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Biomedical subjects

G K Feld

Publications and source records attributed to G K Feld.

At least 19 recordsLinked to original sources
PubMed1992

Activation patterns in experimental canine atrial flutter produced by right atrial crush injury.

OBJECTIVES: This study was designed to localize and characterize the atrial flutter reentrant circuit and the electrophysiologic effects of right atrial crush injury in a new canine model. BACKGROUND: In previous studies sustained atrial flutter was induced in the canine heart by rapid atrial pacing after a linear crush injury was placed in the right atrial free wall. METHODS: Eight dogs (group 1) with three electrode plaques on the right and left atria and Bachmann's bundle and seven dogs (group 2) with a single high density electrode plaque on the right atrium were studied with use of a 64-channel computerized mapping system. RESULTS: At baseline, during sinus rhythm and right and left atrial pacing, activation spread uniformly without areas of slow conduction. Crush injury produced marked conduction delay or complete block during sinus rhythm, increasing the mean difference in activation times across the injury compared with control values (group 1, 31 +/- 4 vs. 14 +/- 5 ms, p less than 0.01; group 2, 28 +/- 10 vs. 7 +/- 2 ms, p less than 0.01). Rapid atrial pacing (S1S1 200 ms) above and below the crush injury revealed a line of complete block across which adjacent electrodes recorded markedly different activation times (33 +/- 5 and 38 +/- 12 ms difference, respectively) and around which activation wave fronts proceeded, colliding opposite the stimulating electrodes. The mean atrial flutter cycle length of 11 episodes induced in group 1 and 14 episodes in group 2 was 157 +/- 16 and 140 +/- 16 ms, respectively (p = NS). Activation mapping revealed a reentrant circuit in the right atrium around the crush injury in all episodes. Although the reentrant circuit did not contain a discrete area of slow conduction, activation time below was longer than that above the crush injury (92 +/- 14 vs. 66 +/- 8 ms and 82 +/- 12 vs. 59 +/- 9 ms in groups 1 and 2, respectively, p less than 0.01 for both). Rapid atrial pacing or premature stimuli produced progressive conduction delay and unidirectional block between the crush injury and the tricuspid anulus, inducing atrial flutter directly in 9 of 25 episodes. In 16 episodes, atrial flutter developed after transient induction of atrial fibrillation. CONCLUSIONS: 1) Atrial flutter in this model is due to reentry in the right atrium; 2) the crush injury functions as an anatomic obstacle around which reentry may occur; and 3) the reentrant circuit does not contain a discrete area of slow conduction but, rather, generally slower conduction below the crush injury.

Animals↗
PubMed1992

A new pacemaker algorithm for continuous capture verification and automatic threshold determination: elimination of pacemaker afterpotential utilizing a triphasic charge balancing system.

A new pacemaker algorithm designed to automatically verify pacemaker capture and determine pacing threshold by detection of a stimulus evoked potential was studied in 20 patients undergoing permanent pacemaker implantation. To eliminate pacing stimulus afterpotential and detect an evoked response, a hardware feedback circuit and a software template matching algorithm were used to produce a triphasic charge-balanced pacing pulse. After charge balancing the pacing lead, a residual artifact is measured. A capture window is defined as the area integral of the first 24 msec of the evoked depolarization, and a capture threshold as one third the amplitude of the capture window. The maximum allowable residual artifact is one eighth the amplitude of the capture window. Once the stimulus afterpotential is eliminated and the evoked response detected, capture threshold is automatically and continuously determined and the algorithm adds a 0.8-V safety margin to the pacemaker output. This algorithm was run automatically and after simulated loss of capture, produced by manually decreasing pacer output below threshold, in the bipolar (13 patients) and unipolar (20 patients) pacing modes. In each patient loss of capture was immediately detected. The data were consistent (P = NS) between algorithm runs. During unipolar pacing the area integral of the first 24 msec of the evoked response was 412 +/- 137 versus 413 +/- 144 and the residual artifact 5.8 +/- 4.8 versus 8.1 +/- 7.5. The resulting ratio (signal/noise) of the two parameters was 150 +/- 141 versus 145 +/- 181. Automatically determined threshold was 0.69 +/- 0.43 V versus 0.69 +/- 0.42.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1992

Mechanism of double potentials recorded during sustained atrial flutter in the canine right atrial crush-injury model.

