Thematische Bibliographien / Antiarrhythmic effect

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  2. Dissertationen
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  5. Konferenzberichte

Auswahl der wissenschaftlichen Literatur zum Thema „Antiarrhythmic effect“

Autor: Grafiati
Veröffentlicht am 29. Juni 2021
Zuletzt aktualisiert am 13. Februar 2022

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Zeitschriftenartikel zum Thema "Antiarrhythmic effect"

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Calvert, Clay A., und John Brown. „Influence of Antiarrhythmia Therapy on Survival Times of 19 Clinically Healthy Doberman Pinschers With Dilated Cardiomyopathy That Experienced Syncope, Ventricular Tachycardia, and Sudden Death (1985–1998)“. Journal of the American Animal Hospital Association 40, Nr. 1 (01.01.2004): 24–28. http://dx.doi.org/10.5326/0400024.

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Overtly healthy Doberman pinschers, having moderate to severe myocardial failure secondary to dilated cardiomyopathy, which experienced ventricular tachycardia, syncope or collapse, and sudden death were studied to determine the effect of antiarrhythmic medication on their clinical outcome. Antiarrhythmia drug therapy may have retarded sudden death in 13 treated dogs compared to the six dogs not administered antiarrhythmia drugs.
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Mont, Lluís. „Antiarrhythmic Effect of Cardiac Resynchronization“. Revista Española de Cardiología (English Edition) 58, Nr. 10 (Oktober 2005): 1139–41. http://dx.doi.org/10.1016/s1885-5857(06)60390-3.

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Pandya, Bejal, und Pier D. Lambiase. „An avoidable antiarrhythmic side effect“. British Journal of Hospital Medicine 67, Sup1 (Januar 2006): M14—M15. http://dx.doi.org/10.12968/hmed.2006.67.sup1.20338.

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Madakasira, Sudhakar. „Cardiac antiarrhythmic effect of nortriptyline“. General Hospital Psychiatry 8, Nr. 2 (März 1986): 123–25. http://dx.doi.org/10.1016/0163-8343(86)90098-8.

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Rusinova, Radda, Roger E. Koeppe und Olaf S. Andersen. „A general mechanism for drug promiscuity: Studies with amiodarone and other antiarrhythmics“. Journal of General Physiology 146, Nr. 6 (16.11.2015): 463–75. http://dx.doi.org/10.1085/jgp.201511470.

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Amiodarone is a widely prescribed antiarrhythmic drug used to treat the most prevalent type of arrhythmia, atrial fibrillation (AF). At therapeutic concentrations, amiodarone alters the function of many diverse membrane proteins, which results in complex therapeutic and toxicity profiles. Other antiarrhythmics, such as dronedarone, similarly alter the function of multiple membrane proteins, suggesting that a multipronged mechanism may be beneficial for treating AF, but raising questions about how these antiarrhythmics regulate a diverse range of membrane proteins at similar concentrations. One possible mechanism is that these molecules regulate membrane protein function by altering the common environment provided by the host lipid bilayer. We took advantage of the gramicidin (gA) channels’ sensitivity to changes in bilayer properties to determine whether commonly used antiarrhythmics—amiodarone, dronedarone, propranolol, and pindolol, whose pharmacological modes of action range from multi-target to specific—perturb lipid bilayer properties at therapeutic concentrations. Using a gA-based fluorescence assay, we found that amiodarone and dronedarone are potent bilayer modifiers at therapeutic concentrations; propranolol alters bilayer properties only at supratherapeutic concentration, and pindolol has little effect. Using single-channel electrophysiology, we found that amiodarone and dronedarone, but not propranolol or pindolol, increase bilayer elasticity. The overlap between therapeutic and bilayer-altering concentrations, which is observed also using plasma membrane–like lipid mixtures, underscores the need to explore the role of the bilayer in therapeutic as well as toxic effects of antiarrhythmic agents.
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Martinez-Hernandez, E., und L. A. Blatter. „Effect of carvedilol on atrial excitation-contraction coupling, Ca2+ release, and arrhythmogenicity“. American Journal of Physiology-Heart and Circulatory Physiology 318, Nr. 5 (01.05.2020): H1245—H1255. http://dx.doi.org/10.1152/ajpheart.00650.2019.

