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Biomedical subjects

G J Klein

Publications and source records attributed to G J Klein.

At least 127 records · Page 7Linked to original sources

Junctional tachycardia: a useful marker during radiofrequency ablation for atrioventricular node reentrant tachycardia.

OBJECTIVES: The aim of this study was to evaluate junctional tachycardia as a useful marker during radiofrequency ablation for atrioventricular (AV) node reentrant tachycardia. BACKGROUND: Junctional tachycardia appears to be a response of the atrioventricular node to injury and is seen during both radiofrequency AV node ablation and slow and fast pathway ablation for AV node reentrant tachycardia. We hypothesized that junctional tachycardia heralding AV node block and that associated with slow or fast pathway ablation may have different characteristics that could be useful in preventing inadvertent AV block. METHODS: Characteristics of junctional tachycardia were examined after 59 radiofrequency ablation sessions in 53 consecutive patients with a mean age (+/- SD) of 41.6 +/- 16.5 years. Type 1 junctional tachycardia was followed by transient second- or third-degree AV block (n = 5) or permanent third-degree AV block (n = 1). Type 2 junctional tachycardia was followed by normal AV conduction (n = 53). RESULTS: Fifty-one patients had typical AV node reentrant tachycardia, and two patients had atypical tachycardia. Fast pathway ablation was attempted during 6 sessions and slow pathway ablation during 53 sessions. Patients underwent 15.3 +/- 10 radiofrequency applications, with a mean duration of 24 +/- 9.7 s. Junctional tachycardia was observed an average of 2.8 +/- 1.8 times per ablation session. Type 1 junctional tachycardia had a significantly faster rate than that of type 2 (cycle length 363 +/- 44 vs. 558 +/- 116, p < 0.001). In addition, type 1 junctional tachycardia was associated with predominantly ventriculoatrial block whereas type 2 was associated with predominantly 1:1 ventriculoatrial conduction (2 of 6 vs. 47 of 53 episodes, p < 0.05). CONCLUSIONS: We conclude that junctional tachycardia leading to AV block can be recognized by a faster junctional rate and ventriculoatrial block. This is a useful marker of impending AV block during slow and fast pathway ablation.

Adult↗

Biphasic versus sequential pulse defibrillation: a direct comparison in humans.

It has been demonstrated recently that both biphasic and sequential pulse defibrillation shocks are superior to monophasic defibrillation shocks in animals and humans. There is little information directly comparing these two waveforms when pulse characteristics, subjects, and total electrode surface areas are kept constant. We determined the defibrillation threshold intraoperatively in 12 patients undergoing arrhythmia surgery, with the use of two or three patch electrodes (Medtronic 6891 and 6892), while keeping the electrode surface area constant. Patients were randomized in a crossover design for determinations of defibrillation threshold by means of biphasic and sequential pulse shocks. Leading-edge delivered current and delivered energy were significantly lower with sequential pulse shocks than with biphasic shocks (delivered energy means +/- SEM 3.6 +/- 0.7 joules vs 5.5 +/- 0.9 joules, respectively). We conclude that sequential pulse defibrillation with three defibrillating electrodes provides an important current delivery system not matched by biphasic shocks with two electrodes when subjects, waveform characteristics, and total electrode surface areas are kept constant.

Adult↗

Defibrillation shocks produce different effects on Purkinje fibers and ventricular muscle: implications for successful defibrillation, refibrillation and postshock arrhythmia.

