Marwan Bahu

Effect of an irregular ventricular rhythm on cardiac output

Impairment of cardiac function in atrial fibrillation has been attributed to loss of atrial contraction and to a rapid ventricular rate. The results of this study suggest that irregularity of the ventricular rhythm, independent of the ventricular rate, may also contribute to impairment of cardiac function during atrial fibrillation.

Effect of Verapamil and Procainamide on Atrial Fibrillation–Induced Electrical Remodeling in Humans

BACKGROUND Atrial fibrillation (AF) shortens the atrial effective refractory period (ERP) and predisposes to further episodes of AF. The purpose of this study was to determine the effect of verapamil and procainamide on these manifestations of AF-induced electrical remodeling. METHODS AND RESULTS In adult patients without structural heart disease, the atrial ERP was measured before and after AF after pharmacological autonomic blockade and administration of verapamil (17 patients), procainamide (10 patients), or saline (20 patients). AF was then induced by rapid pacing. Immediately on AF conversion, the post-AF ERP was measured at alternating drive cycle lengths of 350 and 500 ms. In the saline group, the pre-AF and first post-AF ERPs at the 350-ms drive cycle length were 206+/-19 and 179+/-27 ms (P<.0001), respectively, and at the 500-ms drive cycle length, the values were 217+/-16 and 183+/-23 ms, respectively (P<.0001). There was a similar significant shortening of the first post-AF ERP in the procainamide group. In the verapamil group, however, there was no difference between the pre-AF and the first post-AF ERP at the 350-ms (226+/-15 versus 227+/-22 ms, P=.8) or 500-ms (230+/-17 versus 232+/-20 ms, P=.6) drive cycle length. During determinations of the post-AF ERP, 105 secondary episodes of AF were unintentionally induced in 12% of verapamil patients compared with 90% and 80% of saline and procainamide patients (P<.01 versus verapamil). CONCLUSIONS Pretreatment with the calcium channel antagonist verapamil, but not the sodium channel antagonist procainamide, markedly attenuates acute, AF-induced changes in atrial electrophysiological properties. These data suggest that calcium loading during AF may be at least partially responsible for AF-induced electrical remodeling.

A Prospective Evaluation of Catheter Ablation of Ventricular Tachycardia as Adjuvant Therapy in Patients With Coronary Artery Disease and an Implantable Cardioverter-Defibrillator

BACKGROUND Implantable cardioverter-defibrillator (ICD) therapy is integral to current therapy for ventricular tachycardia. Patients with an ICD frequently require concomitant antiarrhythmic drug therapy. Despite this, some patients still receive frequent ICD therapies for ventricular tachycardia. Therefore, the purpose of this prospective study was to determine the utility of ablation of ventricular tachycardia in patients with an ICD who experience frequent ICD therapies. METHODS AND RESULTS Twenty-one consecutive patients with frequent ICD therapies despite antiarrhythmic drug therapy were the subjects of this study. The mean age was 69+/-6 years, and 17 were men. The mean ejection fraction was 0.22+/-0.08, and all patients had coronary artery disease. During the 36+/-51 days (range, 4 days to 7 months) preceding the ablation procedures, the patients received 34+/-55 ICD therapies for the clinical ventricular tachycardia, or a mean of 25+/-88 ICD therapies per month. The patients underwent radiofrequency ablation of the presumed clinical ventricular tachycardia by inducing the tachycardia and mapping according to endocardial activation, continuous electrical activity, pace mapping, concealed entrainment, or mid-diastolic potentials. Ablation of the clinical arrhythmia was successful in 76% of patients during 1.4+/-0.6 (range, 1 to 3) ablation procedures and required 12.5+/-9.2 applications of energy. During 11.8+/-10.0 months of follow-up, the frequency of ICD therapies per month decreased from 60+/-80 before successful ablation to 0.1+/-0.3 ICD therapies per month after ablation (P=.01). A quality-of-life assessment demonstrated a significant improvement after successful (P=.02) but not unsuccessful ablation (P=.9). CONCLUSIONS Radiofrequency ablation of ventricular tachycardia as adjuvant therapy in patients with coronary artery disease and an ICD has a reasonable success rate, significantly reduces ICD therapies, and appears to be associated with an improved quality of life.

