[Thrombosis during thrombopoietin receptor agonist treatment for immune thrombocytopenia. A French multicentric observational study]. / Thromboses sous agonistes du récepteur de la thrombopoïétine au cours du purpura thrombopénique immunologique. Étude rétrospective multicentrique en France.

INTRODUCTION: Thrombopoietin-receptor agonists (TPO-RA) are marketed for immune thrombocytopenia (ITP). They have been associated to thrombosis occurrence in randomized controlled trials. However, the characteristics of these thromboses in the real-life practice as well as their management are poorly known. The objectives of this study were to determine the risk factors, circumstances and management of thrombosis occurring during exposure to TPO-RA in ITP. METHODS: We carried out a multicentre retrospective study in France. Moreover, all cases reported to the French pharmacovigilance system were also analyzed. RESULTS: Overall, 41 thrombosis (13 arterial) in 36 ITP patients (14 males and 22 females, mean age: 59 years) were recorded between January 2009 and October 2015. Twenty patients were treated with romiplostim, 15 with eltrombopag and 1 was treated by both medications. Thirty-three (92%) of the patients had another risk factor for thrombosis. Ten (28%) had an history of thrombosis and 13 (36%) received immunoglobulin in the month preceding the thrombotic event. Three had antiphospholipid antibodies; congenital low-risk thrombophilia was found in 4 cases; 18 patients (50%) were splenectomized. Median platelet count at the time of thrombosis was 172G/l (1-1049G/l). In 22 patients (56%), a good prognosis was associated with the thrombosis and was not linked with TPO-RA withdrawal. Bleeding events occurred in 14% of the patients treated with antiplatelet or anticoagulant drug, including 5% serious events (1 death of intracranial haemorrhage, 1 death of haemorrhagic shock). CONCLUSIONS: The thrombotic risk may be carefully assessed before starting TPO-RA in ITP patients. The impact of antiphospholipid antibodies and of congenital thrombophilia remains to be defined. Thrombosis evolution seems independent of TPO-RA management. Bleeding manifestations seem rare. Poor prognosis was mainly due to ischemic sequelae.

Comparison of naive sixth-grade children with trained professionals in the use of an automated external defibrillator.

BACKGROUND: Survival after out-of-hospital cardiac arrest (OHCA) is strongly influenced by time to defibrillation. Wider availability of automated external defibrillators (AEDs) may decrease response times but only with increased lay use. Consequently, this study endeavored to improve our understanding of AED use in naive users by measuring times to shock and appropriateness of pad location. We chose sixth-grade students to simulate an extreme circumstance of unfamiliarity with the problem of OHCA and defibrillation. The children's AED use was then compared with that of professionals. METHODS AND RESULTS: With the use of a mock cardiac arrest scenario, AED use by 15 children was compared with that of 22 emergency medical technicians (EMTs) or paramedics. The primary end point was time from entry onto the cardiac arrest scene to delivery of the shock into simulated ventricular fibrillation. The secondary end point was appropriateness of pad placement. All subject performances were videotaped to assess safety of use and compliance with AED prompts to remain clear of the mannequin during shock delivery. Mean time to defibrillation was 90+/-14 seconds (range, 69 to 111 seconds) for the children and 67+/-10 seconds (range, 50 to 87 seconds) for the EMTs/paramedics (P<0.0001). Electrode pad placement was appropriate for all subjects. All remained clear of the "patient" during shock delivery. CONCLUSIONS: During mock cardiac arrest, the speed of AED use by untrained children is only modestly slower than that of professionals. The difference between the groups is surprisingly small, considering the naïveté of the children as untutored first-time users. These findings suggest that widespread use of AEDs will require only modest training.

Multicenter experience with a pectoral unipolar implantable cardioverter-defibrillator. Active Can Investigators.

