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Biomedical subjects

W Schoels

Publications and source records attributed to W Schoels.

35 records · Page 2Linked to original sources

Multisite pacing for prevention of atrial tachyarrhythmias: potential mechanisms.

OBJECTIVES: To determine the effects of single-, dual-, triple- and quadruple-site atrial pacing on atrial activation and refractoriness in normal canine hearts. BACKGROUND: Multisite pacing has been suggested to be superior to single-site pacing for prevention of atrial tachyarrhythmias. However, the underlying electrophysiological mechanisms are undetermined at the moment, as is the rationale for the selection of pacing locations and the number of pacing sites. METHODS: In 13 normal beagle dogs, an epicardial multielectrode (128 bipoles) and a multiplexer mapping system were used to reconstruct epicardial atrial activation patterns obtained during simultaneous stimulation from up to four electrodes located in the high and low right and left atrium, respectively. For all pacing modes (single-, dual-, triple- and quadruple-site pacing), total activation times and local effective refractory periods at eight randomly selected sites as well as local recovery intervals were determined. In a subgroup of five dogs, total epicardial activation times were also obtained during single-site septal stimulation (septal group). RESULTS: Activation times and local recovery intervals were minimized by triple-site stimulation, whereas a fourth site did not produce further shortening. Septal stimulation produced epicardial activation times comparable to quadruple-site stimulation. Local refractory periods and their dispersion always remained unaffected. Functional conduction blocks apparent during single-site were found to resolve during multisite stimulation. CONCLUSIONS: Multisite pacing can prevent functional conduction blocks by multidirectional excitation and a reduction in total activation time. Triple-site and, possibly, septal pacing modes are expected to be most efficient because both minimize total activation times and maximize the multidirectionality of excitation. In spite of unaffected local refractory periods, the shortening of local recovery intervals might homogenize atrial repolarization and, thus, contribute to the preventive effects of multisite pacing.

Animals↗

Role of sodium channels in ventricular fibrillation: a study in nonischemic isolated hearts.

Because the role of sodium channels in the initiation and maintenance of VF is not fully elucidated, we studied the significance of sodium channel activity in VF using sodium channel blockers. In nonischemic isolated feline hearts, the following electrophysiologic parameters were measured before and after application of tetrodotoxin (5 x 10(-7) M, n = 6) or lidocaine (1 x 10(-5) M, n = 8): (a) during pacing, epicardial conduction time; refractoriness; the fastest rate for 1:1 pacing/response capture, and all tissue resistivity, indirectly reflecting intercellular electrical resistance; (b) during 8 min of electrically induced tachyarrhythmias, all tissue resistivity; peak frequency (to measure average frequency based on fast-Fourier transformation analysis); and normalized entropy (to measure the degree of arrhythmia organization). In nonischemic isolated rabbit hearts (n = 4), three-dimensional mapping was performed before and after application of lidocaine (1 x 10(-5) M). In feline hearts, lidocaine and tetrodotoxin application resulted in: (a) more spontaneous arrhythmia termination (63-67%) than in nontreated hearts (7%); (b) transformation from mainly VF into ventricular tachycardia with increased organization; and (c) prolongation of conduction time (155-248%) (p < 0.01 for all parameters). The ventricular refractory period was slightly prolonged by tetrodotoxin in the right ventricle and exhibited rate-dependent shortening in control and with lidocaine. Tetrodotoxin and lidocaine reduced the pacing rate for 1:1 pacing/response capture, and all tissue resistivity was not significantly affected. Peak frequency was decreased by tetrodotoxin and lidocaine mainly in the left ventricle (p < 0.01). In nontreated left ventricles, peak frequency was increased over time but was attenuated by lidocaine. In isolated rabbit hearts, several simultaneous wave fronts were detected during VF in nontreated hearts and were reduced to only one or two major wavefronts after application of lidocaine. Suppression of sodium channel activity that primarily slowed conduction time and had little or no effect on ventricular refractory period and all tissue resistivity resulted in less stable and more organized arrhythmias and reduced tachyarrhythmia rate compared with nontreated hearts. These results suggest an active role for sodium channels in the maintenance of ventricular fibrillation.

