How to manage the patient with a high defibrillation threshold.
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Biomedical subjects
Publications and source records attributed to David J Callans.
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BACKGROUND: Atrial fibrillation (AF) manifests disorganized atrial activity and irregular R-R intervals on electrocardiogram (ECG). Variation in R-R intervals can also be seen with other supraventricular tachycardias that may mimic AF. OBJECTIVE: We report our observations on three patients who were referred to our center to undergo pulmonary vein (PV) isolation for erroneously diagnosed AF in the setting of dual atrio-ventricular (AV) nodal pathways manifesting as AV nodal reentrant tachycardia (AVNRT) and/or double response during sinus rhythm. METHODS AND RESULTS: These three subjects (two females) were derived from a group of 456 consecutive patients undergoing AF ablation at our center over a 3-year period. All three patients had been symptomatic for over 2 years, having failed two or more antiarrhythmic medications. In each case AF was initially diagnosed on ECG and/or recordings from ambulatory monitoring. However, in all three cases the correct diagnosis was established during the invasive electrophysiologic study. In one patient during the stimulation protocol, two narrow complex tachycardias were serially induced (cycle lengths: 305 and 360 msecs; VA time: 60 and 240 msecs). The latter was confirmed to be atypical AVNRT and during this tachycardia, block in upper pathway was observed. In the other two patients, sinus rhythm with repetitive runs of double response and isolated junctional beats were observed in the absence of retrograde conduction. Successful slow pathway modification was performed in each subject and all three patients have remained arrhythmia free over a mean follow-up of 31 +/- 16 months off antiarrhythmic medications. CONCLUSIONS: AF can be erroneously diagnosed in patients with dual AV nodal pathways manifesting double response and/or AVNRT. Incorporating a stimulation protocol as a part of the AF ablation procedure may help in diagnosing these rare clinical presentations that can be cured by slow pathway modification alone.
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OBJECTIVES: The purpose of this study was to (1) determine how often implantable cardioverter-defibrillator (ICD) system modifications were needed to obtain an adequate safety margin for defibrillation, (2) identify how often and for what indications defibrillation threshold (DFT) testing was not performed, and (3) identify factors predicting the need for modification. BACKGROUND: Ventricular fibrillation (VF) typically is induced at the time of ICD insertion. Although DFT testing often is minimized, a safety margin of 10 J has been utilized as a standard of care. However, current devices offer technology such as biphasic waveforms and high outputs, and the need for testing has been questioned. METHODS: We reviewed the records of the last 1,139 patients undergoing initial ICD placement, generator replacement, or revision. RESULTS: Seventy-one patients (6.2%) were identified as having an unacceptably high DFT (<10 J safety margin) requiring intervention, and some required >1 modification. Use of a high-output device alone was not enough to obtain an adequate DFT in 48% (34/71) of patients who required modifications (3% of the total population). No arrhythmia inductions were performed in 54 patients (4.7%) because of well-defined clinical conditions. Patients who required system modification had a lower ejection fraction, were younger, were less likely to have coronary artery disease, were more likely to be undergoing upgrade/generator replacement, and were more likely to be taking amiodarone. Long-term mortality was not different between the group of patients who required modification compared with those who did not (17% vs 20%, P = NS). CONCLUSIONS: Routine VF induction and documentation of effective defibrillation still remains a reasonable part of ICD placement because an inadequate safety margin may occur in >6% of patients. The incidence of patients who were inappropriate for testing based on well-defined clinical conditions is small (<5%) in this unselected large series. Although some clinical features may predict the need for system modification, additional studies are needed to better define "acceptable efficacy" of ICDs in preventing sudden death prior to altering these standards in selected patients.
BACKGROUND: Idiopathic ventricular tachycardias (IVTs) can originate from the basal left ventricle (LV). OBJECTIVE: To determine if using magnetic electroanatomic mapping (MEAM) for accurate localization (1) unique ECG morphologies on pace maps from medial and lateral sites in basal LV could be identified and (2) this ECG information would facilitate VT localization. METHODS: In 12 patients with structurally normal hearts undergoing ablation for IVT, detailed MEAM of LV was constructed in sinus rhythm and pace-mapping was done from the septal-parahisian (S-P) region, aortomitral continuity (AMC), and superior, superolateral, and lateral mitral annular (MA) locations. Pace maps were analyzed for ECG morphologies in limb leads and transition patterns in precordial leads. RESULTS: Medial pacing sites (S-P and AMC) compared with lateral sites (superolateral and lateral MA) demonstrated narrower QRS complexes (134 +/- 24 msec vs. 182 +/- 18 msec; P < .05) with initial negative forces in lead V1 and predominantly positive forces in lead I (amplitude 0.59 +/- 0.27 mV vs. 0.16 +/- 0.34 mV; P < .05). The ratio of QRS complexes in leads II and III was >1 for all (12 of 12) S-P pace maps and 11 of 12 lateral MA pace maps but remained < or =1 for pace maps from 10 of 12 AMC locations, 11 of 12 superior MA locations, and 10 of 11 superolateral MA locations. Using these ECG criteria, a blinded reviewer was able to accurately localize the site of origin (SOO) of clinical arrhythmia (successful ablation site on MEAM) in 10 of 12 cases (83%) of IVT originating from basal LV. CONCLUSION: Pace maps from basal LV endocardium manifest site-dependent ECG morphologies that can help differentiate medial from lateral locations and can predict the SOO of clinical arrhythmias from this region.