Long-term follow-up after radiofrequency modification of the atrioventricular node in patients with atrial fibrillation.

OBJECTIVES The purpose of this study was to describe the long-term follow-up results in 62 patients with atrial fibrillation and an uncontrolled ventricular rate, who underwent radiofrequency modification of the atrioventricular (AV) node. BACKGROUND Previous studies in small numbers of patients have suggested that radiofrequency modification may be effective in controlling the ventricular rate in patients with atrial fibrillation, but long-term follow-up data have been lacking. METHODS The subjects of this study were 62 consecutive patients (mean age +/- SD 65 +/- 14 years; 43 with structural heart disease) who underwent an attempt at radiofrequency modification of the AV node because of symptomatic, drug-refractory atrial fibrillation with an uncontrolled ventricular rate. The atrial fibrillation was chronic in 46 patients and paroxysmal in 16. Radiofrequency energy was applied to the posteroseptal or mid-septal right atrium to lower the ventricular rate in atrial fibrillation to 120 to 130 beats/min during an infusion of 4 micrograms/min of isoproterenol. RESULTS Short-term control of the ventricular rate was successfully achieved without the induction of pathologic AV block in 50 (81%) of 62 patients. Inadvertent high degree AV block occurred in 10 (16%) of 62 patients, with the AV block occurring at the time of the procedure in 6 patients and 36 to 72 h after the procedure in 4. During 19 +/- 8 months of follow-up (range 4 to 33), 5 (10%) of 50 patients had a symptomatic recurrence of an uncontrolled rate during atrial fibrillation. Overall, adequate rate control at rest and during exertion, without pathologic AV block, was achieved long term in 45 (73%) of 62 patients. Among 37 patients with a successful outcome, left ventricular ejection fraction increased from (mean +/- SD) 0.44 +/- 0.14 to 0.51 +/- 0.10 one year later (p < 0.001). Complications other than AV block included polymorphic ventricular tachycardia 10 to 24 h after the procedure in two patients who had a predisposing factor for ventricular tachycardia and sudden death 1 to 5 months after the procedure in two patients with idiopathic dilated cardiomyopathy, one of whom had a pacemaker for AV block. CONCLUSIONS In approximately 70% of properly selected patients with atrial fibrillation and an uncontrolled ventricular rate, radiofrequency modification of the AV node results in excellent long-term control of the ventricular rate at rest and during exertion.

Comparison of Effective and Ineffective Target Sites That Demonstrate Concealed Entrainment in Patients With Coronary Artery Disease Undergoing Radiofrequency Ablation of Ventricular Tachycardia

BACKGROUND Concealed entrainment has been useful in guiding catheter ablation of monomorphic ventricular tachycardia in patients with coronary artery disease. However, not all sites with concealed entrainment result in successful ablation of the targeted ventricular tachycardia. The purpose of this prospective study was to identify factors at sites that demonstrate concealed entrainment that differentiate effective from ineffective target sites. METHODS AND RESULTS In 14 consecutive patients with hemodynamically stable monomorphic ventricular tachycardia and coronary artery disease, radiofrequency ablation of 26 ventricular tachycardias was performed. Ablation was attempted at 46 sites that demonstrated concealed entrainment. Twenty-five of the targeted ventricular tachycardias (96%) were successfully ablated. The positive predictive value of concealed entrainment for successful ablation was 54%; it increased to 72% in the presence of a stimulus-QRS interval/ventricular tachycardia cycle length ratio of < or = 70%, to 82% in the presence of a match of the stimulus-QRS and electrogram-QRS interval, and to 89% in the presence of isolated mid diastolic potentials that could not be dissociated from ventricular tachycardia during entrainment. CONCLUSIONS The positive predictive value of concealed entrainment for identification of successful ablation sites in patients with sustained ventricular tachycardia and coronary artery disease can be significantly enhanced by the presence of associated mapping criteria, particularly an isolated mid diastolic potential that cannot be dissociated from the tachycardia.