OBJECTIVES: The purpose of this study was to prospectively examine in a multicenter study the methods of use, efficacy and complications of a unipolar cardioverter-defibrillator in patients at risk for sudden cardiac death. BACKGROUND: Implantation of cardioverter-defibrillators in the pectoral region offers a significant opportunity to improve the management of patients with life-threatening arrhythmias. Unipolar, single-lead, pectoral implantable cardioverter-defibrillators might decrease related mortality, morbidity and costs in the care of such patients. METHODS: From November 3, 1993 to May 8, 1995, a unipolar defibrillator (Medtronic model 7219C) was selected for use in 473 patients from 74 centers (386 [82%] men, 87 [18%] women; mean [+/- SD] age 59 +/- 13 years, range 16 to 88). The clinical indication for use was ventricular fibrillation in 157 patients, sustained ventricular tachycardia in 236, both ventricular tachycardia and ventricular fibrillation in 53 and syncope or inducible ventricular tachycardia/ventricular fibrillation in 27. Coronary artery disease was present in 323 patients (68%). The mean left ventricular ejection fraction was 0.36 +/- 0.15 (range 0.10 to 0.85). The distribution of New York Heart Association congestive heart failure was class I = 34%; class II = 45%; class III = 17%; and class IV = 2%. RESULTS: The unipolar cardioverter-defibrillator was inserted successfully in 464 (98%) of 473 candidates. Effective defibrillation occurred with the first shock polarity tested in 88% of patients, after a polarity switch in 8% and after lead or generator repositioning in 2%. The stored energy defibrillation threshold was obtained at implantation in 339 patients (72%) and was 11.5 +/- 6.1 J, with 72% of patients having a defibrillation threshold < or = 12 J. The mean "skin-to-skin" implantation time was 96 +/- 45 min (range 25 to 335 min). Complications occurred in 29 patients (6%). Device therapy for 2,160 spontaneous ventricular tachycardia or fibrillation episodes occurred in 128 patients (27%) over a 2,732 device-month experience (range 0 to 17.2) and was effective in 98.7% of episodes. There were 14 deaths (10 nonsudden cardiac, 3 sudden cardiac, 1 noncardiac). Cumulative survival, on an intention-to-treat basis from all causes of death at 17.2 months, was 94.4%. CONCLUSIONS: Unipolar pectoral implantable cardioverter-defibrillators can be inserted with a high likelihood of success in a relatively brief procedure. Defibrillation thresholds are low, morbidity is modest, and survival rates are good with this new type of implantable cardioverter-defibrillator.

Sustained ventricular arrhythmias: differences between survivors of cardiac arrest and patients with recurrent sustained ventricular tachycardia.

Clinical, angiographic, echocardiographic and electrophysiologic data were examined in 101 patients with a history of sustained ventricular arrhythmia not associated with acute myocardial infarction. These patients included 66 survivors of out of hospital cardiac arrest and 35 patients presenting with hemodynamically well tolerated sustained ventricular tachycardia. On univariate analysis, patients in the cardiac arrest group had a lower incidence of previous myocardial infarction and left ventricular aneurysm and a higher ejection fraction compared with the ventricular tachycardia group. During electrophysiologic testing, the arrhythmia induced in the patients in the cardiac arrest group was fast and polymorphic and frequently degenerated into ventricular fibrillation. In contrast, in the ventricular tachycardia group, a slower, monomorphic and hemodynamically well tolerated ventricular tachycardia was commonly induced. On multivariate analysis, a polymorphic pattern of the induced ventricular arrhythmia was the only independent variable that distinguished the survivors of cardiac arrest from those presenting with sustained ventricular tachycardia. These results suggest that 1) the survivors of cardiac arrest and patients presenting with sustained well tolerated ventricular tachycardia are clinically distinct groups; and 2) the polymorphic tachycardia induced during programmed electrical stimulation in the survivors of cardiac arrest may indicate an unstable tachycardia mechanism. This may explain why these patients present with ventricular fibrillation and cardiac arrest, whereas others present with hemodynamically stable ventricular tachycardia.

