A multi-center experience of ablation index for evaluating lesion delivery in typical atrial flutter.

BACKGROUND: Anatomical studies demonstrate significant variation in cavotricuspid isthmus (CTI) architecture. METHODS: Thirty-eight patients underwent CTI ablation at two tertiary centers. Operators delivered 682 lesions with a target ablation index (AI) of 600 Wgs. Ablation parameters were recorded every 10-20 ms. Post hoc, Visitags were trisected according to CTI position: inferior vena cava (IVC), middle (Mid), or ventricular (V) lesions. RESULTS: There were no complications. 92.1% of patients (n = 35) remained in sinus rhythm after 14.6 ± 3.4 months. For the whole CTI, peak AI correlated with mean impedance drop (ID) (R2  = 0.89, p < .0001). However, analysis by anatomical site demonstrated a non-linear relationship Mid CTI (R2  = 0.15, p = .21). Accordingly, while mean AI was highest Mid CTI (IVC: 473.1 ± 122.1 Wgs, Mid: 539.6 ± 103.5 Wgs, V: 486.2 ± 111.8 Wgs, ANOVA p < .0001), mean ID was lower (IVC: 10.7 ± 7.5Ω, Mid: 9.0 ± 6.5Ω, V: 10.9 ± 7.3Ω, p = .011), and rate of ID was slower (IVC: 0.37 ± 0.05 Ω/s, Mid: 0.18 ± 0.08 Ω/s, V: 0.29 ± 0.06 Ω/s, p < .0001). Mean contact force was similar at all sites; however, temporal fluctuations in contact force (IVC: 19.3 ± 12.0 mg/s, Mid: 188.8 ± 92.1 mg/s, V: 102.8 ± 32.3 mg/s, p < .0001) and catheter angle (IVC: 0.42°/s, Mid: 3.4°/s, V: 0.28°/s, p < .0001) were greatest Mid CTI. Use of a long sheath attenuated these fluctuations and improved energy delivery. CONCLUSIONS: Ablation characteristics vary across the CTI. At the Mid CTI, higher AI values do not necessarily deliver more effective ablation; this may reflect localized fluctuations in catheter angle and contact force.

Differences in the upslope of the precordial body surface ECG T wave reflect right to left dispersion of repolarization in the intact human heart.

BACKGROUND: The relationship between the surface electrocardiogram (ECG) T wave to intracardiac repolarization is poorly understood. OBJECTIVE: The purpose of this study was to examine the association between intracardiac ventricular repolarization and the T wave on the body surface ECG (SECGTW). METHODS: Ten patients with a normal heart (age 35 ± 15 years; 6 men) were studied. Decapolar electrophysiological catheters were placed in the right ventricle (RV) and lateral left ventricle (LV) to record in an apicobasal orientation and in the lateral LV branch of the coronary sinus (CS) for transmural recording. Each catheter (CS, LV, RV) was sequentially paced using an S1-S2 restitution protocol. Intracardiac repolarization time and apicobasal, RV-LV, and transmural repolarization dispersion were correlated with the SECGTW, and a total of 23,946 T waves analyzed. RESULTS: RV endocardial repolarization occurred on the upslope of lead V1, V2, and V3 SECGTW, with sensitivity of 0.89, 0.91, and 0.84 and specificity of 0.67, 0.68, and 0.65, respectively. LV basal endocardial, epicardial, and mid-endocardial repolarization occurred on the upslope of leads V6 and I, with sensitivity of 0.79 and 0.8 and specificity of 0.66 and 0.67, respectively. Differences between the end of the upslope in V1, V2, and V3 vs V6 strongly correlated with right to left dispersion of repolarization (intraclass correlation coefficient 0.81, 0.83, and 0.85, respectively; P <.001). Poor association between the T wave and apicobasal and transmural dispersion of repolarization was seen. CONCLUSION: The precordial SECGTW reflects regional repolarization differences between right and left heart. These findings have important implications for accurately identifying biomarkers of arrhythmogenic risk in disease.

Pharmacological Modulation of Right Ventricular Endocardial-Epicardial Gradients in Brugada Syndrome.