OBJECTIVES: To understand the mechanisms of postdefibrillation arrhythmias and failed defibrillation, we studied the cellular effects of high voltage shocks on different cardiomyocytes in the dog. BACKGROUND: The causes of postdefibrillation arrhythmias and unsuccessful defibrillation are not clear. METHODS: High voltage shocks with voltage differentials of 9.3 to 97.6 V/cm were delivered to isolated canine papillary muscles with attached Purkinje fibers. Transmembrane potentials were recorded simultaneously from the Purkinje fiber and the ventricular muscle using standard microelectrode techniques. RESULTS: After delivery of high voltage shocks, significant depolarization and rapid firing were observed in Purkinje fibers. The maximal rate of the rapid firing in the Purkinje fibers correlated with shock intensity (r = 0.69, p < 0.05). In contrast, in ventricular muscle, only slight depolarization and a transient refractory state were observed after the shock. The incidence of the refractory state was correlated with both the shock intensity and the rate of the rapid firing in the Purkinje fiber (r = 0.89 and 0.74, p < 0.01 and 0.05, respectively). Propranolol at a concentration sufficient for complete beta-blockade (1 mg/liter) did not change the tissue response to shocks but suppressed or abolished the shock-induced rapid firing of Purkinje fibers at a higher concentration (3 mg/liter). Blockade of the slow calcium channel with verapamil (400 micrograms/dl) did not alter the responsiveness of the preparation to shocks. CONCLUSION: These results indicate that high voltage shocks induce different responses in Purkinje fibers and ventricular muscle. The shock-induced rapid firing in the Purkinje fiber may contribute to postshock arrhythmias and possibly refibrillation in some cases. The shock-induced transient refractory state in the ventricular muscle may prevent the ventricle from responding to the rapid firing and thus may decrease the incidence of postshock arrhythmias.

Action Potentials↗

A placebo-controlled trial of intravenous and oral disopyramide for prevention of neurally mediated syncope induced by head-up tilt.

OBJECTIVES: A double-blind randomized trial was designed to determine the efficacy of intravenous and oral disopyramide phosphate in preventing neurally mediated syncope induced by a head-up tilt test. BACKGROUND: Neurally mediated syncope is a frequent cause of syncope and may be induced by head-up tilt testing. Recent uncontrolled trials have suggested that disopyramide may be an effective therapy in patients with neurally mediated syncope. METHODS: Twenty-two consecutive patients with recurrent neurally mediated syncope and two or more successive positive head-up tilt test responses were randomly allocated to receive either intravenous disopyramide or placebo. Head-up tilt testing at 60 degrees was performed for 15 min. If presyncope or syncope was not provoked, isoproterenol infusion was started at a rate of 1 microgram/min and the rate gradually increased until a 25% increase in heart rate was achieved. Eleven patients were subsequently randomized in crossover fashion to receive oral disopyramide (800 mg/day) or placebo during 1 week. The primary end point was prevention of syncope or presyncope provoked by head-up tilt testing. RESULTS: Head-up tilt test results were positive for syncope in 12 (75%) of 16 patients receiving intravenous placebo and in 12 (60%) of 20 patients receiving disopyramide (p = 0.55 Fisher exact test, 95% confidence interval [CI] -14% to 40%). In the intravenous phase, complete crossover was achieved in 15 patients. Head-up tilt test results during this phase were positive in 13 patients (87%) receiving placebo and in 12 patients (80%) receiving disopyramide (p = 0.50 Fisher exact test, 95% CI -19% to 32%) and were positive in all patients receiving their initially randomized drug or placebo. In the oral phase, head-up tilt results were positive in only two patients (18%) assigned to placebo and in three patients (27%) receiving disopyramide (p = 0.54 Fisher exact test, 95% CI -42% to 24%). A mean follow-up time of 29 +/- 8 months was obtained in 21 of the 22 patients. Syncope recurred in 3 (27%) of the 11 patients receiving disopyramide and 3 (30%) of the 10 patients not treated pharmacologically (p > 0.05). CONCLUSIONS: Intravenous disopyramide was ineffective for the prevention of neurally mediated syncope provoked by head-up tilt testing. No significant effect was observed after oral therapy with disopyramide. There was a striking decrease in the incidence of positive tilt test results over time regardless of intervention, thus discouraging the use of head-up tilt as the single method of assessing therapeutic efficacy. Recurrence of syncope after the investigative protocol was infrequent over long-term follow-up regardless of treatment group.

Administration, Oral↗

Elimination of slow pathway conduction: an accurate indicator of clinical success after radiofrequency atrioventricular node modification.