Anesthetics, Local↗

[Catheter ablation of supraventricular tachyarrhythmias: experimental findings].

In the majority of cases, atrial fibrillation seems to depend on multiple, simultaneously active reentrant circuits. Their pathlength is defined by local refractory periods and conduction velocities. Active circuits experience constant changes in number, location and dimension. Ablative interventions targeting individual circuits are, therefore, not likely to be successful. Current approaches aim at multiple, electrically isolated atrial segments providing insufficient space for the given minimal size of potential reentrant circuits. Pharmacologic interventions either result in conduction delay and subsequent conduction block, or in prolongation of local refractoriness increasing the size of existing circuits. Creation of isolated atrial segments by endocardial catheter ablation implies the feasibility of extended, contiguous transmural lesions. Mapping studies in healthy dogs demonstrated that contiguous anatomic lesions are very hard to achieve with conventional catheter techniques. Functional conduction blocks, however, may be obtained. Furthermore, application of radiofrequency energy induces prolongation of local refractoriness even at a distance from the actual anatomic lesion. Thus, in the interventional therapy of atrial fibrillation, functional effects of radiofrequency ablation might at least serve to facilitate the strenuous implementation of the isolation concept.

Animals↗

Mechanisms of pacing interventions in atrial fibrillation.

Atrial flutter is due to large single reentrant loops, typically oriented around the caval veins and a line of functional conduction block in between. These reentrant circuits can easily be terminated by properly timed extra beats colliding in the antidromic direction with the reentrant orthodromic wavefront and being blocked in the orthodromic direction within the area of slow conduction. Due to the complex situation in atrial fibrillation with multiple, ever-changing wavelets and a marked functional inhomogeneity of the atrial tissue, these simple concepts do not apply. However, regional control of atrial tissue by rapid pacing is feasible during atrial fibrillation, and through a multisite approach, this pacing modality might lead to a situation where the remaining nonentrained atrial tissue is just no longer reaching the critical mass. Single-site, dual-site, and biatrial pacing seems to reduce the incidence of atrial fibrillation recurrences. Specific advantages and disadvantages of each approach still need to be elucidated. Apart from preventing bradycardia, preventive pacing modes reduce intra-atrial conduction times and might reduce intra-atrial dispersion of refractoriness. Still, the specific mechanisms relevant for their effectiveness need further clarification.

Atrial Fibrillation↗

Differential effects of d-sotalol on normal and infarcted myocardium: an experimental study using epicardial mapping.

OBJECTIVE: The aim of the study was to investigate the differential effects of the class III agent, d-sotalol, on conduction and refractoriness on normal and infarcted areas of the canine ventricle. METHODS: Epicardial mapping studies were performed in 6 dogs 5-7 days after ligation of the left descending coronary artery using a specially designed patch electrode which contained 192 bipolar electrodes. Normal and infarcted areas were differentiated with respect to their macroscopic appearance and electrophysiological properties. Activation maps and local effective refractory periods (ERP) were determined before and after the administration of d-sotalol (1.5 mg/kg) at cycle lengths of 250, 300 and 350 ms. RESULTS: Conduction and refractoriness were relatively homogeneous in the normal zone (NZ), contrasting with inhomogeneity in the infarct zone (IZ). In 2 dogs d-sotalol produced regional delay and block of conduction, exclusively in the IZ. The relative increase in refractoriness (delta ERP) after d-sotalol was significantly more pronounced in the IZ than in vs the NZ. In the NZ, delta ERP was most prominent at the longest (350 ms) and least prominent at the shortest (250 ms) basic pacing cycle lengths (11.5 +/- 2.8 vs. 7.3 +/- 1.4%; P < 0.05). The effect of d-sotalol in the IZ was independent of the basic pacing cycle length. CONCLUSIONS: d-Sotalol preferentially prolonged refractoriness in the IZ of the canine ventricle. This effect and the lack of rate-dependence in the IZ could provide a possible explanation for both the potent antiarrhythmic and potential antiarrhythmic effect of d-sotalol.

