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Biomedical subjects

G J Klein

Publications and source records attributed to G J Klein.

At least 163 records · Page 9Linked to original sources
PubMed1991

Reduction in defibrillator shocks with an implantable device combining antitachycardia pacing and shock therapy.

Implantable defibrillators reduce the risk of sudden death in patients with malignant ventricular arrhythmias, but significant restriction in quality of life can occur as a result of frequent device activation. To determine if a device that provides both antitachycardia pacing and shock therapy can safely reduce the frequency of shocks after implantation, 46 consecutive patients undergoing initial implantation of a defibrillator were studied. In all patients, the implanted device provided antitachycardia pacing and shock therapy. Detected tachycardia characteristics and the results of therapy were stored in the device's memory. There were 42 men and 4 women, aged 26 to 71 years (mean 58.7 +/- 13.5). Left ventricular ejection fraction ranged from 13% to 67% (mean 32.2 +/- 13.4%) and 31 patients had experienced one or more episodes of cardiac arrest. Induced arrhythmias included sustained monomorphic ventricular tachycardia in 38 patients, nonsustained polymorphic ventricular tachycardia in 2 and ventricular fibrillation in 4. Over a total follow-up period of 255 patient-months (range 1 to 13, mean 6.1), 25 patients experienced spontaneous arrhythmic events. In 22 patients, 909 episodes of tachycardia were treated by antitachycardia pacing, which was successful on 840 occasions (92.4%). Acceleration of ventricular tachycardia by pacing therapy was estimated to have occurred 39 times. Syncope occurred once during pacing-induced acceleration of ventricular tachycardia. Forty-four episodes of tachycardia in seven patients were treated directly by shocks because of short tachycardia cycle length; 88% of all detected tachycardias were treated without the need for shocks. Four patients died from cardiorespiratory failure and one patient died suddenly without any detected tachyarrhythmia.(ABSTRACT TRUNCATED AT 250 WORDS)

Anti-Arrhythmia Agents↗
PubMed1991

Effects of lidocaine on defibrillation threshold in the pig: evidence of anesthesia related increase.

Some antiarrhythmic drugs may influence the ability of a shock to defibrillate a patient but the effect of lidocaine on defibrillation efficacy has been controversial, suggesting multiple influencing factors. We determined the effects of three doses of lidocaine on defibrillation thresholds, using single and sequential shocks, in 36 open chest halothane-anesthetized pigs. An additional eight pigs were anesthetized with barbiturate and received the highest infusion regime of lidocaine. Shocks were delivered through three mesh electrodes sutured over the anterior right ventricle, posterior right ventricle, and lateral left ventricle for sequential pulse shocks and between a lateral right to a lateral left ventricular mesh electrode for single pulse shocks. Triplicate defibrillation thresholds (DFTs) were obtained before and after lidocaine (n = 32) or saline (n = 12) administration, either with halothane or barbiturate anesthesia. Lidocaine did not alter DFT at any dose with either the single pulse (control 17.4 +/- 3.7 joules [J], highest dose of lidocaine 13.5 +/- 1.7 J, P = NS) or sequential pulse shocks (control 7.6 +/- 0.8 J, highest dose lidocaine 6.6 +/- 0.7 J, P = NS), when halothane anesthesia was used. Similar results were obtained with lower doses. In contrast, lidocaine in pentobarbital anesthetized pigs produced a significant increase of the DFT with single (control 13.7 +/- 1.9, during lidocaine 16.6 +/- 3.1, P less than 0.01) and sequential shocks (control 11.1 +/- 2.2, during lidocaine 14.5 +/- 3.4, P less than 0.01). Interaction between barbiturates and lidocaine, and/or pH may account for the inconsistency in previous studies and must be considered for animal and clinical experiments.

Anesthesia↗
PubMed1991

Hypothesis testing as an approach to the analysis of complex tachycardias--an illustrative case of a preexcitation variant.