Background We explored the hypothesis that increased cholinergic tone exerts its proarrhythmic effects in Brugada syndrome (BrS) through increasing dispersion of transmural repolarization in patients with spontaneous and drug-induced BrS. Methods BrS and supraventricular tachycardia patients were studied after deploying an Ensite Array in the right ventricular outflow tract and a Cardima catheter in the great cardiac vein to record endo and epicardial signals, respectively. S1-S2 restitution curves from the right ventricular apex were conducted at baseline and after edrophonium challenge to promote increased cholinergic tone. The local unipolar electrograms were then analyzed to study transmural conduction and repolarization dynamics. Results The study included 8 BrS patients (5 men:3 women; mean age, 56 years) and 8 controls patients with supraventricular tachycardia (5 men:3 women; mean age, 48 years). Electrophysiological studies in controls demonstrated shorter endocardial than epicardial right ventricular activation times (mean difference: 26 ms; P<0.001). In contrast, patients with BrS showed longer endocardial than epicardial activation time (mean difference: -15 ms; P=0.001). BrS hearts, compared with controls, showed significantly larger transmural gradients in their activation recovery intervals (mean intervals, 20.5 versus 3.5 ms; P<0.01), with longer endocardial than epicardial activation recovery intervals. Edrophonium challenge increased such gradients in both controls (to a mean of 16 ms [ P<0.001]) and BrS (to 29.7 ms; P<0.001). However, these were attributable to epicardial and endocardial activation recovery interval prolongations in control and BrS hearts, respectively. Dynamic changes in repolarization gradients were also observed across the BrS right ventricular wall in BrS. Conclusions Differential contributions of conduction and repolarization were identified in BrS which critically modulated transmural dispersion of repolarization with significant cholinergic effects only identified in the patients with BrS. This has important implications for explaining the proarrhythmic effects of increased vagal tone in BrS, as well as evaluating autonomic modulation and epicardial ablation as therapeutic strategies.

Ventricular stimulus site influences dynamic dispersion of repolarization in the intact human heart.

The spatial variation in restitution properties in relation to varying stimulus site is poorly defined. This study aimed to investigate the effect of varying stimulus site on apicobasal and transmural activation time (AT), action potential duration (APD) and repolarization time (RT) during restitution studies in the intact human heart. Ten patients with structurally normal hearts, undergoing clinical electrophysiology studies, were enrolled. Decapolar catheters were placed apex to base in the endocardial right ventricle (RVendo) and left ventricle (LVendo), and an LV branch of the coronary sinus (LVepi) for transmural recording. S1-S2 restitution protocols were performed pacing RVendo apex, LVendo base, and LVepi base. Overall, 725 restitution curves were analyzed, 74% of slopes had a maximum slope of activation recovery interval (ARI) restitution (Smax) > 1 (P < 0.001); mean Smax = 1.76. APD was shorter in the LVepi compared with LVendo, regardless of pacing site (30-ms difference during RVendo pacing, 25-ms during LVendo, and 48-ms during LVepi; 50th quantile, P < 0.01). Basal LVepi pacing resulted in a significant transmural gradient of RT (77 ms, 50th quantile: P < 0.01), due to loss of negative transmural AT-APD coupling (mean slope 0.63 ± 0.3). No significant transmural gradient in RT was demonstrated during endocardial RV or LV pacing, with preserved negative transmural AT-APD coupling (mean slope -1.36 ± 1.9 and -0.71 ± 0.4, respectively). Steep ARI restitution slopes predominate in the normal ventricle and dynamic ARI; RT gradients exist that are modulated by the site of activation. Epicardial stimulation to initiate ventricular activation promotes significant transmural gradients of repolarization that could be proarrhythmic.

Effect of mental stress on dynamic electrophysiological properties of the endocardium and epicardium in humans.