A prospective, randomized evaluation of effect of ventricular fibrillation duration on defibrillation thresholds in humans.

The effect of ventricular fibrillation duration in humans on defibrillation efficacy as it pertains to the time of intervention of an automatic implantable defibrillator is unknown. If a difference in defibrillation efficacy exists in the early period after ventricular fibrillation onset, it may affect algorithms used by antiarrhythmic devices for arrhythmia detection and therapy. Therefore, a prospective, randomized evaluation was performed of the effect of ventricular fibrillation durations of 10 s and 20 s on defibrillation thresholds in 10 survivors of sudden cardiac arrest undergoing implantation of an automatic cardioverter defibrillator. The initial duration of ventricular fibrillation was chosen randomly. Subsequently, each patient served as his or her own control for the alternate duration of ventricular fibrillation to that chosen initially. The mean leading edge defibrillation threshold voltage was 411 +/- 114 V when ventricular fibrillation persisted for 10 s and 419 +/- 125 V when it persisted for 20 s (p = 0.73). The mean defibrillation threshold current was 11.4 +/- 2.8 A when ventricular fibrillation persisted for 10 s and 11.4 +/- 3.2 A when it persisted for 20 s (p = 0.97). The delivered energy defibrillation threshold was 11.5 +/- 5.9 J when ventricular fibrillation persisted for 10 s and 12.0 +/- 6.9 J when it persisted for 20 s (p = 0.67). These findings show that the defibrillation threshold does not change between 10 and 20 s of ventricular fibrillation in out-of-hospital survivors of cardiac arrest at the time of surgical implantation of an automatic defibrillator. The data may have influence on the programming of defibrillator detection algorithms.

An effective and adaptable transvenous defibrillation system using the coronary sinus in humans.

With use of a coronary sinus catheter electrode, a right ventricular catheter electrode and a chest wall patch electrode system, defibrillation threshold voltage, current and energy were measured with four distinct transvenous defibrillation techniques delivered in random sequence in each of 12 survivors of cardiac arrest immediately before implantation of a standard epicardial patch defibrillation system. The four transvenous defibrillation techniques were 1) single pathway monophasic pulsing, 2) single pathway biphasic pulsing, 3) dual pathway sequential pulsing, and 4) dual pathway simultaneous pulsing. A transvenous defibrillation method was considered to be potentially useful only if the defibrillation threshold was less than or equal to 500 V (less than or equal to 15 J delivered energy). The 500 V value would allow a 2:1 defibrillation safety margin for a device with a maximal output of 30 J. No single transvenous pulsing technique was uniformly superior in efficacy. However, by choosing the best pulsing technique for each patient, it was possible to obtain an average defibrillation threshold of 410 +/- 135 V leading edge voltage, 7.2 +/- 2.5 A leading edge current and 11.3 +/- 7.4 J delivered energy for the group of 12 patients. With the ability to vary defibrillation technique, transvenous antiarrhythmic device implantation would have been possible in 10 (83%) of the 12 patients at or below a 15 J defibrillation threshold cutoff point. In contrast, if only one transvenous defibrillation method had been used, as few as 5 and at most 8 of the 12 patients would have been candidates for a transvenous defibrillation system given a 15 J defibrillation threshold cutoff point for insertion.(ABSTRACT TRUNCATED AT 250 WORDS)

Tocainide for drug-resistant sustained ventricular tachyarrhythmias.

Eighty-two patients with drug-resistant ventricular tachycardia or fibrillation were treated with oral tocainide. Treatment in 54 patients, all with inducible ventricular tachycardia or fibrillation at baseline electrophysiologic testing, was based on the results of invasive electrophysiologic testing. Twenty-eight additional patients with frequent spontaneous ventricular tachycardia or no inducible arrhythmia during electrophysiologic testing were treated on the basis of the findings of electrocardiographic (ECG) Holter monitoring. Tocainide was effective in 7 (13%) and partially effective in 5 (8%) of the 54 patients in the electrophysiologic study group and was effective in 17 (61%) of the 28 patients in the ECG monitoring group. History of previous myocardial infarction and failure of response to lidocaine correlated with failure to respond to tocainide. Side effects were common both during initial therapy and during long-term treatment and necessitated discontinuation of tocainide therapy in 17% of the patients. At a mean follow-up period of 14 months, 13 patients are still receiving tocainide and are arrhythmia-free. In conclusion, the usefulness of oral tocainide in the management of drug-refractory sustained ventricular tachycardia or fibrillation is limited because of its low effectiveness and frequent side effects.

