Monophasic Action Potential Catheter Research Articles

Effects of adenosine on local stimulus-response latency and induction of atrial fibrillation by premature stimuli.

Premature atrial stimuli delivered during the relative refractory or "vulnerable" period exhibit increased local stimulus-response latency and may occasionally induce atrial arrhythmias. The use of adenosine to treat supraventricular tachycardias may also provoke atrial arrhythmias. In this study we investigated the effects of adenosine on the latency of premature complexes in relation to repolarization and induction of atrial arrhythmias in 14 patients without structural heart disease. A monophasic action potential catheter was used for recording in the right atrium and introducing premature stimuli (S2) at twice diastolic threshold after eight paced (S1) complexes. At short coupling intervals, S2 latency increased relative to S1 latency. S2 was delivered repeatedly at a fixed coupling interval (producing maximal local response latency) and adenosine (6 mg) was given intravenously. Adenosine decreased S2 latency significantly (23+/-5 to 11+/-3 ms, P<0.01), to values similar to S, latency. However, despite the decrease in S2 latency, the combination of adenosine and S2 more often resulted in transient atrial arrhythmias (11 of 14 patients vs 2 of 14 patients without adenosine, P<0.05). Adenosine had no effect on S, latency (9+/-2 vs. 9+/-2 ms) but decreased monophasic action potential duration from 202+/-37 to 158+/-38 ms (P<0.01). Adenosine was also given to 10 patients with S2 introduced at a coupling interval 40-50 ms less than the baseline effective refractory period. This resulted in a decrease in atrial refractoriness and capture of S2 in all cases. Latency for S2 was significantly greater than Si latency (21+/-12 vs. 9+/-2 ms, P<0.01) and transient atrial arrhythmias were induced in 9 of 10 patients. We conclude that for a given S2 coupling interval, adenosine decreases local stimulus-response latency but increases atrial vulnerability to transient atrial arrhythmias. Decreased latency may be related to a shift in the zone of relative refractoriness associated with an adenosine-mediated decrease in monophasic action potential duration. Induction of atrial arrhythmias in the presence of adenosine occurs independently of increased latency and is therefore not dependent on S2 falling within the relative refractory period at the site of stimulation.

Electrical Remodeling in Human Atrial Fibrillation Influences Post-Cardioversion Atrial Mechanical Dysfunction and Early Relapse

Background:It has been demonstrated that atrial fibrillation (AF induces shortening of atrial refractory period, which was known as electrical remodeling, resulting in an increased vulnerability for reinduction of AF. Atrial mechanical function does not restore immediately after cardioversion, atrial stunning exists during this period in chronic AF. We hypothesized that electrical remodeling in chronic AF determines the atrial mechanical dysfu- nction after cardioversion and early relapse of AF. Method:Patients with chronic atrial fibrillation (CAF, n =17 who have been done transthoracic DC cardioversion, paroxysmal AF (PAF, n=11, and normal control (CON, n=5 were studied. Using MAP (monophasic action potential catheter, MAP duration 90% repolari- zition (MAPD90 and atrial effective refractory period (AERP were measured at 9 different sites in the right atrium. Magnitude of dispersion of these parameters was calculated by SD 2 (variance. Assessment of mitral inflow variables (peak velosities of A, E wave, and A/E ratio was performed at immediately after DC cardio- version, 1st day, 3rd days, 1 week, 4 weeks and 8 weeks by transthoracic pulse wave Doppler. Result:MA- PD90 significantly shortened in patients with CAF (235.4±38.1 ms compared with that of PAF (270.9±45.2 ms and control (274.0±51.9 ms, whereas AERP did not show significant differences. The magnitude of dispersion of MAPD90 and AERP was not different among the groups. AF recurred in 9 of 17 (53% patients with CAF particularly in whom A/E ratio was 0.4(250.9±52.9 ms, p=0.05. Conclusion:Electrical remodeling in chronic human AF characterized by shortening of monophasic action potential duration is one of the main factors that determines the atrial mechanical dysfunction after cardioversion and early relapse into AF. (Korean Circulation J 1999;29(8 :788-795

Induction of ventricular fibrillation by T wave shocks: observations from monophasic action potential recordings.