BACKGROUND: During atrial flutter, double potentials may be recorded at specific sites in the atria. It has been suggested that double potentials represent sequential activations at the center of the reentrant circuit. An alternative hypothesis is that double potentials represent electrical activity in an area of slow conduction. Understanding their mechanism is important because double potentials have been considered a possible indicator of target sites for catheter ablation. METHODS AND RESULTS: We systematically studied double potentials in our canine model of atrial flutter produced by right atrial crush injury using a 64-channel computerized mapping system with 56 electrodes on the right atrium in seven mongrel dogs under general anesthesia. Activation maps were recorded during sinus rhythm before and after crush injury, during rapid pacing above and below the crush injury, and during sustained atrial flutter, entrainment of atrial flutter, and termination of atrial flutter induced with D-sotalol (2 mg/kg). During sinus rhythm before crush injury, activation was uniform, and double potentials were not recorded in any dog. After crush injury, activation proceeded up to and around the crush injury, and narrowly split double potentials were recorded in two of seven dogs. During rapid pacing above and below the crush injury, double potentials were recorded in five dogs. During 14 episodes of atrial flutter (mean cycle length, 140 +/- 16 msec), double potentials were recorded at electrodes along the crush injury. The activation time of the early x component of the double potentials (25 +/- 13 msec) was similar to that of adjacent electrodes above the crush injury (24 +/- 11 msec), and the activation time of the late y component (89 +/- 13 msec) was similar to that of adjacent electrodes below the crush injury (91 +/- 14 msec). The timing of the x and y components was dependent on the location of the recording electrode, with x and y widely spaced at the end of the crush injury near the area of earliest atrial activation during atrial flutter, more equally timed at the center of the crush injury, and more closely timed at the end of the crush injury opposite the area of earliest activation. During transient entrainment, double potentials were accelerated to the pacing rate, but their activation time relative to adjacent electrodes was maintained. During abrupt termination of atrial flutter, the early x component of the double potential was always recorded, but the late y component was not, because of conduction block below the posterior end of the crush injury. CONCLUSIONS: This study has shown in our canine model of atrial flutter that double potentials are recorded from the center of the reentrant circuit and that they represent sequential activations as the reentrant wave front passes on either side of the crush injury.

Action Potentials↗
PubMed1992

Radiofrequency catheter ablation for the treatment of human type 1 atrial flutter. Identification of a critical zone in the reentrant circuit by endocardial mapping techniques.

