MRI Mode Programming for Safe Magnetic Resonance Imaging in Patients With a Magnetic Resonance Conditional Cardiac Device.

Although diagnostically indispensable, magnetic resonance imaging (MRI) has been, until recently, contraindicated in patients with an implantable cardiac device. MR conditional cardiac devices are now widely used, but the mode programming needed for safe MRI has yet to be established. We reviewed the details of 41 MRI examinations of patients with a MR conditional device. There were no associated adverse events. However, in 3 cases, paced beats competed with the patient's own beats during the MRI examination. We describe 2 of the 3 specific cases because they illustrate these potentially risky situations: a case in which the intrinsic heart rate increased and another in which atrial fibrillation occurred. Safe MRI in patients with an MR conditional device necessitates detailed MRI mode programming. The MRI pacing mode should be carefully and individually selected.

Assessment of Efficacy and Necessity of Routine Defibrillation Threshold Testing in Patients Undergoing Implantable Cardioverter-Defibrillator (ICD) Implantation.

Defibrillation threshold (DFT) testing is performed routinely in patients undergoing implantable cardioverter-defibrillator (ICD) implantation to verify the ability of the ICD to terminate ventricular fibrillation (VF). However, neither the efficacy nor the safety of DFT testing has been proven; thus, the necessity of such testing is controversial. We conducted a retrospective study of the efficacy of DFT testing, particularly with respect to long-term outcomes of ICD implantation.The study included 150 patients (125 men, 25 women, aged 59.0 ± 17.6 years) who underwent ICD or cardiac resynchronization therapy defibrillator implantation, with (n = 73) or without (n = 77) intraoperative DFT testing, between June 1996 and September 2007. VF was induced by delivery of a T-wave shock, and a 20-25-J shock was then delivered. If the 20-25-J shock failed to terminate VF, 30 J was delivered. We assessed whether undersensed VF events occurred during DFT testing and/or during patient follow-up and checked for any association between undersensing and delayed shock delivery. During DFT testing, fine VF was sensed, and shocks were delivered in a timely manner. Nevertheless, 2 patients in the DFT testing group died from VF within 3 years after device implantation.DFT testing, in comparison to non-DFT testing, appeared to have no influence on the long-term outcomes of our patients, suggesting that DFT testing at the time of ICD implantation is limited.

Clarifying the arrhythmogenic substrate for Brugada syndrome.

The right ventricular outflow tract (RVOT) is considered the arrhythmogenic region that gives rise to Brugada syndrome. To obtain a better understanding of this substrate, we performed electroanatomic mapping of the right ventricle (RV) in patients with Brugada syndrome. The RV was mapped electroanatomically with the CARTO system in 11 patients with asymptomatic Brugada syndrome but in whom ventricular fibrillation was induced by programmed ventricular stimulation, and in 5 control patients. The low voltage zone area (< 1.5 mV) was larger (16.1% versus 7.8%, P < 0.01) and the bipolar electrogram duration was greater (81.6 ± 7.8 ms versus 53.4 ± 5.6 ms, P < 0.01) in the patients with Brugada syndrome versus the control patients; the bipolar electrogram duration was greater in the septal portion and free wall of the RVOT. Our data suggest that regional endocardial conduction slowing based on structural abnormalities exists at the RVOT in Brugada syndrome.

Effects of quinidine on the action potential duration restitution property in the right ventricular outflow tract in patients with brugada syndrome.

BACKGROUND: On a cellular level, Brugada syndrome has been attributed to a deep phase 1 notch and subsequent shallow and prolonged repolarization in the right ventricular outflow tract (RVOT). A sodium channel mutation that leads to early inactivation of the late sodium current has been identified in some patients. Thus, drugs that inhibit the transient outward current (I(to)) responsible for the phase 1 notch and/or enhance the late sodium current might suppress arrhythmic events in patients with Brugada syndrome. The effects of quinidine gluconate, a potent inhibitor of I(to), on RVOT action potential duration (APD) restitution kinetics in patients with Brugada syndrome were evaluated. METHODS AND RESULTS: Programmed ventricular stimulation was performed in 9 Brugada syndrome patients by delivering up to 3 extrastimuli from the right ventricular apex and RVOT. RVOT monophasic action potentials (MAPs) were recorded before and after intravenous administration of quinidine (n=6) or ibutilide (n=3). All patients had inducible ventricular fibrillation (VF) before drug administration. Both quinidine and ibutilide increased steady-state and minimum RVOT MAP duration during programmed stimulation. Quinidine decreased the maximum slope of the RVOT APD restitution curve and VF could not be induced after administration of quinidine in 5 of the 6 patients. CONCLUSIONS: Quinidine appears to suppress the induction of VF by increasing RVOT MAP duration and decreasing the maximum slope of the restitution curve.