Shocks given during the vulnerable period of cardiac repolarization may induce ventricular fibrillation (VF). However, the relationship of the vulnerable period and the monophasic action potential (MAP) has not yet been reported in humans. The purpose of this study was, therefore, to determine how the monophasic action potential recorded from the right ventricle correlates with inducibility of VF using T wave shocks during ventricular pacing. Eleven patients undergoing implantable cardioverter defibrillator (ICD) implantation had a MAP catheter positioned in the right ventricle (RV). The local monophasic action potential duration at 90% repolarization (MAP90) duration was measured during pacing at 400 ms. VF induction was attempted by pacing at 400 ms for 10 cycles and then giving a 1.0 joule monophasic T wave shock at varying coupling intervals (CI) to the last paced stimulus. The maximum and minimum CI that induced VF were determined and mapped in relation to the MAP90 recording. The average paced MAP duration was 275 +/- 20 ms. The minimum and maximum CI to induce VF were 255 +/- 24 ms and 325 +/- 36 ms respectively. This ranged from 93% to 118% of the MAP90 duration but because of delay in conduction time to the MAP catheter, shocks that induced ventricular fibrillation occurred between 74% and 99% of local repolarization time. VF is inducible with low energy T wave shocks falling during the last 25% of the right ventricular MAP90 recording. This corresponds with VF initiation during phase III repolarization.

Effects of antiarrhythmic drugs on the monophasic action potential of the canine isolated, blood-perfused ventricular septum preparation.

The present study was designed to combine the monophasic action potential (MAP) recording technique with a well-established canine isolated, blood-perfused ventricular septum preparation for examining, simultaneously, electrical and mechanical drug-induced changes. A MAP catheter was positioned onto the base of a papillary muscle for recording the local MAP, using a manual micromanipulator together with a commercially available catheter sheath to keep the optimal contact pressure against the ventricular wall. The catheter sheath was filled with saline to eliminate the background electrical noise. Tetrodotoxin, disopyramide, lidocaine, and verapamil were used to clarify the potential utility of the preparation. Tetrodotoxin and lidocaine shortened the MAP duration, while disopyramide prolonged it. Verapamil slightly shortened the MAP duration but not significantly. Each drug showed negative inotropic and coronary vasodilator effects. Sodium channel blockers slowed intraventricular conduction and decreased the maximum upstroke velocity of MAP, while verapamil showed no effects. These results suggest that utilization of the blood-perfused ventricular septum preparation together with MAP recording will become a valuable model for evaluating drugs with multiple sites of action on cardiac muscles.

Optimizing the Geometry of Implantable Leads for Recording the Monophasic Action Potential with Fractally Coated Electrodes

This study investigates the influence of various lead geometry on intracardial signals like the monophasic action potential (MAP) to optimize the geometry of implantable MAP leads. The experimental results were compared with a field theoretical approach to the origin of MAP from the transmembrane potential (TAP). During the experiments several lead geometries (tip surface: 1.3 to 12 mm2; tip-ring distance: 0.8 mm to 25 cm; ring surface: 1.8 mm2 to 40 mm2) were investigated in endo- and epicardial positions in 12 dogs (17 +/- 9 kg). The electrodes were fixed passively (tines) or actively (screws). MAP was recorded during several interventions and correlated with MAP measured using an Ag-AgCl MAP catheter. The experimental results showed that small tips provided high MAP amplitudes with less pressure. No difference was observed using active and passive fixations. A tip-ring distance smaller than 5 mm with a ring surface smaller than the tip (< 5 mm2) avoided artifacts in the repolarization course. For the theoretical approach the quasistatic, anisotropic bidomain model was calculated in small unity volumes Vi where the TAP phi mi was constant and represented by the current density Ji. Two solutions for electrode positions at and outside the heart were achieved. By superposition of each solution phi ei the summed potential at the electrode position was calculated. The theoretical findings show in good correlation with the experimental results that a larger distance than 10 mm leads to distortions in repolarization course by signals proportional to phi out.

Pinacidil's Effects on Defibrillation Outcomes: Role of Increased Potassium Conductance Via the K(ATP) Channel.