Prospective comparison of sequential pulse and single pulse defibrillation with use of two different clinically available systems.

Sixteen out-of-hospital survivors of ventricular fibrillation underwent a prospective, randomized, intraoperative comparison of sequential pulse and single pulse defibrillation with use of two distinct electrode systems and waveform shapes currently available for clinical use. Defibrillation was tested alternately with either the single pulse or the sequential pulse system 10 s into an episode of ventricular fibrillation. Sequential pulse defibrillation was performed with two 4 ms truncated exponential pulses of constant duration delivered to three equally spaced oval epicardial patch electrodes composed of concentric coils. The posterior left ventricular electrode served as the common cathode. The first anode was over the anterior right ventricle and the second anode was over the anterior left ventricle. Single pulse defibrillation was performed with the standard intracardiac defibrillation system with use of a single truncated exponential pulse with a fixed 65% tilt delivered across two rectangular, wire mesh epicardial patch electrodes positioned over the anterior right ventricle and posterolateral left ventricle. During defibrillation threshold determination, voltage and current waveforms were recorded and used to determine pulsing resistance and delivered and stored energy. Average defibrillation threshold leading edge voltage for the single pulse technique was 273 +/- 101 V compared with 246 +/- 67 V (11% less) for the sequential pulse technique (p = 0.136). Defibrillation threshold leading edge current for the single pulse technique was 6.7 +/- 2.5 A compared with 5.2 +/- 1.7 A (29% less) for the sequential pulse method (p = 0.005). The defibrillation threshold delivered energy was 5.6 +/- 4.0 J for the single pulse technique and 3.5 +/- 1.8 J (38% less) for the sequential pulse technique (p = 0.021).(ABSTRACT TRUNCATED AT 250 WORDS)

A prospective randomized evaluation of biphasic versus monophasic waveform pulses on defibrillation efficacy in humans.

Biphasic waveforms have been suggested as a superior waveform for ventricular defibrillation. To test this premise, a prospective randomized intraoperative evaluation of defibrillation efficacy of monophasic and biphasic waveform pulses was performed in 22 survivors of out of hospital ventricular fibrillation who were undergoing cardiac surgery for implantation of an automatic defibrillator. The initial waveform used in a patient for defibrillation testing, either monophasic or biphasic, was randomly selected. Subsequently, each patient served as his or her own control for defibrillation testing of the other waveform. The defibrillation threshold was defined as the lowest pulse amplitude that would effectively terminate ventricular fibrillation with a single discharge delivered 10 s after initiation of an episode of ventricular fibrillation induced with alternating current. Each defibrillation pulse was recorded oscilloscopically, and defibrillation pulse voltage, current, resistance and stored energy were measured. Fifteen (68%) of the 22 patients had a lower defibrillation threshold with the biphasic pulse, 3 (14%) had a lower threshold with the monophasic pulse and 4 (18%) had equal defibrillation thresholds (within 1.0 J) regardless of waveform. The mean leading edge defibrillation threshold voltage was 317 +/- 105 V when the monophasic pulse was used and 267 +/- 102 V (16% less) when the biphasic pulse was used (p = 0.008). Mean leading edge defibrillation threshold current was 7.9 +/- 3.7 A when the monophasic pulse was used and 6.8 +/- 3.8 A (14% less) when the biphasic pulse was used (p = 0.051).(ABSTRACT TRUNCATED AT 250 WORDS)

Clinical predictors of the defibrillation threshold with the unipolar implantable defibrillation system.