A new criteria differentiating type 2 and 3 Brugada patterns from ordinary incomplete right bundle branch block.

The type 1 (coved) ECG pattern is diagnostic for Brugada syndrome; types 2 and 3 require antiarrhythmic drug challenge to confirm its presence. We evaluated a 12-lead ECG-based criterion to differentiate between ordinary incomplete right bundle branch block (iRBBB) and true type 2 and 3 patterns that evolve toward type 1 during drug challenge. The subjects were 22 patients (21 men, 1 woman; mean age, 46.8 ± 13.2 years) referred for drug challenge (1 mg/kg pilsicainide, iv). In magnified ECG lead V1 and/or V2 with an iRBBB pattern, the baseline angle defined as the cross section of the upslope of the r' wave with the downslope of the r' wave was measured and compared between patients responding negatively versus positively to drug challenge, and was found to be significantly smaller in patients responding negatively (20.9 ± 12.9°, n = 6, versus 38.7 ± 16.5°, n = 13; P = 0.009). This ECG-based method successfully discriminates between the ordinary iRBBB pattern and drug-induced evolution toward a type 1 Brugada ECG.

Prolonged QRS duration in lead V2 and risk of life-threatening ventricular Arrhythmia in patients with Brugada syndrome.

Brugada syndrome is an inherited disorder that predisposes some patients to sudden cardiac death. It is not well established which Brugada syndrome patients are at risk of life-threatening arrhythmias. We investigated whether standard 12-lead electrocardiograms (ECG) can identify such patients. The subjects were 35 men with Brugada syndrome (mean age, 50.1 ± 12.4 years). Documented ventricular fibrillation or aborted sudden cardiac arrests were judged to be related to the Brugada syndrome. Ten patients (mean age, 49.6 ± 14.9 years) were symptomatic, and 25 (mean age, 50.3 ± 11.5 years) were asymptomatic. We determined the PR interval, QRS duration, and QT interval from baseline 12-lead ECG leads II and V2 as well as the J point elevation amplitude of lead V2. The QRS interval was measured from QRS onset to the J point in leads II and V2. The only significant difference between the symptomatic and asymptomatic patients was the QRS duration measured from lead V2. The mean QRS interval was 129.0 ± 23.9 ms in symptomatic patients versus 108.3 ± 15.9 ms in asymptomatic patients (P = 0.012). A QRS interval in lead V2 ≥ 120 ms was found to be a possible predictor of a life-threatening ventricular arrhythmia and/or syncope (P = 0.012). Prolonged QRS duration as measured on a standard 12-lead ECG is associated with ventricular arrhythmia and could serve as a simple noninvasive marker of vulnerability to life-threatening cardiac events in patients with Brugada syndrome.

Temperature-controlled cooled-tip radiofrequency linear ablation of the atria guided by a realtime position management system.