BACKGROUND: It has been shown that the inhibition of potassium ion conductance decreases defibrillation threshold. We postulated that if potassium conductance is a primary mechanism affecting defibrillation threshold values, then increasing potassium ion conductance will increase defibrillation values. The primary objective of this study was to determine if the ATP-dependent potassium (K(ATP)) channel opener pinacidil would increase defibrillation threshold values. The second objective was to prove that the observed changes were due to potassium conductance by using the K(ATP) inhibitor, glyburide, to reverse the electrophysiologic actions of pinacidil. The third objective was to determine if the electrophysiology action sof pinacidil correlate with changes in defibrillation threshold value. METHODS AND RESULTS: Domestic farm swine (n = 14) were anesthetized and intubated. Subsequently, they were instrumented with monophasic action potential catheters and epicardial defibrillation patches. Defibrillation threshold values, action potential duration, effective refractory period, and ventricular fibrillation cycle length were determined at baseline and during treatment phase 1 and treatment phase 2. Pigs were randomized into 2 groups: group 1 (n = 6) received D(5)W in treatment phase one followed by D(5)W in treatment phase 2 and group 2 (n = 8) received pinacidil in treatment phase one followed by the addition of glyburide in treatment phase two. DFT(ED50) did not change at baseline, treatment phase one or treatment phase two for group 1 (10.5 +/- 2, 11.1 +/- 1.7, 10.5 +/- 1.0 J) or for group 2 (10.1 +/- 2.2, 11.4 +/- 4.2, 11.4 +/- 3.0 J). Electrophysiologic parameters )QRS, effective refractory period, action potential duration(90), and ventricular fibrillation cycle length) were not significantly changed from baseline in group 1. In contrast, effective refractory period, action potential duration(90), and ventricular fibrillation cycle length significantly decreased at all recorded sites after the administration of pinacidil in group 2 (range of 7-13%, 6-9%, and 12-17%, respectively). However, pinacidil did not change the basal level of dispersion in effective refractory period, action potential duration, and ventricular fibrillation cycle length during paced rhythm or ventricular fibrillation. Glyburide reversed pinacidil's electrophysiologic actions. CONCLUSIONS: Pinacidil does not alter defibrillation threshold, but it reduces effective refractory period, action potential duration, and ventricular fibrillation cycle length and does not increase electrical heterogeneity. Therefore, changes in potassium channel conductance as well as shortening repolarization are unlikely primary mechanisms for elevating defibrillation threshold.

Combining Monophasic Action Potential Recordings With Pacing to Demonstrate Delayed Afterdepolarizations and Triggered Arrhythmias in the Intact Heart

In the intact heart, methodological difficulties hamper the direct visualization of delayed afterdepolarizations (DADs) responsible for triggered arrhythmias. Therefore, we tested the hypothesis that a combination of pacing and the recording of a monophasic action potential (MAP) could facilitate the recognition of ouabain-induced DADs and triggered arrhythmias by demonstrating an increase in the diastolic baseline slope (dV/dT) of the MAP recording at the end of a pacing train. In anesthetized dogs with chronic atrioventricular block, a right ventricular endocardial MAP was recorded during (1) control (n = 11), (2) 15 to 45 minutes after administration of ouabain (45 +/- 10 micrograms/kg, n = 11), (3) 10 minutes after administration of lidocaine (3 mg/kg, n = 5), and (4) during lidocaine washout (n = 3). Pacing was performed with the MAP catheter. Also, the protocol was performed in 3 dogs with conducted sinus rhythm during control and ouabain circumstances. During control, the slope value was 2 +/- 2 mV/s (mean +/- SD), the incidence of DADs after the stimulation train was 6%, and no ventricular tachycardias (VTs) were induced in dogs with atrioventricular block. During ouabain administration, the slope and DAD incidences increased to, respectively, 26 +/- 14 mV/s and 74% (P < .05 for both). VTs were induced frequently. Lidocaine prevented VT induction by decreasing the slope and the incidence of DADs. This effect disappeared after lidocaine washout. During conducted sinus rhythm, similar results were found. By combining pacing and MAP recordings, the diastolic slope observed on MAP recordings in ouabain-intoxicated hearts can be used as a marker for DADs and triggered arrhythmias. This finding may be helpful in identifying triggered activity in the intact heart.