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Here we show that the clinically widely used β-blocker carvedilol has profound effects on Ca2+ signaling and ion currents, but also antiarrhythmic effects in adult atrial myocytes. Carvedilol inhibits sodium and calcium currents and leads to failure of ECC but also prevents spontaneous Ca2+ release from cellular sarcoplasmic reticulum (SR) Ca2+ stores in form of arrhythmogenic Ca2+ waves. The antiarrhythmic effect occurs by carvedilol acting directly on the SR ryanodine receptor Ca2+ release channel.
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Frustaci, Andrea, Marina Caldarulo, Valerio di Rienzo, Matteo A. Russo und Nicola Gentiloni. „Antiarrhythmic Effect of H-2 Antihistamines“. Chest 99, Nr. 1 (Januar 1991): 262–63. http://dx.doi.org/10.1378/chest.99.1.262.

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HAYAKAWA, KOICHI. „Evaluation of drug effect of antiarrhythmic agents. a. Guideline of evaluation of effect of antiarrhythmic agents.“ Rinsho yakuri/Japanese Journal of Clinical Pharmacology and Therapeutics 17, Nr. 2 (1986): 413–14. http://dx.doi.org/10.3999/jscpt.17.413.

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Wang, Jie, Jun Li und Bo Feng. „Shen Song Yang Xin Capsule Combined with Antiarrhythmic Drugs, a New Integrative Medicine Therapy, for the Treatment of Frequent Premature Ventricular Contractions (FPVC): A Meta-Analysis of Randomized Controlled Trials“. Evidence-Based Complementary and Alternative Medicine 2014 (2014): 1–9. http://dx.doi.org/10.1155/2014/976713.

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Objective. To evaluate the beneficial and adverse effects of Shen Song Yang Xin Capsule (SSYX Capsule) combined with antiarrhythmic drugs for the treatment of frequent premature ventricular contractions (FPVC).Methods. Seven electronic databases were searched to retrieve any potential randomized controlled trials (RCTs) designed to evaluate the clinical efficacy of SSYX Capsule combined with Antiarrhythmic Drugs for FPVC reported in any language, with total effect for FPVC and number of ventricular premature contraction as the main outcome measure. The methodological quality of the included studies was assessed using criteria from the Cochrane Handbook for Systematic Review of Interventions, Version 5.1.0, and analysed using RevMan 5.1.0 software.Results. Sixteen RCTs of SSYX Capsule were included. The methodological quality of the trials was generally evaluated as low. The results of meta-analysis showed that SSYX Capsule combined with antiarrhythmic drugs was more effective in total effect for FPVC and number of ventricular premature contraction compared with Antiarrhythmic Drugs in patients with FPVC or FPVC complicated by other diseases. Ten of the trials reported adverse events, indicating that the safety of SSYX Capsule is still uncertain.Conclusions. There is some but weak evidence about SSYX Capsule combined with antiarrhythmic drugs appearing to be more effective in total effect for FPVC and number of ventricular premature contraction in patients with FPVC and its complications.
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Mirzoyan, Ruben S., Antonina I. Turilova, Tamara S. Gan’shina, Nina I. Avdyunina, Boris M. Pyatin, Alexandra D. Meshchaninova, Anastasia S. Rodina, Olga Yu Shagaleeva, Valentin I. Zolotarev und Pavel V. Sutyagin. „New Antiarrhythmic Agent to Stabilize Functional Activity of Rat Heart Sinus Node Cardiomyocytes“. Research Results in Pharmacology 6, Nr. 4 (06.11.2020): 19–27. http://dx.doi.org/10.3897/rrpharmacology.6.58520.

