Sean S. O'Nunain

Treatment of ventricular tachycardia by transcatheter radiofrequency ablation in patients with ischemic heart disease.

BACKGROUND Recurrent sustained ventricular tachycardia (VT) is not responsive to antiarrhythmic drugs in the majority of patients, who therefore need therapy with nonpharmacological methods. We evaluated prospectively the feasibility, safety, and efficacy of transcatheter radiofrequency (RF) ablation of VT in 21 selected patients with ischemic heart disease and VT. METHODS AND RESULTS Twenty-one patients with ischemic heart disease and recurrent, drug-refractory VT documented by 12-lead ECG were selected who had sufficient hemodynamic tolerance of VT to undergo transcatheter mapping. Documented clinical VT was reproduced by programmed cardiac stimulation (PCS), and the site of origin was localized by a combination of techniques, including pace mapping, activation-sequence mapping, recordings of middiastolic potentials, and application of resetting and entrainment principles. RF current at 55 V was applied (3.8 +/- 3.1 applications per patient) for as long as 30 seconds at a time to target sites. Twenty-four distinct clinical VTs (mean cycle length, 445 +/- 52 milliseconds) were mapped and ablated in 21 patients. In 17 of 21 patients (81%), the procedure was acutely successful, and the target clinical VT could no longer be induced by PCS after the procedure, whereas in 4 patients, clinical VT remained inducible. By contrast, VTs with shorter cycle length and different QRS morphology than the ablated VT could still be induced by PCS in 12 of 21 patients. One patient died in intractable congestive heart failure 10 days after the procedure, and the remaining 20 are alive at the end of the follow-up period. The majority of the patients continued to be treated with at least one additional mode of antiarrhythmic therapy; 12 patients were still taking antiarrhythmic drugs, and 9 patients received an implantable cardioverter/defibrillator. During a mean follow-up period of 13.2 +/- 5.0 months, 9 of 20 patients (45%) had recurrent VT. In 4 patients, the recurrent VT was different than the previously ablated one. Clinical VT recurred in all 4 patients in whom RF ablation had been acutely unsuccessful. Four patients with recurrent VT underwent repeat RF ablation procedures that were acutely successful and had no further recurrence. CONCLUSION Transcatheter RF ablation is feasible but has only moderately high efficacy in a small, selected group of patients with ischemic heart disease and drug-refractory, highly frequent, hemodynamically tolerated, sustained VT. In the majority of the patients, this treatment technique is palliative rather than definitive, and many of the patients continue to require other methods of antiarrhythmic therapy.

Subclavian Crush Syndrome Complicating Transvenous Cardioverter Defibrillator Systems

Subclavian crush syndrome, described with pacemaker leads implanted via subclavian puncture, may occur when conductor fractures and insulation breaches develop by compression of a lead between the first rib and clavicle. We reviewed our experience in 164 patients who underwent intended implantation of transvenous defibrillator systems to determine the clinical relevance of subclavian crush syndrome in defibrillator patients. Venous access was obtained via subclavian puncture in 114 patients (70%) and via cephalic cut‐down in 50 patients (30%). Nonthoracotomy lead systems, with or without subcutaneous patch, were successfully implanted in 131 of 164 patients (79.9%). Thoracotomy was required in 32 patients (19.5%) and subxiphoid patch in 1 patient (0.6%). Over a mean of 12.9 months (range 1–62 months), 3 patients (1.8%) required revision of the rate sensing lead/coil or superior vena cava coil after development of lead compression fractures in the region of the clavicle and first rib. In all 3 patients the leads had been implanted via subclavian puncture (2.6% of patients in whom the subclavian technique was utilized). Two patients presented with spurious shocks. One patient was asymptomatic. Conclusions: When venous access is obtained via subclavian puncture, subclavian crush syndrome may develop in patients with transvenous defibrillator systems. Patients may be asymptomatic and lead fractures may go unrecognized. When implanting transvenous defibrillator systems, strong consideration should be given to obtaining venous access primarily via the cephalic cut‐down technique.

