q interval was longer than that of the first PVC (53 vs. 130ms), suggesting that a conduction delay inside the Purkinje network occurred (Panel C). A radiofrequency application to the earliest site of the PP, where a perfect pace map was obtained, successfully eliminated the PVC and VT. Discussion: A PVC couplet originating from the surviving Purkinje network initiated the VT. The first PVC, which rapidly spread to the entire LV, did not initiate the VT. A conduction delay in the Purkinje network induced by the short-coupled second PVC might be important for the initiation of the VT.
S257 resuscitation she developed severe hypoxic cerebral damage. Prior medical history was uneventful, particularly with respect to syncope or clinical signs of tachycardia. Due to a reduced LVEF (40%) on admission, the initial diagnosis of pregnancy-associated cardiomyopathy was made and the patient underwent implantation of an ICD before discharge. During long-term neuro-rehabilitation, an anti-psychotic poly-pharmacotherapy including several QT prolonging drugs was initiated due to severe neurologic disorder. Clinical Course: During a first regular ICD interrogation on an outpatientbasis, several episodes of TdP ventricular tachycardia and VF resulting in several appropriate ICD shock discharges were confirmed. The EGMs (Fig.1) showed several episodes of short-long-short sequences initiating the arrhythmic events as well as pronounced prolongation of the QT interval. The 12-lead ECG showed marked changes in T-wave morphology. These findings led to the clinical diagnosis of LQT-2 syndrome. Beta blocker dosage was increased, and the antipsychotic drug regimen was modified. Molecular Genetic Analysis: Genotyping revealed a novel mutation [Leu413Pro] in Exon 6 of the HERG gene, confirming the clinical diagnosis of LQT-2-syndrome. The patient’s family is currently being tested for LQT phenotype and genotype and undergoes risk stratification. Conclusion: Cardiac arrest may be the first clinical event in patients with inherited LQT syndrome. Female patients with a HERG mutation are at increased risk of postpartal arrhythmic events. These may be precipitated by hormonal alterations affecting delayed rectifier function subsequently leading to an increased propensity to cardiac events.
P4-116 INAPPROPRIATE ICD THERAPY DUE TO TRANSCUTANEOUS PACING DURING CPR Rajjit Abrol, MD, George N. Carayannopoulos, MD and Robert C. Kowal, MD, PhD. Baylor University Medical Center, Dallas, TX and Hospital St. Catherine of Siena, Stony Brook University Hospital, Long Island, NY.
P4-115 POSTPARTUM CARDIAC ARREST AS A FIRST MANIFESTATION OF INHERITED LONG QT SYNDROME WITH A NOVEL HERG MUTATION Thomas Klingenheben, MD, Karin Mayer, PhD and Joachim R. Ehrlich, MD. Praxis fu¨r Kardiologie, Bonn, Germany, Centre of Human Genetics, Martinsried, Germany and J. W. Goethe University, Frankfurt, Germany. Case Presentation: An 18-year old woman was resuscitated from documented VF arrest, 10 days after having given birth to a healthy boy. Following
A 69 year old man with ischemic cardiomyopathy and a biventricular ICD was admitted with resuscitated cardiac arrest. The patient was found by EMS with pulseless electrical activity and regained circulation with CPR. EMS reported several brief episodes of VT followed by an ICD discharge. ICD interrogation revealed two episodes in the VT zone treated, in sum, with 4 ATPs and 1 shock. Review of the electrograms (EGMs) revealed a distinctly anomalous pattern of activation. In the atrial channel (Fig: A), alternating 15 mV and 3 mV EGMs were observed. Similarly, in the ventricular channel (Fig: V), alternating 15 mV and 8 mV EGMs were present. The 15 mV EGMs were simultaneous in both the A and V channels with a coupling interval of 740 msec (Fig: vertical arrows). The 3mV (A) and 8 mV (V) EGMs were linked with an AV interval of 210 msec, consistent with sinus rhythm and intrinsic ventricular conduction (Fig: P and R). These EGMs were dissociated from the 15 mV signals. Interpretation: The 15 mV EGMS were thought to be most consistent with an external electrical source (Fig: ES). Indeed, the use of transcutaneous pacing (TCP) during CPR was later confirmed. Therefore, we concluded that TCP without capture led the ICD to count both the TCP and intrinsic activation, triggering therapy when the coupling intervals fell in the VT zone. The “VT” noted by EMS was actually ATP prior to the ICD shock. Post-shock, capture by the TCP was noted on the interrogation EGMs and prevented further ICD therapy (not shown). Crosstalk between implanted pacemakers and ICDs is well described. To our knowledge, this is the first
