• 【[胺碘酮作为甲状腺毒性低钾血症周期性麻痹 (反应) 的原因]。】 复制标题 收藏 收藏
    DOI:10.1157/13107958 复制DOI
    作者列表:Blanco Jarava A,Moreno Rodríguez A,Cano Llorente V,Espinosa Magro P,Sánchez Castaño A,González Moraleja J
    BACKGROUND & AIMS: -2
    背景与目标: -2
  • 【通过利用循证实践降低胺碘酮相关静脉炎的发生率。】 复制标题 收藏 收藏
    DOI:10.1111/wvn.12470 复制DOI
    作者列表:Murphy K,Murphy J,Fischer-Cartlidge E
    BACKGROUND & AIMS: BACKGROUND:Intravenous (IV) amiodarone has multiple indications including treatment of hemodynamically unstable patients and the prevention of atrial or ventricular arrhythmias after thoracic surgery. Inflammation of the vein, or phlebitis, is the most common adverse event associated with peripherally administered amiodarone. In 2017, a rise in reported phlebitis incidents was occurring at one large academic medical center. AIM:This evidence-based quality improvement initiative aimed to decrease and enhance early detection of phlebitis in patients receiving amiodarone. METHODS:Due to the variation in assessment and management standards, evidence-based practice (EBP) methodology was utilized to establish a process for quality improvement. A thorough literature search was completed, identifying evidence-based interventions to decrease phlebitis and enhance early detection. Thorough critiques of the literature and synthesis of the evidence were completed. Multidisciplinary guidelines based on the literature were created. The guidelines included interventions such as an increase in IV assessment frequency, vein selection criteria, and the utilization of a standardized grading tool for assessment. RESULTS:Phlebitis was reduced by 30%-88%. In the first 6 months post-intervention, there was a 48% reduction in phlebitis cases. In addition, the severity of phlebitis and the quality of reporting also improved dramatically. LINKING EVIDENCE TO ACTION:This evidence-based quality improvement process led to identifying relevant knowledge gaps in care that could be streamlined into everyday nursing practice to decrease patient harm. This paper describes an in-depth process of how EBP helped to quickly take a clinical inquiry and adapt change based on findings from the evidence. Other organizations can utilize EBP to solve patient safety concerns using similar processes.
    背景与目标:
  • 【甲状腺功能减退对犬心室颤动易感性的影响: 与胺碘酮的比较研究。】 复制标题 收藏 收藏
    DOI:10.1007/BF02627962 复制DOI
    作者列表:Liu P,Fei L,Wu W,Li J,Wang J,Zhang X
    BACKGROUND & AIMS: It has been shown that thyroid hormone has a significant effect on the heart and that suppression of thyroid function may contribute to the antiarrhythmic effect of amiodarone. The study was aimed at investigating the effects of hypothyroidism, compared with those of amiodarone, on vulnerability to ventricular fibrillation in dogs. In this study, 25 adult dogs were randomly divided into three groupsa hypothyroid group following total thyroidectomy (n = 9), an amiodarone group (n = 8, 400 mg per day, 4 weeks), and a control group (n = 8). Both amiodarone and control groups were subjected to sham surgery. Five to 8 weeks after surgery, ventricular fibrillation threshold and other electrophysiological parameters were determined. Right ventricular effective refractory period, monophasic action potential duration, and ventricular fibrillation threshold were significantly increased in both the thyroidectomized and amiodarone-treated animals. There was no significant change in monophasic action potential duration dispersion. The incidence of ventricular fibrillation during ischemia and reperfusion was significantly reduced in both treated groups compared with the sham-operated euthyroid controls. These observations suggest that hypothyroidism has a significant antifibrillatory effect in dogs. Homogeneous prolongation of repolarization and refractoriness may contribute to the antifibrillatory action of hypothyroidism.