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Introduction: The aim of this study was to explore the antiarrhythmic activity of the new antiarrhythmic drug, succinic acid ester of 5-hydroxyadamantane-2-one (ADK-1110) and its effect on the functional activity of rat heart sinus node. Materials and methods: Experiments were performed on 80 non-linear white awake male rats weighing 200 g, using calcium chloride and aconitine arrhythmia models. The ECG was recorded from all the animals in the II standard lead before the start of the experiment. The effect of ADK-1110 on the electrical activity characteristics of rat heart sinus node pacemakers in vitro was studied on 26 outbred Wistar rats of both sexes with a body weight of 160 to 200 g, using the microelectrode technique. Results and discussion: The compound significantly exceeds the known reference drugs in terms of the antiarrhythmic index. The agent also surpasses our previously proposed adamantane derivative ADK-1100 on calcium chloride model and is not inferior to the aconitine one. The electrophysiological analysis of the sinus node pacemaker cardiomyocytes characteristics in vitro under the influence of ADK-1110 revealed that the compound expands the area occupied by true pacemakers. Discussion: The obtained data indicate the presence of properties of antiarrhythmics of classes I, III, and IV in ADK-1110. The indicated functional remodeling stabilizes the functional activity of the central part of the sinus node. Conclusion: ADK-1110 stabilizes the functional activity of the central part of the sinus node. ADK-1110 also has a cerebrovascular anti-ischemic property.
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Dissertationen zum Thema "Antiarrhythmic effect"

1

Das, Kumuda C. „Amelioration of oxidative lung injury by antiarrhythmic agents“. Diss., Virginia Tech, 1992. http://hdl.handle.net/10919/39844.

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Crockett, Thomas Robert. „The mechanism(s) underlying the antiarrhythmic effect of drugs acting on endothelin receptors in myocardial ischaemia and reperfusion“. Thesis, University of Strathclyde, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.248261.

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El-Eraky, Hala Mohammed Tawfik. „The effect of gender on the pharmacokinetic and pharmacodynamic properties of drugs affecting cardiac repolarization : a study of antiarrhythmic drugs“. Thesis, University of Newcastle Upon Tyne, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.394683.

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Sylwan, Gustafsson Magdalena. „Den antiarytmiska effekten av magnesium : En litteraturstudie relaterat till magnesiumform, dos och typ av arytmi“. Thesis, Linnéuniversitetet, Institutionen för kemi och biomedicin (KOB), 2021. http://urn.kb.se/resolve?urn=urn:nbn:se:lnu:diva-105440.

