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  • 1
    Electronic Resource
    Electronic Resource
    The Dynamic Behavior of the Diastolic Slope of Monophasic Action Potential Can be Related to the Occurrence and Maintenance of Delayed Afterdepolarization Dependent Arrhythmias (1999)
    Oxford, UK : Blackwell Publishing Ltd
    Pacing and clinical electrophysiology 22 (1999), S. 0 
    Details
    ISSN: 1540-8159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: We have described the value of the diastolic slope of the MAP recording at the end of a pacing train as a qualifying marker for the induction of delayed afterdepolarization (DAD) dependent arrhythmias. In the present study (1) the behavior of the slope at different time points during a pacing train was quantified and related to the arrhythmogenic outcome (group A) and (2) termination of DAD dependent VT was related to changes in the slope steepness (group B). In dogs with chronic complete AV block, a MAP was recorded during (1) ventricular pacing, before and after ouabain administration (group A) and (2) 6 spontaneous and 6 lidocaine induced VT terminations (group B). During control (group A), the slope at the end of pacing train was 5 ± 3 mV/s (mean ± SD), independent of the pacing duration. During ouabain, this increased to 20 ± 15 mV/s (P 〈 0.05), varying with the duration of pacing. The slope was steeper after pacing for 4 seconds, compared to 20 seconds (26 ± 12 mV/s vs 16 ± 13 mV/s, P 〈 0.05) which corresponded with more frequent VT induction. In spontaneously terminating VTs (group B), CL increased from 353 ± 54 ms at the start to 434 ± 78 ms (P 〈 0.05) before VT termination. This corresponded with a decreasing steepness of the slope from 19 ± 10 mV/s to 6 ± 5 mV/s (P 〈 0.05). In lidocaine induced VT termination, the CL and the steepness of the slope showed an identical behavior. There is a dynamic variation in the steepness of the diastolic slope during pacing, which depends on the duration of pacing and predicts arrhythmogenic outcome. Furthermore, a decrease in steepness of the slope during DAD dependent VT can be used to predict VT termination.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1540-8159.1999.tb00299.x
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  • 2
    Electronic Resource
    Electronic Resource
    Rate Dependent Effects of Procainamide on the Threshold Current for Pacing in the Setting of Postrepolarization Refractoriness in Dogs (1999)
    Oxford, UK : Blackwell Publishing Ltd
    Pacing and clinical electrophysiology 22 (1999), S. 0 
    Details
    ISSN: 1540-8159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Normally, ventricular APD exceeds the VERP. However, under specific circumstances this relation may change and can become inverse. This phenomenon of postrepolarization refractoriness may be caused by a decrease in excitability. The threshold current (TC) for pacing has never been quantified as a possible explanation for these observations. Using a MAP pacing catheter in the right ventricular apex, the rate dependent behavior of TC, VERP, and APD before and after procainamide (dose 20 mg/kg in 10 min + 5 mg/min infusion) was determined in 17 dogs with chronic complete AV block. Initially, TC was determined with 0.1 mA accuracy. Using a pacing current of at least twice TC, VERP and APD showed a similar, rate dependent shortening for PCLs 800, 575, and 350 ms. Procainamide treatment led to an equal, rate independent VERP and APD increase: no post repolarization refractoriness. Subsequently, accuracy for TC determination was increased to 0.01 mA. Comparing PCLs 800 and 250 ms, TC doubled from 0.05 ± 0.01 to 0.10 ± 0.09 mA during control and almost tripled from 0.06 ± 0.02 to 0.17 ± 0.10 mA (P 〈 0.05) after procainamide. Using a fixed pacing current of exactly twice TC found at 800 ms PCL during control, VERP exceeded APD after procainamide treatment at 300 and 250 ms PCL: postrepolarization refractoriness. Increasing the pacing current to twice the rate dependent TC, the relation between VERP and APD normalized: no postrepolarization refractoriness. We conclude that after procainamide, rate dependent TC increase is of major importance for the phenomenon of postrepolarization refractoriness.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1540-8159.1999.tb00441.x
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  • 3