BACKGROUND: Striking temporal associations exist between ventricular arrhythmia and acute mental stress, for example, during natural disasters, or defibrillator shocks associated with stressful events. We hypothesized that electrophysiological changes in response to mental stress may be exaggerated at short coupling intervals and hence relevant to arrhythmia initiation. OBJECTIVE: The aim of this study was to determine the dynamic response in human electrophysiology during mental stress. METHODS: Patients with normal hearts and supraventricular tachycardia underwent electrophysiological studies avoiding sedation. Conditions of relaxation and stress were induced with standardized psychometric protocols (mental arithmetic and anger recall) during decremental S1S2 right ventricular (RV) pacing. Unipolar electrograms were acquired simultaneously from the RV endocardium, left ventricular (LV) endocardium (LV endo), and epicardium (LV epi), and activation-recovery intervals (ARIs) computed. RESULTS: Twelve patients ( 9 women; median age 34 years) were studied. During stress, effective refractory period (ERP) reduced from 228 ± 23 to 221 ± 21 ms (P < .001). ARIs reduced during mental stress (P < .001), with greater reductions in LV endocardium than in the epicardium or RV endocardium (LV endo -8 ms; LV epi -5 ms; RV endo -4 ms; P < .001). Mental stress depressed the entire electrical restitution curve, with minimal effect on slope. A substantial reduction in minimal ARIs on the restitution curve in LV endo occurred, commensurate with the reduction in ERP (LV endo ARI 195 ± 31 ms at rest to 182 ± 32 ms during mental stress; P < .001). Dispersion of repolarization increased sharply at coupling intervals approaching ERP during stress but not at rest. CONCLUSION: Mental stress induces significant electrophysiological changes. The increase in dispersion of repolarization at short coupling intervals may be relevant to observed phenomena of arousal-associated arrhythmia.

Can old dogs learn new "transfusion requirements in critical care": a survey of packed red blood cell transfusion practices among members of The American Association for the Surgery of Trauma.

BACKGROUND: The objective of this study was to characterize variations in packed red blood cell (PRBC) transfusion practices in critically ill patients and to identify which factors influence such practices. We hypothesized that significant variation in transfusion triggers exists among acute care surgeons. METHODS: A survey of PRBC transfusion practices was administered to the American Association for the Surgery of Trauma members. The scenarios examined hemoglobin thresholds for which participants would transfuse PRBCs. RESULTS: A hemoglobin threshold of less than or equal to 7 g/dL was adopted by 45% of respondents in gastrointestinal bleeding, 75% in penetrating trauma, 66% in sepsis, and 62% in blunt trauma. Acute care surgeons modified their transfusion trigger significantly in the majority of the modifications of these scenarios, often inappropriately so. CONCLUSIONS: This study documents continued evidence-practice gaps and wide variations in the PRBC transfusion practices of acute care surgeons. Numerous clinical factors altered such patterns despite a lack of supporting evidence (for or against).

Dynamic conduction and repolarisation changes in early arrhythmogenic right ventricular cardiomyopathy versus benign outflow tract ectopy demonstrated by high density mapping & paced surface ECG analysis.

AIMS: The concealed phase of arrhythmogenic right ventricular cardiomyopathy (ARVC) may initially manifest electrophysiologically. No studies have examined dynamic conduction/repolarization kinetics to distinguish benign right ventricular outflow tract ectopy (RVOT ectopy) from ARVC's early phase. We investigated dynamic endocardial electrophysiological changes that differentiate early ARVC disease expression from RVOT ectopy. METHODS: 22 ARVC (12 definite based upon family history and mutation carrier status, 10 probable) patients without right ventricular structural anomalies underwent high-density non-contact mapping of the right ventricle. These were compared to data from 14 RVOT ectopy and 12 patients with supraventricular tachycardias and normal hearts. Endocardial & surface ECG conduction and repolarization parameters were assessed during a standard S1-S2 restitution protocol. RESULTS: Definite ARVC without RV structural disease could not be clearly distinguished from RVOT ectopy during sinus rhythm or during steady state pacing. Delay in Activation Times at coupling intervals just above the ventricular effective refractory period (VERP) increased in definite ARVC (43 ± 20 ms) more than RVOT ectopy patients (36 ± 14 ms, p = 0.03) or Normals (25 ± 16 ms, p = 0.008) and a progressive separation of the repolarisation time curves between groups existed. Repolarization time increases in the RVOT were also greatest in ARVC (definite ARVC: 18 ± 20 ms; RVOT ectopy: 5 ± 14, Normal: 1 ± 18, p<0.05). Surface ECG correlates of these intracardiac measurements demonstrated an increase of greater than 48 ms in stimulus to surface ECG J-point pre-ERP versus steady state, with an 88% specificity and 68% sensitivity in distinguishing definite ARVC from the other groups. This technique could not distinguish patients with genetic predisposition to ARVC only (probable ARVC) from controls. CONCLUSIONS: Significant changes in dynamic conduction and repolarization are apparent in early ARVC before detectable RV structural abnormalities, and were present to a lesser degree in probable ARVC patients. Investigation of dynamic electrophysiological parameters may be useful to identify concealed ARVC in patients without disease pedigrees by using endocardial electrogram or paced ECG parameters.