OBJECTIVES: The purpose of this study was to determine the optimal end point of radiofrequency atrioventricular (AV) node modification using anatomically guided slow pathway approaches in patients with AV node reentrant tachycardia. BACKGROUND: The optimal end point for AV node modification using radiofrequency energy is uncertain, although elimination of inducible AV node reentrant tachycardia has been used. METHODS: We followed up 51 consecutive patients (40 women, 11 men, mean age +/- SD 41 +/- 16 years) with symptomatic AV node reentrant tachycardia for 12 +/- 6 months (range 4 to 24) after radiofrequency AV node modification using an anatomically guided slow pathway approach. Inducible AV node reentrant tachycardia was eliminated in all patients, whereas residual slow pathway conduction persisted in 12 patients (24%) after ablation. One study was complicated by complete AV block and two patients were lost to follow-up (one with and one without residual slow pathway conduction). RESULTS: Clinical recurrence of AV node reentrant tachycardia was documented in seven patients (14%) 3 days to 3 months (median 1 month) after ablation. The recurrence rate was significantly higher in patients with than in those without residual slow pathway conduction (6 [55%] of 11 vs. 1 [3%] of 37, p < 0.01). The recurrence rate was not different between patients with only residual slow pathway conduction and those with residual slow pathway conduction and inducible single echo cycles (three [60%] of five in both groups, p = NS). The number of radiofrequency energy applications was not significantly different between those without and those with recurrence (20 +/- 17 vs. 16 +/- 9, p = NS). Junctional tachycardia during application of radiofrequency energy tended to be more frequently observed in those with a successful outcome (77% vs. 57%, p > 0.05). Of the 22 patients who underwent modification before 1992, residual slow pathway conduction was present in 9 (41%) of 22 patients. Atrioventricular node reentrant tachycardia recurred in five (56%) of these nine patients. A greater effort made in 1992 to eliminate slow pathway conduction in 29 patients resulted in residual slow pathway conduction in only 3 (11%) with recurrence in 2 (4%). CONCLUSIONS: Complete elimination of slow pathway conduction is feasible in the majority of patients. Elimination of slow pathway conduction is highly predictive of long-term success after AV node modification using an anatomically guided approach.

Adult↗

Effects of flecainide on defibrillation threshold in pigs.

Flecainide has been reported to decrease defibrillation efficacy in pentobarbital-anesthetized dogs. Conversely, flecainide did not alter defibrillation energy requirements in halothane-anesthetized pigs. We wished to determine whether these discrepancies were related to defibrillation technique, interaction with the anesthetic regimen, or animal species. The effects of three doses of flecainide on defibrillation threshold (DFT) were determined using single- and sequential-pulse shocks in halothane-anesthetized open-chest pigs. Triplicate DFTs were obtained before and after three doses of flecainide (n = 34) or saline (n = 13) infusion. Similarly, the effects of the highest dose of flecainide were determined using barbiturate-anesthetized animals (n = 10). Flecainide did not alter DFT at any dose with either the single-pulse shock (control 17.7 +/- 2.1 J, highest dose of flecainide 19.1 +/- 3.2 J, p = NS) or sequential-pulse shock (control 9.2 +/- 1.0 J, highest dose of flecainide 8.4 +/- 1.4 J, p = NS) when halothane anesthesia was used. Similar results were obtained using barbiturate anesthesia either with sequential (control 8.7 +/- 0.9 vs. 8.2 +/- 0.6 J, p = NS) or single shocks (control 13.2 +/- 0.8 vs. 13.7 +/- 1.0 J, p = NS). Flecainide did not alter DFT in our model, regardless of defibrillation technique or anesthetic regimen.

Animals↗

Ethanol increases defibrillation threshold in pigs.