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Bakgrund: Arytmi innebär en avvikande rytm hos hjärtat, alltså att det uppstått en avvikelse i impulsbildning och/eller impulsfortledning. Det kan inverka negativt på livskvalitén, orsaka följdsjukdomar eller leda till livshotande tillstånd. Utöver den konventionella behandlingen finns det behov av ytterligare alternativ. Magnesium är ett essentiellt mineralämne som är viktigt för hjärtats elektrofysiologi. Det har i tidigare studier visat sig att magnesium har haft effekt på postoperativt uppkomna arytmier och att låga nivåer av magnesium hos en frisk population har ökat risken för utvecklandet av olika arytmier. Magnesiums föreslagna antiarytmiska egenskaper är därför av intresse att studera vidare.  Syfte: Syftet med studien är att studera om magnesium har någon antiarytmisk effekt hos individer med arytmi.  Metod: En litteraturstudie genomfördes avseende relevanta artiklar publicerade i databasen PubMed från år 2000 och framåt. En relevansbedömning och kvalitetsgranskning genomfördes med utgångspunkt från Statens beredning för medicinsk och social utvärderings (SBU) metodbok.  Resultat: Tolv artiklar inkluderades i litteraturstudien varav sju uppvisade en antiarytmisk effekt av magnesium. En antiarytmisk effekt vid förmaksflimmer uppvisades i samtliga studier där det administrerades mer än 4 gram intravenöst magnesium. Eftersom magnesium i olika former har olika biotillgänglighet skulle formen eventuellt också kunna vara en bidragande faktor till effekten men studiematerialet var för litet gällande olika magnesiumformer. Vidare går det inte att särskilja om magnesium har olika effekt på olika arytmier då representationen av respektive arytmi var för liten. Slutsats: Magnesium har en antiarytmisk effekt vid administrering över 4 gram intravenöst. Huruvida detta gäller för fler arytmier än förmaksflimmer framkommer inte av denna litteraturstudie. Det finns ett behov av fler studier för att dels undersöka vilken som är den eventuella optimala formen och dosen av magnesium, dels för att utreda vilka typer av arytmier som verkar mottagliga för magnesium som behandlingsalternativ.
Background: Arrhythmia means a deviating rhythm in the heart, either in impulse formation and/or impulse conduction. It can adversely affect the quality of life, cause sequelae or lead to life-threatening conditions. In addition to the conventional treatment, there is a need for alternatives. Magnesium is an essential mineral that is important for the electrophysiology of the heart. Previous studies have shown that magnesium has had an effect on postoperative arrhythmias and that low levels of magnesium in a healthy population have increased the risk of developing various arrhythmias. The proposed antiarrhythmic properties of magnesium are therefore of interest for further study.  Aim: The aim of the study is to investigate whether magnesium has any antiarrhythmic effect in individuals with arrhythmias.  Methods: A literature study was conducted regarding relevant articles published in the PubMed database from the year 2000 and until today. Relevance assessment and quality review were carried out on the basis of  Swedish Agency for Health Technology Assessment and Assessment of Social Services (SBU) method book.  Results: Twelve articles were included in the literature study, seven of which showed an antiarrhythmic effect. An antiarrhythmic effect in atrial fibrillation was shown in all studies where more than 4 grams of intravenous magnesium was administered. Since magnesium in different forms has different bioavailability, the form could possibly also be a contributing factor to the effect, but the study material was too small for different forms of magnesium. Furthermore, it is not possible to distinguish whether magnesium has different effects on different arrhythmias as the representation of each arrhythmia was too small.  Conclusions: Magnesium has antiarrhythmic effect when administrated in excess of 4 gram intravenously. Whether this applies to more arrhythmias than atrial fibrillation does not emerge from this literature study. There is a need for more studies to investigate the possible optimal form and dose of magnesium, and to investigate which types of arrhythmias seem susceptible to magnesium as a treatment alternative.
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Spiers, James Paul. „The cardiovascular effects of a novel antiarrhythmic drug (UK-52,046)“. Thesis, Queen's University Belfast, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.356976.

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Sun, Wei. „Antiarrhythmic effects of ischaemic preconditioning in anaesthetised rats : studies on the roles of bradykinin and nitric oxide“. Thesis, University of Strathclyde, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.249783.

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Yong, Sandro Luis. „A series of amino-2-cyclohexyl esters, their electrophysiological and antiarrhythmic effects as related to actions on ischemia-induced arrhythmias“. Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape4/PQDD_0021/NQ56650.pdf.

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Bugana, Marco. „Mathematical Modeling to Investigate Antiarrhythmic Drug Side Effects: Rate-Dependence Role in Ionic Currents and Action Potentials Shape in the O’Hara Model“. Master's thesis, Alma Mater Studiorum - Università di Bologna, 2012. http://amslaurea.unibo.it/3529/.

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Sudden cardiac death due to ventricular arrhythmia is one of the leading causes of mortality in the world. In the last decades, it has proven that anti-arrhythmic drugs, which prolong the refractory period by means of prolongation of the cardiac action potential duration (APD), play a good role in preventing of relevant human arrhythmias. However, it has long been observed that the “class III antiarrhythmic effect” diminish at faster heart rates and that this phenomenon represent a big weakness, since it is the precise situation when arrhythmias are most prone to occur. It is well known that mathematical modeling is a useful tool for investigating cardiac cell behavior. In the last 60 years, a multitude of cardiac models has been created; from the pioneering work of Hodgkin and Huxley (1952), who first described the ionic currents of the squid giant axon quantitatively, mathematical modeling has made great strides. The O’Hara model, that I employed in this research work, is one of the modern computational models of ventricular myocyte, a new generation began in 1991 with ventricular cell model by Noble et al. Successful of these models is that you can generate novel predictions, suggest experiments and provide a quantitative understanding of underlying mechanism. Obviously, the drawback is that they remain simple models, they don’t represent the real system. The overall goal of this research is to give an additional tool, through mathematical modeling, to understand the behavior of the main ionic currents involved during the action potential (AP), especially underlining the differences between slower and faster heart rates. In particular to evaluate the rate-dependence role on the action potential duration, to implement a new method for interpreting ionic currents behavior after a perturbation effect and to verify the validity of the work proposed by Antonio Zaza using an injected current as a perturbing effect.
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Hung, Chi-Feng, und 洪啟峰. „Electromechanical effect of two antiarrhythmic agents, JKL 1067 and N-allylsecoboldine, on cardiac tissue“. Thesis, 1994. http://ndltd.ncl.edu.tw/handle/51832110654720344978.