Cardiac arrhythmias continue to pose a major medical challenge and significant public health burden. Atrial fibrillation, the most prevalent arrhythmia, affects more than two million Americans annually and is associated with a twofold increase in mortality. In addition, more than 250,000 Americans each year suffer ventricular arrhythmias, often resulting in sudden cardiac death. Despite the high incidence and societal impact of cardiac arrhythmias, presently there are insufficient insights into the molecular mechanisms involved in arrhythmia generation, propagation, and/or maintenance or into the molecular determinants of disease risk, prognosis, and progression. In addition, present therapeutic strategies for arrhythmia abatement often are ineffective or require palliative device therapy after persistent changes in the electrical and conduction characteristics of the heart have occurred, changes that appear to increase the risk for arrhythmia progression. This article reviews our present understanding of the complexity of mechanisms that regulate cardiac membrane excitability and cardiac function and explores the role of derangements in these mechanisms that interact to induce arrhythmogenic substrates. Approaches are recommended for future investigations focused on providing new mechanistic insights and therapeutic interventions.
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BACKGROUND: Idiopathic "fascicular" left ventricular tachycardia (IFLVT) is frequently not inducible or nonsustained at the time of planned catheter ablation. The mechanism of the arrhythmia has been suggested to be reentry involving a sizable area of the LV inferior septum extending from base toward the apex. OBJECTIVE: We tested the ability of a series of radiofrequency lesions delivered in a linear fashion to the inferior-mid septum to control ventricular tachycardia not amenable to standard mapping ablation strategies. METHODS: Programmed stimulation both at baseline state and with isoproterenol after heart rate was increased by at least 25% was performed in all patients. The patients included in the study were either non-inducible or only had brief nonsustained VT not amenable to "traditional" mapping. A detailed electroanatomic map of the LV was performed in sinus rhythm. The location of the linear lesion along the inferior septum was guided by the presence of Purkinje potentials, with pacemapping as an additional guide. A linear lesion was placed perpendicular to the long axis of the ventricle approximately midway from the base to the apex in the region of the mid to mid-inferior septum. Radiofrequency lesions were delivered using a 4mm tip catheter at 50 Watts and 52 degrees for 60-90 seconds. RESULTS: Of 122 consecutive patients who underwent ablation of idiopathic VT from 1999 to 2003, 15 had IFLVT based on standard diagnostic criteria. Six of the 15 patients (40%) had nonsustained or no inducible VT in the EP lab. The number of RF lesions ranged from 7 to 15 (mean 9). The length of the effective linear lesion ranged from 1.2 to 2.2 cm (mean 1.7 cm). Development of left posterior fascicular block was noted in two of the six patients. However, despite the absence of development of left posterior fascicular block in the other four patients, no VT or premature ventricular beats could be induced after ablation using the same provocation maneuvers as performed in the baseline state. No spontaneous arrhythmias occurred during follow-up to 16 +/- 8 months (range 6 to 30 months). CONCLUSION: In patients with difficult to induce or nonsustained VT with the typical right bundle branch block pattern and a superiorly directed axis on 12-lead ECG, RF energy ablation delivered in a linear fashion approximately midway to two thirds toward the apex along the mid to inferior septum and perpendicular to the plane of the septum is safe and effective for VT control.