Animals↗

Echocardiographic Fourier phase and amplitude imaging for quantification of ischemic regional wall asynergy: an experimental study using coronary microembolization in dogs.

OBJECTIVES: This study investigated whether echocardiographic Fourier phase and amplitude imaging can be used to evaluate ischemia-related regional wall asynergy. BACKGROUND: Because myocardial ischemia delays the onset and peak of endocardial inward motion and reduces its magnitude, Fourier phase and amplitude analysis of two-dimensional echocardiograms may be used to evaluate regional wall motion abnormalities objectively by analyzing temporal sequence and magnitude of endocardial motion. METHODS: Digital cine loops of left ventricular long- and short-axis views were obtained in six anesthetized dogs at baseline and 1 to 30 min after coronary microembolization and were mathematically transformed using a first-harmonic Fourier algorithm to obtain phase angles and amplitudes of endocardial segments. Mean phase angles and amplitudes were compared with visual wall motion analysis based on a scoring system and quantitative analysis based on segmental fractional area shortening derived from planimetry. RESULTS: Microembolization delayed segmental phase angles by 47 +/- 44 degrees in mild to moderate hypokinesia (fractional shortening [mean +/- SD] 41 +/- 13%) and by 77 +/- 63 degrees in severe hypokinesia (fractional shortening 13 +/- 5%) and reduced segmental amplitudes from 80 +/- 36 gray level intensity at baseline to 53 +/- 34 in segments developing mild to moderate hypokinesia, and from 93 +/- 36 to 35 +/- 28 gray level intensity in segments developing severe hypokinesia. Shifts in segmental phase angles correlated better with dynamic shifts in segmental fractional area shortening than did changes in wall motion score (r = -0.65 vs. r = 0.52, p < 0.001). CONCLUSIONS: Echocardiographic Fourier phase imaging can be used to evaluate ischemia-related regional wall asynergy, displaying contraction sequence and magnitude in a simple, objective format.

Algorithms↗

Circus movement atrial flutter in the canine sterile pericarditis model. Relation of characteristics of the surface electrocardiogram and conduction properties of the reentrant pathway.

OBJECTIVES: This study was designed to elucidate the basis for the electrocardiographic (ECG) appearance of atrial flutter in the canine sterile pericarditis model. BACKGROUND: During atrial flutter, the surface ECG may show typical F waves or isolated P waves of any polarity. METHODS: Electrocardiographic leads II, III and aVF and epicardial atrial activation maps constructed from 127 simultaneously recorded bipolar electrograms were compared in 20 dogs with sterile pericarditis and inducible atrial flutter. RESULTS: In 10 dogs with F wave atrial flutter, single loop reentry occurred around combined functional/anatomic obstacles that included one or both caval veins and a vertically oriented arc of functional conduction block. In 10 dogs with P wave atrial flutter, a merely functional (n = 4) or combined (n = 6) obstacle involving any atrial vessel and more vertically (n = 5) or more horizontally (n = 5) oriented arcs of block was present. The isoelectric interval between P waves corresponded to the conduction time within the slow zone of the reentrant circuit (96 +/- 27 vs. 100 +/- 24 ms, mean +/- SD). Slow conduction accounted for 65 +/- 8% of the cycle length in P wave atrial flutter, but for only 29 +/- 7% in F wave atrial flutter (p < 0.05). Slow conduction was usually associated with activation of fewer than five epicardial electrodes per 10-ms isochronal interval, reflecting only a small amount of atrial tissue. The polarity of P or F waves was determined by the direction of the major wave front activating the most electrodes per 10-ms isochronal interval, irrespective of whether the right or the left atrium was activated. CONCLUSIONS: The F waves result from reentrant activation at a relatively constant speed around a vertically oriented functional/anatomic obstacle involving one or both caval veins. The P waves occur when the circuit contains a marked area of slow conduction.