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碩士
國立臺灣大學
藥理學研究所
82
JKL 1067 和 N-Allylsecoboldine(STL-1)是兩個合成生物鹼，發現具有 增強收縮力及減慢心跳頻率之作用。 論文主要研究它們在心臟組織之電 生理及增強心收縮力之效果，並且評估它們的抗心律不整的活性。在大白 鼠心房及心室肌組織，1 到 30 uM JKL 1067 會使收縮力隨濃度增加而增 強，然而，其心房自發性跳動頻率則被減慢。 在大白鼠、天竺鼠的實驗 中，會使因冠狀動脈結紮再灌流及ouabain所誘發之心律不整恢復為正常 心律。 之效果，不會因前處理腎腺素阻斷劑而發生改變，但是會被前處 理的鉀管道阻斷劑所減弱 。 在大白鼠心室細胞中， 動作電位期間會隨 JKL 1067 濃度的增加而延長，且減慢伴隨動作電位去極化速率。JKL 1067可減少鈉電流，並且使鈉電流穩定狀態不活化曲線向負電位方向漂移 。 其恢復之時間常數也受影響而延長。 對於瞬時外流鉀電流，可使其尖 峰電流值減少，且明顯加速此電流的不活化速率。 另外，其穩定狀態不 活化曲線也受影響而向負電位方向漂移。 此藥物對鉀電流之抑制程度隨 鉗定時間延長而增加，結果表示 JKL1067 之抑制作用，可能是在此管道 打開狀態下進行。在較高的濃度下(10uM)對L型鈣電流沒有影響，上述三 種電流抑制敏感程度Ito>INa>>ICa。在低濃度下(小於 10 uM)可增加內向 整流鉀電流。 由以上結果顯示，JKL 1067 可能藉著對 Ito 的抑制作用 ，進而延長動作電位期間而產生增強收縮力之效果，其抗心律不整的活性 是由於對INa及 Ito的抑制，加上部分活化 IK1 的作用而產生。 STL-1可 產生增強心收縮力的作用，且可減慢自發性跳動頻率。增強收縮力的效果 不被前處理? 及?接受體阻斷劑所影響，但卻被前處理的鉀管道抑制劑 所抑制。在大白鼠的心室細胞，STL-1會使其動作電位期間延長。對離子 電流抑制大小程度為 INa>Ito>ICa>> IK1。對於鈉電流的抑制 ，伴隨著 使其穩定不活化狀態曲線向負電位方向移動。 抑制瞬時外流鉀電流是隨 濃度的增加而增加，且會加速瞬時外流鉀電流不活化速率， 使其穩定不 活化狀態曲線向負電位方向移動 ，但是對於其從不活化狀態恢復的速度 則不影響 。在較高濃度下，10 uM STL-1 只輕微地使鈣電流的不活化狀 態曲線向負電位方向移動。而濃度達 10uM以上時才會對內向整流鉀電流 有少部分的抑制作用 。在天竺鼠心房細胞中, 也會使其動作電位期間延 長，此延 內向整流鉀電流，及遲開性外流鉀電流的抑制有關。STL-1對 ouabain誘發之心律不整也有對抗之效果 The effects and antiarrhythmic activities of JKL 1067 and N- allylsecoboldine (STL-1), two synthetic alkaloids with positive inotropic and negative chronotropic activities, were assessed in cardiac tissues. JKL 1067 (1-30 uM) decreased heart rate and increased twitch tension in rat atria and ventricular strips. The inotropic effect was uneffected by adrenoceptor antagonist, but was reduced by K+ channel blocker. In guinea pig and rat hearts, ischemic reperfusion and ouabain induced arrhythmia was reverted to sinus rhythm. In rat ventricular cells, JKL 1067 prolonged action potential with a decrease in (dV/dt)max and INa and shifted inactivation curves in the negative direction. The recovery time constant was also prolonged. JKL 1067 reduced Ito with increased rate of inactivation and a negative shift of inactivation curve. The fractional inhibition increased with time, suggesting that JKL 1067 interacts with open Ito channels. At 10 mM, JKL 1067 did not affect ICa but caused a slight negative shift of inactivation curve. The sensitivity to JKL 1067 block was: Ito> INa>> ICa. In contrast, lower concentration of JKL 1067 (<10 uM) increased IK1. These results suggest that JKL 1067 increases contraction by inhibition of Ito and exerts antiarrhythmic activity by inhibition of Ito and INa with a partial increase of IK1. STL-1 (3-30uM) decreased heart rate, prolonged action potential and caused positive inotropic effect in rat atrial and ventricular muscles. The inotropic effect was abolished by K+ channel blocker. In rat ventricular cells, the sensitivity to block was INa> Ito> ICa>> IK1. STL-1 decreased INa with a nega- tive shift in its inactivation curve. STL-1 reduced Ito with an acceleration and a negative shift in inactivation curve. The rate of recovery from inactivation state, however, was unaffected.
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Wu, Adonis Zhi-Yang, und 吳智陽. „Underlying Ionic Channel Mechanism of Antiarrhythmic Effect by a Green Tea Polyphenol, (-)-Epicatechin-3-gallate“. Thesis, 2012. http://ndltd.ncl.edu.tw/handle/17957081558289252085.

