1994
DOI: 10.1016/0002-8703(94)90076-0
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Interactions between drugs and devices: Experimental and clinical studies

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Cited by 62 publications
(27 citation statements)
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“…From previous studies, we know that amiodarone increases the DFT [26, 27, 28]and thus potentially reduces the effectiveness of a PCD in terminating malignant ventricular arrhythmias. Some class III anti-arrhythmic agents, such as sotalol, have been shown to decrease DFT, while class I agents have the opposite effects [10]. Studies of DFT in pure class III anti-arrhythmic drugs suggest an inverse relationship between the prolonged refractory stage from potassium channel blockade and the amount of energy required to overcome the fibrillation [9].…”
Section: Discussionmentioning
confidence: 99%
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“…From previous studies, we know that amiodarone increases the DFT [26, 27, 28]and thus potentially reduces the effectiveness of a PCD in terminating malignant ventricular arrhythmias. Some class III anti-arrhythmic agents, such as sotalol, have been shown to decrease DFT, while class I agents have the opposite effects [10]. Studies of DFT in pure class III anti-arrhythmic drugs suggest an inverse relationship between the prolonged refractory stage from potassium channel blockade and the amount of energy required to overcome the fibrillation [9].…”
Section: Discussionmentioning
confidence: 99%
“…Conventional drug therapy is used in these individuals to decrease the frequency of spontaneous ventricular tachyarrhythmias, slow the rate of the ventricular tachycardia once breakthrough occurs, suppress supraventricular tachy-arrhythmias (SVT) and lower the ventricular response if the SVT is non-suppressible. Most importantly, concomitant anti-arrhythmic therapy in patients with a PCD is also thought to reduce the incidence of PCD shocks and thus minimize patient discomfort [10]. …”
Section: Introductionmentioning
confidence: 99%
“…Amiodarone appears to have a less consistent effect [41,42]; however, in selected individuals, it appears to be associated with potentially life-threatening increase in defibrillation threshold when administered chronically [43][44][45][46]. The Low Energy Safety Study [47] assessed the efficacy and safety of programming chronic ICD shock energy levels based on defibrillation threshold.…”
Section: Antiarrhythmic Drugs Causing Increase In Defibrillation Thrementioning
confidence: 99%
“…The data on the effects of antiarrhythmic drugs on defibrillation thresholds are incomplete, and often largely based on animal data, which may be species specific and have limited extrapolation to humans. Different results have often been obtained with different animal models, ie, dogs and pigs, employing different kinds of anesthesia (Table 1) [31,[36][37][38][39][40][41][42][43][44][45][46]. In a prospective parallel design human study, long-term therapy with mexiletine had no effect on defibrillation thresholds [46]; more recent data dispute this suggesting that mexiletine may elevate defibrillation threshold even more than amiodarone [47].…”
Section: Defibrillation Therapiesmentioning
confidence: 99%