Due to the difficulty in producing a transmural linear lesion and the possibility of complications such as thrombus formation leading to thromboembolism, the catheter-based maze procedure remains problematic. We tested, in pigs, the possibility of using a temperature-controlled cooled-tip radiofrequency (RF) ablation system together with a realtime position management (RPM) system to create a transmural linear lesion uncomplicated by thrombus formation.Nine pigs underwent insertion of two electrode catheters (each with two ultrasound electrodes), one into the coronary sinus (CS) and one into the right ventricular apex (references for ultrasound-based non-fluoroscopic three-dimensional mapping). A cooled-tip catheter (with two ultrasound electrodes) was introduced into the right atrium. Linear right atrial ablation was performed with a custom radiofrequency (RF) generator. The catheter was perfused with 0.66 mL/second of saline. RF was delivered for 60 seconds at a target temperature of 40°C. A linear ablation line was created between the superior vena cava and inferior vena cava. Three-dimensional isochronal maps were created during CS pacing before and after ablation. In 4 of the 9 pigs, a transmural linear ablation line was confirmed by three-dimensional mapping and postmortem macroscopic examination. No endocardial thrombus formation was noted. Temperature-controlled cooled-tip RF linear ablation guided by an RPM system appears to have potential for creating linear lesions in the atria. Further studies are needed to determine whether such an ablation technique and the parameters used will facilitate successful completion of the catheter-based maze procedure.

A quantitative and qualitative analysis of the virtual unipolar electrograms from non-contact mapping of right or left-sided outflow tract premature ventricular contractions/ventricular tachycardia origins.

OBJECTIVE: This study was conducted to examine the virtual unipolar electrogram configuration of right/left outflow tract (OT) premature ventricular contraction (PVC)/ventricular tachycardia (VT) origins obtained from a non-contact mapping system (NCMS). METHODS: The subjects consisted of 30 patients with OT-PVCs/VT who underwent NCMS-guided ablation. We evaluated the virtual unipolar electrograms of the origin on 3D right ventricular (RV)-OT isochronal maps. RESULTS: Successful ablation was achieved from the RV in 20 patients (RVOT group), and it failed in 10 (non-RVOT group: including left-sided/pulmonary artery/deep RVOT foci). On the virtual unipolar electrograms, the earliest activation (EA) preceded the QRS onset by 11.2 ± 2.6 ms in the RVOT group and by 7.4 ± 10.5 ms in the non-RVOT group (P = 0.138). The negative slope of the electrogram at the EA site (EA slope(5)), quantified by the virtual unipolar voltage amplitude 5 ms after the EA onset, was significantly steeper in the RVOT group than in the non-RVOT group (0.66 ± 0.52 mV vs. 0.14 ± 0.17 mV, P = 0.005). Cutoff values for the EA-to-QRS onset time and EA slope(5) of ≥ 8 ms and >0.3 mV, respectively, completely differentiated the RVOT group from the non-RVOT group. A lesser EA slope(5) was associated with a greater radiofrequency energy delivery required to terminate RVOT-PVCs/VT. CONCLUSIONS: These demonstrate the importance of the virtual unipolar electrograms from OT-PVC/VT origins obtained with the NCMS. The virtual EA predicts both successful and potentially difficult ablation sites from the RV side.

Functional atrioventricular conduction block in an elderly patient with acquired long QT syndrome: elucidation of the mechanism of block.

The long QT syndrome (LQTS) is occasionally complicated by impaired atrioventricular (AV) conduction. This form of LQTS can manifest before birth or during neonatal life, and no previous report has demonstrated LQTS complicated by impaired AV conduction in elderly patient. This case report describes an elderly patient with an acquired form of LQTS who developed ventricular fibrillation that was successfully defibrillated during admission to the hospital. Electrophysiologic study demonstrated that HV interval was 38 milliseconds and QT interval was 635 milliseconds during sinus rhythm cycle length of 1167 milliseconds. 1:1 AV conduction was maintained to a pacing cycle length of 545 milliseconds with an AH interval of 144 milliseconds, HV interval of 44 milliseconds, and right ventricular monophasic action potential duration of 360 milliseconds. However, 2:1 HV block developed at a pacing cycle length of 500 milliseconds. Intravenous administration of mexiletine decreased the cycle length of developing HV block to 360 milliseconds.

Ventricular fibrillation induced by radiofrequency ablation for slow ventricular tachycardia associated with left ventricular dysfunction.