Pseudo-pacemaker syndrome following inadvertent fast pathway ablation for atrioventricular nodal reentrant tachycardia.

Pseudo‐Pacemaker Syndrome After AV Nodal Ablation. Atrioventricular nodal reentrant tachycardia that is refractory to drug treatment has recently been treated with radiofrequency catheter ablation. In this case report we describe a patient with atrioventricular nodal reentrant tachycardia in whom radiofrequency ablation of slow pathway was attempted, with inadvertent damage to the fast pathway. The patient developed marked first‐degree atrioventricular block associated with symptoms mimicking pacemaker syndrome.

The treatment of patients with infected implantable cardioverter-defibrillator systems

OBJECTIVE The purpose of this study was to evaluate the treatment of patients with infected implantable cardioverter-defibrillator systems. METHODS Retrospective analysis was done of the cases of 21 patients treated for implantable cardioverter-defibrillator infection during an 11-year period. RESULTS Of 723 cardioverter-defibrillator implantations (550 primary implants, 173 replacements), nine (1.2%) were complicated by early postoperative device-related infections. Late infections developed in two patients 19 and 22 months, respectively, after implantation. Ten other patients were transferred to our institution for treatment of cardioverter-defibrillator infection. The time from implantation to overt infection was 2.2 +/- 1.3 months, excluding the two late infections. The responsible organisms were Staphylococcus aureus (9), Staphylococcus epidermidis (6), Streptococcus hemolyticus (1), gram-negative bacteria (3), Candida albicans (1), and Corynebacterium (1). All patients were treated with intravenous antibiotic drugs. Total system removal was done in 15 patients and partial removal in 2; in 4, the cardioverter-defibrillator system was not explanted. There were no perioperative deaths. A new implantable cardioverter-defibrillator system was reimplanted in 7 patients after 2 to 6 weeks of antibiotic therapy. Ten patients were treated without reimplantation (2 arrhythmia operation, 8 antiarrhythmic drugs). Four patients (3 patients without explantation and 1 with partial system removal) were treated with maintenance long-term antibiotic therapy. During a mean follow-up of 21 +/- 2.8 months, no patient had clinical recurrence of infection. One patient treated with antiarrhythmic drugs without system reimplantation died suddenly. CONCLUSIONS Infections that involve implantable cardioverter-defibrillator systems can be safely managed by removing the entire system with reimplantation after intravenous antibiotic therapy. In selected patients in whom the risk for system explantation is high and anticipated life expectancy is short, long-term antibiotic therapy to suppress low-virulence infections may represent an acceptable alternative.