Alcohol ingestion has been associated with cardiac arrhythmias and may initiate fibrillation in patients with automatic defibrillators. The effect of alcohol on defibrillation efficacy is unknown. To assess the acute effects of alcohol on defibrillation efficacy, triplicate defibrillation thresholds (DFTs) were determined before and after intravenous administration of 25% ethanol. Fifty-two pigs were randomized into four groups: (1) control, 6 mL/kg of saline over 10 minutes (n = 12); (2) low dose, 6 mL/kg of 25% ethanol over 10 minutes (n = 12); (3) mid dose, 0.45 mL/kg per minute for 30 minutes followed by 0.045 mL/kg per minute for 45 minutes (n = 12); and (4) high dose, 0.6 mL/kg per minute for 30 minutes followed by 0.06 mL/kg per minute for 45 minutes (n = 16). Three coil defibrillating electrodes (Medtronic 6888) were sutured to the epicardium of the right and left ventricles for defibrillation shocks. Ventricular fibrillation was induced using alternating current and after 10 seconds of fibrillation, the minimum energy for defibrillation was established using sequential pulse defibrillation. Triplicate determinations were obtained before and after saline or ethanol infusion. Alcohol elevated DFT in a dose related manner. Control and low dose groups thresholds were unchanged, but the mid dose approached statistical significance (6.8 +/- 0.7 vs 7.6 +/- 0.9 J, 0.05 < P < 0.1) and the high dose was significantly elevated (8.5 +/- 0.7 vs 11.2 +/- 1.1 J, P < 0.01). Ventricular effective refractory periods and cycle lengths between fibrillatory waves did not differ before and after the high dose ethanol.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Supraventricular tachycardias: the role of surgery.

Because of its high efficacy and low morbidity radiofrequency energy catheter ablation techniques have toppled the hierarchy of choice in the electrophysiological intervention armamentum. This review assesses current role of surgery and its foreseeable future. Most accessory AV pathways can be attained by endocardial manipulation and ablated. Surgical dissection of accessory pathways on the beating heart had documented that most pathways were paraannular, although right-sided pathways may be distant to the annulus. Results of accessory pathway ablation have shown that right-sided pathways are difficult to approach and ablate. Surgical ablation may currently be considered after failed catheter ablation. AV nodal modification using catheter ablation also yields excellent results. Radiofrequency energy creates a discrete lesion associated with discrete electrophysiological alteration. Surgical dissection is associated with more diffuse and extensive anatomical and electrophysiological changes and is no longer used even after failed catheter ablation. The arrhythmogenic anatomical substrate associated with atrial flutter is not yet well delineated in the coronary sinus os region. How to extend tissue modification for uniform success here is not yet known. Further surgical approach combined with extensive intraoperative cardiac mapping may ultimately prove a valuable guide for subsequent catheter technique. Atrial fibrillation is the last surgical frontier unchallenged by catheter techniques. Arrhythmogenic anatomical substrate is diffuse spreading over the entire atrial myocardium without a discrete target. The associated pathology is diffuse, severe, and progressive and present even in the so-called lone atrial fibrillation. Progression of underlying pathology can nullify the best designed surgical rationale in terms of sinus node chronotropic function, and atrial contractility. Currently used surgical techniques, i.e., the corridor and the Maze operations, have contributed to a better selection of patients. Surgery is still associated with significant morbidity and relative efficacy, and may be improved before becoming the electrophysiological intervention of choice for atrial fibrillation. In conclusion, atrial fibrillation is a greater surgical challenge, but has to be met with the same standard used for other supraventricular tachycardias.

Atrial Fibrillation↗

Malposition of transvenous pacing lead in the left ventricle.

Malposition of pacemaker leads has been described in several locations but rarely in the left ventricle. The incidence and clinical course of this pacemaker complication are unknown. We describe clinical, electrocardiographic, chest X ray, and echocardiographic findings in four patients in whom the transvenous pacing lead was inadvertently placed through the interatrial septum and mitral valve into the left ventricle. In these patients, lead misplacement was not recognized at the time of implantation and lead malposition was diagnosed a mean of 2 years later. All four patients had right bundle branch block configuration paced complexes. In retrospect, chest X rays suggested atypical lead position in all, but the initial posterior-anterior and lateral chest X rays were misinterpreted and contributed to the delay in diagnosis. When lead misplacement in the left ventricle was considered it was confirmed by two-dimensional echocardiography. One patient subsequently presented with a stroke and the remainder were diagnosed when they presented with other unrelated problems. Pacing thresholds were normal at the time of implantation and behaved normally during follow-up. The patient presenting with stroke was anticoagulated and the other three have been managed expectantly without anticoagulation. Diagnosis of left ventricular lead malposition is not difficult but requires a high index of suspicion. A 12-lead ECG and posterior-anterior and lateral chest X rays after implantation can be diagnostic. Patients with pacing lead in the left ventricle may remain asymptomatic with normal lead function during long-term follow-up. Anticoagulation should be considered when this problem comes to attention for the first time during follow-up.

