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Biomedical subjects

C J Kirchhof

Publications and source records attributed to C J Kirchhof.

At least 19 recordsLinked to original sources
PubMed1998

Carotid sinus massage as a diagnostic and therapeutic tool for atrial flutter-fibrillation.

Alterations in vagal tone can influence the atrial fibrillatory process by changing the atrial refractory period. We observed in a patient with paroxysmal atrial fibrillation (AF) that carotid sinus massage (CSM) changed a "coarse" type of fibrillation into a "fine" type, followed by termination of the arrhythmia. Although coincidental conversion of AF into sinus rhythm could not be excluded, we concluded that it is worth while to try CSM in every patient presenting with AF prior to other interventions to restore sinus rhythm.

Aged↗
PubMed1997

Electrophysiological effects of acute dilatation in the isolated rabbit heart: cycle length-dependent effects on ventricular refractoriness and conduction velocity.

BACKGROUND: Acute ventricular dilatation has important electrophysiological effects: Dilatation shortens action potential duration and refractoriness without an apparent effect on conduction velocity. These effects have been implicated as a potential mechanism of arrhythmias in patients with congestive failure. Because the influence of cycle length on these phenomena has not been studied, we examined the effects of dilatation during ventricular pacing at cycle lengths from 1000 to 150 ms. METHODS AND RESULTS: Thin epicardial layers were created in isolated, perfused rabbit left ventricles (n=7). A fluid filled latex balloon was secured in the left ventricle to dilate the left ventricle. Mapping was performed with 248 epicardial electrodes. Longitudinal conduction velocity (76+/-1 cm/s; mean+/-SEM) and transverse conduction velocity (26+/-1 cm/s) were not influenced by dilatation at any cycle length. In contrast, the effects of dilatation in decreasing left ventricular effective refractory period (ERP) were significantly greater at shorter drive cycle lengths: The decrease in ERP was 2+/-2 ms (a 1% change) at a drive cycle length of 1000 ms and 18+/-4 ms (a 20% change) at a drive cycle length of 150 ms. In 10 additional intact, isolated perfused rabbit hearts, dilatation decreased ERP to a greater degree during 250 ms drive cycle length pacing than during pacing at 400 ms (25+/-4 versus 16+/-3 ms; P=.01). CONCLUSIONS: Acute dilatation exaggerates the normal rate-dependent shortening of refractoriness but does not influence transverse or longitudinal conduction velocity. This observation suggests that the electrophysiological effects of acute dilatation may be greater during tachycardia than at slower cycle lengths. This may have implications for arrhythmias in patients with congestive heart failure.

Acute Disease↗
PubMed1997

Electrical remodeling due to atrial fibrillation in chronically instrumented conscious goats: roles of neurohumoral changes, ischemia, atrial stretch, and high rate of electrical activation.

BACKGROUND: Recently, we developed a goat model of chronic atrial fibrillation (AF). Due to AF, the atrial effective refractory period (AERP) shortened and its physiological rate adaptation inversed, whereas the rate and stability of AF increased. The goal of the present study was to evaluate the role of (1) the autonomic nervous system, (2) ischemia, (3) stretch, (4) atrial natriuretic factor (ANF), and (5) rapid atrial pacing in this process of electrical remodeling. METHODS AND RESULTS: Twenty-five goats were chronically instrumented with multiple epicardial atrial electrodes. Infusion of atropine (1.0 mg/kg; n=6) or propranolol (0.6 mg/kg; n=6) did not abolish the AF-induced shortening of AERP or interval (AFI). Blockade of K+(ATP) channels by glibenclamide (10 micromol/kg; n=6) slightly increased the AFI from 95+/-4 to 101+/-5 ms, but AFI remained considerably shorter than during acute AF (145 ms). Glibenclamide had no significant effect on AERP after electrical cardioversion of AF (69+/-14 versus 75+/-15 ms). Volume loading by 0.5 to 1.0 L of Hemaccel (n=12) did not shorten AERP. The median plasma level of ANF increased from 42 to 99 pg/mL after 1 to 4 weeks of AF (n=6), but ANF infusion (0.1 to 3.1 microg/min, n=4) did not shorten AERP. Rapid atrial pacing (24 to 48 hours; n=10) progressively shortened AERP from 134+/-10 to 105+/-6 ms and inversed its physiological rate adaptation. CONCLUSIONS: Electrical remodeling by AF is not mediated by changes in autonomic tone, ischemia, stretch, or ANF. The high rate of electrical activation itself provides the stimulus for the AF-induced changes in AERP.