    背景与目标: 研究表明,甲状腺激素对心脏有重要作用,甲状腺功能的抑制可能有助于胺碘酮的抗心律失常作用。该研究旨在研究甲状腺功能减退症与胺碘酮相比对犬心室颤动的影响。在这项研究中,将25只成年犬随机分为三组,即全甲状腺切除术后甲状腺功能减退组 (n = 9),胺碘酮组 (n = 8,每天400 mg,4周) 和对照组 (n = 8)。胺碘酮和对照组均接受假手术。术后5 ~ 8周,测定心室颤动阈值及其他电生理参数。在甲状腺切除和胺碘酮治疗的动物中,右心室有效不应期,单相动作电位持续时间和心室颤阈值均显着增加。单相动作电位持续时间离散度无明显变化。与假手术的甲状腺功能正常对照组相比,两个治疗组在缺血和再灌注期间心室纤颤的发生率均显着降低。这些观察结果表明,甲状腺功能减退症对狗具有明显的抗纤颤作用。复极化和难治性的均匀延长可能有助于甲状腺功能减退的抗纤作用。
  • 【抗心律失常药胺碘酮显示抗真菌活性,诱导不规则的钙反应和黑曲霉的细胞内酸化-胺碘酮靶向黑曲霉的钙和pH稳态。】 复制标题 收藏 收藏
    DOI:10.1016/j.fgb.2012.07.007 复制DOI
    作者列表:Bagar T,Benčina M
    BACKGROUND & AIMS: :The rapidly developing resistance of fungi to antifungal drugs is a serious health problem. Today's drugs mainly target cell membrane composition and synthesis. Moreover, some of them have serious side effects. New antifungal drugs targeting different molecular pathways are necessary. Amiodarone, an FDA approved antiarrhythmic drug displays antifungal activity. It targets calcium and pH homeostasis. In concentrations above 25 μM, it inhibits the growth of the filamentous fungi Aspergillus niger. It triggers a biphasic calcium response accompanied by a high [Ca(2+)](c) resting level and an intracellular acidification from 7.5 to 6.0, both of which are concentration dependent. Both extracellular calcium and calcium from intracellular organelles are sources of the transient second cytosolic calcium peak, whose amplitude is 0.12 μM for cells treated with 0.1mM amiodarone. In P-type ATPase deficient A. niger strains pmrAΔ and pmcAΔ, the [Ca(2+)](c) resting level after amiodarone treatment is at least twice as high as that of the wild type, which correlates with fungal viability and hypersensitivity to amiodarone. A combination of amiodarone and amphotericin B is additive in terms of cell viability and cytosolic calcium influx. In contrast, a combination of azole drugs and amiodarone has a synergistic effect on the viability of fungi.
    背景与目标: : 真菌对抗真菌药物的耐药性迅速发展,是一个严重的健康问题。当今的药物主要是靶向细胞膜的组成和合成。此外,其中一些有严重的副作用。针对不同分子途径的新型抗真菌药物是必要的。胺碘酮是FDA批准的抗心律失常药物,具有抗真菌活性。它的目标是钙和pH稳态。在25μm以上的浓度下,它会抑制丝状真菌黑曲霉的生长。它触发双相钙反应,伴随着高 [Ca(2)](c) 静息水平和从7.5到6.0的细胞内酸化,两者均取决于浓度。细胞外钙和来自细胞内细胞器的钙都是瞬时第二个胞质钙峰的来源,对于用0.1毫米胺碘酮处理的细胞,其振幅为0.12 μ m。在P型atp酶缺陷型黑曲霉菌株pmrAΔ 和pmca Δ 中,胺碘酮处理后的 [Ca(2)](c) 静息水平至少是野生型的两倍,这与真菌活力和对胺碘酮的超敏反应有关。胺碘酮和两性霉素b的组合在细胞活力和胞质钙内流方面是累加的。相反,唑类药物和胺碘酮的组合对真菌的生存能力具有协同作用。
  • 【人周围肺上皮细胞中胺碘酮和去乙基胺碘酮之间的细胞毒性相互作用。】 复制标题 收藏 收藏
    DOI:10.1016/j.cbi.2013.05.006 复制DOI
    作者列表:Roth FC,Mulder JE,Brien JF,Takahashi T,Massey TE
    BACKGROUND & AIMS: :The potent and efficacious anti-dysrhythmic agent amiodarone (AM) can cause potentially life-threatening lung damage (amiodarone-induced pulmonary toxicity; AIPT), which is characterized by cell death in the lungs, followed by inflammation and fibrosis. AM's major metabolite, desethylamiodarone (DEA), has a greater toxic potency than AM and it has been suggested that DEA may act synergistically with AM to cause lung toxicity. The objective of this study was to determine the type of cytotoxic interaction between AM and DEA in HPL1A human peripheral lung epithelial cells. Cytotoxicity was measured by lactate dehydrogenase release. AM and DEA caused concentration-dependent cytotoxicity in HPL1A cells. The concentration of drug causing 50% cell death (LC50) and the Hill slope factor, which represents steepness of the concentration-cell death curve, were significantly different between AM and DEA (12.4μM and 1.98; 5.07μM and 5.43, for AM and DEA, respectively) indicating that they may induce cytotoxicity through different mechanisms. A combined concentration of 7.13μM AM plus DEA, equivalent to 41% of each compound's individual LC50 value, resulted in 50% cell death. Isobolographic analysis revealed this effect to be additive, although the combined concentrations were only slightly higher than the concentrations that defined the threshold of synergy (threshold of synergy=4.21±1.98μM AM plus 1.73±1.05μM DEA; experimental data point=5.06±0.47μM AM plus 2.07±0.47μM DEA). The cytotoxic interaction between AM and DEA may be clinically relevant in the development of AIPT.