OBJECTIVES: The purpose of this study was to determine the relation between clinical variables and the defibrillation threshold by using a standardized testing protocol and a uniform implantable defibrillator system. BACKGROUND: Past studied have not revealed useful correlations between clinical variables and the energy required to terminate ventricular fibrillation. Most of these studies did not use a uniform implantable defibrillator system or a standardized protocol to measure the defibrillation threshold and, thus, did not control for the influence of these technical influences. We postulated that defibrillator and defibrillation threshold measurement-based sources of variability overshadowed important clinical predictors. METHODS: The defibrillation threshold was measured by using a standardized protocol in 101 consecutive patients. We used a transvenous unipolar pectoral defibrillation system that employed a single endocardial right ventricular defibrillation coil as the anode and the shell of an 80-cm3 pulse generator as the cathode to deliver a 65% tilt biphasic pulse. RESULTS: Several clinical variables were found to be significantly associated with the defibrillation threshold: patient gender, height, weight, body surface area, heart rate at rest, QRS and corrected QT (QTc) intervals, left ventricular mass and several measures of heart and chest size by chest roentgenogram. None of these variables had a correlation coefficient > 0.45 with the defibrillation threshold. On multivariate analysis, left ventricular mass and heart rate at rest were the only independent predictors of the defibrillation threshold and explained only 25% of the observed variability. CONCLUSIONS: Despite the use of a uniform transvenous defibrillation system and a standardized protocol to measure the defibrillation threshold, no clinically relevant correlation was found between clinical variables and the defibrillation threshold. The defibrillation threshold is probably a function of a complex interaction of anatomic, physiologic and cellular variables that are not adequately represented by easily obtainable clinical information. It is probably not possible to predict defibrillation outcome from standard clinical variables.

Surface electrocardiographic clues suggesting presence of a nodofascicular Mahaim fiber.

Standard electrocardiograms from 87 consecutive patients with tachycardia of left bundle branch block configuration were analyzed retrospectively for features that might be characteristic of tachycardia utilizing a nodofascicular Mahaim fiber. The study group consisted of 13 patients with nodofascicular tachycardia, 34 with supraventricular tachycardia and aberrant conduction over the His-Purkinje system, 22 with ventricular tachycardia and 18 with antidromic tachycardia utilizing a right-sided accessory atrioventricular pathway. Six variables present during tachycardia of left bundle branch block configuration were predictive of a nodofascicular fiber: cycle length between 220 and 450 ms, QRS axis of 0 to -75 degrees, QRS duration 0.15 second or less, R wave in lead I, rS wave in precordial lead V1 and a precordial transition from a negative to a positive QRS complex after lead V4. All six criteria were present in 16 of the 87 patients. No patient with ventricular tachycardia satisfied these criteria, whereas 3 of 34 with supraventricular tachycardia, 1 of 18 with antidromic tachycardia and 12 of 13 with tachycardia using a nodofascicular fiber did. It is concluded that analysis of the surface electrocardiogram during tachycardia may suggest the presence of a nodofascicular fiber.

Long-term outcome in patients who survive out of hospital ventricular fibrillation and undergo electrophysiologic studies: evaluation by electrophysiologic subgroups.