    Electronic Resource
    Electronic Resource
    Steady-State and Dynamic Behavior of Ventricular Repolarization and Refractoriness in the Dog: The Effect of Multiple Cycle Length Changes and d-Sotalol Administration (1998)
    Oxford, UK : Blackwell Publishing Ltd
    Pacing and clinical electrophysiology 21 (1998), S. 0 
    Details
    ISSN: 1540-8159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: In anesthetized dogs with chronic, complete AV block we studied the characteristics of ventricular repolar-ization and refractoriness. Therefore, we determined: (1) steady-state values of ventricular effective refractory period (VERP), action potential duration (APD), and stimulus T interval (STI) before and after d-sotalol treatment at various pacing cycle lengths (PCLs); and (2) the dynamics of VERP, APD, and STI before and after d-sotalol treatment after the abrupt PCL decreases. VEHP, APD, and STI showed a normal frequency dependency. All three parameters increased significantly after d-sotalol administration. During steady-state and dynamic measurements, STI was always longer than APD and APD was always longer than VERP in an individual animal, irrespective of PCL and conditions. Standard deviations of steady-state and dynamic values indicated a considerable interindividual variation. However, the dynamics of VERP, APD, and STI after an abrupt decrease in PCL were highly correlated (linear regression analysis: r2± 0.93). The best mathematical model to describe these dynamics was a bi-exponential model (r2± 0.98) with a very short first and a much longer second time constant. We found that there was a very consistent relation between VERP, APD, and STI, not only during steady-state but also in the dynamic situation after various abrupt PCL decreases. This relation does not change after the administration ofd-so-talol. Therefore, STI could be used to predict steady-state and dynamic values of VERP and APD. Since STI can be made available online in implantable pacing systems this could lead to the development of new features in these devices.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1540-8159.1998.tb00277.x
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  • 4
    Electronic Resource
    Electronic Resource
    Mechanism-Specific Antiarrhythmic Effects of the Potassium Channel Activator Levcromakalim Against Repolarization-Dependent Tachycardias (1994)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of cardiovascular electrophysiology 5 (1994), S. 0 
    Details
    ISSN: 1540-8167
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Mechanism-Specific Action of Levcromakalim. Introduction: The hypothesis that levcromakalim. a potassium channel (IK-ATP.) activator with antihypertensive properties, has a mechanism-specific antiarrhythmic action against repolarization-dependent ventricular tachycardias (VTs) was tested in dogs. Methods and Results: A low dose of leveromakalim (0.01 mg/kg) was selected, which decreased blood pressure by 25% but had almost no electrophysiologic effect on AV nodal or ventricular conduction or effective refractory period. In dogs with chronic AV block, the antiarrhythmic action of this dose of levcromakalim was evaluated in three models of abnormal impulse formation: (I) dsotalol (2 mg/kg) induced torsades de pointes VT, initiated by early afterdepolarizations (EADs). (2) sustained ouabain-induced VTs, which are dependent on delayed after depolarizations (DADs), and (3) VT occurring 24 hours after left anterior descending coronary artery occlusion, which are likely based on abnormal automaticity. Levcromakalim abolished d-sotalol induced U waves, ventricular ectopic beats, and self-terminating bouts of torsades de pointes. Induction of torsades de pointes by pacing was also completely prevented. The cycle length of the idioventricular rhythm, which was lengthened after d-sotalol from 1490 ± 515 to 1700 ± 610 msec (P 〈 0.05), remained similar after levcromakalim (1655 ± 580 msec). The QT(U) duration, which was increased after d-sotalol from 410 ± 55 to 550 ± 40 msec (P 〈 0.05), normalized to 405 ± 70 msec (P 〈 0.05). Lcvcromakulim did not suppress but rather enhanced ouabain-induced VT by decreasing the cycle length slightly from 315 ± 35 to 290 ± 35 msec (P 〈 0.05). Pretreatment with a beta Mocker prevented this acceleration in rate. Finally, levcromakalim had no effect on VT 24 hours after infarction. Conclusion: A low dose of levcromakalim has specific antiarrhythmic properties against repolarization-dependent arrhythmias, but it does not affect VTs based on other mechanisms of abnormal impulse formation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1540-8167.1994.tb01196.x