BACKGROUND: Recent studies of human type 1 atrial flutter demonstrated reentry in the right atrium and an area of slow conduction in the low posteroseptal right atrium. Direct-current catheter ablation of this area has been only moderately successful in preventing recurrence. Therefore, we performed endocardial activation mapping and entrainment pace mapping during atrial flutter to determine the critical site for radiofrequency ablation of this arrhythmia. METHODS AND RESULTS: Twelve consecutive patients (seven men and five women; age, 21-73 years) with type 1 atrial flutter (mean cycle length, 253 +/- 39 msec) underwent right atrial endocardial activation and entrainment pace mapping using standard transvenous catheter techniques to localize the atrial flutter reentrant circuit, the area of slow conduction, and the exit site from the area of slow conduction. Upon identifying appropriate sites, radiofrequency energy (16-29 W) was applied via a 4-mm tipped catheter. Activation mapping of atrial flutter revealed a counterclockwise reentrant wave front originating just inferior or posterior to the coronary sinus ostium, proceeding superiorly in the atrial septum to the right atrial free wall, then inferiorly toward the tricuspid annulus and finally medially between the inferior vena cava and the tricuspid annulus, where low-amplitude fragmented electrical activity was noted. Entrainment pace mapping from this area produced an exact P wave match to atrial flutter on 12-lead ECG with a long (greater than 40 msec) stimulus-to-P interval indicating slow conduction, whereas pacing just inferior or posterior to the coronary sinus ostium produced an exact P wave match with a short stimulus-to-P interval (less than 40 msec), presumably identifying the exit site from the area of slow conduction. Radiofrequency energy (one to 14 applications) was effective in terminating and preventing reinduction of atrial flutter in 10 patients. In two patients, atrial flutter was not terminated during radiofrequency energy application but during subsequent pacing attempts. Sites where ablation was successful, located just inferior or posterior to the coronary sinus ostium, were characterized by discrete electrograms with activation times of -20 to -50 msec before P wave onset and exact entrainment pace maps with a stimulus-to-P interval of 20 to 40 msec, consistent with the exit site from the area of slow conduction. Follow-up (mean, 16 +/- 9 weeks; range, 2-31 weeks) revealed recurrence of the original atrial flutter in two patients, one of whom underwent repeat ablation without further recurrence, self-limited infrequent recurrence of a new atrial flutter or atrial fibrillation in three suppressed by beta-blocker or digoxin, and no recurrence in seven. CONCLUSIONS: 1) Radiofrequency energy applied to a critical area in the atrial flutter reentrant circuit, inferior or posterior to the coronary sinus ostium, will terminate and prevent arrhythmia reinduction. 2) Long-term follow-up in a larger series of patients will be required to confirm efficacy of this technique, although short-term results look promising.

Adult↗
PubMed1991

Effects of pacing rate and timing of defibrillation shock on the relation between the defibrillation threshold and the upper limit of vulnerability in open chest dogs.

To test the relation between the defibrillation threshold and the upper limit of vulnerability, the shock strength associated with 50% probability of successful defibrillation (DFT50) and that associated with 50% probability of reaching the upper limit of vulnerability (ULV50) were determined in 20 open chest dogs with use of the delayed up-down method, with pacing drive cycle lengths of 150 to 500 ms and either single 6-ms shocks (10 dogs) or 12-ms biphasic shocks (10 dogs) given at the mid-upslope, peak and mid-downslope of the T wave of electrocardiographic lead II. The shocks were given by means of a patch-patch configuration on the anterior and posterior surfaces of the heart, which was paced from a stimulating electrode attached to the left ventricular apex. Analysis of variance showed no statistically significant differences in ULV50 as determined with different pacing cycle lengths. For monophasic shocks, DFT50 (331 +/- 66 V or 5.8 +/- 2.7 J) was not significantly different from ULV50 determined at the mid-upslope of the T wave (318 +/- 64 V or 5 +/- 2 J). The correlation coefficients between the two values were 0.74 (p = 0.014) for voltage and 0.67 (p = 0.034) for energy. In contrast, DFT50 was significantly higher than ULV50 as determined at the peak of the T wave (219 +/- 43 V or 2.3 +/- 1 J) and mid-downslope of the T wave (200 +/- 38 V or 1.9 +/- 0.9 J). In three dogs, ventricular fibrillation could not be induced at the mid-downslope of the T wave with any baseline pacing (Si) cycle length.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗
PubMed1991

Clinical electrophysiological effects of intravenous recainam: an antiarrhythmic drug under investigation for the treatment of ventricular and supraventricular arrhythmias.