Animals↗
PubMed1997

Coronary sinus pacing prevents induction of atrial fibrillation.

BACKGROUND: Atrial fibrillation (AF) is due to reentry, and its incidence has been shown to decrease after dual-site atrial or biatrial pacing. We investigated whether a simpler pacing approach via the distal coronary sinus (CSd) could eliminate AF inducibility by high right atrial (HRA) extrastimuli (APDs). We based our hypothesis on our previous observation that AF inducibility by HRA APDs was associated with conduction delays to the posterior triangle of Koch, whereas AF was never induced with CSd APDs, which were associated with minimal intra-atrial conduction delays. METHODS AND RESULTS: Programmed electrical stimulation was performed from the high right atrium and CSd, and bipolar recordings were obtained from the high right atrium, His bundle, posterior triangle of Koch, and coronary sinus. In 13 patients (age, 44+/-18 years), AF was reproducibly induced with a critically timed HRA APD (220+/-22 ms) delivered during HRA pacing. AF was not induced in any of the patients when HRA APDs were delivered during CSd pacing at the same critical coupling intervals. Coronary sinus APDs delivered during HRA pacing also were not associated with AF induction. The APD coupling interval measured at the posterior triangle of Koch during CSd pacing was significantly prolonged compared with the one measured during HRA pacing and AF induction (381+/-58 versus 263+/-37 ms; P<.0001). CONCLUSIONS: We propose that CSd pacing suppresses the propensity of HRA APDs to induce AF by limiting their prematurity at the posterior triangle of Koch and not allowing local conduction delay and local reentry to occur.

Adolescent↗
PubMed1996

Electrophysiologic mechanisms of perpetuation of atrial fibrillation.

The presence of an excitable gap during atrial fibrillation (AF), although short and variable, may be of potential importance for the development of alternative techniques for termination of AF by rapid pacing. Also the notion that perpetuation of AF may be partly dependent on macroreentry around the natural atrial orifices, may provide a new therapeutic option for the permanent cure of AF by interrupting the anatomical circular pathways in the atria by radiofrequency ablation. In our opinion the rapidly growing understanding of the electrophysiologic mechanisms of AF certainly warrants some optimism about the possibility of cure of AF in the near future without causing too much discomfort and without carrying on unacceptable risk.

Adolescent↗
PubMed1996

Unravelling the electrical mysteries of atrial fibrillation.

Animal experiments have confirmed that a short but variable excitable gap is present during induced atrial fibrillation. The existence of this gap allows atrial fibrillation to be locally captured by rapid pacing. An area of up to 4 cm in diameter can be activated by uniform wave fronts propagating away from the site of stimulation, although the size of this area may be limited by intra-atrial conduction block or by collision with fibrillation waves. Rapid pacing can accelerate atrial fibrillation by inducing local re-entry circuits with a cycle length shorter than the pacing interval. During pacing-induced atrial fibrillation in patients undergoing surgery for Wolff-Parkinson-White syndrome, three types of atrial activation have been identified, which vary in their degree of complexity and in the length of their fibrillation intervals. It appears that the spectrum of varying cycle lengths during atrial fibrillation might be explained by a mixture of different sorts of atrial re-entry patterns, comprising purely functional intra-atrial re-entry, random re-entry, anatomical re-entry, and nodal re-entry.

Animals↗
PubMed1995

Atrial fibrillation begets atrial fibrillation. A study in awake chronically instrumented goats.

BACKGROUND: In this study we tested the hypothesis that atrial fibrillation (AF) causes electrophysiological changes of the atrial myocardium which might explain the progressive nature of the arrhythmia. METHODS AND RESULTS: Twelve goats were chronically instrumented with multiple electrodes sutured to the epicardium of both atria. Two to 3 Weeks after implantation, the animals were connected to a fibrillation pacemaker which artificially maintained AF. Whereas during control episodes of AF were short lasting (6 +/- 3 seconds), artificial maintenance of AF resulted in a progressive increase in the duration of AF to become sustained (> 24 hours) after 7.1 +/- 4.8 days (10 of 11 goats). During the first 24 hours of AF the median fibrillation interval shortened from 145 +/- 18 to 108 +/- 8 ms and the inducibility of AF by a single premature stimulus increased from 24% to 76%. The atrial effective refractory period (AERP) shortened from 146 +/- 19 to 95 +/- 20 ms (-35%) (S1S1, 400 ms). At high pacing rates the shortening was less (-12%), pointing to a reversion of the normal adaptation of the AERP to heart rate. In 5 goats, after 2 to 4 weeks of AF, sinus rhythm was restored and all electrophysiological changes were found to be reversible within 1 week. CONCLUSIONS: Artificial maintenance of AF leads to a marked shortening of AERP, a reversion of its physiological rate adaptation, and an increase in rate, inducibility and stability of AF. All these changes were completely reversible within 1 week of sinus rhythm.