The correct elucidation of the electrophysiological substrate and mechanism(s) responsible for a complex arrhythmia requires a systematic approach to the analysis of the electrophysiological data. One approach calls for the formulation of a set of hypotheses that could explain the data obtained during the study. The hypotheses are then tested for compatibility with phenomena observed and the one that agrees with the majority of the findings would represent the most tenable explanation. We present the case of a young girl with a wide QRS complex tachycardia and a history of ventricular preexcitation that illustrates this approach. The complexities were resolved only after intraoperative analysis and surgical ablation of a right-sided accessory pathway with decremental properties, and provides further insight into our understanding of the nodoventricular Mahaim fiber.

Anti-Arrhythmia Agents↗
PubMed1991

Defibrillation shocks increase myocardial pacing threshold: an intracellular microelectrode study.

Defibrillation is known to cause inability to pace the heart acutely, but the mechanism is unknown. This study used microelectrode techniques to directly evaluate the effect of defibrillation shocks on the pacing threshold and membrane potentials from superfused guinea pig papillary muscles. Failure of pacing stimuli to induce action potentials (pacing failure) followed shocks of 50-200 V/cm, with pacing failure duration correlated with shock intensity. Increasing pacing strength from one to three times diastolic threshold decreased the incidence and duration of pacing failure. Decreased extracellular calcium concentration and verapamil added to the superfusate increased the duration of pacing failure. Membrane potential depolarization occurred after shock, but pacing failure did not correlate with depolarization magnitude. We conclude that defibrillation shocks directly cause shock intensity-dependent increase of myocardial pacing threshold. The pacing threshold of the myocardium can be increased after defibrillation shock independent of hypoxia or shock-induced depolarization and may involve membrane changes in calcium handling.

Action Potentials↗
PubMed1991

Defibrillation efficacy. Comparison of defibrillation threshold versus dose-response curve determination.

When an automatic defibrillator is implanted, it is essential to determine the efficacy of the defibrillating system accurately, while balancing the need to keep the number of fibrillation episodes to a minimum. Two methods have evolved to assess defibrillation efficacy: 1) the "defibrillation threshold," which requires few ventricular fibrillation episodes, and 2) the "dose-response curve," which requires many ventricular fibrillation episodes and relates percent success to energy. The purpose of this study was to compare these two methods directly. Twenty open-chest anesthetized pigs had triplicate defibrillation threshold determinations. To produce a dose-response curve, six shocks then were delivered at 0.5, 0.75, 1.0, 1.25, 1.5, and 2.0 times the mean defibrillation threshold, in a balanced randomized order, during separate episodes of ventricular fibrillation. The data were fitted by logistic regression, conversions of the logistic regression, and a saturable exponential and nonsaturable growth exponential. A comparison was made of the mean defibrillation threshold and the 50% point on the dose-response curve (ED50) for each model, for each animal. In addition, the reliability of each measure was assessed by comparing the coefficients of variation. There was no statistical difference between the group defibrillation threshold (6.6 +/- 0.5 J) and group ED50 values (ED50 range of the models, 5.7 +/- 1.9 to 7.0 +/- 0.9 J). However, the variability about the defibrillation threshold was less than that of the ED50 values for all mathematical models except the true logistic equation, which was virtually the same.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Catheter ablation of idiopathic exercise-induced right bundle branch block and left axis deviation ventricular tachycardia.

Catheter ablation of ventricular tachycardia was performed in a patient without evidence of structural heart disease. ECG showed ventricular tachycardia and a right bundle branch block QRS configuration with left axis deviation induced by exercise and atrial pacing. At electrophysiology, presystolic activation was found in the low septal region of the left ventricle. Radiofrequency energy delivered to this site failed to prevent tachycardia. Three direct current shocks (total energy 400 J) delivered in this region rendered the tachycardia noninducible. There were no complications. During the follow-up period of six months the patient has remained free from arrhythmia on no medication. This report expands the use of catheter ablation to patients with idiopathic ventricular tachycardia ('verapamil responsive' ventricular tachycardia) originating in the left ventricle.

Bundle-Branch Block↗
PubMed1990

Right ventricular pressure during ventricular arrhythmias in humans: potential implications for implantable antitachycardia devices.

