Optimal transseptal puncture location for robot-assisted left atrial catheter ablation.

BACKGROUND: The preferred method of treatment for atrial fibrillation (AF) is by catheter ablation, in which a catheter is guided into the left atrium through a transseptal puncture. However, the transseptal puncture constrains the catheter, thereby limiting its manoeuvrability and increasing the difficulty in reaching various locations in the left atrium. In this paper, we address the problem of choosing the optimal transseptal puncture location for performing cardiac ablation to obtain maximum manoeuvrability of the catheter. METHODS: We have employed an optimization algorithm to maximize the global isotropy index (GII) to evaluate the optimal transseptal puncture location. As part of this algorithm, a novel kinematic model for the catheter has been developed, based on a continuum robot model. Pre-operative MR/CT images of the heart are segmented using the open source image-guided therapy software, 3D Slicer, to obtain models of the left atrium and septal wall. These models are input to the optimization algorithm to evaluate the optimal transseptal puncture location. RESULTS: The continuum robot model accurately describes the kinematics of the catheter. Simulation and experimental results for the optimal transseptal puncture location are presented in this paper. The optimization algorithm generates discrete points on the septal wall for which the dexterity of the catheter in the left atrium is maximum, corresponding to a GII of 0.4362. CONCLUSION: We have developed an optimization algorithm based on the GII to evaluate the optimal position of the transseptal puncture for left atrial cardiac ablation.

Relationship between serum potassium concentration and risk of recurrent ventricular tachycardia or ventricular fibrillation.

INTRODUCTION: Electrolyte abnormalities are considered a correctable cause of a life-threatening ventricular arrhythmia according to American Heart Association/American College of Cardiology Practice Guidelines, and ventricular tachycardia or ventricular fibrillation in the setting of an electrolyte abnormality is considered a class III indication for defibrillator implantation. However, there are little data to support this recommendation. The purpose of this study was to determine the risk of a recurrent sustained ventricular arrhythmia in patients with a low serum potassium concentration at the time of an initial episode of a sustained ventricular arrhythmia. METHODS AND RESULTS: One hundred sixty-nine consecutive patients who presented with a sustained ventricular arrhythmia and a serum potassium concentration determined on the day of the arrhythmia underwent defibrillator implantation. All patients had structural heart disease and left ventricular ejection fraction of 0.32+/-0.15. On the day of the index arrhythmia, 30% of the patients had a serum potassium concentration <3.5 or >5.0 mEq/L, including 7% who had a serum potassium concentration <3.0 or >6.0 mEq/L. For the entire cohort of patients, freedom from a recurrent sustained ventricular arrhythmia was 18% at 5 years and was not significantly different among patients with a serum potassium concentration <3.5 mEq/L (23%), between 3.5 and 5.0 mEq/L (16%), and >5.0 mEq/L (5%; P = 0.1). CONCLUSION: The results of the present study suggest that patients with structural heart disease and an abnormal serum potassium concentration at the time of an initial episode of sustained ventricular tachycardia or ventricular fibrillation are at high risk for a recurrent ventricular arrhythmia; therefore, implantable defibrillator therapy may be reasonable.

Differentiation of atypical atrioventricular node re-entrant tachycardia from orthodromic reciprocating tachycardia using a septal accessory pathway by the response to ventricular pacing.

OBJECTIVES: The purpose of this study was to determine whether the response to ventricular pacing during tachycardia is useful for differentiating atypical atrioventricular node re-entrant tachycardia (AVNRT) from orthodromic reciprocating tachycardia (ORT) using a septal accessory pathway. BACKGROUND: Although it is usually possible to differentiate atypical AVNRT from ORT using a septal accessory pathway, a definitive diagnosis is occasionally elusive. METHODS: In 30 patients with atypical AVNRT and 44 patients with ORT using a septal accessory pathway, the right ventricle was paced at a cycle length 10 to 40 ms shorter than the tachycardia cycle length (TCL). The ventriculo-atrial (VA) interval and TCL were measured just before pacing. The interval between the last pacing stimulus and the last entrained atrial depolarization (stimulus-atrial [S-A] interval) and the post-pacing interval (PPI) at the right ventricular apex were measured on cessation of ventricular pacing. RESULTS: All 30 patients with atypical AVNRT and none of the 44 patients with ORT using a septal accessory pathway had an S-A-VA interval >85 ms and PPI-TCL >115 ms. CONCLUSIONS: The S-A-VA interval and PPI-TCL are useful in distinguishing atypical AVNRT from ORT using a septal accessory pathway.