Animals↗
PubMed1994

Experimental models of arrhythmias: toys or truth?

In this communication two new experimental models of atrial fibrillation are described. One model (artificial maintenance of atrial fibrillation in conscious goats) points to the electrophysiological changes caused by prolonged atrial fibrillation. It shows that within 24 h of atrial fibrillation the atrial refractory period becomes markedly shortened and the duration of atrial fibrillation markedly prolonged. In the other model, experimentally induced atrial fibrillation in the dog is regionally entrained by local rapid pacing. However, termination of atrial fibrillation by local overdrive pacing was never observed. The possible implication of these new experimental models for prevention and treatment of clinical atrial fibrillation are discussed.

Animals↗
PubMed1994

Interaction of acute ventricular dilatation and d-sotalol during sustained reentrant ventricular tachycardia around a fixed obstacle.

BACKGROUND: Antiarrhythmic therapy of ventricular tachycardia is associated with decreased efficacy and increased proarrhythmia in patients with congestive heart failure, but the explanation for these observations is not known. This study examined the interaction of ventricular dilatation and d-sotalol in a model of reentry ventricular tachycardia. METHODS AND RESULTS: Thin epicardial layers of anisotropic myocardium were created in Langendorff-perfused rabbit left ventricles by a cryo procedure. A fluid-filled, latex balloon was secured within the left ventricle to change ventricular volume. Sustained reentrant ventricular tachycardia, around a central cryolesion, was induced by rapid pacing in all preparations (n = 7). Epicardial mapping was performed through 248 electrodes. Single premature beats introduced within the reentry circuit were used to define the excitable gap. Dilatation did not influence ventricular tachycardia cycle length or conduction velocity. A 1.25-mL increase in left ventricular volume widened the excitable gap by 12% (range, 5% to 29%) (P < .001) because of a decrease in myocardial refractoriness. d-Sotalol (final concentration, 10 mg/L) narrowed the excitable gap 18% (range, 7% to 29%) (P = .002) in the undilated left ventricle. d-Sotalol was less effective in the dilated left ventricle, narrowing the excitable gap only 9%, a difference that was not statistically significant. During pacing to induce or terminate tachycardia, tachycardia acceleration was observed significantly more frequently in the dilated than in the undilated ventricle. Ventricular tachycardia acceleration was due to the development of double-wave reentry (two successive waves traveling in the same circuit in the same direction). d-Sotalol, which narrowed the excitable gap, prevented tachycardia acceleration and double-wave reentry. CONCLUSIONS: Antiarrhythmic efficacy may be decreased by dilatation because of widening of the initial excitable gap and a decrease in the gap-narrowing effect of these agents. Double-wave reentry, more likely with a widening of excitable gap, may partially explain tachycardia acceleration in the dilated ventricle.

Animals↗
PubMed1994

High-density mapping of electrically induced atrial fibrillation in humans.

BACKGROUND: Mapping studies in animals have suggested that atrial fibrillation (AF) is based on multiple reentering wavelets. Little information is available about the patterns of activation during AF in humans. The objective of the present study was to reconstruct and classify the patterns of human right atrial (RA) activation during electrically induced AF. METHODS AND RESULTS: AF was induced by rapid atrial pacing in 25 patients with Wolff-Parkinson-White syndrome undergoing surgery for interruption of their accessory pathway(s). The free wall of the RA was mapped using a spoon-shaped electrode containing 244 unipolar electrodes. The activation of the RA during AF showed large interindividual differences. Based on the complexity of atrial activation, three types of AF were defined. In type I (40% of patients), single broad wave fronts propagated uniformly across the RA. Type II (32%) was characterized by one or two nonuniformly conducting wavelets, whereas in type III (28%), activation of the RA was highly fragmented and showed three or more different wavelets that frequently changed their direction of propagation as a result of numerous arcs of functional conduction block. There were significant differences (P < .05) among the three types of AF in median intervals (174 +/- 28, 150 +/- 14, and 136 +/- 16 milliseconds), variation in AF intervals (P5-95) (54 +/- 25, 94 +/- 21, and 104 +/- 22 milliseconds), incidence of electrical inactivity (42 +/- 11%, 21 +/- 4%, and 8 +/- 4%) and reentry (3 +/- 7%, 36 +/- 28%, and 99 +/- 36%), and average conduction velocity during AF (61 +/- 6, 54 +/- 4, and 38 +/- 10 cm/s). CONCLUSIONS: During pacing-induced AF in humans, the RA is activated by one or multiple wavelets propagating in different directions. Three types of RA activation during AF were identified. From type I to type III, the frequency and irregularity of AF increased, and the incidence of continuous electrical activity and reentry became higher. These various types of AF in humans appear to be characterized by different numbers and dimensions of the intra-atrial reentrant circuits.