Animals↗

Advances in follow-up techniques for implantable defibrillators.

The complexity of newer implantable defibrillators has made device follow-up increasingly more intricate. Extensive data-logging capacity provides specific information on recorded events, which facilitates more accurate determination of patient arrhythmias. This helps the clinician judge whether the device is detecting and treating arrhythmias appropriately, or whether false sensing of external signals or supraventricular rhythms is occurring. There is also a record of the efficacy of delivered therapy from the device that helps in optimizing subsequent programming. Programming itself has become much more complicated, with multiple independently programmable therapy zones, each with numerous available therapeutic modalities. In addition, defibrillator status information has been improved. Accurate battery voltage measurements give a reasonable estimate of remaining device life, and pace/sense and shock lead impedances can be measured to provide information on total system integrity. Together, these advances allow more specific programming of the device to the individual patient's condition but require increasing experience and expertise of the physician.

Defibrillators, Implantable↗

Acute efficacy and chronic follow-up of patients with non-thoracotomy third generation implantable defibrillators.

Non-thoracotomy implantation of implantable cardioverter defibrillators (ICDs) has simplified the process of device insertion, promising to decrease associated procedural complications while providing sudden death protection at least equal to epicardial systems. This study presents the acute and chronic results of 110 patients who underwent attempted non-thoracotomy ICD implantation with the Medtronic Transvene lead system and PCD model 7217 or 7219. Of the 110 patients attempted, 100 (91%) had the system successfully implanted without the need for an epicardial patch. One patient died 1 week postoperatively of septic shock related to the implantation (0.9% perioperative mortality). During follow-up of 16 +/- 11 months, 45% of the patients had an event detected as ventricular tachycardia; 26% of these detections were felt clinically to be due to supraventricular rhythms. Of the remainder, 87% were successfully treated with the first VT therapy, and 98% were terminated by the final therapy; 66% of the patients had at least one episode of ventricular fibrillation, of which 5% were felt to be inappropriate detections; 85% of the appropriate episodes were successfully treated with the first VF therapy, and all were converted by the final therapy. Total mortality at 6, 12, and 24 months was 3%, 11%, and 19% respectively. Only one patient had sudden cardiac death, occurring at 13 months postimplant. Overall, the non-thoracotomy lead system for this ICD displayed infrequent implant complications and proved to be reliable at terminating arrhythmias and maintaining a low rate of sudden cardiac death in this high risk population.

Adult↗

A unified functional/anatomic substrate for circus movement atrial flutter: activation and refractory patterns in the canine right atrial enlargement model.

OBJECTIVES: This study was designed to test the concept of a functional/anatomic interaction in a canine model of reentry based on right atrial enlargement and to elucidate the electrophysiologic basis for functional conduction block. BACKGROUND: The monotonic feature of atrial flutter suggests a uniform substrate for the arrhythmia. Atrial flutter in the sterile pericarditis model is due to single-loop circus movement around a functional or a functional/anatomic obstacle near the atrioventricular (AV) ring. Sustained circus movement requires a critical interaction of a functional arc of block, a natural obstacle, the AV ring and a zone of slow conduction. The location of the inferior vena cava predisposes the lower right atrium to single-loop reentry. METHODS: In 11 dogs with right atrial enlargement, 127 bipolar epicardial electrograms were obtained during atrial flutter. For correlation of activation and refractory maps, the effective refractory period under each electrode was determined using the extrastimulus technique. RESULTS: Atrial flutter was due to single-loop reentry around functional arcs of block near the AV ring (n = 2) or around functional/anatomic obstacles (n = 8) involving the inferior vena cava. A slow zone was located between the arc and the AV ring and between the inferior vena cava and AV ring, respectively. During initiation, the arc joined the AV ring, forcing activation to proceed around the free end of the arc before breaking through the arc near the AV ring. Arrhythmia termination required the arc of block to rejoin the AV ring. Inducibility of sustained atrial flutter was associated with a marked spatial dispersion of refractoriness. The configuration of the functional arc of block was critically dependent on the spatial pattern of refractoriness. CONCLUSIONS: Atrial flutter requires a similar functional or functional/anatomic substrate independent of the underlying etiology. The spatial distribution of refractoriness in enlarged canine atria provides an adequate substrate for the development of functional conduction block.