Noncontact mapping guided ablation of right ventricular outflow tract ectopy in a patient with interruption of the inferior vena cava and azygos continuation.

A 58-year-old woman with symptomatic multiple monomorphic premature ventricular beats of a right ventricular outflow tract origin was referred for ablation. An inferior vena cava interruption with azygos continuation was discovered during catheter placement. This case describes positioning of the noncontact mapping array and successful radiofrequency ablation in this challenging anatomy.

High-density substrate mapping in Brugada syndrome: combined role of conduction and repolarization heterogeneities in arrhythmogenesis.

BACKGROUND: Two principal mechanisms are thought to be responsible for Brugada syndrome (BS): (1) right ventricular (RV) conduction delay and (2) RV subepicardial action potential shortening. This in vivo high-density mapping study evaluated the conduction and repolarization properties of the RV in BS subjects. METHODS AND RESULTS: A noncontact mapping array was positioned in the RV of 18 BS patients and 20 controls. Using a standard S(1)-S(2) protocol, restitution curves of local activation time and activation recovery interval were constructed to determine local maximal restitution slopes. Significant regional conduction delays in the anterolateral free wall of the RV outflow tract of BS patients were identified. The mean increase in delay was 3-fold greater in this region than in control (P=0<0.001). Local activation gradient was also maximally reduced in this area: 0.33+/-0.1 (mean+/-SD) mm/ms in BS patients versus 0.51+/-0.15 mm/ms in controls (P<0.0005). The uniformity of wavefront propagation as measured by the square of the correlation coefficient, r(2), was greater in BS patients versus controls (0.94+/-0.04 versus 0.89+/-0.09 [mean+/-SD]; P<0.05). The odds ratio of BS hearts having any RV segment with maximal restitution slope >1 was 3.86 versus controls. Five episodes of provoked ventricular tachycardia arose from wave breaks originating from RV outflow tract slow-conduction zones in 5 BS patients. CONCLUSIONS: Marked regional endocardial conduction delay and heterogeneities in repolarization exist in BS. Wave break in areas of maximal conduction delay appears to be critical in the initiation and maintenance of ventricular tachycardia. These data indicate that further studies of mapping BS to identify slow-conduction zones should be considered to determine their role in spontaneous ventricular arrhythmias.

The effect of dofetilide on ventricular defibrillation thresholds.

INTRODUCTION: High defibrillation threshold (DFT) with an inadequate defibrillation safety margin remains an infrequent but troubling problem associated with defibrillator implantation. Dofetilide is a selective class III antiarrhythmic drug that reduces DFTs in a canine model. We hypothesized that dofetilide would reduce DFTs in humans, obviating the need for complex lead systems. METHODS AND RESULTS: Sixteen consecutive patients with DFTs > or =20 J delivered energy at implant-received dofetilide therapy and underwent follow-up DFT testing acutely following drug loading and/or chronically (128 +/- 94 days). Amiodarone was discontinued in four patients at implantation. With dofetilide, DFTs decreased from 28 +/- 4 J to 19 +/- 7 J (P < 0.0001), resulting in a safety margin of 15 +/- 8 J for the implanted devices. Five patients subsequently had spontaneous arrhythmias terminated successfully with shocks. CONCLUSION: Dofetilide reduces DFTs sufficiently to prevent the need for more complex lead systems. This strategy should be considered when an inadequate defibrillation safety margin is present.

Sustained ventricular tachycardia following alcohol septal ablation for hypertrophic obstructive cardiomyopathy.