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  • 5
    Electronic Resource
    Electronic Resource
    The Effect of Flunarizine and Ryanodine on Acquired Torsades de Pointes Arrhythmias in the Intact Canine Heart (1995)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of cardiovascular electrophysiology 6 (1995), S. 0 
    Details
    ISSN: 1540-8167
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Flunarizine and Ryanodine in Acquired TdP. Introduction: Ryanodine, a specific blocker of the Ca2+ release channel of the sarcoplasmic reticulum, and flunarizine, a[Ca2+], overload blocker, possess antiarrhythmic effects against delayed after depolarizations (DADs) and DAD-dependent arrhythmias. In vitro controversy exists about their effect on early after depolarizations (EADs): no effect was reported on cesium-induced EADs, while ryanodine did prevent EADs induced by isoproterenol. To study the possible role of intracellular Ca2+ overload in acquired EAD-dependent torsades de pointes (TdP) arrhythmias, we tested the effects of flunarizine and ryanodine in our animal model of TdP. Methods and Results: Anaesthetized dogs with chronic AV block received d-sotalol or almokalant followed by pacing. A subset of dogs with reproducible TdP (≥ 3 times) were selected to receive flunarizine (2 mg/kg per 2 min) or ryanodine (10 μg/kg per 10 min). After dsotalol, TdP was induced at a mean cycle length of the idioventricular rhythm (CL-IVR) of 2070 ± 635 msec and a QT(U) interval of 535 ± 65 msec. Induction of TdP was prevented by flunarizine in all experiments (8/8): electrophysiologically this was associated with a decrease in CL-IVR, QT(U), and QTc interval (390 ± 100 to 320 ± 45, P 〈 0.05). Ryanodine prevented TdP induction in 4 of 5 experiments and decreased the CL-IVR, QT(U), and the QTc interval from 385 ± 75 to 320 ± 20 msec (P 〈 0.05). Both drugs also suppressed the almokalant-induced EADs and related ectopic activity. This antiarrhythmic action corresponded with the inability to reinduce TdP by pacing. Conclusions: Blockade of the Ca2+ release channel of the sarcoplasmic reticulum by ryanodine or the reduction of [Ca2+] overload by flunarizine prevents induction of EAD-dependent acquired TdP arrhythmias, suggesting a role for [Ca2+]i overload in acquired TdP.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1540-8167.1995.tb00770.x
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  • 6
    Electronic Resource
    Electronic Resource
    Atrial-Specific Drugs: (2004)
    350 Main Street , Malden , MA 02148-5018 , USA , and 9600 Garsington Road , Oxford OX4 2DQ , UK . : Blackwell Science Inc
    Journal of cardiovascular electrophysiology 15 (2004), S. 0 
    Details
    ISSN: 1540-8167
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1540-8167.2004.04569.x
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  • 7
    Electronic Resource
    Electronic Resource
    Hybrid Action Potential Etiology (2000)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of cardiovascular electrophysiology 11 (2000), S. 0 
    Details
    ISSN: 1540-8167
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1540-8167.2000.tb00082.x
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  • 8
    Electronic Resource
    Electronic Resource
    High Uniformity of Left and Right Ventricular Repolarization Dynamics Induced by an Abrupt Decrease in Pacing Cycle Length in a Dog is not Affected by Left Ventricular Ischemia (2000)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of cardiovascular electrophysiology 11 (2000), S. 0 
    Details
    ISSN: 1540-8167