The long-term outcome of 241 survivors of out of hospital ventricular fibrillation who underwent programmed electrical stimulation was evaluated. Patients were categorized according to the rhythm induced at baseline drug-free electrophysiologic testing. Ventricular fibrillation was induced in 39 patients (16%) (Group 1), sustained ventricular tachycardia in 66 patients (27%) (Group 2) and nonsustained ventricular tachycardia in 34 patients (14%) (Group 3); 102 patients (42%) (Group 4) did not have an arrhythmia inducible at baseline electrophysiologic testing. Antiarrhythmic drugs were administered over the long term to 92% of patients in Group 2, 91% of patients in Group 1 and 47% of patients in Group 4. At a mean follow-up time of 30 +/- 15 months, recurrent sudden cardiac death or nonfatal ventricular fibrillation occurred in 11 (28%) of 39 patients with inducible ventricular fibrillation (Group 1), 14 (21%) of 66 patients with inducible sustained ventricular tachycardia (Group 2), 4 (12%) of 34 patients with inducible nonsustained ventricular tachycardia (Group 3) and 16 (16%) of 102 patients without inducible arrhythmias (Group 4). Actuarial analysis revealed a 2 year cumulative arrhythmia-free survival rate of 65% for patients in Group 2, 71% for patients in Group 1, 79% for patients in Group 3 and 81% for patients in Group 4 (p = 0.02). Actuarial survival of patients with inducible sustained ventricular tachycardia or ventricular fibrillation suppressed by electrophysiologically guided drug therapy was not significantly different from that in patients whose arrhythmia was not suppressed. Multivariate regression analysis revealed that only the presence of congestive heart failure was an independent predictor of outcome in these patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Localization of septal pacing sites in the dog heart by epicardial mapping.

To examine whether different septal pacing sites could be distinguished by their epicardial activation patterns, six to eight stimulating electrodes were placed throughout the septum in seven open chest dogs. Unipolar electrograms were obtained from 52 epicardial electrodes during pacing from each stimulating electrode and isochronous epicardial maps were constructed. The location of each stimulating electrode was found by dissection, and its distance from the overlying epicardium was measured. To allow comparison among epicardial maps, the septum was conceptually subdivided into nine regions to which stimulating electrodes were assigned. Epicardial activation patterns from the same region were similar and these patterns allowed the region containing a stimulating electrode to be identified in many cases. Three other variables were found to have additional localizing value. There were: 1) the time from the stimulus to epicardial breakthrough, 2) the duration of epicardial activation, and 3) the area of epicardium activated in the first 5 ms after epicardial breakthrough. For those stimulating electrodes that could not be localized by their epicardial activation patterns, the distance of the stimulating electrode beneath the epicardium was well fit from these three variables by multiple regression (correlation coefficient [r] = 0.97). Thus, using all the previous factors, localization of septal pacing sites was possible in the noninfarcted dog heart by epicardial mapping.

Reducing mortality from sudden cardiac death in the community: lessons from epidemiology and clinical applications research.

The reduction of mortality from sudden cardiac death (SCD) in the community remains a challenge. Clinical-epidemiologic studies have identified a range of factors that are associated with an increased risk of SCD. While of potential etiologic and prognostic importance, these factors have limited sensitivity and a low positive predictive value for SCD. On the other hand, clinical trials have suggested that a variety of interventions, including risk factor reduction, nutritional interventions, drug therapies, cardiac procedures, and new technologies, have the potential to reduce mortality from SCD. In this review, we examine what is known about the epidemiology and clinical application of interventions to reduce mortality from SCD; and, we consider the impact of both prevention and clinical interventions on mortality from SCD from a community perspective. There is mounting evidence that supports both public health and clinical efforts to prevent the occurrence of SCD. There also is evidence suggesting that new technologies, such as automated external defibrillators, have the potential to reduce case-fatality from SCD. Further progress will depend on improved methods to identify persons-at-risk, reduction of risk factors, and application of techniques -- both simple and advanced -- to improve survival in victims of SCD.

Implantable defibrillators and antiarrhythmic drugs in patients at risk for lethal arrhythmias.

The high mortality rate and frequency of ventricular arrhythmias in patients with congestive heart failure has prompted numerous clinical trials aimed at reducing mortality by addressing arrhythmic death. Recently completed trials have suggested that for patients who have survived cardiac arrest, the preferred treatment may be an implantable cardioverter defibrillator (ICD). From the standpoint of primary prevention, implantable defibrillators and amiodarone have received the most attention. It remains unclear, however, to which patients these studies apply, and if and how the results might be generalized. No available studies confirm an additional benefit of pharmacologic or device-based antiarrhythmic therapy beyond that offered by optimal treatment with beta blockers, angiotensin-converting enzyme inhibitors, and lipid-lowering drugs in the majority of patients with cardiomyopathy. Clinical trials are ongoing to address these issues.