A 49-year-old man with a history of hypertrophic obstructive cardiomyopathy (HOCM) presented in sustained monomorphic ventricular tachycardia (SMVT) 8 days post-alcohol septal ablation. A dual chamber implantable cardioverter defibrillator ICD was implanted and the patient experienced another episode of VT 3 weeks later, which was terminated by an ICD shock. This case demonstrates probable scar-induced reentrant VT post-alcohol septal ablation, a likely rare but hypothesized complication of this procedure.

Electroanatomic mapping of the right atrium with a right atrial basket catheter and three-dimensional intracardiac echocardiography.

The ablation of arrhythmias progresses towards an approach based upon application of linear lesions between nonconducting anatomic/electrical areas. Hence the identification of detailed anatomy together with electrical behavior becomes increasingly important. This study aims to achieve true electroanatomic mapping by the use of three-dimensional intracardiac imaging of the right atrium combined with use of a right atrial basket to obtain detailed electrical information. We studied nine patients, seven requiring atrial flutter ablation. A 9 Fr, 9 MHZ intracardiac echo catheter was pulled back from SVC to IVC using respiratory and ECG gating. The images, recorded on a Clearview ultrasound machine, were reconstructed using commercially available software. The intracardiac basket was placed into the atrium using the markers and fluoroscopy to allow orientation. Isochronal maps were obtained from the basket in sinus rhythm, pacing from different sites within the atrium and in atrial flutter. Isochronal maps were constructed and superimposed on the ICE image. The maps with pacing were consistent with that which was expected, confirming the validity of this approach. We were able to visualize changes in activation sequence following the placement of bidirectional isthmus block. True electroanatomic mapping is possible by the use of three-dimensional ICE reconstruction of the right atrium with electrical activation obtained from an intracardiac basket. This has significance for anatomically based arrhythmia ablations such as the ablation of atrial flutter, atrial fibrillation, with transcatheter MAZE procedures and pulmonary vein isolation. Further developments in software will allow such maps to be produced simultaneously with greater rapidity.

Comparison of impedance minute ventilation and direct measured minute ventilation in a rate adaptive pacemaker.

Respiration rate (RR) and minute ventilation (MV) provide important clinical information on the state of the patient. This study evaluated the accuracy of determining these using a pacemaker impedance sensor. In 20 patients who were previously implanted with a Guidant PULSAR MAX group of pacemakers, the telemetered impedance sensor waveform was recorded simultaneously with direct volume respiration waveforms as measured by a pneumatometer. Patients underwent 30 minutes of breathing tests while supine and standing, and a 10-minute ergonometer bicycle exercise test at a workload of 50 W. Breathing tests included regular and rapid-shallow breathing sequences. RR was determined by a computerized algorithm, from impedance and respiration signals. The mean RR by impedance was 21.3 +/- 7.7 breaths/min, by direct volume was 21.1 +/- 7.6 breaths/min, range 7-66, the mean difference of RR measured by the impedance sensor, as compared with the true measurement, being 0.2 +/- 2.1 breaths/min. During the entire exercise, the mean correlation coefficient between impedance (iMV) and direct measured MV was 0.96 +/- 0.03, slope 0.13 +/- 0.05 L/Omega and range 0.07-0.26 L/Omega. Bland-Altman limits of agreement were +/- 4.6 L/min for MV versus iMV with each patient calibrated separately. The correlation coefficient for iMV versus MV over the entire 10 minutes of exercise, including the initial 4 minutes of exercise, was 0.99. The transthoracic impedance sensor of an implanted pacemaker can accurately detect respiration parameters. There was a large variation between subjects in the iMV versus MV slope during a bicycle exercise test, whereas for each subject, the slope was stable during submaximal bicycle exercise.

Occurrence of atrial fibrillation after flutter ablation: the significance of intra-atrial conduction and atrial vulnerability.