BACKGROUND: Both focal and macroreentrant atrial tachycardia (ATs) can occur after pulmonary vein (PV) isolation for treatment of atrial fibrillation (AF). We report the response to pacing and pharmacologic maneuvers performed in patients with stable focal ATs after segmental PV isolation. OBJECTIVES: The purpose of this study was to determine the mechanism of focal ATs occurring after PV isolation. METHODS: Patients with persistent left AT after cessation of antiarrhythmic drug therapy presented for mapping and ablation. Electroanatomic mapping during AT was performed. Entrainment was performed from multiple right and left atrial sites. Single-beat resetting was performed. Adenosine was infused intravenously to determine the effect on the tachycardia. RESULTS: Five patients (3 men and 2 women; age 65 +/- 10 years) had focal left AT that persisted in response to pacing maneuvers. Four patients had ATs (cycle length 265 +/- 18 ms) that demonstrated focal areas of early activation at the septal aspect of the right lower (3 patients) or right upper (1 patient) PV ostium. Resetting demonstrated a flat-plus increasing curve in two patients. Adenosine was infused with transient AV block and no change to the tachycardia cycle length in three patients. Tachycardias were entrained from multiple left atrial sites. Recordings from the ablation catheter at the critical isthmus typically demonstrated mid-diastolic or long fractionated potentials. One tachycardia with a longer and more variable cycle length (480-598 ms) did not demonstrate fusion during pacing from distant sites. CONCLUSION: Persistent focal left ATs may occur after segmental PV isolation. Many of these tachycardias are caused by a focal reentrant circuit located at the PV ostium; however, focal nonreentrant rhythms also may occur.
INTRODUCTION: A 10% incidence of left atrial (LA) thrombus formation has been detected using intracardiac echocardiography (ICE) imaging monitoring during LA ablation for atrial fibrillation (AF). The aim of this study was to determine if the intensity of anticoagulation reduces LA thrombus formation during pulmonary vein isolation procedure in patients with AF and spontaneous echo contrast (SEC). METHODS AND RESULTS: We studied 511 patients (age 56 +/- 10 years) undergoing pulmonary vein ostial isolation/ablation using radiofrequency energy. SEC was detected in 179 of 511 patients with ICE imaging before dual transseptal catheterization. All patients were anticoagulated with heparin to achieve activated clotting time (ACT) 250-300 seconds (group I) or >300 seconds (group II) confirmed at 30-minute intervals. SEC was detected in 49/294 (16.7%) patients in group I versus 130/217 (59.9%) in group II (P < 0.0001). LA thrombus was observed in 33/294 (11.2%) patients in group I versus 6/217 (2.8%) in group II (P < 0.05). For those patients with SEC, LA thrombus was observed in 22/49 (44.9%) in group I versus 2/61 (4.6%) in group II (P < 0.0001). There were no significant differences in age, number of unsuccessful drugs, persistent AF, left ventricular ejection fraction, and LA diameter between the two groups. No clinical embolic event was observed with withdrawal of LA thrombus to the RA. CONCLUSION: ICE-diagnosed SEC before transseptal catheterization identifies an increased risk of LA thrombus. Increased intensity of heparin anticoagulation (ACT >300 seconds) during LA ablation for AF may prevent LA thrombus formation especially in patients with SEC.
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BACKGROUND: Recent studies have demonstrated spatiotemporal organization in atrial fibrillation (AF), with a left-to-right atrial frequency gradient during AF in isolated sheep hearts. We hypothesized that human AF would also manifest a left-to-right atrial frequency gradient. METHODS AND RESULTS: Thirty-one patients aged 56.7+/-10.5 years with a history of paroxysmal or persistent (>1 month) AF were included. Recordings were made at each pulmonary vein (PV) ostium and simultaneously from the coronary sinus (CS) and posterior right atrium (RA) during AF. Sequential fast Fourier transforms (FFTs) were performed. FFT profiles were analyzed to determine the dominant frequency (DF). There were 18 patients with paroxysmal AF and 13 with persistent AF. In the paroxysmal group, there was a significant left-to-right atrial DF gradient, with DF highest at the PV/left atrial (LA) junction, intermediate at the CS, and lowest in the RA (6.2+/-0.8, 5.5+/-0.7, and 5.1+/-0.6 Hz, respectively; P<0.001). There were no patients in whom DF was greater at the RA than the PV/LA junction. In the persistent group, there was no significant difference between DF recorded from the LA/PV junction, CS, and RA (6.1+/-0.7, 5.8+/-0.6, and 5.8+/-0.6 Hz, respectively; P=NS). CONCLUSIONS: In humans with paroxysmal AF, DFs are highest at the PV/LA junction, intermediate in the CS, and slowest in the posterior RA. These findings agree with animal models that suggest that the posterior LA may play an important role in maintaining paroxysmal AF. The role of the posterior LA in persistent AF requires further study.