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博士
國防醫學院
生命科學研究所
101
The voltage-gated sodium currents (INa) contribute to cardiac spontaneous action potential (sAP) upstroke, influence AP duration (APD), and may be responsible for early afterdepolarization (EAD). (-)-Epicatechin-3-gallate (ECG), a polyphenol extracted from green tea, has been proposed as an effective compound for improving cardiac contractility. However, the therapeutic potential of ECG on arrhythmia remains unknown. I furnished a definition for the temporal involvement of INa on the characterized ontogenic sAP in primary culture of neonatal rat ventricular myocytes, a hypertrophic model of myocardial arrhythmias, by employing whole-cell patch clamp configurations. Two stages of sAP alterations were observed, including the suppression of amplitude and frequency about one week in early, whereas APD prolongation in late culture periods. With a culture time increase, the temporal alterations of INa properties were observed in decrease of INa density, negative shift of steady-state inactivation curve, and prolongation of the recovery time constant. ECG enhanced the slowly inactivation of INa in a concentration-dependent manner (0.1-100 uM) with an EC50 value of 3.8uM. ECG increased the firing rate of normal sAP about twofold without waveform alteration. The bradycardia-dependent EAD could be significantly restored by ECG in fast firing rate to normal sAP waveform. The results revealed that INa suppression leads to the retardation of automaticity, APD prolongation, and EAD occurrence. The dissertation further explicates how ECG may act as a promising candidate in clinical applications. The data reveal that ECG, the novel INa agonist, can be as an effective treatment for cardiac bradyarrhythmias.
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Bücher zum Thema "Antiarrhythmic effect"

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Luc, Hondeghem, Hrsg. Molecular and cellular mechanisms of antiarrhythmic agents. Mount Kisco, NY: Futura Pub. Co., 1989.

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Wijdicks, Eelco F. M., und Sarah L. Clark. Antihypertensives and Antiarrhythmics. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190684747.003.0013.