Asystole after exercise in healthy persons

Exercise-related syncope is infrequent in healthy persons, although vasodepressor syncope reproduced by positive head-up tilt testing has been reported in small series of healthy persons [1] and athletes [2] with syncope after exercise. Whether vasodepressor syncope may also occur during exercise is controversial and is now an issue of public debate [3]. Asystole after exercise is an extremely rare finding in healthy persons, and single cases without clear proof of the underlying mechanisms have been reported during the past 20 years [4-7]. We describe three patients with recurrent exercise-related syncope in whom prolonged asystole after exercise was documented. Positive head-up tilt table testing in all three patients suggested neurocardiogenic syncope as the underlying mechanism. Case Reports Patient 1 A 34-year-old man had atypical chest pain and a history of multiple episodes of syncope and presyncope, all related to physical stress. Two syncopal episodes occurred immediately after weight lifting. Submaximal exercise test results did not indicate ischemia. However, 1.5 minutes into recovery, the patient developed sudden asystole (lasting for 32 seconds) with rare ventricular escape beats (Figure 1). This resulted in respiratory arrest, and chest massage was initiated by the supervising physician; the patient recovered just before being intubated. Fifteen months later, he had another syncopal episode while walking into the bathroom at night. A chest radiograph, a 12-lead electrocardiogram, 24-hour Holter monitoring, and an echocardiogram all yielded normal test results. Head-up tilt testing was done, and, after 4 minutes in the upright position, the patient became abruptly asystolic for 23 seconds without previous symptoms or hypotension (blood pressure before asystole, 123/92 mm Hg; heart rate, 92 beats per minute). He lost consciousness and made a slow recovery after returning to the supine position. With avoidance of strenuous exercise, the patient has remained free of syncope without drug or pacemaker therapy during 9 months of follow-up surveillance. Figure 1. The rhythm strip starts 1. Patient 2 A 22-year-old man had four episodes of syncope in a 1-year period, all occurring during or immediately after playing basketball. During warm-up before a game, he had a syncopal spell while standing still after running. He reported several similar episodes that he shortened by lying supine. Echocardiography showed moderate concentric left ventricular hypertrophy without evidence of outflow tract obstruction and showed a left ventricular ejection fraction of 75%. The surface electrocardiogram was consistent with left ventricular hypertrophy, but arterial blood pressure measurements were repeatedly normal. One minute after maximal exercise testing, he developed a sudden onset of bradycardia associated with near syncope, and several 4- to 6-second periods of asystole were documented followed by sinus bradycardia with first-degree atrioventricular block. Thallium imaging results were normal. The results of a comprehensive electrophysiologic study were also normal. Ten minutes into head-up tilt table testing, the patient had vasodepressor syncope (systolic blood pressure, 60 mm Hg) accompanied by mild bradycardia (43 beats per minute). A repeated exercise test, with a scopolamine patch in place, showed normal results. Scopolamine was prescribed but was subsequently discontinued because of side effects. The patient has taken oral disopyramide for 38 months and has had an uneventful course during this time; he continues to play basketball. Patient 3 A 35-year-old man had two presyncopal episodes, one immediately after strenuous exercise and the second after fighting a fire. His clinical evaluation was unremarkable. Echocardiographic results showed mild mitral valve prolapse without mitral regurgitation and showed normal left ventricular function. Exercise radionuclide ventriculographic results were normal. Eight minutes into recovery, while seated, the patient had sudden asystole for 15 seconds with a brief loss of consciousness followed by a slow sinus recovery at a rate of 10 to 20 beats per minute. Respiratory arrest occurred, but cardiac and respiratory function returned spontaneously. Comprehensive electrophysiologic study results were entirely normal. Head-up tilt table testing at baseline was unremarkable, but repeated testing using intravenous isoproterenol (0.025 g/kg per minute) provoked vasodepressor syncope (blood pressure, 80/60 mm Hg) with relative bradycardia (heart rate decrease from 120 to 64 beats per minute) after 15 minutes in the upright position. The patient started receiving atenolol (25 mg per day); repeated head-up tilt test and exercise test results (maximal heart rate, 148 beats per minute; Bruce stage 8) were normal. While receiving atenolol, the patient has remained free of recurrent syncope after 9 months of follow-up. Discussion Single cases of asystole after exercise have been described previously, but the underlying mechanisms have been uncertain [4-7]. Our findings of positive head-up tilt test results in all three patients suggest that a variant of neurocardiogenic syncope may be one mechanism of asystole after exercise, but additional abnormalities in the autonomic control of the cardiovascular system seem to be involved. Blood pressure control at rest and also in response to changing posture is mainly regulated through the baroreceptor reflex [8]. The response to exercise involves additional mechanisms [9] (such as increased sympathetic activity) that have been partly ascribed to the so-called metaboreflex activated by metabolites from ischemic muscles [10, 11]. After exercise, the heart rate decreases to baseline, although the blood pressure remains increased, despite continuing activation of this reflex by ongoing muscle ischemia. This phenomenon has been attributed to an exercise-induced up-regulation of the parasympathetic efferent tone, which, in the period after exercise, selectively depresses the heart rate without affecting the vascular bed and blood pressure [9, 11]. The mechanisms provoking neurocardiogenic syncope are probably initiated by a progressive decrease in venous return in the upright position, which is responsible for maximal stimulation of the sympathetic system. Echocardiographic studies have documented a progressive decrease in end-diastolic and end-systolic volumes during head-up tilt table testing, with a maximal increase in fractional shortening before syncope [12]. The strong sympathetic drive in the setting of a relatively empty heart leads to vigorous myocardial contraction, which, in susceptible persons, activates mechanoreceptors in the left ventricular wall (C-fibers) and causes a profound response of the afferent vagal nerve [13]. This vagal stimulus may trigger a sudden withdrawal of the neural efferent sympathetic activity (negative feedback loop) and may increase the efferent parasympathetic tone with subsequent vasodilation and progressive hypotension [14]. Because arterial hypotension usually precedes bradycardia, inactivation of the sympathetic efferent tone and consequent vasodilation may be the primary mechanism of syncope [15]. Bradycardia and asystole, as markers of the increased parasympathetic tone, play only a secondary role in most patients with vasodepressor syncope. This view is further supported by the fact that, in most patients, hypotension and syncope cannot be avoided by atrioventricular sequential pacing [15]. Infrequently, however, cardioinhibition leading to profound bradycardia or asystole may be the dominant mechanism responsible for symptoms. In our patients, syncope and asystole typically occurred in the recovery period of exercise, when venous return was diminished (sitting position). The findings of positive results from head-up tilt testing suggest that all three patients had a low threshold to trigger an abnormal afferent parasympathetic response to decreased venous return, suggesting that venous pooling after exercise may have been one of the mechanisms triggering their asystole. However, the long latency between maximal activation of the mechanoreceptors (peak exercise) and the onset of syncope during late recovery in one of our patients (8 minutes after exercise) and in another of the previously reported patients (10 minutes after exercise) suggests that other mechanisms, such as inappropriate control of the sympathetic tone after exercise (for example, diminished sympathetic response to muscle ischemia after exercise), may play an additional role in some patients. Based on these patients and the current understanding of neurocardiogenic syncope, it appears that asystole after exercise in otherwise healthy persons may represent a variant of this syndrome, in which the effect of increased efferent parasympathetic tone predominates over the effect of sympathetic withdrawal. The optimal management of patients with vasodepressor syncope is unknown. In theory, if initiation of the vasodepressor reflex can be prevented, the hypotension and bradycardia that follow its activation should be eliminated. Accordingly, therapy is generally directed at the underlying mechanisms rather than at the outcome. Although several drugs (including -blockers [16], disopyramide [17], and scopolamine [18]) have been used, no consensus exists about whether drug therapy or implantation of pacemakers is beneficial in treating patients with this condition [19].