Adenosine-Induced Atrial Arrhythmia: A Prospective Analysis

Adenosine is safe and effective for the termination of paroxysmal supraventricular tachycardia (PSVT). This agent is recommended for termination of narrow and wide QRS-complex tachycardias of unknown cause in the setting of hemodynamic stability [1-6]. However, anecdotal experience suggests that adenosine can precipitate atrial fibrillation and atrial flutter [7-14]. The frequency of adenosine-induced atrial arrhythmias has not been well defined. We therefore sought to identify the frequency with which adenosine administered during PSVT causes atrial arrhythmias and the mechanisms by which these arrhythmias are induced. Methods Patients The study participants were 200 consecutive patients (74 men and 126 women) with PSVT who were referred for an electrophysiology procedure and possible ablation. The mean (SD) patient age was 43 16 years. No patient had structural heart disease. These patients had had symptoms from PSVT for a mean of 13.7 12.1 years before the electrophysiology procedure. No patient had a clinical history of atrial fibrillation or atrial flutter. The mechanism responsible for PSVT during electrophysiologic evaluation was typical (n = 114) or atypical (n = 10) atrioventricular nodal reentrant tachycardia in 124 patients, atrioventricular reciprocating tachycardia with a manifest accessory pathway in 40 patients, a concealed accessory pathway in 28 patients, and atrial tachycardia in 8 patients. Electrophysiologic Testing The investigational protocol was approved by the Committee for Human Research at the University of Michigan. Patients gave informed consent for all procedures. Electrophysiology procedures were performed in the fasting state after therapy with all antiarrhythmic medications had been discontinued for at least 5 half-lives. Three 7-French quadripolar electrode catheters were inserted into the right femoral vein and positioned in the high right atrium, across the tricuspid valve to record the His-bundle electrogram, and in the right ventricle. Leads V1, II, and III and the intracardiac electrograms were displayed on an oscilloscope and recorded on a Mingograph 7 recorder (Siemens-Elema, Solna, Sweden) at a paper speed of 100 mm/s. Pacing was performed with a programmable stimulator (Bloom Associates, Reading, Pennsylvania). The goal of electrophysiologic testing was to induce and determine the mechanism of PSVT and to measure the conduction properties and the refractory periods of the atrioventricular node [15]. If tachycardia could not be provoked in the baseline state, isoproterenol (2 g/min) was given intravenously and programmed stimulation of the right atrium and right ventricle was repeated. Isoproterenol was required for tachycardia induction in 71 patients. The likelihood of requiring isoproterenol for the induction of tachycardia was similar in patients with atrioventricular nodal reentrant tachycardia (n = 44 [57%]), those with atrioventricular reentrant tachycardia (n = 23 [54%]), and those with atrial tachycardia (n = 4 [50%]) (P > 0.2). Study Protocol Eligible patients were presumed to have PSVT and were referred for an electrophysiology procedure and possible ablation. Only patients with a history of reactive airway disease were excluded. After the mechanism of PSVT was determined, the investigational protocol was performed. During tachycardia, 12 mg of adenosine (Fujisawa USA, Inc., Deerfield, Illinois) was administered as a bolus as quickly as possible through a sheath positioned in the femoral vein. The adenosine bolus was immediately followed by a 20-mL bolus of normal saline. Termination of tachycardia and development of atrial fibrillation or atrial flutter were noted. The cycle length of atrial fibrillation or atrial flutter and the type of atrial fibrillation were determined [16]. The types of atrial fibrillation were defined as follows: type I, discrete atrial electrograms of variable structure with an isoelectric baseline; type II, discrete atrial electrograms of variable structure with a nonisoelectric baseline; type III, neither discrete atrial electrograms nor an isoelectric baseline; and type IV, a combination of type III and either type I or type II atrial electrograms [16]. The occurrence of atrial or ventricular premature complexes was also noted. Upon termination of PSVT by adenosine and upon induction of atrial fibrillation, the time from the preceding atrial complex to the premature atrial complex that induced atrial fibrillation was measured. The ratio of the coupling interval of the premature complex to the preceding cycle length was determined, as was the total duration of atrial fibrillation or atrial flutter. If atrial fibrillation persisted for more than 10 minutes, sinus rhythm was restored with cardioversion. Statistical Analysis Continuous variables are expressed as the mean SD and were compared by using an unpaired t-test. The frequency of induction of atrial fibrillation or atrial flutter with adenosine, based