Aged↗

Comparative atrioventricular node properties after radiofrequency ablation and operative therapy of atrioventricular node reentry.

The anatomical substrate for atrioventricular (AV) node reentry is unclear. To gain insights into the mechanism of cure of AV node reentry by nonpharmacological techniques, we compared AV node properties in 53 patients undergoing operative therapy (perinodal dissection) and 43 undergoing radiofrequency ablation (28 posterior approach, 15 anterior approach). Anterior radiofrequency ablation was associated with significant AH prolongation (62 +/- 18 msec vs 136 +/- 64 msec, P < 0.0001), loss of "fast" pathway physiology, and no change in the anterograde refractory period of the AV node (273 +/- 24 msec vs 268 +/- 28 msec, P = NS). Posterior radiofrequency ablation did not change the AH interval (67 +/- 17 msec vs 68 +/- 17 msec, P = NS), prolonged AV node effective refractory period (275 +/- 48 msec vs 320 +/- 55 msec, P < 0.0001), and was associated with loss of "slow pathway" physiology. Operative treatment prolonged the AH interval (66 +/- 18 msec vs 83 +/- 37 msec, P < 0.0001) and the AV node effective refractory period (264 +/- 52 msec vs 364 +/- 112 msec, P < 0.0001), and affected dual pathway physiology inconsistently. These data support the view that the "fast" and "slow" pathways are distinct perinodal entities that can be selectively ablated. The operative approach causes more diffuse and variable injury to the AV node region.

Adolescent↗

Arrhythmogenic effects of catecholamines are decreased in heart failure induced by rapid pacing in dogs.

Increased circulating catecholamines are considered to be arrhythmogenic in heart failure. It is unclear whether increased circulating catecholamines contribute directly to ventricular arrhythmias or are only markers of the severity of heart failure. The present study determined the sensitivity of the failing heart to the arrhythmogenic effect of exogenous norepinephrine in a rapid pacing-induced model of heart failure in dogs (240 beats for 4 wk, n = 14). A similarly operated, non-paced group served as controls (n = 9). Cardiac sensitivity to the arrhythmogenic effect of catecholamines was determined by measuring the minimal dose of exogenous norepinephrine that induced ventricular tachycardia (arrhythmogenic threshold dose, ATD). ATD significantly increased after development of heart failure in heart-failure group (1.62 +/- 0.32 microgram/kg at baseline vs. 16.65 +/- 3.48 micrograms/kg at restudy, P < 0.01), whereas no significant change was noted in the control group (1.08 +/- 0.36 microgram/kg at baseline vs. 2.53 +/- 0.36 micrograms/kg at restudy, P > 0.10). Action potential duration was unchanged by superfusion with 10(-7) M isoproterenol in both ventricular muscles (230.2 +/- 6.1 vs. 229.7 +/- 5.3 ms, P = NS) and Purkinje fibers (273.2 +/- 6.5 vs. 283.8 +/- 4.2 ms, P = NS) from the failing hearts, although isoproterenol induced a shortening in the control group (204.8 +/- 0.9 vs. 181.3 +/- 1.6 ms in ventricular muscles, P < 0.01; 313.8 +/- 6.5 vs. 279.5 +/- 5.7 ms in Purkinje fibers, P < 0.01). We conclude that the failing heart has a decreased sensitivity to the arrhythmogenic effect of catecholamines.

Action Potentials↗

Heart transplantation after cardioverter-defibrillator implantation. A case control study.