Atrial vulnerability and intra-atrial conduction delay are important substrates for paroxysmal atrial fibrillation (AFib); however, their significance is unknown in patients undergoing atrial flutter ablation. Antegrade (high right atrium to coronary sinus: HRA-CS) and retrograde (CS-HRA) intra-atrial conduction times and AFib inducibility were assessed in 61 patients undergoing ablation for type I atrial flutter. Twenty-three patients had structural heart disease and 18 AFib before the procedure. After 16 +/- 12 months of follow-up 17 patients experienced AFib, 5 of which progressed into chronic AFib. During the study, AFib was easily inducible in 14 patients, 7 of which developed AFib (P =.03). Patients with post- ablation AFib were older (59 +/- 11 vs. 44 +/- 15 years, P =.001), had longer intra-atrial conduction times before (98 +/- 17 ms vs. 68 +/- 20 ms, P <.001) and after ablation (91 +/- 19 ms vs. 73 +/- 21 ms, P =.01) than those without AFib. Discriminant analysis revealed that only age, previous AFib and inta-atrial conduction delay (>90 ms) were independent predictors of postablation AFib. Patients without a history of AFib and with normal intra-atrial conduction had a 3% risk of AFib, while patients with both factors had a 90% risk of AFib after ablation. Intra-atrial conduction delay is an important electrophysiological factor predicting atrial fibrillation after successful flutter ablation.

A randomized prospective study of single coil versus dual coil defibrillation in patients with ventricular arrhythmias undergoing implantable cardioverter defibrillator therapy.

ICD implantation is standard therapy for malignant ventricular arrhythmias. The advantage of dual and single coil defibrillator leads in the successful conversion of arrhythmias is unclear. This study compared the effectiveness of dual versus single coil defibrillation leads. The study was a prospective, multicenter, randomized study comparing a dual with a single coil defibrillation system as part of an ICD using an active pectoral electrode. Seventy-six patients (64 men, 12 women; age 61 +/- 11 years) were implanted with a dual (group 1, n = 38) or single coil lead system (group 2,n = 38). The patients represented a typical ICD cohort: 60% presented with ischemic cardiomyopathy as their primary cardiac disease, the mean left ventricular ejection fraction was 0.406 +/- 0.158. The primary tachyarrhythmia was monomorphic ventricular tachyarrhythmia in 52.6% patients and ventricular fibrillation in 38.4%. There was no significant difference in terms of P and R wave amplitudes, pacing thresholds, and lead impedance at implantation and follow-up in the two groups. There was similarly no difference in terms of defibrillation thresholds (DFT) at implantation. Patients in group 1 had an average DFT of 10.2 +/- 5.2 J compared to 10.3 +/- 4.1 J in Group 2, P = NS. This study demonstrates no significant advantage of a dual coil lead system over a single coil system in terms of lead values and defibrillation thresholds. This may have important bearing on the choice of lead systems when implanting ICDs.

Coronary ischemia induced by radiofrequency ablation in the left atrium.

INTRODUCTION: We report three cases of transient, reversible coronary ischemia occurring after radiofrequency ablation in the left atrium. METHODS AND RESULTS: A 56-year-old man with a left atrial tachycardia that was mapped to the septum and roof of the atrium using a noncontact mapping developed 5-mm ST elevation in the anterolateral leads. Coronary angiography showed an occluded diagonal that was opened using intracoronary nitrate, which led to resolution of the ST changes. A 57-year-old man undergoing right upper pulmonary vein ablation developed 6-mm ST elevation in leads V1-V4, II, III, and aVF. Coronary angiography showed normal coronaries with slow flow into the left anterior descending artery, which resolved with nitrates. A 50-year-old man undergoing left lower pulmonary vein ablation developed 3-mm reversible inferior ST elevation. All patients were adequately anticoagulated after transseptal access to the left atrium. CONCLUSION: Ablation in the left atrium, at the roof, septum, and left inferior wall, can cause transient coronary ischemia, possibly due to spasm, which can be reversed with intracoronary nitrates. This phenomenon has not been previously described.

Can we predict which patients with implantable cardioverter defibrillators receive appropriate shock therapy? A study of 155 patients.