This open-label, multicenter study was designed to assess the electrophysiological properties of intravenous recainam, an investigational Class I antiarrhythmic agent. In 25 patients undergoing electrophysiological studies for the evaluation of arrhythmias, recainam was administered intravenously in a loading infusion (0.1 mg/kg/min) for 40 minutes, followed by a maintenance infusion (0.02 mg/kg/min) until the completion of the study. Electrophysiological measurements were obtained at baseline, 30 minutes after initiation of the loading infusion, and 30 minutes after termination of the infusion during washout. Conduction intervals, refractory periods, and sinus node recovery times were measured during sinus rhythm and during atrial or ventricular pacing. Vital signs were obtained and recorded before, during, and after recainam infusion. The results showed no change in mean arterial pressure, but heart rate increased slightly by 4 beats/min following recainam infusion. Recainam produced a generalized slowing of intracardiac conduction. The mean intraatrial conduction time, measured at an atrial paced cycle length of 600 msec, increased during recainam loading infusion by 44%, from 38.8% +/- 2.8 to 53.0 +/- 5.4 msec; intranodal conduction time increased by 10%, from 102.0 +/- 5.5 to 112.1 +/- 5.2 msec; and infranodal conduction time increased by 31% from 53.1 +/- 3.0 to 70.7 +/- 3.8 msec. Slowed conduction persisted during washout. The mean right atrial effective refractory period was significantly prolonged (+7% at 600 msec cycle length and +8% at 450 msec cycle length, P less than 0.05 and P less than 0.01, respectively) during recainam loading and remained so during washout.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Epicardial activation and repolarization patterns in patients with right ventricular hypertrophy.

To map global epicardial repolarization patterns and test the "SI" model of T wave generation, the patterns of epicardial activation and repolarization in patients with chronic pulmonary thromboembolism and right ventricular hypertrophy were studied by computerized mapping techniques and monophasic action potential (MAP) recording. The ventricular activation patterns were characterized by delayed right ventricular activation and the absence of normal early epicardial ventricular breakthrough in some cases. The repolarization patterns were characterized by nonuniform distribution of T wave morphologies. The T waves were predominantly positive over the left ventricular epicardium and negative or biphasic over the right ventricular epicardium. The activation-recovery (A-R) intervals were measured from the local activation to the maximal dV/dt of the upstroke of the T waves (Wyatt method). The difference between the A-R intervals and the MAP from onset of activation to 90% repolarization (MAP90) varies according to T wave morphology and could be as high as 96 msec with positive T waves, despite significant correlations (r = 0.56-0.90) between MAP90 and A-R intervals for each morphology. Better overall correlations were found if the minimal dV/dt on the downslope of the positive T waves was chosen to estimate the time of local repolarization (alternative method). Using this method, the mean A-R intervals were the same over the right and left ventricles. Cardiopulmonary bypass significantly prolonged the action potential duration equally at all parts of the epicardium. We conclude that in patients with right ventricular hypertrophy, the time of local repolarization can be estimated by our alternative method; the right ventricle completes activation and repolarization later than the left ventricle, and the distribution of T wave morphologies is nonuniform, with predominantly positive T waves observed over the left ventricle and negative or biphasic T waves observed over the right ventricle. These findings are compatible with the SI model of the generation of T waves.

Action Potentials↗
PubMed1990

Demonstration of accessory pathway interaction by computerized mapping in preexcitation syndrome.

While interaction between the normal conduction system and an accessory pathway (AP) has been reported, interaction between two APs has not been well documented. With the assistance of computerized mapping techniques, we recently operated on a patient with two APs. One of these two APs had slow anterograde conduction velocity and was concealed during sinus rhythm and atrial pacing. Intraoperative computerized mapping studies revealed that the interaction between the APs was responsible for the anterograde conduction block of the slow AP during sinus rhythm and atrial pacing. This is the first direct demonstration of inhibition of conduction of one AP by the other AP in a patient with preexcitation syndrome.

Adult↗
PubMed1989

Oral N-acetylprocainamide compared to quinidine plus digoxin in the chronic suppression of atrial flutter in humans.