767-5 Differential Effects of Lidocaine on Defibrillation Threshold with Monophasic and Biphasic Waveforms

Antiarrhythmic drugs can interfere with electrical defibrillation using monophasic non-sequential shocks (MS). It is unknown if these drugs affect the efficacy of biphasic defibrillation shocks (BS). Since MS and BS waveforms can exhibit disparate effects on myocardial excitability and refractoriness (properties which may influence defibrillation efficacy), it is possible that antiarrhythmic drugs, such as lidocaine (L), will affect defibrillation threshold (DFT) of one waveform differently than another. We studied 25 pentobarbital anesthetized farm swine who had endocardial pacing and monophasic action potential catheters placed into the right ventricle. Pacing was used to induced sustained ventricular fibrillation (5-8 s) which was followed by defibrillation via epicardial electrodes. Each pig was assigned to one of four treatment groups; 1) MS + D5W (n = 7), 2) MS + L (n = 7) 3) BS + D5W (n = 5), or 4) BS + L (n = 7). DFTs were measured at baseline (Base) and subsequently during treatment (D5W or L). DFT values (joules) predicting 50% success at baseline were: + D5W = 7.34 ± 1.59, MS + L= 7.11 ± 1.5, BS + D5W = 5.28 ± 1.55 and BS + L = 3.86 ± 1.2. The figure depictsDownload : Download high-res image (130KB)Download : Download full-size imagetreatment DFT values as percent of baseline. In the MS groups, the change in DFT from Base to L was 92 ± 28% vs the change from Base to D5W of 0.6 ± 29% (p &lt; 0.0001). In the BS groups, however, the change in DFT from Base to L was similar to the change from Base to D5W (-6.7 ± 15 vs -29 ± 17%, p = 0.08). Compared to D5W, L increased DFT in the biphasic group by a magnitude that was ¼ that seen in the monophasic group. Clinical Implications: The effect of antiarrhythmic drugs on DFT (especially increased DFT values) may be less of a concern when using implantable devices employing biphasic waveforms.

Effects of adenosine on atrial refractoriness and arrhythmias

Transient atrial fibrillation is sometimes observed following adenosine administration and adenosine is known to shorten atrial action potential duration and refractory period. This study was designed to characterise the dose-response relationship of adenosine on these variables relative to arrhythmia induction with single atrial premature stimuli. The effects of adenosine during sustained atrial flutter were also determined. Intravenous bolus doses of adenosine were given to pentobarbitone anaesthetised dogs following cervical vagotomy and autonomic blockade with atropine and nadolol. Monophasic action potential catheter recordings were obtained from the right atrium and a programmable stimulator was used for pacing. Placebo had no effect on monophasic action potential duration (MAPD) or atrial effective refractory period (ERP) and no arrhythmias were observed. Adenosine (0.1-1.0 mg.kg-1) produced dose related decreases in MAPD and ERP and transient atrial fibrillation (5-122 s) was repeatedly and reproducibly induced in 12 dogs. In six dogs, intravenous dipyridamole (0.25 mg.kg-1) enhanced the effects of adenosine on MAPD and ERP and increased the incidence of atrial fibrillation. In another six dogs, 8-sulphophenyltheophylline (5.0 mg.kg-1, intravenously) markedly blunted the effects of adenosine, and atrial fibrillation could no longer be induced by premature stimuli. In a separate series of experiments the effects of adenosine were evaluated in seven dogs in which sustained atrial flutter could reproducibly be induced by rapid atrial pacing. Administration of placebo never caused termination of the arrhythmia, whereas intravenous boluses of adenosine (0.1-1.0 mg.kg-1) decreased and produced variation in atrial flutter cycle length, and then terminated the arrhythmia in all cases. These effects of adenosine were also enhanced by dipyridamole and antagonised by 8-sulphophenyltheophylline. Adenosine produces a receptor mediated shortening of monophasic action potential duration and refractoriness which increases vulnerability to transient atrial arrhythmias. During sustained atrial flutter, these effects may also contribute to destabilisation and termination of the arrhythmia.

Prostaglandin modulation of early afterdepolarizations and ventricular tachyarrhythmias induced by cesium chloride combined with efferent cardiac sympathetic stimulation in dogs