BACKGROUND: Appropriate shock therapy (AST) occurs in the minority of patients with implantable cardioverter defibrillators (ICDs). We assessed which patients received AST and whether there were any predictive factors. METHODS: We retrospectively analysed data from 155 patients implanted with ICDs at our institution from a period from February 1984 to February 2001. Stored electrogram data were analysed. We sub-divided patients on the basis of underlying cardiac disease. Various clinical echocardiographic and electrophysiological variables were studied. RESULTS: AST occurred in 53 (34%) of patients (Group 1) and no AST in 102 (64%) of patients (Group 2). Impaired LV function was significantly associated with AST. Group 1 patients had a lower ejection fraction (EF) compared to Group 2 (37.5+/-13% vs. 47.8+/-14%, P<0.0001). Seventy-two percent of patients with AST had an EF <40% vs. 35% of patients in Group 2 (P<0.0001). NYHA Class was also associated with AST, 42% of Group 1 were in NYHA Class III/IV vs. 12% in Group 2 (P<0.001). Programmed electrical stimulation (PES) was a predictor of AST. PES was positive in a greater proportion of patients in Group 1 vs. 2 (88% vs. 64%, P<0.0006). Sub-group analysis showed that patients with dilated cardiomyopathy (DCM) had a high incidence of AST (80%). In these patients PES was a poor predictor of AST being positive in only 25%. CONCLUSION: AST occurs in the minority of our patients. Certain pre-procedural variables predict AST. PES does not appear useful in predicting shock therapy in DCM patients and a negative PES should not preclude ICD implantation in this group.

Effect of adrenergic stimulation on action potential duration restitution in humans.

BACKGROUND: Enhanced sympathetic activity facilitates complex ventricular arrhythmias and fibrillation. The restitution properties of action potential duration (APD) are important determinants of electrical stability in the myocardium. Steepening of the slope of APD restitution has been shown to promote wave break and ventricular fibrillation. The effect of adrenergic stimulation on APD restitution in humans is unknown. METHODS AND RESULTS: Monophasic action potentials were recorded from the right ventricular septum in 18 patients. Standard APD restitution curves were constructed at 3 basic drive cycle lengths (CLs) of 600, 500, and 400 ms under resting conditions and during infusion of isoprenaline (15 patients) or adrenaline (3 patients). The maximum slope of the restitution curves was measured by piecewise linear regression segments of sequential 40-ms ranges of diastolic intervals in steps of 10 ms. Under control conditions, the maximum slope was steeper at longer basic CLs; eg, mean values for the maximum slope were 1.053+/-0.092 at CL 600 ms and 0.711+/-0.049 at CL 400 ms (+/-SEM). Isoprenaline increased the steepness of the maximum slope of APD restitution, eg, from a maximum slope of 0.923+/-0.058 to a maximum slope of 1.202+/-0.121 at CL 500 ms. The effect of isoprenaline was greater at the shorter basic CLs. A similar overall effect was observed with adrenaline. CONCLUSIONS: The adrenergic agonists isoprenaline and adrenaline increased the steepness of the slope of the APD restitution curve in humans over a wide range of diastolic intervals. These results may relate to the known effects of adrenergic stimulation in facilitating ventricular fibrillation.

Reversion and maintenance of sinus rhythm in patients with permanent atrial fibrillation by internal cardioversion followed by biatrial pacing.

Patients in atrialfibrillation (AF) who fail external cardioversion are usually regarded as in permanent AF. Internal cardioversion may revert many such patients into sinus rhythm (SR) but the majority relapse rapidly into AF. We investigated whether internal cardioversion followed by biatrial pacing is an effective to restore and subsequently maintain SR in patients with permanent AF. Patients in permanent AF underwent internal cardioversion that was followed by biatrial temporary pacing for 48 hours. Those who remained in SR received a permanent biatrial pacemaker programmed to a rate responsive mode with a lower rate 90 beats/min. Primary end point of the study included maintenance in SR 3 months after internal cardioversion. Sixteen patients (14 men, 57 +/- 11 years) were cardioverted. The median duration of AF was 24 months (quartiles, Q1 = 8.5 and Q3 = 102) and mean left atrium diameter was 48 +/- 04 mm. A permanent biatrial pacemaker was implanted in 11 patients. At a mean fallow-up of 15 months (range 4 to 24), 8 patients remained in SR for more than 3 months. AF was eliminated in 5 patients, while in two a second internal cardioversion on amiodarone was required. Antiarrhythmic therapy was used in half of our population and did not predict the long-term maintenance of SR. Following internal cardioversion with continuous biatrial pacing, 50% of patients with permanent AF were maintained for prolonged periods in SR. This is a new modality of treatment of permanent AF directed to the maintenance of SR that provides a further therapeutic option in end-stage AF.