A 59-year-old man with premature ventricular contractions (PVCs) and slow ventricular tachycardia (VT) underwent electrophysiologic testing. The left ventricular ejection fraction was 27%. Activation mapping showed the site of earliest activation to be the posterolateral site of the right ventricle inflow tract, and we considered this to be the focal mechanism underlying the PVCs/slow VT. Radiofrequency current delivered at this site induced a cluster of rapid ventricular beats (sustained VT) with the same QRS morphology as the PVCs, followed by ventricular fibrillation. The PVC/VT focus might have served as an abnormal automatic trigger and driver for the ventricular fibrillation.

Upper turnaround point of the reentry circuit of common atrial flutter--three-dimensional mapping and entrainment study.

BACKGROUND: Although the anterior and posterior boundaries of cavotricuspid isthmus-dependent atrial flutter (AFL) are reported to be located at the tricuspid annulus and sinus venosa region or crista terminalis, the exact upper turnaround point of the AFL circuit remains unclear. The aim of this study was to determine the upper turnaround site of the AFL circuit by means of three-dimensional (3D) mapping and entrainment pacing. METHODS: Subjects were 21 patients with counter-clockwise AFL in whom high-density mapping of the high right atrium (RA) and superior vena cava (SVC) orifice was performed with an electroanatomical or non-contact mapping system. Entrainment pacing was performed around the SVC-RA junction. RESULTS: In 20 of the 21 patients, the wavefront from the septal RA split into two wavefronts: one that traveled anterior to the SVC and another that traveled to the posterior RA where it was blocked. In the remaining patient, the wavefront from the septal RA split into two wavefronts: one that propagated through the anterior portion of the SVC orifice and another that propagated transversely across the posterior portion of the SVC orifice. The two wavefronts joined in the lateral RA. Entrainment pacing from the SVC-RA junction demonstrated that the anterior boundary was within the circuit in all patients, but the posterior boundary also constituted a circuit in four patients. CONCLUSIONS: We surmise that the upper turnaround site of the AFL circuit is located in the anterior portion of the SVC-RA junction in the majority of patients with AFL.

Electrical remodeling in fibrillating canine atrium: action potential alternans during rapid atrial pacing and late phase 3 early afterdepolarization after cessation of rapid atrial pacing.

Sustained atrial fibrillation (AF) was induced by atrial burst pacing, and monophasic action potentials (MAPs) were recorded. MAP alternans was observed at a cycle length (CL) of 167.5 ± 28.2 msec before burst pacing and 201.3 ± 40.2 msec after burst pacing. AF > 5 minutes duration was induced in 1 dog in the control condition but in all 8 dogs after burst pacing. The difference in RA MAPD(80) of the first spontaneous beat and steady-state sinus rhythm was significantly larger after atrial burst pacing than before atrial burst pacing (31.5 ± 15.9 msec versus 8.2 ± 9.0 msec) In 4 dogs, late phase 3 early after depolarization was observed after rapid atrial pacing. Rapid atrial pacing-induced electrical remodeling includes APD alternans during rapid atrial pacing and also causes an increase in the MAPD of the initial several beats and the development of late phase 3 early afterdepolarizations after a sudden increase in CL.

Abnormal atrial repolarization and depolarization contribute to the inducibility of atrial fibrillation in Brugada syndrome.

Brugada syndrome is often accompanied by atrial tachyarrhythmia, such as atrial fibrillation (AF). The aim of this study was to examine atrial vulnerability in patients with Brugada syndrome. Two groups of patients were compared: 18 patients with Brugada syndrome (Brugada syndrome group) and 11 age-matched patients with neither organic heart disease nor AF episodes (control group). Programmed electrical stimulation was performed from the right atrium (RA), and the effective refractory period of the right atrium (ERP-RA), interatrial conduction time (IACT), monophasic action potentials (MAPs) at the high RA, and the inducibility of AF lasting > 30 seconds were studied. MAP duration at 80% repolarization (MAPD(80)) was calculated. AF was induced with a single extrastimulus or double extrastimuli in all patients with Brugada syndrome but in none of the control patients. The ERP-RA did not differ between the groups. IACT at the shortest diastolic interval was significantly increased in the Brugada syndrome group compared to that in the control group. The maximum slope of the MAPD(80) restitution curve was significantly steeper in the Brugada syndrome group than in the control group (2.4 + or - 2.0 versus 0.82 + or - 0.36, P < 0.02). Ventricular fibrillation was induced with ventricular programmed stimulation in all Brugada syndrome patients. Both abnormal interatrial conduction and steep restitution of action potential duration may contribute to the atrial arrhythmogenicity in Brugada syndrome.