Animals↗

Spontaneous and inducible ventricular arrhythmias in a canine model of chronic heart failure: relation to haemodynamics and sympathoadrenergic activation.

The relationship between the incidence, frequency and complexity of spontaneous ventricular arrhythmias and the extent of haemodynamic compromise and sympathoadrenergic hyperactivity was evaluated in a canine model of chronic heart failure produced by multiple sequential intracoronary microembolizations. Ambulatory ECG Holter monitoring recorded during chronic heart failure in 18 dogs revealed spontaneous ventricular arrhythmias ranging from single ventricular premature beats (VPBs) to non-sustained episodes of ventricular tachycardia (VT). Single VPBs were present in 94% of dogs, couplets in 67%, triplets in 28% and spontaneous episodes of non-sustained VT in 33%. Dogs with > 28 VPBs.h-1 (n = 9) had a markedly higher plasma norepinephrine (PNE) concentration (1001 +/- 185 vs 561 +/- 31 pg.ml-1) (P < 0.03), and a higher pulmonary artery wedge pressure (PAWP) (18 +/- 2 vs 12 +/- 1 mmHg) (P < 0.03) than dogs with < or = 28 VPBs.h-1 (n = 9). Dogs that developed spontaneous episodes of VT also had significantly higher PNE levels (1119 +/- 247 pg.ml-1) compared to dogs that did not develop VT (612 +/- 64 pg.ml-1) (P < 0.02). Programmed ventricular stimulation performed in seven of 18 dogs resulted in the development of sustained monomorphic VT in three and ventricular fibrillation in three dogs each (43%, 43%). Dogs with inducible sustained monomorphic VT had a significantly higher number of ambient arrhythmias and higher PAWP compared to dogs that did not develop sustained VT. The observed complexity, frequency and incidence of spontaneous and inducible ventricular arrhythmias in this canine model are similar to those described in patients with chronic heart failure.

Animals↗

Circus movement atrial flutter in canine sterile pericarditis model. Activation patterns during entrainment and termination of single-loop reentry in vivo.

BACKGROUND: Recently, we used a custom designed "jacket" electrode with 127 bipolar electrodes in a flexible nylon matrix to map the total atrial epicardial surface in the in situ canine heart. Atrial flutter in dogs with sterile pericarditis was shown to be due to a single wave front circulating around a combined functional/anatomic obstacle, with the arc of functional conduction block contiguous with one or more of the atrial vessels. METHODS AND RESULTS: In the present study, this model was used to analyze the activation pattern during pacing-induced entrainment and termination of single reentrant loops in a syncytium without anatomically predetermined pathways. Sustained atrial flutter was induced in five dogs with 3-5-day-old sterile pericarditis. Atrial pacing at a cycle length 5-30 msec shorter than the spontaneous cycle length entrained the arrhythmia and could result in a "classical" activation pattern, characterized by an antidromic stimulated wave that collided with the reentrant orthodromic wave front of the previous beat at a constant site. However, two variations of this classical activation pattern were also observed: 1) Pacing at short cycle lengths could lead to localized conduction block in antidromic direction, forcing a change in the pathway of the antidromic wave front. This could prevent the expected shift of the site of collision in antidromic direction. 2) The stimulated orthodromic wave front could also use a pathway different from that of the original reentrant impulse, so that a different circuit was active during the pacing period. Termination of atrial flutter by rapid atrial stimulation was associated with progressive slowing and finally blocking of the paced orthodromic wave front and a progressive shift of the site of collision in antidromic direction. The occurrence of conduction block was determined by the cycle length of stimulation and the number of stimulated beats. A longer train at the critical cycle length or the critical number of beats at a shorter cycle length could reinduce the same reentrant circuit or a different reentrant circuit, respectively, during stimulated cycles following the beat that terminated reentry. CONCLUSIONS: The epicardial activation sequence during entrainment of reentrant arrhythmias does not necessarily follow a standard activation pattern. Instead, the stimulated orthodromic as well as the antidromic wave front might use a pathway different from that of the original reentrant wave front. The mechanisms of termination, failure of termination, and reinitiation of single-loop reentry are similar to those in the "figure-eight" reentrant circuit.