on the mechanism of PSVT, was compared by using analysis of variance. Nominal variables were compared by using the Fisher exact test. A P value less than 0.05 was considered statistically significant. Results Main Findings Paroxysmal supraventricular tachycardia terminated after adenosine administration in 198 patients (99% [95% CI, 96% to 100%]) (Figure 1). Adenosine administration resulted in atrial fibrillation (n = 22) or atrial fibrillation and atrial flutter (n = 2) in 24 patients (12% [CI, 7.5% to 16.5%]) a mean of 6.3 6.2 seconds (range, 0.4 to 20.7 seconds) after PSVT termination (Figure 2). The rhythm preceding the atrial premature complex that provoked the atrial arrhythmia was sinus rhythm in 21 patients and an atrial ectopic complex in 3 patients. When atrial fibrillation or atrial flutter occurred, 20 patients had atrioventricular block and 4 patients had a prolonged P-R interval. In 1 patient, atrial fibrillation lasting 22 seconds precipitated atrial flutter that lasted 3.4 minutes; in another patient, atrial flutter lasting 1.5 minutes provoked atrial fibrillation that lasted 5.3 minutes. Figure 1. A representative example of electrocardiographic recordings of paroxysmal supraventricular tachycardia (PSVT) termination after adenosine administration. Figure 2. Electrocardiographic recordings showing atrial fibrillation that developed 8.8 seconds after paroxysmal supraventricular tachycardia (PSVT) was terminated by adenosine administration (shown in ). arrow Type I atrial fibrillation occurred in 1 patient, type III occurred in 10 patients, type IV occurred in 13 patients, and atrial flutter occurred in 2 patients. No patient had type II atrial fibrillation. The mean ventricular rate during atrial fibrillation was 107 43 beats/min. The mean duration of the atrial arrhythmias was 5.6 6.7 minutes (range, 8 seconds to 20.7 minutes). Sinus rhythm was restored spontaneously in 16 patients (67%), and cardioversion was required to restore sinus rhythm in 8 patients (33%). Risk Factors for Adenosine-Induced Atrial Arrhythmias Among the 24 patients who developed atrial fibrillation or both atrial fibrillation and atrial flutter, 13 had atrioventricular nodal reentrant tachycardia (11% of all patients with atrioventricular nodal reentrant tachycardia), 9 had atrioventricular reentrant tachycardia (13% of all patients with atrioventricular reentrant tachycardia), and 2 had atrial tachycardia (25% of all patients with atrial tachycardia) (P > 0.2). The frequency of atrial arrhythmia induction was similar in patients with typical (11%) and atypical (10%) atrioventricular nodal reentrant tachycardia (P = 1.0) and in patients with manifest (15%) and concealed (11%) accessory pathways (P > 0.2). During the electrophysiology procedure, atrial fibrillation or atrial flutter only developed immediately after the administration of 12 mg of adenosine. No patient had a history of atrial fibrillation or atrial flutter. After PSVT termination, one or more ventricular or atrial premature complexes occurred in 17% and 63% of patients, respectively. Occurrence of a ventricular premature complex was not associated with the development of atrial fibrillation (P = 0.2). However, atrial premature complexes occurred in all 24 patients who developed atrial fibrillation or both atrial fibrillation and atrial flutter and in 102 of the 176 patients (58%) who did not develop an atrial arrhythmia (P < 0.001) (Figure 2). The time from the preceding beat to premature atrial complex was 265 124 milliseconds (range, 80 to 530 milliseconds) when atrial fibrillation or atrial flutter developed (Figure 2) and 436 141 milliseconds (range, 200 to 920 milliseconds) when atrial fibrillation or atrial flutter did not develop (P < 0.001). Furthermore, the ratio of the coupling interval of the atrial premature complex to the preceding atrial cycle length was 0.37 0.16 when atrial fibrillation was induced after adenosine administration (Figure 2) and 0.49 0.16 when atrial fibrillation was not induced (P = 0.002). The development of an atrial arrhythmia after the administration of adenosine was not associated with age, sex, PSVT cycle length, the requirement of isoproterenol infusion for PSVT induction, the atrioventricular block cycle length, the ventriculoatrial block cycle length, or the R-R interval immediately preceding the development of atrial fibrillation (P > 0.2 for the first six variables; P = 0.2 for the last variable). In addition, atrial overdrive pacing was used to terminate PSVT 6.2 3.1 times per patient (range, 5 to 20 times per patient) and never led to atrial fibrillation or atrial flutter. Ventricular Response during Adenosine-Induced Atrial Fibrillation The mean ventricular rate during adenosine-induced atrial arrhythmias was similar in patients with atrioventricular nodal reentrant tachycardia (105 46 beats/min), those with atrioventricular reentrant tachycardia (114 41 beats/min), and those with atrial tachycardia (91 24 beats/min) (P > 0.2). Amo