Should an abnormal serum potassium concentration be considered a correctable cause of cardiac arrest?

According to American Heart Association/American College of Cardiology Practice Guidelines, electrolyte abnormalities, including abnormal serum potassium concentrations, are considered a correctable cause of a life-threatening ventricular arrhythmia. Ventricular defibrillator therapy in this situation is a class III indication, and thought to be ineffective and perhaps harmful, although there are minimal data to support this recommendation. The steady-state serum potassium concentration frequently changes during a cardiac arrest. Additionally, the vast majority of cardiac arrest patients have structural heart disease and are commonly treated with a variety of medications that can alter the serum potassium concentration. In the Antiarrhythmics Versus Implantable Defibrillators (AVID) trial, patients with a correctable cause of an electrolyte imbalance were excluded from study participation but were followed in the AVID registry. Similar outcomes were observed among patients in the AVID registry and the main trial. Spironolactone therapy in patients with congestive heart failure decreases all-cause mortality and sudden and nonsudden cardiac death. In a preliminary study of 169 patients with an episode of a sustained ventricular arrhythmia treated with an implantable defibrillator, freedom from appropriate defibrillator therapy was 18% after five years. The probability of appropriate defibrillator therapy was independent of the initial serum potassium concentration. For these reasons, our current clinical practice is to use an implantable defibrillator to treat an initial episode of sustained ventricular tachycardia or ventricular fibrillation that occurs in a patient with structural heart disease and an abnormal serum potassium concentration.

Noninvasive diagnosis of a wide QRS complex tachycardia mechanism by programmed atrial and ventricular stimulation using a dual chamber defibrillator.

Stored atrial and ventricular electrograms retrieved from dual chamber implantable defibrillators facilitate the diagnosis of arrhythmias. This case also illustrates the usefulness of programmed atrial and ventricular stimulation for noninvasive rhythm diagnosis in patients with a wide QRS tachycardia and an implantable defibrillator.

Electrogram polarity and cavotricuspid isthmus block during ablation of typical atrial flutter.

INTRODUCTION: The atrial activation sequence around the tricuspid annulus has been used to assess whether complete block has been achieved across the cavotricuspid isthmus during radiofrequency ablation of typical atrial flutter. However, sometimes the atrial activation sequence does not clearly establish the presence or absence of complete block. The purpose of this study was to determine whether a change in the polarity of atrial electrograms recorded near the ablation line is an accurate indicator of complete isthmus block. METHODS AND RESULTS: Radiofrequency ablation was performed in 34 men and 10 women (age 60 +/- 13 years [mean +/- SD]) with isthmus-dependent, counterclockwise atrial flutter. Electrograms were recorded around the tricuspid annulus using a duodecapolar halo catheter. Electrograms recorded from two distal electrode pairs (E1 and E2) positioned just anterior to the ablation line were analyzed during atrial flutter and during coronary sinus pacing, before and after ablation. Complete isthmus block was verified by the presence of widely split double electrograms along the entire ablation line. Complete bidirectional isthmus block was achieved in 39 (89%) of 44 patients. Before ablation, the initial polarity of E1 and E2 was predominantly negative during atrial flutter and predominantly positive during coronary sinus pacing. During incomplete isthmus block, the electrogram polarity became reversed either only at E2, or at neither E1 nor E2. In every patient, the polarity of E1 and E2 became negative during coronary sinus pacing only after complete isthmus block was achieved. In 4 patients (10%), the atrial activation sequence recorded with the halo catheter was consistent with complete isthmus block, but the presence of incomplete block was accurately detected by inspection of the polarity of E1 and E2. CONCLUSION: Reversal of polarity in bipolar electrograms recorded just anterior to the line of isthmus block during coronary sinus pacing after ablation of atrial flutter is a simple, quick, and accurate indicator of complete isthmus block.