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Acute brain injury can precipitate a hypertensive response, which for the most part is the result of stress-induced, increased sympathetic activity. Acute stroke with hypertension may not be a response but more often a prior, untreated hypertension or a patient with no access to medication. This hypertensive response may wane quickly, and aggressive treatment of these temporary surges in blood pressure could have unwanted consequences. Important characteristics of most antihypertensive drugs used in the neurosciences intensive care unit are cost, having a rapid onset with a short duration of action, and having a low incidence of adverse side effects. Many of the antiarrhythmic drugs also have antihypertensive effects, so these drug classes are best combined in one chapter. This chapter discusses blood pressure targets, the most appropriate antihypertensive medications to use for acute management, and clinically relevant cardiac arrhythmias and their treatment.
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Billman, George E., Hrsg. The Effects of Omega-3 Polyunsaturated Fatty Acids on Cardiac Rhythm: Antiarrhythmic, Proarrhythmic, Both or Neither? Frontiers Media SA, 2013. http://dx.doi.org/10.3389/978-2-88919-088-1.

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LeMaitre, John, und Jan Kornder. Anti-arrhythmics in critical illness. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0038.

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Anti-arrhythmic drugs (AADs) are an important component of the pharmacological arsenal used in the management of the critically-ill patient. The benefits of AADs, as well as their potential disadvantageous side effects, largely depend on their effects upon the cardiac action potential. AADs can be broadly grouped according to their cellular actions, upon which their clinical effects depend. However, there is substantial cross-over amongst the groups in terms of these actions and efficacy for particular arrhythmias, and also for side effects. Amiodarone exhibits a broad spectrum of antiarrhythmic activity and is often the most useful AAD for the critically-ill patient where short-term use reduces concerns relating to toxic side effects associated with chronic administration. However, each of the other available AADs have their uses for particular scenarios in the critically-ill patient, although attention needs to be paid to comorbidities to attenuate the risk of adverse response. AADs are pro-arryhthmic in 5-10% of patients with potential lethal consequences, and the use of AADs in the critically-ill patient should be considered very carefully as correction of the underlying substrate may be sufficient in some circumstances to resolve the index arryhthmia.
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Buchteile zum Thema "Antiarrhythmic effect"

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Massarella, J. W., und K. C. Khoo. „Effect of Age on the Clinical Pharmacokinetics of Antiarrhythmic Drugs“. In Drug Studies in the Elderly, 207–47. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-1253-6_11.

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Campbell, Ronald W. F. „Sudden Cardiac Death — Failure or Effect of Antiarrhythmic Drug Therapy?“ In Cardiac Arrhythmias: New Therapeutic Drugs and Devices, 191–200. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4613-2595-6_12.

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Arad, Michael, Tatiana Oxman, Ron Leor und Babeth Rabinowitz. „Protaglandins and the antiarrhythmic effect of preconditioning in the isolated rat heart“. In Biochemical Mechanisms in Heart Function, 249–55. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4613-1279-6_32.

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Jennings, Robert B., und Keith A. Reimer. „Measurement of Infarct Size: Effect of Reperfusion with Arterial Blood“. In Risk/Benefit Analysis for the Use and Approval of Thrombolytic, Antiarrhythmic, and Hypolipidemic Agents, 3–13. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4613-1605-3_1.

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Honerjäger, P. „The contribution of Na channel block to the negative inotropic effect of antiarrhythmic drugs“. In Controversial issues in cardiac pathophysiology, 33–37. Heidelberg: Steinkopff, 1986. http://dx.doi.org/10.1007/978-3-662-11374-5_4.

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Herzig, S., und H. Lüllmann. „Effects of Cardiac Glycosides at the Cellular Level“. In Antiarrhythmic Drugs, 545–63. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-73666-7_25.

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Raasmaja, Atso, Antti Talo, Heimo Haikala, Erkki Nissinen, Inge-Britt Lindén und Pentti Pohto. „Biochemical Properties of OR-1259 - A Positive Inotropic and Vasodilatory Compound with an Antiarrhythmic Effect“. In Excitation-Contraction Coupling in Skeletal, Cardiac, and Smooth Muscle, 423. Boston, MA: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4615-3362-7_63.