Heart Rhythm, Vol 3, No 5, May Supplement 2006
P4-113 TWO VENTRICULAR TACHYCARDIAS WHICH SHOWED THE OPPOSITE AXIS SHARED THE CRITICAL ISTHMUS IN A PATIENT WITH DOUBLE OUTLET RIGHT VENTRICLE AFTER RASTELLI PROCEDURE Yoko Hagiwara, MD, Kyoko Soejima, MD, Seiji Takatsuki, MD, Kojiro Tanimoto, MD, Akiko Kase, RN, Kotaro Fukumoto, MD, Masaki Ieda, MD, Toshiaki Sato, MD, Shunichiro Miyoshi, MD, Hideo Mitamura, MD and Satoshi Ogawa, MD. Keio University School of Medicine, Tokyo, Japan and Saiseikai Central Hospital, Tokyo, Japan. A 33-year-old male, s/p Rastelli procedure at the age of 9 y/o for double outlet right ventricle (DORV) was admitted to our hospital due to ventricular tachycardia (VT). The morphology of clinical VT was LBBB, superior axis (CL 410 ms). During the EP study, 2 types of VTs including the clinical VT were induced. VT2 had LBBB with inferior axis (CL 440 ms). Activation mapping was performed both in VT1 and VT2, early-diastolic potential during VT1 and mid-diastolic potential during VT2 were recorded at the same channel in LVOT. Entrainment mapping confirmed the site being the central portion of the isthmus for VT1 and the exit portion of the isthmus for VT2. Interestingly, pace mapping at this site showed the perfect pace matches to VT2 with gradual prolongation of S-QRS interval, and QRS morphology changed to that of VT1. RF application at this site abolished both VT1 and 2. From this observation, this small channel was shared with two types of VTs which had different CL and exits.
P4-114 THE ACTIVATION PATTERN OF THE PREMATURE VENTRICULAR CONTRACTIONS TRIGGERING AN ELECTRICAL
Poster 4 STORM IN A PATIENT WITH REMOTE MYOCARDIAL INFARCTION Kenji Yodogawa, MD, Yasushi Miyauchi, MD, Yoshinori Kobayashi, MD, Koji Katoh, MD, Yuki Iwasaki, MD, Takeshi Yamamoto, MD, Hiroshi Taniguchi, MD, Tsutomu Horie, MD, Yasuhiro Hirasawa, MD, Norishige Morita, MD, Meiso Hayashi, MD, Mitsunori Maruyama, MD, Naoki Satoh, MD, Keiji Tanaka, MD, Takao Katoh, MD and Teruo Takano, MD. Nippon Medical School, Tokyo, Japan. Background: Premature ventricular contractions (PVCs) triggering electrical storms in patients with a myocardial infarction (MI) often originate from the Purkinje network in the ischemic border zone. However, the activation pattern of such PVC has not been reported in detail. Case Report: A 68-year-old male with a remote MI and frequent unifocal PVCs triggering electrical storms underwent an electrophysiologic study. The PVC had a QRS complex with a right bundle branch block and superior axis configuration and a duration of 130msec. The VT was initiated by a PVC couplet, but not single PVCs. The activation pattern of the single PVCs was visualized using an electroanatomical mapping system. A spiky Purkinje potential (PP) that preceded the onset of the QRS could be recorded over a wide area of the MI border zone (0.5-1.5mV) in the anteroseptal to inferior endocardial LV (white tags in panel A). During the PVC, the earliest PP preceded the onset of the QRS complex by 53msec, and rapidly spread to the entire Purkinje network (Panel A). Then the ventricular depolarization involving ⬎85% of the endocardial LV (except for the dense scar in the inferobasal LV) occurred within the first 50 ms of the QRS complex (Panel B). During the second PVC that initiated the VT, the PP-Q interval was longer than that of the first PVC (53 vs. 130ms), suggesting that a conduction delay inside the Purkinje network occurred (Panel C). A radiofrequency application to the earliest site of the PP, where a perfect pace map was obtained, successfully eliminated the PVC and VT. Discussion: A PVC couplet originating from the surviving Purkinje network initiated the VT. The first PVC, which rapidly spread to the entire LV, did not initiate the VT. A conduction delay in the Purkinje network induced by the short-coupled second PVC might be important for the initiation of the VT.