Adult↗
PubMed1993

Electrophysiologic effects of ORG 30701 (dopropidil) on rabbit ventricular myocardium.

The electrophysiologic effects of ORG 30701 (1-8 x 10(-6) M) were tested in a thin, two-dimensional sheet of ventricular myocardium. Special attention was paid to a possible promotion of reentrant excitation. The drug did not increase the degree of inhomogeneity of conduction and because of the marked effect on refractoriness prevent fast rates (either spontaneously or driven). If the extracellular potassium concentration was lowered (from 5.6 to 2.0 mM), the enhancement of refractoriness by the drug was more marked. The changes in refractoriness do not appear to be based on lengthening of the repolarization of the action potential, but rather on post-repolarization refractoriness; therefore, the occurrence of triggered activity (early afterdepolarizations) is not anticipated. ORG 30701 is a cardioactive drug that because of its calcium antagonistic action acts as an antianginal drug and, in addition, exhibits antiarrhythmic properties.

Animals↗
PubMed1992

Sinus node automaticity during atrial fibrillation in isolated rabbit hearts.

BACKGROUND: It is still unclear what role the sinus node may play in the genesis or perpetuation of atrial fibrillation. Therefore, we studied the electrical activity in different regions of the sinus node during atrial fibrillation. METHODS AND RESULTS: In Langendorff-perfused rabbit hearts, paroxysms of atrial fibrillation were induced by burst pacing. Standard microelectrode techniques were used to record transmembrane potentials from different regions of the sinus node. We found that during atrial fibrillation, a high degree (5:1) of sinoatrial entrance block was present that protected the pacemaker fibers in the center of the sinus node against the high rate of fibrillatory impulses. As a result, the true pacemaker fibers in the center of the node were activated with only a slightly higher average rate than during sinus rhythm. Spontaneous diastolic depolarization was still present but was modulated by electrotonic depolarizations due to intranodal conduction block of atrial fibrillatory impulses. Incidentally, phase 4 depolarization resulted in the generation of spontaneous action potentials in the sinus node. However, the high activation rate in the sinoatrial border during atrial fibrillation prevented these spontaneous impulses to exit from the sinus node. Because of the minimal degree of sinus node overdrive suppression (9%) and the presence of concealed automaticity during atrial fibrillation, spontaneous termination of atrial fibrillation was promptly followed by resumption of normal sinus rhythm. CONCLUSIONS: During atrial fibrillation, sinus automaticity still is present in the center of the sinus node and hardly overdrive suppressed due to a high degree of sinoatrial entrance block.

Animals↗
PubMed1991

Reentrant excitation around a fixed obstacle in uniform anisotropic ventricular myocardium.

BACKGROUND: The purpose of this study was to investigate the role of tissue anisotropy and dispersion of refractoriness on initiation of reentrant ventricular tachycardia (VT). METHODS AND RESULTS: A ring of perfused uniform anisotropic ventricular epicardium in Langendorff-perfused rabbit hearts was created by an endocardial freezing technique. High-resolution mapping (248 channels) was used to analyze epicardial activation of the left ventricle. One to three premature beats were induced at a total of 272 points in 17 experiments (16 different points around the ring in each experiment). Reentrant VT could be initiated at 43 of the 272 points tested. The cycle length of VT was stable and ranged from 128 to 198 msec (mean, 161 +/- 19 msec). Correlation between conduction velocity and the angle between the circulating activation wave and epicardial fiber orientation showed that in segments of the ring where conduction was perpendicular to the fiber axis, mean conduction velocity was 25 +/- 5 cm/sec compared with 60 +/- 7 cm/sec when conduction was parallel to the fiber orientation. Analysis of the site of unidirectional conduction block showed that in 41 of 43 cases, block occurred while the impulse was propagating parallel to the fiber orientation. Measurement of the refractory periods at either side of the line of unidirectional block showed that only in 12 of 43 cases did block occur while the impulse was propagating into an area with a longer (more than 10 msec) refractory period. CONCLUSIONS: In uniform anisotropic ventricular myocardium, reentrant VT is initiated because lowering the stimulating efficacy of the depolarization wave by premature beats leads to preferential conduction block parallel to the fiber orientation.