Animals↗

Circus movement atrial flutter in the canine sterile pericarditis model. Differential effects of procainamide on the components of the reentrant pathway.

To evaluate the mechanisms of action of procainamide on the components of the reentrant pathway, drug-induced changes in activation patterns, effective refractory periods (ERPs), and stimulation thresholds were analyzed in nine dogs with sterile pericarditis and sustained atrial flutter. Activation maps were based on 127 close bipolar recordings from a special "jacket" electrode. From the control map, 22 +/- 2 sites covering the slow zone and the normal zone of the reentrant circuit were selected to measure ERPs and thresholds. The excitable gap was estimated from the longest ERP during pacing at the tachycardia cycle length. During atrial flutter, epicardial activation proceeded as a single wave around an arc of functional conduction block in the proximity of the atrioventricular (AV) ring or around a combined functional/anatomic obstacle, with the arc being contiguous with one of the venae cavae. An area of slow conduction, which accounted for 53 +/- 15% of the revolution time within 35 +/- 15% of the total length of the reentrant pathway, was bordered by the arc of block and the AV ring or a caval vein and the AV ring, respectively. Procainamide (5-10 mg/kg i.v.) prolonged the cycle length of atrial flutter from 144 +/- 17 to 190 +/- 24 msec (p less than 0.05) and then terminated the arrhythmia in all studies. The increase in cycle length was due to an increase in conduction time in the slow zone by 37 +/- 11 msec (86 +/- 17% of the total cycle length increase). During the last reentrant beat, conduction failed in the slow zone, with the arc of block joining the AV ring. At termination, procainamide had prolonged conduction time, stimulation threshold, and ERP in the normal zone by 11 +/- 18%, 40 +/- 80%, and 5 +/- 15%, respectively, compared with 51 +/- 16%, 86 +/- 93%, and 14 +/- 21%, respectively, in the slow zone (p less than 0.05 for all three parameters). The duration of the excitable gap did not change significantly. We conclude that procainamide preferentially affected the slow zone of single loop reentrant circuits. The drug terminated circus movement atrial flutter without abolishing the excitable gap, and its effect on conduction seemed the major determinant of the antiarrhythmic action.

Animals↗

Therapy assessment for sustained ventricular tachyarrhythmias: how many electropharmacological tests are appropriate?

Surgery, implantable devices or catheter ablations offer therapeutic choices for the treatment of malignant ventricular tachyarrhythmias (VT) resistant to antiarrhythmic drugs. The number of electropharmacological (EP) tests that should precede consideration of a nonpharmacological therapy has not been defined. We performed serial EP tests in 94 patients with inducible sustained VT until an effective drug was identified or all available drugs had failed to suppress VT induction. With up to 11 tests in individual patients, suppression of VT inducibility was finally achieved in 66 patients (70%). In 47 of these 66 patients (70%), only one or two tests were necessary to identify an effective regimen. However, in 40%, 28%, 18%, and 9% of the patients still inducible after 2, 3, 4, and 5 drug tests, respectively, an effective agent could be identified during subsequent tests. No critical number of unsuccessful EP tests clearly separated responders and nonresponders to medical therapy. During follow-up (34 +/- 11 months), 14 patients placed on antiarrhythmic drugs predicted to be effective had symptomatic VT recurrence. VT recurrence was unrelated to the type or the number of unsuccessful EP tests preceding identification of the prescribed drug. Extensive EP testing with all available agents might therefore be worthwhile in selected patients. An "appropriate" number of EP studies has to be determined individually for each patient, based on the chance of finding an effective drug during subsequent studies and the risk and benefit of the therapeutic choices.