Implantable defibrillators use algorithms based on ventricular electrographic data to detect the onset and termination of arrhythmias, but these algorithms do not always differentiate hemodynamically stable from unstable arrhythmias. Although, ideally, left ventricular function should be used to assess the hemodynamic state, right ventricular pulse pressure can be assessed in humans on a long-term basis with a transvenous lead. The potential utility of right ventricular pulse pressure to assess hemodynamic stability was studied in 22 patients with induced ventricular arrhythmias. Right ventricular pressure was measured with use of a transvenous right ventricular endocardial pacing lead with a piezoelectric bender pressure sensor 3 cm from its tip. Single ventricular premature paced beats administered in up to a bigeminal frequency did not alter the mean right ventricular pulse pressure (control 33.7 +/- 26, bigeminy 35.7 +/- 26 mm Hg). Twenty-one episodes of induced ventricular tachycardia were studied in the electrophysiology laboratory. Five seconds after tachycardia induction, hemodynamically stable ventricular tachycardia had a longer cycle length (294 +/- 41 ms) and the right ventricular pulse pressure ratio was higher (0.55 +/- 0.26) than that in unstable ventricular tachycardia (cycle length 256 +/- 55 ms, p = 0.06; pulse pressure ratio 0.26 +/- 0.09, p less than 0.05). Twenty episodes of ventricular fibrillation were induced in eight patients. One second after induction, right ventricular pulse pressure decreased from 25 +/- 5 to 6 +/- 3 mm Hg (p less than 0.05). On the first beat after defibrillation, right ventricular pulse pressure increased to 24 +/- 14 mm Hg, a level not significantly different from that before the induction of ventricular fibrillation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Value of a revised procainamide test in the Wolff-Parkinson-White syndrome.

A shortest preexcited RR interval less than 250 ms during atrial fibrillation identifies the patient with Wolff-Parkinson-White syndrome potentially at risk for ventricular fibrillation. Loss of preexcitation after infusion of up to 10 mg/kg of procainamide during sinus rhythm has been reported to correlate with a slow ventricular response during atrial fibrillation and has been proposed as a noninvasive test to establish risk of sudden death in these patients. Others have failed to establish this relation and have questioned the usefulness of the procainamide test. Such conflicting results were hypothesized to be a result of differing dosages and methodology. Consequently, this study tested the effect of incremental doses of procainamide (to a cumulative dose of 1 g) on the anterograde effective refractory period of the accessory pathway and related the reliability of the procainamide test to the dose at which preexcitation was lost. The effect of procainamide on the anterograde effective refractory period of the accessory pathway was dose dependent; patients who lost preexcitation had a steeper dose-response curve. Loss of preexcitation by a cumulative dose of 550 mg provided the best balance for sensitivity (60%) and specificity (89%) in identifying patients with preexcited shortest RR greater than 250 ms. Specificity fell steeply after this dosage and higher doses were not useful. The diagnostic accuracy of the procainamide test is critically related to dosage and method of infusion.

Adolescent↗
PubMed1990

Intravenous adenosine triphosphate during wide QRS complex tachycardia: safety, therapeutic efficacy, and diagnostic utility.

PURPOSE: Inappropriate administration of intravenous verapamil to patients with wide QRS complex tachycardia due to ventricular tachycardia or atrial fibrillation with Wolff-Parkinson-White syndrome occurs frequently because of misdiagnosis, and may precipitate a cardiac arrest. We evaluated the safety and the diagnostic and therapeutic utility of adenosine triphosphate administered to a consecutive series of 34 patients during wide QRS complex tachycardia due to a variety of mechanisms. PATIENTS AND METHODS: Patients who had a hemodynamically and electrically stable, monomorphic, wide (greater than 120 msec) QRS complex tachycardia induced during an invasive cardiac electrophysiologic test were studied. Hemodynamic stability was defined by a systolic blood pressure greater than 80 mm Hg and no clinical evidence of cerebral or myocardial ischemia. Adenosine triphosphate, 20 mg, was administered as a rapid intravenous bolus via a peripheral vein during wide QRS complex tachycardia. Five surface electrocardiogram leads, at least three intracardiac electrograms, and blood pressure were monitored. RESULTS: Ventricular tachycardia was present in 14 patients (mean age 50.6 +/- 19 years, cycle length 326 +/- 67 msec) and adenosine triphosphate terminated the arrhythmia in one case. Ventricular tachycardia cycle length did not change. Among 10 patients with supraventricular tachycardia with mechanisms not involving the AV node (average ventricular cycle length 346 +/- 82 msec), one case of ectopic atrial tachycardia was terminated. The ventricular rate was transiently increased in patients with Wolff-Parkinson-White syndrome and atrial fibrillation (average R-R interval 351 +/- 84 msec in control and 317 +/- 82 msec after adenosine triphosphate, p less than 0.001). Reentrant tachycardias involving the AV node (cycle length 302 +/- 52 msec) terminated in seven of 10 patients. The drug was well tolerated, and no patient developed hemodynamic compromise necessitating cardioversion as a result of adenosine triphosphate. CONCLUSION: In the setting of electrophysiology testing, adenosine triphosphate is a safe agent, even when administered inappropriately during arrhythmias for which it is relatively ineffective, such as ventricular tachycardia, and Wolff-Parkinson-White syndrome with atrial fibrillation. It is an effective agent in terminating supraventricular tachycardia involving the AV node. Tachycardia termination following adenosine triphosphate, when used as a diagnostic test to indicate obligatory participation of the AV node, had a sensitivity of 70%, specificity of 92%, and a positive predictive accuracy of 85%. Thus, adenosine triphosphate also has diagnostic utility, but should be used after the appropriate arrhythmia diagnosis has been made based on the clinical history and analysis of the 12-lead electrocardiogram.