Effects of intravenous adenosine in patients with preexcited functional tachycardias: Therapeutic efficacy and incidence of proarrhythmic events

Abstract It is concluded that adenosine is effective in terminating preexcited junctional tachycardias, but may be complicated by serious proarrhythmic effects in these patients. These proarrhythmic effects of adenosine (1) preclude its use as the agent of first choice in the acute treatment of arrhythmias in which this diagnosis is suspected, and (2) highlight the need for continuous electrocardiographic monitoring and availability of direct-current cardioversion when adenosine is used as a diagnostic agent in wide-complex tachycardias of unknown origin.

Ventricular Pacing Induced Ventricular Tachycardia in Patients with Implantable Cardioverter Defibrillators

Appropriately timed noncompetitive ventricular pacing potentially may initiate ventricular tachycardia in patients prone to these arrhythmias. The combination of bradycardia pacing and stored electrograms in a currently available cardioverter defibrillator provides an opportunity to evaluate the occurrence of such pacing induced ventricular tachycardia. During a surveillance period of 18.7 ± 11.4 months, stored electrograms documented 302 episodes of ventricular tachycardia in 77 patients. Five patients (6.5%) demonstrated 25 episodes (1–16 per patient) of ventricular tachycardia that were immediately preceded by an appropriately paced ventricular beat (8.3% of all episodes of ventricular tachycardia). All five patients had prior myocardial infarctions and a history of monomorphic ventricular tachycardia occurring both spontaneously and in response to programmed electrical stimulation. Antitachycardia pacing terminated pacing induced ventricular tachycardia in 22 episodes; in one episode antitachycardia pacing accelerated ventricular tachycardia. In two cases shock therapy was aborted for nonsustained ventricular tachycardia. We conclude that, in selected postinfarction patients with recurrent sustained monomorphic ventricular tachycardia treated with implantable cardioverter defibrillators, appropriately timed ventricular pacing may induce ventricular tachycardia.