Prostaglandins inhibit efferent cardiac sympathetic nerve effects by acting at presynaptic sites and may act to suppress some arrhythmias. In the present study, the effects of intravenous administration of prostacyclin (PGI2) and prostaglandin E2(PGE2) on early afterdepolarization and ventricular tachycardia induced by cesium chloride (0.5 mmol/liter per kg body weight intravenously) combined with stimulation of bilateral ansae subclaviae in anesthetized dogs were examined. The right atrium was paced at a constant cycle length of 600 ms. A left ventricular endocardia! monophasic action potential catheter was used to detect early afterdepolarizations.Prostacyclin (0.2 μg/kg per min) reduced the amplitude of the early afterdepolarizations (39.2 ± 8.4% of the monophasic action potential amplitude during control study to 28.7 ± 5.5%, n = 10; p < 0.001) as well as the prevalence of ventricular tachycardia (11 of 14 dogs during control study to 5 of 14 dogs; p = 0.031). Prostaglandin E2(0.2 to 0.6 μg/kg per min) did not significantly reduce the early afterdepolarization amplitude (34.7 ± 8.9% to 25.1 ± 10.7%, n = 8; p = 0.085) or the prevalence of ventricular tachycardia (8 of 10 versus 6 of 10 dogs; p = 0.50).Alpha- and beta-adrenoceptor blockade with combined intravenous administration of propranolol (0.5 mg/kg) and phentolamine (0.3 mg/kg) decreased the amplitude of the early afterdepolarizations induced by cesium chloride and bilateral ansae subclaviae stimulation from 38.6 ± 11.2% to 18.8 ± 3.3% (n = 6; p = 0.005). Additional administration of PGI2further reduced the early afterdepolarization amplitude from 18.8 ± 3.3% to 9.8 ± 4.8% (n = 6; p = 0.001). In control dogs, the amplitude of the early afterdepolarizations and the prevalence of ventricular tachycardia did not change over time with repeated doses of cesium chloride and bilateral ansae subclaviae stimulation.Thus, exogenous PGI2suppresses early afterdepolarization amplitude and reduces the prevalence of ventricular tachycardia induced by cesium chloride combined with bilateral ansae subclaviae stimulation in dogs, even after alpha- and beta-adrenoceptor blockade. A direct action on the cesium chloride-induced repolarization abnormality, unrelated or in addition to sympathetic neural modulation, is likely to be involved in the PGI2effect.

A new single catheter technique for simultaneous measurement of action potential duration and refractory period in vivo

In vivo correlations of action potential duration measured by a monophasic action potential catheter and effective refractory period measured by a separate pacing catheter have been poor, probably because of the known variability of both action potential duration and effective refractory period between different ventricular sites. In this study, a new quadripolar contact electrode catheter designed for simultaneous pacing and monophasic action potential recording at closely adjacent sites (2 mm separation between recording electrodes and pacing electrodes) was tested in five closed chest dogs and four patients. Dog studies: Pacing thresholds were extremely low, ranging from 0.02 to 0.25 mA (mean +/- SD 0.099 +/- 0.051, n = 36) and were stable over time (less than 20% increase during 1 h of continuous pacing). Because of the close proximity of pacing and recording electrodes, the pacing artifact nearly coincided with the monophasic action potential upstroke. Because of the low pacing threshold, however, pacing artifacts were small (33 +/- 17% of the monophasic action potential amplitude at twice diastolic threshold strength) and did not affect the duration or configuration of the simultaneously recorded monophasic action potential. The short stimulus response time and the undisturbed monophasic action potential signal fidelity during pacing allowed precise simultaneous measurements of action potential duration and effective refractory period at the same endocardial site.(ABSTRACT TRUNCATED AT 250 WORDS)

Persistent Functional Atrioventricular Block in Two Patients with Prolonged QT Intervals; Elucidation of the Mechanism of Block

This article describes two infants with prolonged QT interval and intermittent second-degree atrioventricular block. An asymptomatic 14-month-old child with persistent 2:1 atrioventricular conduction since birth underwent electrophysiology study including measurements with a contact monophasic action potential catheter. During 2:1 conduction, atrioventricular block occurred distal to the site of the His-bundle recording. Monophasic action potential duration was closely related to prior RR intervals. Single premature atrial or ventricular depolarizations during 1:1 conduction followed by a pause, lead to monophasic action potential prolongation and subsequent 2:1 atrioventricular conduction, which was perpetuated by the resulting long RR intervals. Paired premature ventricular contractions or short bursts of ventricular pacing elicited monophasic action potential shortening and subsequent 1:1 atrioventricular conduction that was perpetuated by the resulting short RR intervals. A second infant presented at birth with a prolonged QT interval, ventricular tachycardia, and episodes of second-degree atrioventricular block with persistent 2:1 atrioventricular conduction. The atrioventricular block was repeatedly elicited by single premature ventricular contractions and terminated by ventricular couplets. We conclude that the atrioventricular block in both patients is functional in nature and results from the interrelationships between ventricular rate, action potential duration, and His-Purkinje system refractoriness.