A case control study was performed to determine whether previous implantable cardioverter-defibrillator (ICD) insertion adversely affects outcome after heart transplantation. Six male heart transplant recipients who had undergone ICD insertion 12 +/- 5 months before heart transplantation were compared to a cohort of six heart transplant recipients who were matched according to age, preoperative status and hemodynamics, date of transplantation, graft ischemic time, history of a previous cardiac operation, and duration of follow-up. There were no significant differences in operating room time, chest tube drainage, time to extubation, and the duration of intensive care unit or hospital stay between the two groups. Furthermore, there were no significant differences in the number of units of packed cells, fresh frozen plasma, platelets and cryoprecipitate transfused. The number of treated rejection episodes and the number of patients requiring intravenous antibiotics for infection in the first 90 days was identical between groups. It was concluded that heart transplantation after ICD implantation did not appear to carry more risk than heart transplantation after a previous cardiac operation. Our limited experience supports the potential use of the ICD in patients with life-threatening ventricular dysrhythmias who are awaiting transplantation.

Blood Loss, Surgical↗

Classification and terminology of supraventricular tachycardia. Diagnosis and management of the atrial tachycardias.

This article describes some of the historical approaches to classifying supraventricular tachycardias and the evolution of the nomenclature as the knowledge of tachycardias improved. A classification scheme that is mechanistically based and favored by the authors, diagnostic criteria, clinical presentation, and therapy of the atrial tachycardias is also presented.

Humans↗

Biphasic versus sequential pulse defibrillation: a direct comparison in pigs.

It has recently been demonstrated that both biphasic and sequential pulse defibrillation shocks are superior to monophasic defibrillation shocks in animals and humans. There is little information directly comparing these two waveforms when pulse characteristics, subject, and total electrode surface area are kept constant. Pigs were randomized in a cross-over design for triplicate determinations of defibrillation threshold using biphasic and sequential pulse shocks and both large and small epicardial electrodes. Anesthetized pigs weighing 18 to 28 kg had sets of defibrillating electrodes (TX-7) with total surface areas of 13 cm2 (group 1, n = 16) and 26 cm2 (group 2, n = 16), respectively, attached to the heart. Leading edge delivered voltage, current, and energy were significantly lower with sequential pulse shocks than with biphasic shocks for both electrode sets (delivered energy means +/- standard error of the mean: 13.3 +/- 1.6 versus 22.4 +/- 3.0 joules, and 9.9 +/- 1.5 versus 14.2 +/- 1.6 joules, respectively). In addition, six of the pigs could not be defibrillated with 900 stored V using biphasic shocks, although all pigs were defibrillated with less than 800 stored V using sequential pulse defibrillation. We conclude that sequential pulse defibrillation using three defibrillating electrodes provides an important current delivery system not matched by biphasic shocks using two electrodes when subject, waveform characteristics, and total electrode surface area are kept constant.

Animals↗

Effects of acute and prolonged administration of propafenone on internal defibrillation in the pig.

Some antiarrhythmic sodium channel blocking drugs have been found to increase the energy necessary for internal defibrillation. Propafenone is a new drug that has been shown to be efficacious in the therapy of supraventricular and ventricular arrhythmias, and is of potential use in patients with defibrillators. The effects of short-term and prolonged propafenone administration on the internal defibrillation threshold (DFT) were determined in 43 pigs randomized to one of four groups: saline infusion (n = 10); propafenone infusion (n = 10); placebo administration for 8 days (n = 10); or propafenone administration for 8 days (n = 13). Two mesh electrodes were sutured on the right lateral and left lateral epicardial surface and current was delivered from the right electrode to the left electrode. Triplicate DFTs were obtained before and at 40 and 80 minutes after infusion of drug or placebo. In pigs receiving long-term administration, after baseline DFTs were obtained the electrodes were removed and the chest was closed. Following 8 days of drug or placebo administration, DFTs were redetermined. No changes were observed in the short- or long-term control groups. DFTs were lower after propafenone administration: either short-term infusion (20 +/- 6.2 joules at baseline; 15.6 +/- 5 joules at 40 minutes, p less than 0.05; 10.2 +/- 6 joules at 80 minutes, p less than 0.001) or long-term administration (17.8 +/- 2.6 joules at baseline versus 12 +/- 3.2 joules on drug, p less than 0.002). Decreased ventricular cycle lengths were found with acute administration of propafenone. Three pigs died during long-term administration of propafenone.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