Probability of Successful Defibrillation at Multiples of the Defibrillation Energy Requirement in Patients With an Implantable Defibrillator

BACKGROUND The probability of successful defibrillation has been determined in normal animals but not in patients undergoing defibrillator implantation. Therefore, the purpose of this prospective study was to determine the probability of successful defibrillation in humans on the basis of a step-down defibrillation energy requirement. METHODS AND RESULTS Fifty-three consecutive patients underwent five separate inductions of ventricular fibrillation after the defibrillation energy requirement was determined with the use of small decrements and a step-down protocol (20, 15, 12, 10, 8, 6, 5, 4, 3, 2, 1, and 0.8 J). The first shock energy for defibrillation was either 1.0, 1.3, 1.5, 1.7, or 2.0 times the defibrillation energy requirement, and the likelihoods of successful defibrillation were 70+/-27%, 84+/-12%, 86+/-25%, 80+/-29%, and 88+/-32%, respectively (P=.03). The frequencies of uniformly successful defibrillation (5 of 5 defibrillation attempts) were 30%, 27%, 60%, 64%, and 73%, respectively (P=.01). Seven patients in whom the defibrillation energy requirement was <4 J had an overall rate of successful defibrillation of 54+/-20% compared with 86+/-20% in the remaining 47 patients (P=.002). The likelihood of successful defibrillation at twice the defibrillation energy requirement was 98% in the 46 patients with a defibrillation energy requirement of >4 J and 67% in the 7 patients with a defibrillation energy requirement of <4 J (P=.17). An absolute safety margin of 7 J was associated with a 96% probability of successful defibrillation. CONCLUSIONS The probability of successful defibrillation is 70% at the defibrillation energy requirement. The probability plateaus at 88%, at twice the defibrillation energy requirement. A 96% probability of successful defibrillation is achieved at an absolute safety margin of 7 J, and a 98% success rate is achieved at energies that are twice the defibrillation energy requirement if the defibrillation energy requirement is >4 J. If the defibrillation energy requirement is <4 J, larger multiples of the defibrillation energy requirement are needed to achieve a high probability of successful defibrillation.