Adult↗

Circus movement atrial flutter in the canine sterile pericarditis model. Activation patterns during initiation, termination, and sustained reentry in vivo.

The mechanisms of single-loop reentry in a syncytium without anatomically predetermined pathways have not been shown. Using a "jacket electrode" with 111 bipolar electrodes in a nylon matrix, we mapped in situ the atrial epicardial surface during atrial flutter in dogs with sterile pericarditis. Of 21 episodes of reentrant atrial flutter, only four showed double-loop ("figure-eight") reentry, whereas in 17 episodes a single loop was present. During initiation of single-loop reentry, an arc of functional block extended to the atrioventricular (AV) ring. This forced activation to proceed as a single wave around the free end of the arc, before breaking through the arc close to the AV ring. Activation continued as one loop around an arc close to the AV ring (in eight episodes) or around a combined functional and anatomic obstacle (in nine episodes) when the arc joined an atrial vessel. A zone of slow conduction was consistently bordered by the arc of block and the AV ring or by the anatomic obstacle and the AV ring. Spontaneous termination occurred when conduction failed in this area and the arc rejoined the AV ring. High-density recordings (2 mm) along the arc of block showed double potentials separated by an isoelectric interval, interpreted as local activation and electrotonus due to activation on the opposite side of the arc. Histologically, a diffuse inflammatory reaction involved 50-80% of the atrial wall. A transitional layer of myocardial bundles with preserved cross striation, but separated by edema and inflammatory cells, was enclosed between an epicardial layer of fragmented myocytes and an endocardial layer of grossly intact myocardium. There were no distinctive features at sites of functional conduction block or slowed conduction. In conclusion, single-loop reentry is the common pattern during atrial flutter in this model. Its induction depends on an interaction of the AV ring, a functional arc of block, and a zone of slow conduction. The location of the inferior vena cava predisposes the lower right atrium to this type of reentry.

Animals↗

Conversion of sustained into nonsustained ventricular tachycardia during therapy assessment by programmed ventricular stimulation: criterion for a positive drug effect?

Serial electropharmacologic testing using up to 11 different antiarrhythmic drugs was performed in 130 consecutive patients (107 men, 23 women, ages 56 +/- 12) with inducible sustained ventricular tachycardia (VT). After 4 +/- 2.3 drug tests, complete suppression of VT inducibility (defined as less than 6 consecutive beats, mean 1.4 +/- 1.6) was achieved in 86 patients (66%), whereas in 44 patients (34%) nonsustained VTs (greater than or equal to 6 consecutive beats, less than 30 seconds in duration) were still inducible. There was no statistical difference between both groups regarding age, sex, underlying heart disease, ejection fraction or entry arrhythmia. After a mean follow-up period of 19 +/- 17 months, 24 patients (18%) had died, 8 (6%) suddenly. Eight patients (6%) experienced recurrent sustained VT. Symptomatic recurrences (sudden death or VT) occurred in 10 (11%) and 6 patients (13%, difference not significant), respectively. Probability of arrhythmia-free survival was comparable for patients with 0 to 5, 6 to 10, 11 to 15 and 16 to 32 inducible ventricular complexes with discharge medication. The negative predictive value of electropharmacologic drug testing was about 89%, irrespective of the maximal number of inducible complexes used for the definition of a negative test result. It is therefore concluded that conversion of sustained into nonsustained VT during therapy assessment by programmed ventricular stimulation indicates a positive drug effect.

Anti-Arrhythmia Agents↗