Adenosine Triphosphate↗
PubMed1990

Skeletonization of the atrioventricular node for AV node reentrant tachycardia: experience with 32 patients.

We describe our experience with operative therapy for atrioventricular (AV) node tachycardia using an anatomically guided procedure. The operative rationale was to dissect the AV node from most of its atrial inputs (AV node "skeletonization") with the intent of altering the perinodal substrate and preventing reentry. The anteroseptal and posteroseptal regions were initially approached epicardially to facilitate identification of anatomical structures. Under normothermic cardiopulmonary bypass, the right atrial septum was mobilized and the intermediate AV node was exposed anterior to the tendon of Todaro. Atrioventricular node conduction was monitored electrocardiographically throughout the procedure. Ablation of concomitant accessory pathways was done prior to AV node skeletonization. Thirty-two patients aged 9 to 67 years (mean age, 30 years) underwent operation. Five patients had concomitant accessory pathways in addition to AV node reentry. At electrophysiological study before discharge, no patient had AV block although anterograde and retrograde Wenckebach cycle lengths were significantly prolonged. Six patients had retrograde AV block. Twenty-nine patients are free from arrhythmia and require no antiarrhythmic medication after a follow-up of 1 month to 45 months (mean follow-up, 17 months). Three patients had recurrence of tachycardia ten days, 2 months, and 7 months postoperatively. All patients subsequently had a successful reoperation.

Adolescent↗
PubMed1990

Surgical epicardial ablation of left ventricular pathway using sling exposure.

We report our experience with 43 consecutive patients with left free wall pathways operated on since December 1988 using a modified direct epicardial approach through a medial sternotomy, without the adjunct of normothermic cardiopulmonary bypass. The left atrioventricular sulcus is exposed by dislocating the heart cephalad and to the right using a sling made of a large sponge passed around the ventricle through the transverse sinus. While the arterial pressure is monitored, the heart is positioned to obtain adequate exposure without compromising the ventricular function. The left atrioventricular junction is exposed using a direct approach. The epicardium is incised along the ventricular edge and a plane of dissection is identified and opened using blunt dissection over the ventricular wall. The entire left atrioventricular junction can be exposed. After dissection, electrophysiological testing is repeated to assess accessory pathway conduction. Epicardial cryoablation was used when accessory pathway conduction was not present (42 patients). Transmural cryoablation was used under normothermic cardiopulmonary bypass when accessory pathway conduction persisted after dissection (subendocardial pathway). In all, cardiopulmonary bypass was not used in 41 patients. There was one early relapse that required transmural cryoablation. There were no complications.

Adult↗
PubMed1990

Mode of onset of atrial fibrillation in the Wolff-Parkinson-White syndrome: how important is the accessory pathway?