Physician interpretation of electrocardiographic artifact that mimics ventricular tachycardia.

BACKGROUND: Patients who are misdiagnosed with ventricular tachycardia because of electrocardiographic artifact may be subjected to unnecessary procedures. The purpose of this study was to determine how often electrocardiographic artifact is misdiagnosed as ventricular tachycardia. METHODS: Physicians (n = 766) were surveyed with a case simulation that included a two-lead electrocardiographic monitor tracing of artifact simulating a wide-complex tachycardia. RESULTS: The rhythm strip was not recognized as artifact by 52 of the 55 internists (94%), 128 of the 221 cardiologists (58%), and 186 of the 490 electrophysiologists (38%). One hundred fifty-six of the 181 electrophysiologists (88%), 67 of the 126 cardiologists (53%), and 14 of the 15 internists (31%) who misdiagnosed the rhythm as ventricular tachycardia recommended an invasive procedure for further evaluation or therapy. CONCLUSIONS: This physician survey suggests that electrocardiographic artifact that mimics ventricular tachycardia may frequently result in patients being subjected to unnecessary invasive cardiac procedures. Physicians should include artifact in their differential diagnosis of wide complex tachycardias to minimize unneeded procedures.

Prevalence of central venous occlusion in patients with chronic defibrillator leads.

BACKGROUND: Many patients with previously implanted ventricular defibrillators are candidates for an upgrade to a device capable of atrial-ventricular sequential or multisite pacing. The prevalence of venous occlusion after placement of transvenous defibrillator leads is unknown. The purpose of this study was to determine the prevalence of central venous occlusion in asymptomatic patients with chronic transvenous defibrillator leads. METHODS: Thirty consecutive patients with a transvenous defibrillator lead underwent bilateral contrast venography of the cephalic, axillary, subclavian, and brachiocephalic veins as well as the superior vena cava before an elective defibrillator battery replacement. The mean time between transvenous defibrillator lead implantation and venography was 45 +/- 21 months. Sixteen patients had more than 1 lead in the same subclavian vein. No patient had clinical signs of venous occlusion. RESULTS: One (3%) patient had a complete occlusion of the subclavian vein, 1 (3%) patient had a 90% subclavian vein stenosis, 2 (7%) patients had a 75% to 89% subclavian stenosis, 11 (37%) patients had a 50% to 74% subclavian stenosis, and 15 (50%) patients had no subclavian stenosis. CONCLUSIONS: The low prevalence of subclavian vein occlusion or severe stenosis among defibrillator recipients found in this study suggests that the placement of additional transvenous leads in a patient who already has a ventricular defibrillator is feasible in a high percentage of patients (93%).

Complete atrioventricular block after valvular heart surgery and the timing of pacemaker implantation.

The natural history of patients who developed complete atrioventricular block after valvular heart surgery was investigated to determine the optimal timing for pacemaker implantation. Patients who developed complete atrioventricular block within 24 hours after operation, which then persisted for > 48 hours, were unlikely to recover; such patients could potentially undergo earlier pacemaker implantation if otherwise ready for discharge.

Current approaches to evaluation and management of patients with ventricular arrhythmias.