Acquired cyanotic heart disease secondary to traumatic tricuspid regurgitation. Case report with a review of the literature.

A case of traumatic tricuspid insufficiency leading to right atrial enlargement and to a patent foramen ovale with right to left shunting is presented. Six similar cases previously reported are reviewed. The time course of clinical deterioration was related to the type of tricuspid valve damage incurred. Papillary muscle rupture led to surgery within a year, whereas less severe chordal damage allowed a more benign course that lasted from 10 to 25 years from the time of injury to the time of surgery. Surgical repair of the incompetent tricuspid valve and closure of the atrial septal defect led to significant improvement. The diagnostic usefulness of radionuclide imaging and echocardiography is demonstrated in this case. A mechanism of right to left interatrial shunting in the presence of normal pulmonary arterial pressures is proposed; this invokes phasic increases in right atrial pressure from tricuspid insufficiency and streaming of blood from the inferior vena cava into the left atrium across a patent foramen ovale in a manner that resembles conditions in the fetal circulation.

Developments, complications and limitations of catheter-mediated electrical ablation of posterior accessory atrioventricular pathways.

Nineteen patients with posterior accessory pathways and disabling, refractory arrhythmias, underwent catheter ablation using standard defibrillator pulses at energy settings of 150 to 400 J. Accessory pathway ablation was successful in 13 of 19 (68%). Effective catheter ablation correlated with local ventriculoatrial (VA) intervals determined from the coronary sinus catheter at the site of earliest retrograde atrial activation during orthodromic reciprocating tachycardia. In 12 of the 13 successfully ablated patients, the local VA interval was less than 80 ms. In 4 of the 6 unsuccessfully treated patients, the local VA interval was greater than or equal to 80 ms, p less than 0.01. Transient abnormalities noted with the procedure included sinus bradycardia (3 patients), atrioventricular block (5), accelerated junctional rhythm (3), ectopic atrial tachycardia (2), myocardial depression (1), "ischemic" appearing T-wave inversions (10) and hemodynamically insignificant small pericardial effusions (5) Creatine kinase-MB increased from 3 +/- 2 U/liter to 26 +/- 18 U/liter (p less than 0.001), 4 to 8 hours after ablation. In addition, electrical shorts occurring during the ablation procedure in 2 patients were identified and corrected only with oscilloscopic monitoring of voltage and current waveforms. Significant adverse sequelae were seen in 4 patients. Three patients required sternotomy for control of cardiac tamponade secondary to a ruptured coronary sinus and 1 patient had a small posterior left ventricular infarction related to spasm of a right coronary artery extension branch. Coronary sinus rupture correlated with the ratio of catheter diameter to coronary sinus diameter.(ABSTRACT TRUNCATED AT 250 WORDS)

Prospective evaluation of initially ineffective defibrillation pulses on subsequent defibrillation success during ventricular fibrillation in survivors of cardiac arrest.

