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Functional Properties of Muscle
Published in Nassir H. Sabah, Neuromuscular Fundamentals, 2020
The time course of the ventricular cardiac AP is illustrated in Figure 10.20. The duration of the AP is about 250 ms, which allows the development of maximal force during a twitch. The absolute refractory period, also known as the effective refractory period (ERP), is about 200 ms. Because this exceeds the contraction time, it is not possible to tetanize cardiac muscle. The ERP limits the maximum frequency to about 250–300 beats/min.
Basics of Electrophysiology Study
Published in Andrea Natale, Oussama M. Wazni, Kalyanam Shivkumar, Francis E. Marchlinski, Handbook of Cardiac Electrophysiology, 2020
Jonathan R. Hoffman, Marmar Vaseghi
As mentioned above, in addition to baseline conduction times, the refractory periods of important cardiac structures including the conduction system are also measured. The most commonly measured refractory period is the effective refractory period (ERP), or the longest coupling interval between captured beats, which fails to capture or conduct to a given cardiac structure. For example, when pacing the atrium at a drive train of 600 ms, if both the drive train and extrastimulus beat with an S1S2 coupling interval of 250 ms capture the atrium (eliciting both an A1 and A2), but when the coupling interval is decreased to 240 ms, the S2 fails to capture the atrium (only an A1 is observed), the atrial ERP is reported to be 240 ms at a drive cycle length of 600 ms.
In Vivo and In Vitro Cardiac Preparations Used in Antiarrhythmic Assays
Published in John H. McNeill, Measurement of Cardiovascular Function, 2019
At high doses of antiarrhythmic drugs it may not be possible to reach end points for thresholds and effective refractory period.21,26 The nature of end points may also change. Drugs which increase refractory period, such as tedisamil in rats, prevent induction of ventricular fibrillo-flutter; instead only VT occurs. The act of passing current through the myocardium increases the dispersion of refractoriness and may itself induce arrhythmias. Furthermore, placing electrodes may damage the heart and cause arrhythmias. Appropriate controls are essential to account for these potential sources of variance.
Design, synthesis, and biological evaluation of arylmethylpiperidines as Kv1.5 potassium channel inhibitors
Published in Journal of Enzyme Inhibition and Medicinal Chemistry, 2022
Lingyue Zhao, Qian Yang, Yiqun Tang, Qidong You, Xiaoke Guo
An important mechanism for AF is atrial electrical remodelling, which is characterised by significant shortening of atrial effective refractory period (ERP) and action potential duration (APD)5,6 accompanied by prolonged ventricular conduction. This pathological phenomenon is triggered by the weakening of ultra-rapid delayed rectifier potassium current (IKur) through ultra-rapid delayed rectifier potassium channel encoded by KCNA5 (Kv1.5) gene7–9, which is only expressed in atria10,11. Scientists have discovered that over-expression of Kv1.5 reconstituted a 4-aminopyridine-sensitive outward K+ current, shortened the action potential duration, eliminated early after depolarisations, shortened the QT interval, decreased dispersion of repolarisation, and increased the heart rate6. The underlying therapeutic principle seems clear that Kv1.5 current suppression is expected to lead to an extension in APD and increase the ERP of fibrotic atria12,13.
Slow pathway elimination using antegrade conduction improvement with fast atrial pacing during AVNRT radiofrequency ablation: a proof-of-concept study
Published in Acta Cardiologica, 2022
Sok-Sithikun Bun, Ahmed Mostfa Wedn, Ahmed Taher, Philippe Taghji, Fabien Squara, Karim Hasni, Claudio De Zuloaga, Emile Ferrari
Dual AV node physiology was assessed. The presence of an anterograde AH jump (≥ 50 ms) was confirmed with programmed atrial stimulation (up to three extra-stimuli if needed). Baseline SP and FP effective refractory period were determined, including the corresponding maximal AH values on each pathway before refractoriness was reached (AH-FP and AH-SP). At baseline, AVNRT was induced by programmed atrial stimulation or atrial burst pacing. If AVNRT was not inducible at baseline, isoproterenol was infused. AVNRT diagnosis was definitively confirmed by appropriate electrophysiological manoeuvres (His-bundle refractory ventricular extrastimuli delivered and/or ventricular entrainment during tachycardia; para-hissian pacing to avoid any misdiagnosis with the presence of an accessory pathway).
New methodological approaches to atrial fibrillation drug discovery
Published in Expert Opinion on Drug Discovery, 2021
Potassium channel blockers are classified as class 3 AAD in the Vaughan-William’s classification. Blocking of potassium channels with outward current aims to prolong action potential duration and the effective refractory period, thereby disrupting the reentry mechanisms that underlie AF. AADs with predominantly potassium channel-blocking properties such as ibutilide and dofetilide are used in pharmacological cardioversion of AF; sotalol and dofetilide are used for long-term rhythm control of AF in countries where they are available. Other multi-channel blockers such as amiodarone and dronedarone also have potassium channel blocking properties. Prolongation of QTc interval is common with these agents and carries the risk of Torsades de pointes. There is interest in developing atrial specific potassium channel blockers that will not prolong the QTc interval. Achieving atrial-specificity in potassium channel blockade can theoretically be achieved by focusing on subsets of potassium channels that are predominantly expressed in atrial cardiomyocytes but not in the ventricles. Several agents against potassium channels expressed predominantly in the atrium have been explored and have been summarized in previous reviews. [11,12]