Animals↗
PubMed1990

Ventricular response during irregular atrial pacing and atrial fibrillation.

In the isolated rabbit heart the ventricular response during irregular atrial pacing and atrial fibrillation was studied. Irregular pacing was performed by an algorithm that generated a population of random stimuli within a chosen range of intervals. During incremental regular pacing atrioventricular (AV) Wenckebach conduction occurred at an atrial cycle length of 164 +/- 24 ms (n = 11). During irregular atrial pacing with a variation of 20, 60, and 100 ms second-degree AV block developed at average cycle lengths of 171, 182, and 198 ms, respectively. In contrast, the pacing interval resulting in stable 2:1 AV block was shortened from 131 ms to 120 and 112 ms during irregular pacing with 20- and 60-ms variation. During pacing with 100-ms variation stable 2:1 AV block no longer occurred. Addition of acetylcholine (0.25-0.75 X 10(-6) M) increased the maximal degree of stable AV block during regular pacing. During irregular pacing, however, stable AV block disappeared. Instead, during second-degree AV block a monophasic inverse relationship (r = -1.5 +/- 1.7) between atrial and ventricular rates appeared as a result of an increased occurrence of concealed conduction in the AV junction. Also during electrically induced atrial fibrillation an inverse relationship was found between the atrial and ventricular rate. We conclude that the ventricular rate during atrial fibrillation is not only determined by the properties of the AV node but also by the rate and irregularity of the fibrillatory process.

Acetylcholine↗
PubMed1990

Quantification of spatial inhomogeneity in conduction and initiation of reentrant atrial arrhythmias.

In isolated superfused left atria of the rabbit, inhomogeneity in conduction was quantified using the activation times measured with a high-density mapping system. At each recording site, the maximal difference with neighboring activation times (i.e., phase difference) was calculated. Local phase differences were plotted in a phase map, revealing the spatial distribution of inhomogeneities in conduction, and from each map a total index of inhomogeneity was calculated. During slow pacing (2 Hz) local differences in conduction velocity, depending on the direction of propagation, were found already. Inhomogeneity in conduction increased significantly during single early premature beats (inhomogeneity index increased from 2.3 to 3.1; P less than 0.001). The application of multiple premature beats further increased inhomogeneity in conduction, whereas rapid pacing induced the highest level of inhomogeneity (inhomogeneity index 5.3; P less than 0.001). An analysis of the spatial distribution of maximal phase differences revealed that during premature beats inhomogeneities in conduction were limited to an area of 6 mm around the point of origin of the premature impulse, whereas during rapid pacing inhomogeneities in conduction were found throughout the whole preparation. Phase maps constructed during the initiation of reentrant tachyarrhythmias showed that reentry occurred at sites with the highest phase differences. Quantification of spatial inhomogeneities in conduction is a useful tool to evaluate the vulnerability of the myocardial substrate for reentrant arrhythmias.

Animals↗
PubMed1989

Effects of verapamil, diltiazem and disopyramide on sinus function: a comparison with bepridil.

Cardiac drugs known to affect sinus function mostly exhibit negative chronotropic activity. However, impulse conduction within the sinus node can also be influenced. Recently we studied the direct effects of bepridil on rabbit sinus function. It appeared that sinoatrial impulse conduction was depressed markedly with drug concentrations that did not affect sinus automaticity. In the present study the direct effects of verapamil, diltiazem and disopyramide on rabbit sinus function and atrial conduction properties were studied. Verapamil (8.8 x 10(-8) M) reduced the sinoatrial impulse conduction velocity by 35% and prolonged sinoatrial refractoriness by 36%. On the other hand, the sinus rate and atrial conduction parameters were hardly affected. Diltiazem (5 x 10(-6) M) exerted similar actions on the sinoatrial impulse conduction velocity and caused a simultaneous reduction in the sinus rate of 48%. Atrial conduction remained unaffected. Disopyramide (5 x 10(-5) M) depressed both the atrial and nodal conduction properties markedly, whereas the sinus rate was reduced moderately, by almost 20%. Thus, verapamil, diltiazem and disopyramide act differently on sinus function and atrial conduction, whereby the predominant effect of verapamil and diltiazem on sinoatrial conduction properties favours the occurrence of a sinus exit block.

Animals↗