Antiarrhythmic therapy for the suppression of atrial flutter has conventionally entailed the use of a class Ia agent such as quinidine or procainamide. However, atrial flutter often recurs despite the use of these conventional antiarrhythmic regimens. Experimental and clinical evidence suggests that the pharmacologic suppression of atrial flutter may depend on the prolongation of the atrial action potential duration and consequently the voltage-dependent refractoriness. Therefore, the efficacy and tolerance of the class III antiarrhythmic agent N-acetylprocainamide was compared to that of the conventional regimen of the class Ia agent quinidine combined with digoxin (to control ventricular response) in patients with a history of symptomatic sustained atrial flutter. The study was randomized but nonblinded, with a crossover to the alternate regimen if the first failed. Eighteen patients entered the study and were followed for up to 18 months. Of the 12 receiving N-acetylprocainamide (eight randomized and four crossovers), one (8%) failed therapy due to side effects, but none had atrial flutter. Of the 11 receiving quinidine and digoxin (10 randomized and one crossover), three (28%) had a recurrence of atrial flutter, two of whom also had intolerable side effects, and two more (18%) had side effects alone requiring withdrawal of therapy (total 46% failed). The probability of therapeutic success over time was greater (p less than 0.04) for N-acetylprocainamide than for quinidine and digoxin. The data suggest that N-acetylprocainamide may be more effective and better tolerated than the conventional regimen of quinidine plus digoxin. Therefore, large-scale blinded studies of the efficacy of N-acetylprocainamide in the suppression of atrial flutter may be warranted.

Acecainide↗
PubMed1989

Effect of thyroid replacement therapy on the frequency of benign atrial and ventricular arrhythmias.

Whether thyroid replacement therapy can trigger cardiac arrhythmias in patients with hypothyroidism is not known. In this prospective study, 24 h ambulatory electrocardiographic (ECG) monitoring was used to assess the frequency of atrial and ventricular premature beats in 25 patients with hypothyroidism (5 men and 20 women, aged 56 +/- 3 years) before and 3.5 +/- 0.5 months (mean +/- SEM) after thyroid replacement therapy. Plasma thyroid-stimulating hormone was 73.6 +/- 12.3 and 3.1 +/- 0.6 microU/ml and free thyroxine index was 2.4 +/- 0.4 and 9.8 +/- 0.9 micrograms/100 ml at baseline and after thyroid replacement therapy, respectively. The frequency of ventricular premature beats was not affected by thyroid replacement therapy (from 273 +/- 221 at baseline to 352 +/- 235 beats/24 h after therapy), even in patients with frequent baseline arrhythmias. In contrast, the frequency of atrial premature beats was slightly increased after thyroid replacement therapy (from 47 +/- 17 to 279 +/- 197 beats/24 h), largely as a result of changes seen in three patients. No patient developed new onset of sustained ventricular or supraventricular arrhythmias. Average, basal and maximal heart rates during ECG monitoring increased significantly after thyroid replacement therapy (average 72 +/- 2 to 80 +/- 2; basal 64 +/- 2 to 70 +/- 2; maximal 114 +/- 3 to 130 +/- 3 beats/min, respectively, p less than 0.001). In conclusion, thyroid replacement therapy is safe in patients with common benign cardiac arrhythmias, and does not trigger an increase in arrhythmia frequency except in rare patients with baseline atrial premature beats. It is, however, associated with an increase in basal, average and maximal heart rates.

Adult↗
PubMed1988

Anomalous origin of the circumflex coronary artery in association with the right superior septal artery.

The presence of anomalous coronary arteries is observed infrequently during routine coronary angiography. However, their identification is crucial to the management of the patient with associated coronary artery disease. A case is described in which concomitant anomalous origin of the circumflex coronary artery from the right coronary artery, and a right superior septal coronary artery with a separate ostium occurred in association with severe three-vessel coronary artery disease requiring bypass graft surgery. Clues to the presence of the anomalous vessels were (1) their visualization during left ventriculography and (2) their presence or absence during injection of the normally originating vessels. This particular association of anomalous vessels was previously unreported.

Coronary Angiography↗
PubMed1988

Clinical and electrophysiologic effects of amiodarone in patients with atrial fibrillation complicating the Wolff-Parkinson-White syndrome.