Temperature-controlled cooled-tip radiofrequency ablation in left ventricular myocardium.

Steam pop and intramural charring have been reported during cooled-tip radiofrequency catheter ablation (RFCA). We studied the feasibility of temperature-controlled cooled-tip RFCA in the canine heart.An internally cooled ablation catheter was inserted into the left ventricle. A custom-made radiofrequency (RF) generator capable of controlling the tip-temperature at the preset level by slow increases in the power was used. Temperature-controlled cooled-tip RF applications were performed at a target temperature of 40 degrees C for 90 seconds. Acute study: Intramyocardial temperature was measured at the ablation site in 10 dogs by inserting a fluoroptic probe. Chronic study: Lesion depth and volume were measured in 5 dogs after 3 weeks of survival. In the acute study, no pop or abrupt impedance rise was observed. Maximum intramyocardial temperature was 72.4 + or - 14.4 degrees C at 2-4 mm above the endocardium. No coagulum formation, craters, or intramural charring were observed. Maximum lesion depth was 6.7 + or - 1.5 mm, and lesion volume was 404 + or - 219 mm3. In the chronic study, maximum lesion depth was 5.9 + or - 1.1 mm, and lesion volume was 281 + or - 210 mm(3).Temperature controlled RFCA is feasible with a cooled-tip catheter and an RF generator that slowly increases the RF power until the preset catheter-tip temperature is reached.

Abnormal action potential duration restitution property in the right ventricular outflow tract in Brugada syndrome.

BACKGROUND: Although patients with Brugada syndrome (BS) are at risk of ventricular fibrillation (VF) and ensuing death, the action potential duration (APD) restitution properties of the right ventricular outflow tract (RVOT) in patients with BS remain undetermined. METHODS AND RESULTS: Endocardial monophasic action potentials (MAPs) were obtained from 16 patients with BS and 17 control patients. MAPs were recorded from the RVOT in all patients. The MAP duration at 90% repolarization (MAPD(90)), effective refractory period (ERP), and maximum slope of the APD restitution curve were obtained. VF was induced with up to 3 extrastimuli from the RV apex or RVOT. There was no difference in MAPD(90) between the 2 groups, but the ERP was significantly shorter in patients with BS than in control patients (210.7+/-10.5 vs 223.8+/-13.4 ms, P=0.008). MAPD at the shortest diastolic interval was significantly shorter in patients with BS than in control patients (149.9+/-19.9 vs 179.8+/-13.7 ms, P<0.001). The maximum slope of the APD restitution curve was steeper in patients with BS than in control patients (2.90+/-1.29 vs 1.38+/-0.41, P<0.001). CONCLUSIONS: The shorter ERP, shorter MAPD at the shortest diastolic interval and steeply sloped APD restitution curve in the RVOT appear to be related to the inducibility of VF in patients with BS.

Right ventricular histological substrate and conduction delay in patients with Brugada syndrome.

The reported pathogenesis of Brugada syndrome is phase 2 reentry resulting from shortening of the epicardial action potential duration at the right ventricular outflow tract (RVOT). However, several studies have revealed a high incidence of ventricular late potentials and high rate of ventricular fibrillation (VF) induced by programmed ventricular stimulation (PVS). The aim of the present study was to evaluate the role of slow conduction at the RVOT for the initiation of VF by PVS and any underlying pathological conditions in Brugada syndrome. Endocardial mapping of the RVOT and endomyocardial biopsy of the right ventricle were performed in 25 patients with Brugada syndrome with inducible VF. Late potentials were positive in 11 of the 25 (44%) patients. Low-amplitude fragmented and delayed electrograms were recorded at the RVOT in 13 of 18 (72.2%) patients. Histologic examination of the biopsy samples revealed fatty tissue infiltration, interstitial fibrosis, lymphocyte infiltration, and/or myocyte disorganization in 13 patients. Slow conduction at the RVOT may contribute to the induction of VF by PVS in Brugada syndrome. Various pathomorphologic changes may contribute to slow conduction at the RVOT.