The clinical manifestations of ventricular arrhythmias encompass a broad spectrum, from complete absence of symptoms to sudden death. Although our understanding of the pathophysiology and natural history of these arrhythmias has advanced significantly over the past decade, large gaps in our knowledge remain, especially in patients with heart failure not due to coronary artery disease. We have learned much about the appropriate roles of antiarrhythmic drugs and implantable defibrillators in the prevention of sudden death. Studies performed over the past decade have made clear that the primary treatment for patients at high risk for life-threatening ventricular arrhythmias should be the implantable defibrillator. However, specific syndromes causing ventricular tachyarrhythmias are being recognized, and care must be individualized. Although hospital mortality from acute myocardial infarction has decreased as a result of newer therapies, sudden death after hospital discharge remains an important problem, causing at least 30% of post-infarction deaths, even in patients who have received thrombolytic therapy. Two independent studies have confirmed that patients with asymptomatic non-sustained ventricular tachycardia in the presence of left ventricular ejection fraction < .40 after myocardial infarction who have sustained ventricular tachycardia inducible by electrophysiologic study are at significant risk for sudden death. This risk is significantly reduced by ICD, but not pharmacologic, antiarrhythmic therapy. Our major challenge at this time is not how best to treat high risk patients, but how best to identify them prior to events. Finally, physicians should be aware that many symptomatic ventricular tachycardias are now curable at low risk, using catheters to deliver radiofrequency energy.

Effect of ethanol on defibrillation energy requirements in humans.

The purpose of this double-blind study was to determine the effect of intravenous ethanol administration on defibrillation efficacy in 18 patients with an implantable defibrillator. The equivalent of 60 ml of 100 proof ethanol did not impair defibrillation efficacy.

Effects of digoxin on acute, atrial fibrillation-induced changes in atrial refractoriness.

BACKGROUND: Atrial fibrillation (AF) shortens the atrial effective refractory period (ERP) and predisposes to further episodes of AF. The acute changes in atrial refractoriness may be related to tachycardia-induced intracellular calcium overload. The purpose of this study was to determine whether digoxin, which increases intracellular calcium, potentiates the acute effects of AF on atrial refractoriness in humans. METHODS AND RESULTS: In 38 healthy adults, atrial ERP was measured at basic drive cycle lengths (BDCLs) of 350 and 500 ms after autonomic blockade. Nineteen patients had been treated with digoxin for 2 weeks. After a several-minute episode of AF, atrial ERP was measured serially at alternating BDCLs. Compared with pre-AF ERPs, the first post-AF ERPs were significantly shorter in both the digoxin and the control groups (P:<0.001). The post-AF ERP at a BDCL of 350 ms shortened to a greater degree in the digoxin group (37+/-16 ms) than in the control group (20+/-13 ms, P:<0.001); similar changes occurred at a BDCL of 500 ms. During post-AF determinations of the atrial ERP, secondary AF episodes occurred significantly more often in the digoxin group (32% versus 16%; P:<0. 04). CONCLUSIONS: After a brief episode of AF, digoxin augments the shortening that occurs in atrial refractoriness and predisposes to the reinduction of AF. These effects occur in the setting of autonomic blockade and therefore are more likely to be due to the effects of digoxin on intracellular calcium than to its vagotonic effects.

Diagnostic value of tachycardia features and pacing maneuvers during paroxysmal supraventricular tachycardia.

OBJECTIVES: The purpose of this prospective study was to quantitate the diagnostic value of several tachycardia features and pacing maneuvers in patients with paroxysmal supraventricular tachycardia (PSVT) in the electrophysiology laboratory. BACKGROUND: No study has prospectively compared the value of multiple diagnostic tools in a large group of patients with PSVT. METHODS: One hundred ninety-six consecutive patients who had 200 inducible sustained PSVTs during an electrophysiology procedure were included. The diagnostic values of four baseline electrophysiologic parameters, nine tachycardia features and five diagnostic pacing maneuvers were quantified. RESULTS: The only tachycardia characteristic that was diagnostic of atrioventricular (AV) nodal reentry was a septal ventriculoatrial (VA) time of <70 ms, and no pacing maneuver was diagnostic for AV nodal reentry. An increase in the VA interval with the development of a bundle branch block was the only tachycardia characteristic that was diagnostic for orthodromic tachycardia, but it occurred in only 7% of all tachycardias. An atrial-atrial-ventricular response upon cessation of ventricular overdrive pacing was diagnostic of atrial tachycardia, and this maneuver could be applied to 78% of all tachycardias. Burst ventricular pacing excluded atrial tachycardia when the tachycardia terminated without depolarization of the atrium, but the result could be obtained only in 27% of patients. CONCLUSIONS: This prospective study quantitates the diagnostic value of multiple observations and pacing maneuvers that are commonly used during PSVT in the electrophysiology laboratory. The findings demonstrate that diagnostic techniques rarely provide a diagnosis when used individually. Therefore, careful observations and multiple pacing maneuvers are often required for an accurate diagnosis during PSVT. The results of this study provide a useful reference with which new diagnostic techniques can be compared.