The mode of onset of 103 episodes of atrial fibrillation lasting greater than or equal to 30 s was studied in 79 patients with the Wolff-Parkinson-White syndrome during electrophysiologic study. No patient had organic heart disease, and 31 had clinical atrial fibrillation before study. These 79 patients were then compared with a control group of 53 patients with Wolff-Parkinson-White syndrome in whom atrial fibrillation could not be induced. Ninety-five of the 103 episodes were technically suitable for analysis. Atrial fibrillation invariably began with rapid atrial tachycardia that became progressively disorganized within 10 to 20 cycles. It was initiated during right atrial stimulation (n = 52), right ventricular stimulation (n = 8), reciprocating tachycardia (n = 33) and spontaneously (n = 2). Most episodes started at a high right atrial site regardless of accessory pathway location, with only 19% of episodes starting at the electrode closest to the accessory pathway. During reciprocating tachycardia (n = 33), either atrial (n = 8) or ventricular (n = 5) extrastimuli initiated atrial fibrillation. Atrial fibrillation started at the accessory pathway site in 6 of 20 episodes occurring spontaneously during reciprocating tachycardia. Patients with atrial fibrillation had a longer PA interval (54 +/- 14 versus 42 +/- 12 ms, p less than 0.0001), shorter atrial functional refractory period (226 +/- 38 versus 240 +/- 30 ms, p = 0.049) and shorter anterograde effective refractory period of the accessory pathway (279 +/- 26 versus 304 +/- 75 ms, p = 0.03). Clinical reciprocating tachycardia was documented with equal frequency in both the atrial fibrillation and control groups (59.5% versus 52.9%, p = 0.58).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Termination of acute atrial fibrillation in the Wolff-Parkinson-White syndrome by procainamide and propafenone: importance of atrial fibrillatory cycle length.

The effects of intravenous procainamide (n = 30) or propafenone (n = 25) were evaluated in 55 patients with acute atrial fibrillation and the Wolff-Parkinson-White syndrome. All patients received either procainamide (12 to 15 mg/kg body weight) or propafenone (1 to 2 mg/kg) during sustained (greater than 10 min) atrial fibrillation or after termination of nonsustained atrial fibrillation. Termination of atrial fibrillation was attributed to a drug if it occurred less than or equal to 15 min after infusion. Measurements included mean cycle length of fibrillatory electrograms (mean AA interval) as measured at the high right atrium and shortest RR interval between pre-excited cycles during atrial fibrillation. Atrial fibrillation terminated more frequently after procainamide administration (65%) than after propafenone (46%), although this difference was not significant. Procainamide prolonged the shortest pre-excited RR interval (228 +/- 41 to 339 +/- 23 ms, p = 0.0001) as did propafenone (215 +/- 40 to 415 +/- 198 ms, p = 0.0001) and the magnitude of increase was greater for propafenone (p = 0.048). Patients with sustained atrial fibrillation had shorter mean AA intervals than did their counterparts with nonsustained atrial fibrillation (123 +/- 25 versus 186 +/- 35 ms, p = 0.0001). Termination of sustained atrial fibrillation by either drug was accompanied by prolongation of the mean AA interval but not necessarily by the shortest pre-excited RR interval. Termination of atrial fibrillation was heralded by a 68% increase in the mean AA interval after procainamide administration compared with a 30% increase when the arrhythmia persisted. For propafenone the increases were 90% and 68%, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1990

Anatomically guided surgery to the AV node. AV nodal skeletonization: experience in 46 patients with AV nodal reentrant tachycardia.

We report our combined experience with operative therapy for atrioventricular nodal tachycardia using an anatomically guided procedure. The operative rationale was to dissect the AV node with the intent of modifying perinodal tissues (skeletonization). The anterior septal and posterior septal regions were initially approached epicardially to facilitate endocardial dissection. Under normothermic cardiopulmonary bypass, the right atrial septum was mobilized and the intermediate AV node was exposed anterior to the tendon of Todaro. Ablation of concomitant accessory pathways was done prior to AV nodal skeletonization. Forty-six patients aged 9-71 years (mean 36) were operated upon. Five patients had accessory pathways in addition to AV nodal reentry. At electro-physiological study prior to discharge, no patient had an AV block although anterograde and retrograde Wenckebach cycle lengths were significantly prolonged. Ten patients had a retrograde AV block. The 46 patients were free of arrhythmia and not taking antiarrhythmic medication after a follow-up of 1-45 months (mean 17). Three patients had a recurrence of the tachycardia 10 days, 2 months and 7 months post-operatively, respectively. All patients had a subsequently successful reoperation.