Local conduction block of the atria by premature stimulus in a patient with Brugada syndrome.

A 46-year-old man with type II Brugada electrocardiogram pattern changed to a type I Brugada type electrocardiogram pattern by class I antiarrhythmic drug (pilsicainide) underwent electrophysiologic study. Ventricular fibrillation was induced by double extrastimuli from the right ventricular (RV) apex. Monophasic action potentials (MAPs) were then recorded from the high right atrium. Duration of MAP at a coupling interval of 220 milliseconds was 122 milliseconds, and local activation of S2 spread to the left atrium. However, MAP at a coupling interval of 210 milliseconds was 112 milliseconds, and local activation of S2 failed to spread to the rest of atrium.

Comparison of endocardial and epicardial lesion size following large-tip and extra-large-tip transcatheter cryoablation.

BACKGROUND: The efficacy of transcatheter cryoablation for ventricular tachycardia (VT) remains controversial because of the limited size of the lesion produced. An increased lesion size if the cryoablation catheter profile and catheter tip length were increased was hypothesized. METHODS AND RESULTS: Closed-chest transcatheter cryoablation was applied with 7F, 6-mm tip (n=11, 7F group) and 9F, 8-mm tip (n=8, 9F group) catheters to the left ventricular (LV) endocardium and epicardium. Catheter-tip temperature was set to -70 to -80 degrees C, and cryoablation duration was set to 240 s. In acute experiments in the 7F group, endocardial lesion volume was 144.1 +/-86.0 mm(3) and lesion depth was 5.1 +/-1.6 mm, and epicardial lesion volume was 205.6 +/-157.8 mm(3) and lesion depth was 4.7 +/-2.2 mm. In the 9F group, endocardial lesion volume was 301.5 +/-177.4 mm(3) (P<0.001 vs 7F group) and lesion depth was 8.4 +/-1.9 mm (P<0.001 vs 7F group), and epicardial lesion volume was 375.3 +/-167.6 mm(3) (P<0.01 vs 7F group) and lesion depth was 5.0 +/-2.3 mm. CONCLUSIONS: Transcatheter cryoablation of the LV endocardium and epicardium using a larger profile and longer tip electrode may be useful for treating VT originating from the midmyocardium or epicardium.

Surface ECG characteristics of ventricular tachyarrhythmias before degeneration into ventricular fibrillation in patients with Brugada-type ECG.

This study was designed to evaluate whether the right ventricular outflow tract (RVOT) is the arrhythmogenic focus in Brugada syndrome. We enrolled 45 patients with Brugada-type ECG who underwent programmed ventricular stimulation and inducible ventricular fibrillation (VF). In 25 of these 32 patients, repetitive VT was observed before degeneration into VF. The QRS morphology of surface ECG and intracardiac electrograms were evaluated to determine the origin of the ventricular tachycardia (VT) that degenerated into VF. The VT morphology was a left bundle branch block pattern with an inferior axis in 22 of 28 VTs and the intracardiac conduction sequence during VT revealed activation from the RVOT to the RV apex in these 22 VTs. The majority of the patients with Brugada syndrome showed repetitive VT originating from the RVOT that degenerated into VF. The RVOT may be an arrhythmogenic focus in patients with Brugada syndrome.

Left bundle branch block-type ventricular tachycardia originating from the left ventricular septum in a patient with cardiac sarcoidosis.

This case report describes a left bundle branch block (LBBB)-type ventricular tachycardia (VT) with a unique reentrant circuit in a patient with cardiac sarcoidosis. The VT morphology and pace mapping supported an exit site of the VT from the basal posterior right ventricle (RV) septum. Nonetheless, concealed entrainment was established by pacing from a septal left ventricular (LV) site recording a diastolic potential, opposite site to the RV site. A point ablation at that LV site could successfully terminate the VT, suggesting that a critical isthmus was located on the LV side of the interventricular septum despite the demonstration of an LBBB-type VT.