Effect of chronic amiodarone therapy on defibrillation energy requirements in humans.

INTRODUCTION: The effect of oral amiodarone therapy on defibrillation energy requirements in patients with an implantable defibrillator has not been established. METHODS AND RESULTS: Twenty-one consecutive patients with implantable biphasic waveform defibrillators underwent a step-down determination of the defibrillation energy requirement 211 +/- 12 days before and 73 +/- 22 days after initiation of amiodarone therapy (mean total dose 26.7 +/- 11.1 g). Serum amiodarone and desethylamiodarone concentrations were measured at the time of defibrillation energy requirement determination. The mean defibrillation energy requirement before amiodarone therapy was 9.9 +/- 4.6 J. After initiation of amiodarone therapy, the mean defibrillation energy requirement increased to 13.7 +/- 5.6 J (P = 0.004). A linear relationship between the amiodarone (P = 0.02, r = 0.6), desethylamiodarone (P = 0.02, r = 0.6), and combined amiodarone-desethylamiodarone concentrations (P = 0.01, r = 0.6) and the defibrillation energy requirement was noted. Stepwise regression analysis demonstrated that the combined amiodarone-desethylamiodarone concentration was the only independent predictor of increase in the defibrillation energy requirement. CONCLUSION: Chronic oral amiodarone therapy increases the defibrillation energy requirement by approximately 62% in patients with an implantable defibrillator. The combined amiodarone-desethylamiodarone concentration is directly related to the increase in the defibrillation energy requirement.

A randomized trial comparing heparin initiation 6 h or 24 h after pacemaker or defibrillator implantation.

OBJECTIVES: The purpose of this randomized study was to evaluate the prevalence of pocket hematomas in patients treated with heparin 6 h or 24 h after pacemaker or defibrillator implantation. BACKGROUND: The risks of pocket hematoma and need for evacuation after device implantation have not been defined in patients who require anticoagulation. METHODS: Forty-nine consecutive patients with an indication for anticoagulation with heparin after implantable defibrillator or pacemaker implantation were randomized to receive intravenous heparin either 6 h (n = 26) or 24 h (n = 23) postoperatively. Both groups also received warfarin on a daily basis starting the evening of surgery. Twenty-eight patients who received postoperative warfarin alone and 115 patients who did not receive anticoagulation were followed up in a study registry. RESULTS: A pocket hematoma developed in 6 of 26 patients (22%) who were treated with intravenous heparin 6 h postoperatively, as compared with 4 of 23 patients (17%) who were treated with intravenous heparin 24 h postoperatively (p = 0.7). In total, a pocket hematoma developed in 10 of 49 patients (20%) treated with heparin, 1 of 28 patients (4%) treated with warfarin alone and 2 of 115 (2%) patients who received no anticoagulation (p < 0.001). CONCLUSIONS: Intravenous heparin initiation 6 h or 24 h after pacemaker or defibrillator implantation is associated with a 20% prevalence of pocket hematoma formation. Warfarin therapy or no anticoagulation is associated with only a 2% to 4% risk of pocket hematoma formation.

Prevalence and significance of exit block during arrhythmias arising in pulmonary veins.