TRANSVENOUS SINGLE LEAD ATRIAL DEFIBRILLATION : EFFICACY AND RISK OF VENTRICULAR FIBRILLATION IN AN ISCHEMIC CANINE MODEL

Transvenous atrial defibrillation with multiple atrial lead systems has been shown to be effective in models without the potential for ventricular arrhythmias. The specific aim of this study was to evaluate the efficacy and safety of transvenous single lead atrial defibrillation in a canine model of ischemia cardiomyopathy. Ten dogs had ischemia cardiomyopathy induced by repeated intracoronary micmsphere injections. The mean LV ejection fraction decreased from 71%± 9% to 38%± 14% (P = 0.003). Spontaneous atrial fibrillation (AF) developed in four dogs, and in six AF was induced electrically. Atrial defibrillation thresholds (ADFTs) were determined with synchronous low energy shocks using a transvenous tripolar lead with two defibrillation coils (right ventricle, superior vena cava) and an integrated sensing lead (RV coil vs electrode tip). The ADFTs derived by logistic regression were compared at 50% and 90% probability of success (ED50, ED90): ED50 was 2.4 ±1.7 J and 2.9 ±2.1 J, respectively, for 5‐ and 10‐ms monophasic shocks, and 1.8 ± 0.9 J and 2.1 ± 1.3 J, respectively, for 5‐ and 10‐ms biphasic shocks. Immediately after 3 of 2,179 (0.1%) synchronized shocks, ventricular fibrillation (VF) developed. VF was induced in 3 of 1,062 (0.3%) shocks with integrated sensing (RV coil vs electrode tip) compared to 0 of 1,117 shocks when a separate bipolar RV sensing electrode was used for synchronization. In our canine model of ischemic cardiomyopathy, low energy atrial defibrillation via a transvenous single lead system was highly effective. However, there was a small but definite risk of VF induction, which seemed to be greater when an integrated as opposed to a true bipolar RV sensing was used.

Electrocardiographic pseudo-infarct patterns after implantation of cardioverter-defibrillators

Postoperative electrocardiographic (ECG) changes are frequently present after insertion of implantable cardioverter-defibrillators (ICD) and may mimic perioperative myocardial infarction (MI). The purpose of this study was to assess the incidence and clinical significance of postoperative ECG changes in relation to clinical, laboratory, and implantation data. In 25 (16%) of 156 patients undergoing ICD implantation, significant ECG changes (> or = 50% reduction in R-wave amplitude in > or = 3 leads or new Q waves in > or = 2 leads) were present 1 to 3 days after the operation and persisted at hospital discharge in 12 (8%). Presence of thoracotomy, the total number of induced ventricular fibrillation episodes, and the number of defibrillation shocks required during defibrillation threshold (DFT) testing correlated with postoperative ECG changes. Other factors associated with a significant R-wave loss in the lateral precordial leads included left-sided pleural effusion, lung infiltrates or atelectasis, and large defibrillator patch electrodes over the left ventricle or the lateral chest wall. Myocardial necrosis documented by elevated cardiac enzymes occurred in 6 (5%) of 151 patients without significant ECG changes and in 3 (12%) with (p value not significant). However, postoperative ECG changes associated with elevated enzymes were indistinguishable from changes unrelated to necrosis. Therefore the sensitivity and specificity of the surface ECG for detection of MI after ICD placement is poor. Multiple factors such as thoracotomy, myocardial injury from DFT testing, electric insulation, or shielding of the heart may contribute to the development of electrocardiographic pseudo-infarct patterns.