The clinical and electrophysiologic effects of oral amiodarone were evaluated in 10 patients with a history of spontaneous atrial fibrillation and a rapid ventricular response, complicating the Wolff-Parkinson-White syndrome. Five patients developed ventricular fibrillation during an episode of atrial fibrillation. Seven patients underwent electrophysiology study and arrhythmia induction, both before and during chronic amiodarone treatment. During a mean 30 months of follow-up (range 8 to 59 months), no recurrences of atrial fibrillation or ventricular fibrillation were noted. One patient had recurrent supraventricular tachycardia and underwent surgery. One had serious and five had minor side effects. Arrhythmia suppression was associated with prolongation of the anterograde accessory pathway (+38%, p less than 0.01) and atrial (+34%, p less than 0.01) effective refractory periods. Amiodarone also slowed the ventricular response to induced atrial fibrillation, prolonging the mean (+90%, p less than 0.01) and minimum (+104%, p = 0.01) R-R intervals. Thus, amiodarone is a safe and effective alternative for arrhythmia prevention if surgery is inadvisable or is not desired by the patient.

Adult↗
PubMed1988

Effects of N-acetylprocainamide and recainam in the pharmacologic conversion and suppression of experimental canine atrial flutter: significance of changes in refractoriness and conduction.

The electrophysiologic determinants of the pharmacologic conversion and the prevention of atrial flutter are poorly defined. This study investigated the effects of pharmacologically induced changes in atrial conduction velocity and refractoriness, in the conversion and suppression of atrial flutter induced in the open-chest anesthetized dog by intercaval crush and rapid atrial pacing. The effects of an intravenous infusion of the new class III antiarrhythmic drug N-acetylprocainamide (30 mg/kg over 15 min) and the class Ic antiarrhythmic drug recainam (10 mg/kg over 20 min followed by 10 mg/kg/h) were evaluated. N-acetylprocainamide restored sinus rhythm in 10 of 15 (66%) dogs, while recainam converted only 2 of 10 (20%). N-acetylprocainamide prevented reinduction in 3 (20%), while recainam was effective in none. In the atria, N-acetylprocainamide induced significant increases in effective refractory period (+27%, p less than 0.01), functional refractory period (+22%, p less than 0.01), and in atrial flutter cycle length (+13%, p less than 0.01). Recainam increased effective refractory period (+28%, p less than 0.01), functional refractory period (+20%, p less than 0.01), conduction time at atrial paced cycle length of 150 msec (+70%, p less than 0.01) and atrial flutter cycle length (+56%, p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Acecainide↗
PubMed1987

Hemodynamic and electrophysiologic effects of combined infusion of lidocaine and propafenone in humans.

The hemodynamic and electrophysiologic effect of a combined intravenous infusion of lidocaine (100 mg bolus followed by 2 mg/min infusion) and propafenone (1 or 2 mg/kg) in patients with a history of ventricular arrhythmia was studied. Lidocaine infusion alone significantly increased the mean pulmonary artery (+28%) and pulmonary capillary wedge (+17%) pressure, with no effect on cardiac index. Lidocaine alone produced no consistent change in any measured electrophysiologic parameter, except slight QTc shortening (-2%, P less than .05). Propafenone alone, particularly at the higher dose (2 mg/kg), produced significant increases in mean blood pressure (+14%), right atrial pressure (+78%), pulmonary artery pressure (+50%), pulmonary capillary wedge pressure (+65%), systemic vascular resistance (+29%), and pulmonary vascular resistance (+61%) and a decrease in cardiac index (-12%). Significant prolongation of PR (+9%), AH (+29%), and HV (+23%) intervals, atrial functional refractory period (+12%), ventricular effective (+7%) and functional (+6%) refractory period, and Wenckebach cycle length (+13%) also occurred after the administration of propafenone alone. Only the effects on atrioventricular (AV) node were observed at the lower dose of propafenone (1 mg/kg). Combined infusion of lidocaine with propafenone produced a mild, statistically insignificant additional negative inotropic effect but reversed the prolongation in atrial and ventricular refractoriness produced by propafenone alone. Thus, the data show that lidocaine attenuates certain electrophysiologic effects of propafenone, which might alter its antiarrhythmic efficacy, while producing mild additive negative inotropic effects that may be of hemodynamic significance.

Adult↗