INTRODUCTION: Recent studies described the occurrence of conduction block within pulmonary veins. The purpose of this study was to evaluate the prevalence of exit block during arrhythmias that arise in pulmonary veins. METHODS AND RESULTS: Twenty-five patients with atrial tachycardia/fibrillation underwent successful ablation of 28 arrhythmogenic foci within a pulmonary vein. The prevalence of exit block in the pulmonary veins was determined in 28 arrhythmogenic pulmonary veins and 40 nonarrhythmogenic pulmonary veins. During isolated premature depolarizations, exit block in a pulmonary vein was observed at 50% of arrhythmogenic pulmonary vein sites and was never observed within pulmonary veins that did not generate a tachycardia (P < 0.01). During tachycardia, exit block from a pulmonary vein was observed in 61% of the arrhythmogenic pulmonary veins. The mean cycle length of the pulmonary vein tachycardias associated with exit block was significantly shorter than the cycle length of tachycardias that were not associated with exit block (163 +/- 32 vs 251 +/- 45 msec, P < 0.001). Exit block in two pulmonary veins during the same episode of tachycardia was observed in 3 of the 28 arrhythmogenic pulmonary veins (11%) in three different patients. Simultaneous recordings in the two pulmonary veins demonstrated bursts of tachycardia in both veins that were not synchronized. Radiofrequency catheter ablation of the arrhythmogenic site in one of the pulmonary veins eliminated spontaneous recurrences of tachycardia from the other pulmonary vein. CONCLUSION: Exit block from pulmonary veins is a common observation during tachycardias generated within pulmonary veins and indicates that an arrhythmogenic pulmonary vein has been identified. The occurrence of exit block in more than one pulmonary vein most likely is attributable to simultaneous tachycardias, one or both of which may be tachycardia induced and perpetuated by the other.

Comparison of endocardial activation times at effective and ineffective ablation sites within the pulmonary veins.

INTRODUCTION: Recent studies demonstrated that atrial arrhythmias may be generated within pulmonary veins. The purpose of this study was to compare the endocardial activation times at effective and ineffective ablation sites during radiofrequency catheter ablation of arrhythmias initiated or generated within pulmonary veins. METHODS AND RESULTS: Twenty-one of 28 patients without structural heart disease underwent successful ablation of 23 arrhythmogenic foci within a pulmonary vein. Electrograms were recorded at 75 pulmonary venous sites and categorized into three groups: 23 successful ablation sites; 28 unsuccessful target sites within an arrhythmogenic pulmonary vein; and 24 sites within nonarrhythmogenic pulmonary veins. The endocardial activation time of premature depolarizations arising at successful target sites was significantly earlier than at other sites. During premature depolarizations, an endocardial activation time of -75 msec or earlier had a sensitivity of 83% and a specificity of 79% for identification of a successful ablation site. Endocardial activation times earlier than -100 msec were recorded only at successful ablation sites, and endocardial activation times later than -30 msec were recorded only at sites within nonarrhythmogenic pulmonary veins. The presence of a split potential during sinus rhythm or premature depolarizations was not a specific indicator of a successful ablation site. CONCLUSION: The endocardial activation times of premature depolarizations that arise within pulmonary veins and initiate atrial tachycardia/fibrillation are useful in identifying successful ablation sites.

Unique interaction between an atrial single-chamber pacemaker and a ventricular defibrillator.

A well described interaction between an antibradycardia pacemaker and a ventricular defibrillator is sensing of pacemaker stimuli by the ventricular defibrillator. This report describes an interaction between an atrial demand pacemaker and a ventricular defibrillator that resulted in ventricular asystole and polymorphic ventricular tachycardia. In this case, the ventricular defibrillator sensed atrial pacing stimuli when complete atrioventricular block with a slow ventricular escape rate developed. Defibrillator-based ventricular demand pacing was inhibited, resulting in prolonged periods of ventricular asystole, polymorphic ventricular tachycardia, and multiple defibrillator shocks. Ventricular defibrillator sensing of atrial pacemaker stimuli in the setting of complete atrioventricular block and ventricular asystole cannot be simulated during defibrillator implantation when atrioventricular conduction is intact. Therefore, a pacemaker programmed to atrial demand pacing in a patient with a ventricular defibrillator can result in inappropriate inhibition of ventricular pacing in the setting of complete heart block. Furthermore, this interaction can be avoided with a dual-chamber pacing ventricular defibrillator.