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Ischemia Does Not Alter APD Shortening Dynamics. Introduction: After an abrupt increase in heart rate, action potential duration (APD) will shorten. To assess the effect of ischemia on APD shortening dynamics, we compared right ventricular (RV) and left ventricular (LV) APD shortening induced by an abrupt decrease in pacing cycle length (PCL) during control and LV ischemia. Methods and Results: In eight anesthetized AV block dogs, endocardial LV and RV APD were determined simultaneously after an abrupt PCL decrease from 800 to 350 msec. Measurements were repeated during left anterior descending coronary artery (LAD) occlusion. During control, LV and RV APD shortened 97 ± 27 and 71 ± 14 msec, respectively (P 〈 0.05). Shortening was pronounced in a short initial phase and gradual in the longer secondary phase. Linear regression analysis revealed very high uniformity of LV and RV APD shortening dynamics (r2= 0.96 ± 0.01). During repeated LAD occlusion, ischemia induced a gradual LV APD shortening from 314 ± 25 msec to a new steady-state value of 251 ± 23 msec, whereas RV APD remained stable at 289 ± 28 msec. The additional PCL decrease resulted in LV and RV APD shortening of 72 ± 8 and 68 ± 15 msec, respectively, with the same high uniformity of shortening dynamics as seen during control (r2= 0.94 ± 0.03). Conclusion: There is a pronounced difference in APD shortening dynamics induced by an abrupt decrease in PCL compared with ischemia. LV shortening dynamics induced by a decrease in PCL are not affected by LV ischemia, preserving a high interventricular uniformity of repolarization dynamics.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1540-8167.2000.tb00337.x
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  • 9
    Electronic Resource
    Electronic Resource
    Preclinical Evaluation of Antiarrhythmic Drugs: New Drugs Should be Safe to be Successful (2001)
    Oxford, UK : Blackwell Science Inc
    Journal of cardiovascular electrophysiology 12 (2001), S. 0 
    Details
    ISSN: 1540-8167
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1540-8167.2001.01034.x
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  • 10
    Electronic Resource
    Electronic Resource
    Atrial Fibrillation in the Goat Induces Changes in Monophasic Action Potential and mRNA Expression of Ion Channels Involved in Repolarization (2000)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of cardiovascular electrophysiology 11 (2000), S. 0 
    Details
    ISSN: 1540-8167
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: MAP Changes and Ion Channel Expression in Goat AF. Introduction: Sustained atrial fibrillation (AF) is characterized by a marked shortening of the atrial effective refractory period (AKRP) and a decrease or reversal of its physiolonic adaptation to heart rate. The aim of the present study was to investigate whether the AF-induced changes in AKKP in the goat are associated with changes in the atrial monophasic action potential (MAP) and whether an abnormal expression of specific ion channels underlies such changes.Methods and Results: Following thoracotomy, MAPs were recorded from the free wall of the right atrium hoth before induction of AF (control) and after cardioversion of sustained AF (〉2 months) in chronically instrumented goats. In control goats. MAP duration at 80% repolarization (MAPD80) shortened (P 〈 0.01) from 132 ± 4 msec during slow pacing (400-msec interval) to 86 ± 10 msec during fast pacing (180 msec). After cardioversion of sustained AF, the MAPD80, during slow pacing was as short as 67 ± 5 msec (electrical remodeling). Increasing the pacing rate resulted in prolongation (P = 0.02) of the MAPD80 to 91 ± 6 msec. Also. MAPD20 (20% repolarization) shortened (P = 0.05) from 32 ± 4 msec (400 msec) to 14 ± 7 msec (180 msec) in the control goats, whereas it prolonged (P = 0.03) from 20 ± 3 msec (400 msec) to 33 ± 5 msec (180 msec) in sustained AF, mRNA expression of the L-type Ca2+ channel α1c gene and Kv1.5 potassium channel gene, which underlie Ica, and Ikur respectively, was reduced in sustained.AF compared with sinus rhythm hy 32% (P = 0.01) and 45% (P 〈 0.01). respectively. No significant changes were found in the mRNA levels of the rapid Na+ channel, the Na+/Ca2+ exchanger, or the Kv4.2/4.3 channels responsible for I10.Conclusion: AF-induced electrical remodeling in the goat comprises shortening of MAPD and reversal of its physiologic rate adaptation. Changes in the time course of reploarization of the action potential are associated with changes in mRNA expression of the α subunit genes of the L.-type Ca2+ channel and the Kvl.5 potassium channel.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1540-8167.2000.01262.x
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