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Shenasa, Mohammad, Thomas Fetsch, Jafar Shenasa, Antoni Martínez-Rubio, Martin Borggrefe, Lutz Reinhartd und Günter Breithardt. „The effect of antiarrhythmic drugs on the signal averaged ECG. Does it predict response to therapy?“ In Signal Averaged Electrocardiography, 527–48. Dordrecht: Springer Netherlands, 1993. http://dx.doi.org/10.1007/978-94-011-0894-2_32.

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Schleifer, J. William, und Komandoor Srivathsan. „Proarrhythmic Effects of Antiarrhythmic and Non-antiarrhythmic Drugs“. In Pathophysiology and Pharmacotherapy of Cardiovascular Disease, 1015–38. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-15961-4_48.

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Scholz, H. „Kardiodepressive Effekte der Antiarrhythmika“. In Arrhythmiebehandlung und Hämodynamik, 38–47. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-75335-0_4.

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Konferenzberichte zum Thema "Antiarrhythmic effect"

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SUZUKI, MAKOTO, MITSUHIRO NISHIZAKI, TETSUO ARAKAWA, TAKAHIRO OHARA, AKIHIKO MATSUMURA, YUJI HASHIMOTO und MASAYASU HIRAOKA. „THE SUPPRESSIVE EFFECT OF BEPRIDIL ON ATRIAL FLUTTER ORGANIZED FROM PERSISTENT ATRIAL FIBRILLATION DURING CLASS IC ANTIARRHYTHMIC THERAPY“. In Proceedings of the 31st International Congress on Electrocardiology. WORLD SCIENTIFIC, 2005. http://dx.doi.org/10.1142/9789812702234_0084.

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Saiz, J., J. M. Ferrero, M. Monserrat, J. Gomis-Tena, J. Chorro und A. Ferrero. „Effects of the antiarrhythmic drug dofetilide on myocardial electrical activity: a computer modelling study“. In Computers in Cardiology, 2003. IEEE, 2003. http://dx.doi.org/10.1109/cic.2003.1291148.

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Abbasi, Mitra, und Sebastian Polak. „In Silico Assessment of Antiarrhythmic Effects of Drug Ranolazine on Electrical Activity in Human Ventricular Myocardium“. In 2016 Computing in Cardiology Conference. Computing in Cardiology, 2016. http://dx.doi.org/10.22489/cinc.2016.309-284.

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ISHII, KUNIAKI, KAZUE NAKASHIMA und MASAO ENDOH. „EFFECTS OF ANTIARRHYTHMIC DRUGS ON THE CURRENTS OF XENOPUS OOCYTES EXPRESSING HERG AND KvLQT1/minK CHANNELS“. In Proceedings of the 31st International Congress on Electrocardiology. WORLD SCIENTIFIC, 2005. http://dx.doi.org/10.1142/9789812702234_0068.

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Saiz, J., M. Monserrat, J. M. Ferrero, J. Gomis-Tena, K. Cardona, J. Chorro, V. Hernandez und J. M. Alonso. „Effects of the antiarrhythmic drug dofetilide on regional heterogeneity of action potential duration: a computer modelling study“. In Computers in Cardiology 2004. IEEE, 2004. http://dx.doi.org/10.1109/cic.2004.1442928.

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Beatch, Dickenson, Wood und Tang. „An Automated, On-Line, PC-based System For Analysis Of The Frequency dependent Effects Of Antiarrhythmic Drugs On Action Potential Duration, Refractory Periods, And Conduction Velocity, And On Energy Requirements For Defibrillation“. In Proceedings of the Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 1992. http://dx.doi.org/10.1109/iembs.1992.595870.

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Beateti, Gregory N., David R. Dickenson, Randall H. Wood und Anthony S. L. Tang. „An automated, on-line, PC-based system for analysis of the frequency-dependent effects of antiarrhythmic drugs on action potential duration, refractory periods, and conduction velocity, and on energy requirements for defibrillation“. In 1992 14th Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 1992. http://dx.doi.org/10.1109/iembs.1992.5761256.

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