Mechanisms regulating myocardial oxygen consumption in non-ischemic dilated cardiomyopathy (original) (raw)
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Cardiac Pacing and Electrophysiology
Annals of Internal Medicine, 1991
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Pace-pacing and Clinical Electrophysiology, 1999
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.
British Journal of Pharmacology, 2001
The effects of IKs block by chromanol 293B and L-735,821 on rabbit QT-interval, action potential duration (APD), and membrane current were compared to those of E-4031, a recognized IKr blocker. Measurements were made in rabbit Langendorff-perfused whole hearts, isolated papillary muscle, and single isolated ventricular myocytes.Neither chromanol 293B (10 μM) nor L-735,821 (100 nM) had a significant effect on QTc interval in Langendorff-perfused hearts. E-4031 (100 nM), on the other hand, significantly increased QTc interval (35.6±3.9%, n=8, P<0.05).Similarly both chromanol 293B (10 μM) and L-735,821 (100 nM) produced little increase in papillary muscle APD (less than 7%) while pacing at cycle lengths between 300 and 5000 ms. In contrast, E-4031 (100 nM) markedly increased (30 – 60%) APD in a reverse frequency-dependent manner.In ventricular myocytes, the same concentrations of chromanol 293B (10 μM), L-735,821 (100 nM) and E-4031 (1 μM) markedly or totally blocked IKs and IKr, respectively.IKs tail currents activated slowly (at +30 mV, τ=888.1±48.2 ms, n=21) and deactivated rapidly (at −40 mV, τ=157.1±4.7 ms, n=22), while IKr tail currents activated rapidly (at +30 mV, τ=35.5±3.1 ms, n=26) and deactivated slowly (at −40 mV, τ1=641.5±29.0 ms, τ2=6531±343, n=35). IKr was estimated to contribute substantially more to total current density during normal ventricular muscle action potentials (i.e., after a 150 ms square pulse to +30 mV) than does IKs.These findings indicate that block of IKs is not likely to provide antiarrhythmic benefit by lengthening normal ventricular muscle QTc, APD, and refractoriness over a wide range of frequencies.The effects of IKs block by chromanol 293B and L-735,821 on rabbit QT-interval, action potential duration (APD), and membrane current were compared to those of E-4031, a recognized IKr blocker. Measurements were made in rabbit Langendorff-perfused whole hearts, isolated papillary muscle, and single isolated ventricular myocytes.Neither chromanol 293B (10 μM) nor L-735,821 (100 nM) had a significant effect on QTc interval in Langendorff-perfused hearts. E-4031 (100 nM), on the other hand, significantly increased QTc interval (35.6±3.9%, n=8, P<0.05).Similarly both chromanol 293B (10 μM) and L-735,821 (100 nM) produced little increase in papillary muscle APD (less than 7%) while pacing at cycle lengths between 300 and 5000 ms. In contrast, E-4031 (100 nM) markedly increased (30 – 60%) APD in a reverse frequency-dependent manner.In ventricular myocytes, the same concentrations of chromanol 293B (10 μM), L-735,821 (100 nM) and E-4031 (1 μM) markedly or totally blocked IKs and IKr, respectively.IKs tail currents activated slowly (at +30 mV, τ=888.1±48.2 ms, n=21) and deactivated rapidly (at −40 mV, τ=157.1±4.7 ms, n=22), while IKr tail currents activated rapidly (at +30 mV, τ=35.5±3.1 ms, n=26) and deactivated slowly (at −40 mV, τ1=641.5±29.0 ms, τ2=6531±343, n=35). IKr was estimated to contribute substantially more to total current density during normal ventricular muscle action potentials (i.e., after a 150 ms square pulse to +30 mV) than does IKs.These findings indicate that block of IKs is not likely to provide antiarrhythmic benefit by lengthening normal ventricular muscle QTc, APD, and refractoriness over a wide range of frequencies.British Journal of Pharmacology (2001) 132, 101–110; doi:10.1038/sj.bjp.0703777
The influence of pacing rate on intramyocardial electrograms
1999
possible to stimulate all patients at the same pacing rate (PR), as would be desirable. Some of the parameters obtained from the VERs may be affected by the PR. The objective of the present study was to investigate the influence of PR on parameters of interest obtained from the VERX signal. Methods Data Acquisition Unipolar intramyocardial electrograms were obtained using dual-chamber pacemakers with extended bandwidth capability between 0.3 and 200 Hz (Physios CTM 01), and fractal coated epimyocardial electrodes (ELC 54-UP). The first electrode (E1) was placed at the right ventricular outflow tract and connected to the ventricular channel of the pacemaker. The second electrode (E2) was implanted at the right or at the left ventricle with a distance of at least 4 cm to E1 (Figure 1). The measuring session was performed not earlier than three months after the transplantation, and the patients
Role of the slow current in cardiac electrophysiology
Circulation, 1975
Role of the Slow Current in Cardiac Electrophysiology OVER THE PAST TEN YEARS, the concept has emerged that the ionic currents underlying the cardiac action potential include calcium as well as sodium and potassium. The purpose of this communication is to review the development of this concept and attempt to relate it to our understanding of clinical electrophysiology and the pathogenesis of certain arrhythmias. Basic Electrophysiologic Concepts Twenty-six years ago, Hodgkin and Katz' demonstrated that a large and relatively specific increase in the membrane permeability to sodium ions accounted for the amplitude and rate of voltage change of the depolarization phase of squid nerve action potentials. Using the voltage-clamp technique, Hodgkin and Huxley2 analyzed the currents underlying the nerve action potential. They described two constituentsan inward sodium flow followed by an outward potassium flowand formulated equations to describe how these currents vary with transmembrane voltage potential and time. In the ensuing years, cardiac electrophysiologists, assuming that exclusively sodium and potassium movements were involved, applied the Hodgkin-From the
AJP: Heart and Circulatory Physiology, 2003
Our objective was to create an animal preparation displaying long-term electrical alterations after chronic regional energetic stress without myocardial scarring. An Ameroid (AM) constrictor was implanted around the left circumflex coronary artery (LCx) 2 wk before chronic rapid ventricular pacing (CRP) was initiated at 240 beats/min for 4 wk (CRP-AM). Comparisons were made with healthy canines and canines with either AM or CRP. Unipolar electrograms were recorded from 191 sites in the LCx territory in open-chest, anesthetized animals during sinus rhythm and while pacing at 120–150 beats/min, with bouts of transient rapid pacing (TRP; 240/min). In CRP-AM and AM, ST segment elevation was identified at central sites and ST depression at peripheral sites, both increasing with TRP. In CRP-AM and CRP, the maximum negative slope of unipolar activation complexes was significantly depressed and activation-recovery intervals prolonged. Areas of inexcitability as well as irregular isocontour ...