Slow Pathway Ablation in Patients With Documented but Noninducible Paroxysmal Supraventricular Tachycardia

OBJECTIVES The purpose of this study was to assess the clinical efficacy of radiofrequency ablation of the slow pathway in patients with documented but noninducible paroxysmal supraventricular tachycardia (PSVT) who have evidence of dual atrioventricular (AV) node pathways. BACKGROUND Patients with a documented history of PSVT at times do not have inducible PSVT in the electrophysiology laboratory. Because dual AV node pathways serve as the substrate for AV node reentrant tachycardia (AVNRT), ablation of the slow pathway potentially may be useful in these patients. METHODS The subjects in this prospective study were seven consecutive patients who underwent an electrophysiologic procedure because of documented PSVT and were found to have dual AV node physiology or inducible single AV node echo beats, but no inducible PSVT despite the administration of isoproterenol and atropine. Their mean (+/- SD) age was 33 +/- 13 years, and they had been symptomatic for 12 +/- 12 years. The frequency of the episodes of PSVT ranged from > or = 1/day to 1/month. The rate of the documented episodes ranged from 170 to 260 beats/min, and discrete P waves were not apparent. Slow pathway ablation was performed with 9 +/- 4 applications of radiofrequency energy using a combined anatomic and electrogram mapping approach. RESULTS All evidence of dual AV node pathways was eliminated in six patients, and dual AV node physiology remained present in one patient. During a mean follow-up period of 15 +/- 10 months (range 8 to 27), no patient had a recurrence of symptomatic tachycardia (success rate 95% confidence interval 65% to 100%). CONCLUSIONS Slow pathway ablation may be clinically useful in patients with documented but noinducible PSVT who have evidence of dual AV node pathways.

2: 1 atrioventricular block during atrioventricular node reentrant tachycardia

OBJECTIVES The purpose of this study was to determine the incidence and to clarify the mechanism of 2:1 atrioventricular (AV) block during AV node reentrant tachycardia induced in the electrophysiology laboratory. BACKGROUND In patients with 2:1 AV block during AV node reentrant tachycardia, the absence of a His bundle potential in the blocked beats has been considered evidence of intranodal, lower common pathway block. METHODS In consecutive patients with AV node reentrant tachycardia, the incidence of 2:1 AV block and the response to atropine and a single ventricular extrastimulus was observed. RESULTS Persistent 2:1 AV block occurred in 13 of 139 patients with AV node reentrant tachycardia. A His bundle deflection was present in the blocked beats in eight patients and absent in five. Patients with 2:1 AV block had a shorter tachycardia cycle length than did patients without such block (mean +/- SD 312 +/- 32 vs. 353 +/- 55 ms, p < 0.01). Atropine did not alter the 2:1 block in any patient. In every patient, a single ventricular extrastimulus introduced during the tachycardia converted the 2:1 block to 1:1 conduction. CONCLUSIONS The incidence of induced 2:1 AV block during AV node reentrant tachycardia is approximately 10%. The lack of a response to atropine and the consistent conversion of 2:1 block to 1:1 conduction by a ventricular extrastimulus indicate that, regardless of the presence or absence of a His bundle potential in blocked beats, 2:1 block during AV node reentrant tachycardia is due to functional infranodal block.

Response to pacing at sites of isolated diastolic potentials during ventricular tachycardia in patients with previous myocardial infarction

OBJECTIVES The goal of this study was to determine whether isolated diastolic potentials (IDPs) recorded during ventricular tachycardia (VT) are generated in zones of slow conduction and whether the arcs of block that bound these zones of slow conduction are functional or anatomic in nature. BACKGROUND No previous studies have systematically investigated the response to pacing during VT and sinus rhythm at sites where IDPs are recorded. METHODS The study included 11 patients with a previous infarction who underwent radiofrequency catheter ablation of 15 hemodynamically stable, sustained VTs and in whom an IDP that could not be dissociated from the VT was detected during mapping. RESULTS Pacing during VT at the site where the IDP was recorded resulted in concealed entrainment in each of the 15 VTs. In 10 of the 15 VTs, an IDP was present during sinus rhythm at the same site at which a diastolic potential was recorded during VT. In nine VTs, the isolated potential occurred early in diastole; in these cases, the QRS configuration during pacing in the setting of sinus rhythm was different from that during VT. In six VTs, the isolated potential occurred later in diastole, and in these cases, the QRS configuration during pacing in the setting of sinus rhythm was the same as that during VT. CONCLUSIONS Isolated diastolic potentials may often be generated in an area of slow conduction bounded by arcs of block that are anatomically determined and present during sinus rhythm.