BACKGROUND: Identifying the septal versus lateral site of origin of ventricular tachycardia (VT) with a right bundle-branch block (RBBB)-type pattern and an R-S ratio >1 in lead V1 is difficult with the 12-lead ECG, especially in patients with prior apical infarction. METHODS AND RESULTS: We prospectively evaluated 58 patients with VT. Sixteen patients had apical infarcts (group 1), 29 had nonapical infarcts (group 2), and 13 had no heart disease (group 3). QRS complex onset to activation at the right ventricular apex (stim-RVA) was measured during left ventricular (LV) apical septal and lateral pacing, and 47 RBBB-type VTs (QRS-RVA) were localized to the septal or lateral apex by using entrainment techniques. Pacing and VT site of origin were confirmed by electroanatomic mapping. The stim-RVA time was 59+/-16 ms for septal versus 187+/-24 ms for lateral sites in group 1, P<0.001; 70+/-14 ms for septal versus 169+/-19 ms for lateral sites in group 2, P<0.001; and 42+/-15 ms for septal versus 86+/-16 ms for lateral sites in group 3, P<0.005. The QRS-RVA time was 50+/-13 ms for apical septal VTs versus 178+/-21 ms for lateral VTs in group 1, P<0.001; 71+/-17 ms for apical septal versus 157+/-20 ms for lateral VTs in group 2, P<0.001; and 32+/-12 ms for septal versus 71+/-16 ms for lateral VTs in group 3, P<0.01. CONCLUSIONS: The QRS-RVA differs for the VT site of origin from the LV septal versus lateral apex. These data prove useful in rapidly regionalizing the VT site of origin with a V1 R-S ratio >1, particularly in instances of an apical infarct, where surface ECG distinctions are less identifiable.
BACKGROUND: To gain insight into the pathogenesis of right ventricular (RV) cardiomyopathy and ventricular tachycardia (VT), we determined the clinical and electroanatomic characteristics and outcome of ablative therapy in consecutive patients with (1) RV dilatation, (2) multiple left bundle-branch block (LBBB)-type VTs, and (3) an abnormal endocardial substrate defined by contiguous electrogram abnormalities. METHODS AND RESULTS: All 21 patients had detailed RV bipolar electrogram voltage mapping. Eighteen patients had simultaneous left ventricular (LV) mapping, including all 4 patients with right bundle-branch block (RBBB) VT. VT was ablated in 19 patients by use of focal and/or linear lesions with irrigated-tip catheters in 10 of 19 patients. Eighteen patients were men, age 47+/-18 years, and none had a family history of RV dysplasia. RV volume was 223+/-89 cm3. Electrogram abnormalities extended from perivalvular tricuspid valves (5 patients), pulmonic valves (6 patients), or both valves (10 patients). Electrogram abnormalities always involved free wall, spared the apex, and included the septum in 15 patients (71%). The area of abnormality was 55+/-37 cm2 (range, 12 to 130 cm2) and represented 34+/-19% of the RV. In 52 of 66 LBBB VTs, the origin was from the RV perivalvular region. LV perivalvular low-voltage areas noted in 5 patients were associated with a RBBB VT origin. No VT recurred after ablation in 17 patients (89%) during 27+/-22 months. CONCLUSIONS: In patients with RV cardiomyopathy and VT, (1) perivalvular electrogram abnormalities represent the commonly identified substrate and source of most VT, (2) LV perivalvular endocardial electrogram abnormalities and VT can occasionally be identified, and (3) aggressive ablative therapy provides long-term VT control.
BACKGROUND: A proarrhythmic consequence of pulmonary vein (PV) isolation can be a recurrent organized left atrial (LA) tachycardia after ablation. This arrhythmia is frequently referred to as "left atrial flutter," but the mechanism and best ablation strategy have not been determined. METHODS AND RESULTS: Isolation of arrhythmogenic PVs was initially performed by segmental ostial PV ablation guided by a circular mapping catheter in 341 patients. Patients whose predominant recurrent arrhythmia was a persistent organized tachycardia returned for mapping and ablation. Recurrent organized LA tachycardias (cycle length 253+/-33 ms, range 213 to 328 ms) occurred in 10 (2.9%) of 341 patients (age 59+/-9 years, 1 woman). Mapping was consistent with a focal origin in 8 patients and with macroreentry in 1 patient and was unclear in 1 patient owing to degeneration to atrial fibrillation. Focal tachycardias originated from reconnected segments of prior isolated PVs (6 patients), the posterior LA (1 patient), or the superior septum (1 patient). Focal atrial tachycardias were ablated with point lesions that targeted the earliest activation. All reconnected PVs were also reisolated. Reentrant LA flutter occurred around the left PVs in 1 patient. After 6.7+/-2.3 months of follow-up, 9 (90%) of 10 patients were arrhythmia free (4 of whom were taking antiarrhythmic drug therapy), and one was having recurrent atrial fibrillation. CONCLUSIONS: Recurrent organized LA tachycardia after PV isolation is uncommon and typically has a focal origin from reconnected PV ostia. Reisolation of the PV and ablation of non-PV foci are sufficient to treat this proarrhythmia. Linear lesions are only required when a macroreentrant mechanism is present.
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