The effect of initially ineffective defibrillation pulses on subsequent defibrillation success is not known. Therefore, the voltage, current and energy at the defibrillation threshold were compared with the defibrillation rescue pulse voltage, current and energy that terminated ventricular fibrillation when an ineffective pulse just below the defibrillation threshold had been used initially. This lower amplitude ineffective pulse was termed a "subdefibrillation threshold" pulse. The pulse that restored sinus rhythm after the subdefibrillation threshold pulse was delivered was termed the "subdefibrillation threshold rescue pulse." This comparison was undertaken, intraoperatively, in 14 out-of-hospital cardiac arrest survivors using a sequential-pulse catheter-patch defibrillation system. Each of the 14 patients required higher voltage, current, delivered energy and stored energy for defibrillation with the subdefibrillation threshold rescue pulse than with the defibrillation threshold pulse. The defibrillation threshold voltage was 451 +/- 127 volts compared with a subdefibrillation threshold rescue voltage of 585 +/- 147 volts (p less than 0.00002). The defibrillation threshold current was 5.5 +/- 2.4 amps compared with a subdefibrillation threshold rescue current of 7.2 +/- 2.7 amps (p less than 0.00001). Delivered and stored energies were 10.9 +/- 7.4 and 12.3 +/- 7.2J, respectively, for the defibrillation threshold pulse and were 17.6 +/- 9.4 J (p less than 0.00002) and 20.5 +/- 9.3 J (p less than 0.00005), respectively, for the subdefibrillation threshold rescue pulse. It is concluded that the risk of requiring considerably higher energies than anticipated for defibrillation must be incurred, should defibrillation fail because of an initially insufficient defibrillation pulse.(ABSTRACT TRUNCATED AT 250 WORDS)

Comparison of two-dimensional echocardiographic and angiographic findings in arrhythmogenic right ventricular dysplasia.

Comparison of 2-dimensional (2-D) echocardiographic and right ventricular (RV) angiographic findings was performed in 10 patients with arrhythmogenic RV dysplasia. Diagnosis was based on accepted electrocardiographic and angiographic criteria. Nine patients underwent invasive electrophysiologic study, which confirmed RV source of ventricular tachycardia (VT) in 7. Biopsy findings of RV dysplasia were available in 3 patients. Two-dimensional echocardiography and angiography corresponded closely when diffuse RV enlargement and hypokinesia were present. Such diffuse findings were not invariably present. Localized abnormalities consisting of bulging or sacculation of the RV wall were noted by both techniques, even in the absence of diffuse changes. Echocardiographic evidence of localized disease predicted the presence of similar lesions at angiography, but agreement as to specific location was poor. Subjectivity in interpreting subtle RV abnormalities by either technique and the inherent differences in information provided by the 2 methods probably account for the inconsistencies. In the patient with suspected arrhythmogenic RV dysplasia, 2-D echocardiographic evidence of diffuse RV enlargement, otherwise unexplained, strongly supports the diagnosis and angiography may be avoided. Isolated local changes seen by echocardiography should increase suspicion of RV dysplasia, but complementary angiographic study is warranted.

Effect of damped sine-wave shocks on catheter dielectric strength.

This study evaluated the ability of 24 new standard tripolar and quadripolar U.S. Catheter Instruments catheters to withstand a single damped sinusoidal shock delivered by a standard defibrillator. The schema for energy delivery was meant to simulate possible clinical practices. Delivered peak voltage and current were measured during each shock. Each electrode was examined for pitting and changes in line resistance as a consequence of the shock. Electrode pitting occurred on all selected anodal poles. However, it also was found on "unsolicited" electrodes from 7 catheters, indicating that current had followed unanticipated routes. Electrode line resistance was unmeasurable in 6 of these 7 inappropriately pitted electrodes. Delivered peak voltage and postshock catheter dielectric strength depended on the manner of energy delivery. To simulate a posterior septal accessory pathway ablation procedure, a shock was delivered to 2 proximal (anodal) poles in 16 quadripolar catheters (8 received 200 J and 8 received 360 J). Delivered peak voltage was 3,125 +/- 362 V for the 200-J shock and 4,100 +/- 160 V for the 360-J shock. Postshock catheter dielectric strength for the 200- and 360-J shock was 1,425 +/- 826 V and 601 +/- 707 V, respectively. This was significantly lower than peak delivered voltage (p less than 0.001 for either energy). To simulate His bundle or ventricular tachycardia focus ablation, 8 tripolar catheters each received a single 200-J shock to the tip electrode. This resulted in a delivered peak voltage of 2,900 +/- 351 V, compared with a postshock dielectric strength of 1,325 +/- 1,320 V (p less than 0.002).(ABSTRACT TRUNCATED AT 250 WORDS)