S257 resuscitation she developed severe hypoxic cerebral damage. Prior medical history was uneventful, particularly with respect to syncope or clinical signs of tachycardia. Due to a reduced LVEF (40%) on admission, the initial diagnosis of pregnancy-associated cardiomyopathy was made and the patient underwent implantation of an ICD before discharge. During long-term neuro-rehabilitation, an anti-psychotic poly-pharmacotherapy including several QT prolonging drugs was initiated due to severe neurologic disorder. Clinical Course: During a first regular ICD interrogation on an outpatientbasis, several episodes of TdP ventricular tachycardia and VF resulting in several appropriate ICD shock discharges were confirmed. The EGMs (Fig.1) showed several episodes of short-long-short sequences initiating the arrhythmic events as well as pronounced prolongation of the QT interval. The 12-lead ECG showed marked changes in T-wave morphology. These findings led to the clinical diagnosis of LQT-2 syndrome. Beta blocker dosage was increased, and the antipsychotic drug regimen was modified. Molecular Genetic Analysis: Genotyping revealed a novel mutation [Leu413Pro] in Exon 6 of the HERG gene, confirming the clinical diagnosis of LQT-2-syndrome. The patient’s family is currently being tested for LQT phenotype and genotype and undergoes risk stratification. Conclusion: Cardiac arrest may be the first clinical event in patients with inherited LQT syndrome. Female patients with a HERG mutation are at increased risk of postpartal arrhythmic events. These may be precipitated by hormonal alterations affecting delayed rectifier function subsequently leading to an increased propensity to cardiac events.
P4-116 INAPPROPRIATE ICD THERAPY DUE TO TRANSCUTANEOUS PACING DURING CPR Rajjit Abrol, MD, George N. Carayannopoulos, MD and Robert C. Kowal, MD, PhD. Baylor University Medical Center, Dallas, TX and Hospital St. Catherine of Siena, Stony Brook University Hospital, Long Island, NY.
P4-115 POSTPARTUM CARDIAC ARREST AS A FIRST MANIFESTATION OF INHERITED LONG QT SYNDROME WITH A NOVEL HERG MUTATION Thomas Klingenheben, MD, Karin Mayer, PhD and Joachim R. Ehrlich, MD. Praxis fu¨r Kardiologie, Bonn, Germany, Centre of Human Genetics, Martinsried, Germany and J. W. Goethe University, Frankfurt, Germany. Case Presentation: An 18-year old woman was resuscitated from documented VF arrest, 10 days after having given birth to a healthy boy. Following
A 69 year old man with ischemic cardiomyopathy and a biventricular ICD was admitted with resuscitated cardiac arrest. The patient was found by EMS with pulseless electrical activity and regained circulation with CPR. EMS reported several brief episodes of VT followed by an ICD discharge. ICD interrogation revealed two episodes in the VT zone treated, in sum, with 4 ATPs and 1 shock. Review of the electrograms (EGMs) revealed a distinctly anomalous pattern of activation. In the atrial channel (Fig: A), alternating 15 mV and 3 mV EGMs were observed. Similarly, in the ventricular channel (Fig: V), alternating 15 mV and 8 mV EGMs were present. The 15 mV EGMs were simultaneous in both the A and V channels with a coupling interval of 740 msec (Fig: vertical arrows). The 3mV (A) and 8 mV (V) EGMs were linked with an AV interval of 210 msec, consistent with sinus rhythm and intrinsic ventricular conduction (Fig: P and R). These EGMs were dissociated from the 15 mV signals. Interpretation: The 15 mV EGMS were thought to be most consistent with an external electrical source (Fig: ES). Indeed, the use of transcutaneous pacing (TCP) during CPR was later confirmed. Therefore, we concluded that TCP without capture led the ICD to count both the TCP and intrinsic activation, triggering therapy when the coupling intervals fell in the VT zone. The “VT” noted by EMS was actually ATP prior to the ICD shock. Post-shock, capture by the TCP was noted on the interrogation EGMs and prevented further ICD therapy (not shown). Crosstalk between implanted pacemakers and ICDs is well described. To our knowledge, this is the first