Adolescent↗
PubMed1990

Pulsatile flow in the choroidal circulation: a preliminary investigation.

A preliminary investigation has been made of choroidal blood flow using a computer-aided image analysis approach to interpretation of indocyanine green (ICG) dye choroidal angiograms. The goal of the study was to characterise blood flow through the choroidal arteries vs. choroidal capillaries and veins. The methods of analysis used are briefly reviewed, and preliminary data obtained mainly from monkey eyes are presented. Preliminary conclusions are made regarding the relationship between compliance of choroidal arterial vessels and blood flow through them.

Angiography↗
PubMed1990

Utility of low energy test shocks for estimation of cardiac and electrode impedance with implantable defibrillators.

We assessed the value and safety of using a low voltage test shock to predict cardiac and electrode impedance during subsequent high voltage, transvenous, sequential pulse shocks. Two transvenous defibrillation catheters were inserted in 15 patients undergoing electrophysiology study for the evaluation of ventricular tachycardia/fibrillation. A sequential pulse test shock at stored voltage of 50 or 100 volts was delivered during sinus rhythm and high voltage therapeutic shocks were delivered during induced ventricular tachycardia/fibrillation. The test shocks were well tolerated and caused only minimal discomfort. Peak delivered voltage for each pulse of the test shock ranged from 34 to 116 volts (mean 62 +/- 27) and for each pulse of the therapeutic shocks from 186 to 778 volts (mean 435 +/- 146). There was a very strong relationship between the impedance of the test and the mean impedance of the therapeutic shocks (R = 0.89, P less than 0.001). The mean impedance of the test shock was slightly greater than the mean impedance of the test shock as slightly greater than the mean impedance of the therapeutic shocks (mean 90 +/- 24 ohms compared to 77 +/- 16 ohms, P less than 0.001), with a maximum difference between test and therapeutic shock impedances of 39 ohms (mean difference 8.4 +/- 10.3 ohms). There was a significant inverse relationship between impedance and peak current (R = -0.49, P = 0.001). Cardiac and electrode impedance during transvenous defibrillation can be predicted reliably and safely by a low voltage test shock. This technique provides a safe and simple method to ensure appropriate connections and electrode function for subsequent countershock therapies.

Adult↗
PubMed1990

Correlation between the ventricular electrogram amplitude in sinus rhythm and in ventricular fibrillation.

During testing of implantable defibrillators, ability to sense ventricular fibrillation is assessed by observing electrograms and the emitted ECG interpretation channel during induced ventricular fibrillation. We hypothesized that ventricular electrogram amplitude in sinus rhythm could be used to predict the ventricular electrogram amplitude in ventricular fibrillation and serve as a first approximation of the "safety margin" for sensing ventricular fibrillation. We compared the peak-to-peak epicardial ventricular electrogram during sinus rhythm and ventricular fibrillation in 12 patients undergoing defibrillator implantation. The ventricular electrogram was recorded with an integrated bipolar lead and filtered at 10-50 Hz. Ventricular fibrillation was induced by alternating current and the ventricular electrogram measured from cessation of alternating current to the first countershock. The mean ventricular electrogram amplitude in sinus rhythm was 15.3 +/- 5.4 mV (range 7.1-25.5) and in 37 episodes of ventricular fibrillation was 8.3 +/- 3.6 mV (range 2.1-16.3). There was a significant relationship between the mean ventricular electrogram amplitude in sinus rhythm and in ventricular fibrillation (R = 0.7, P less than 0.001). There was wide variation among individuals in the decrease in the mean ventricular electrogram amplitude during ventricular fibrillation, with the ratio of mean ventricular electrogram in sinus rhythm to mean ventricular electrogram in ventricular fibrillation ranging from 0.29 to 1.05 (mean 0.55 +/- 0.20). This suggests that up to a fourfold decrease may be expected in the mean ventricular electrogram amplitude during ventricular fibrillation.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac Pacing, Artificial↗