    背景与目标: : 有效且有效的抗心律不齐剂胺碘酮 (AM) 可引起潜在的威胁生命的肺损伤 (胺碘酮诱导的肺毒性; AIPT),其特征是肺中的细胞死亡,随后是炎症和纤维化。AM的主要代谢产物去乙基胺碘酮 (DEA) 比AM具有更大的毒性,并且有人建议DEA可能与AM协同作用以引起肺毒性。这项研究的目的是确定HPL1A人周围肺上皮细胞中AM和DEA之间的细胞毒性相互作用的类型。通过乳酸脱氢酶释放来测量细胞毒性。AM和DEA在HPL1A细胞中引起浓度依赖性的细胞毒性。引起50% 细胞死亡的药物浓度 (LC50) 和代表浓度-细胞死亡曲线陡度的希尔斜率因子在AM和DEA之间存在显着差异 (12.4 μ m和1.98; 5.07 μ m和5.43,对于AM和DEA,分别) 表明它们可能通过不同的机制诱导细胞毒性。7.13 μ m AM加上DEA的组合浓度,相当于每种化合物的单独LC50值的41%,导致50% 细胞死亡。等射线照相分析显示这种效应是累加的,尽管组合浓度仅略高于定义协同作用阈值的浓度 (协同作用阈值 = 4.21 ± 1.98 μ m AM加1.73 ± 1.05 μ m DEA; 实验数据点 = 5.06 ± 0.47 μ m AM加2.07 ± 0.47 μ m DEA)。AM和DEA之间的细胞毒性相互作用可能与AIPT的发展有关。
  • 【洛伐他汀与胺碘酮和四氯化碳在离体大鼠肝细胞中相互作用的体外研究。】 复制标题 收藏 收藏
    DOI:10.3748/wjg.v13.i15.2198 复制DOI
    作者列表:Krasteva AZ,Mitcheva MK,Kondeva-Burdina MS,Descatoire VA
    BACKGROUND & AIMS: AIM:To investigate the interactions at a metabolic level between lovastatin, amiodarone and carbon tetrachloride in isolated rat hepatocytes. METHODS:For cell isolation two-step collagenase liver perfusion was performed. Lovastatin was administered alone in increasing concentrations (1 mumol/L, 3 mumol/L, 5 mumol/L and 10 mumol/L) and in combination with CCl(4) (86 mumol/L). The cells were also pretreated with 14 mumol/L amiodarone and then the other two compounds were added. RESULTS:Lovastatin promoted concentration-dependent significant toxicity estimated by decrease in cell viability and GSH level by 45% and 84%, respectively. LDH-activity increased by 114% and TBARS content by 90%. CCl(4)induced the expected severe damage on the examined parameters. CCl(4) induced toxicity was attenuated after lovastatin pretreatment, which was expressed in less increased values of LDH activity and TBARS levels, as well as in less decreased cell viability and GSH concentrations. However, the pretreatment of hepatocytes with amiodarone abolished the protective effect of lovastatin. CONCLUSION:We suggest that the observed cytoprotective effect was due to interactions between lovastatin, CCl(4) and amiodarone at a metabolic level.
    背景与目标:
  • 【胺碘酮治疗儿童心脏手术后交界性异位性心动过速: 两例报告并文献复习。】 复制标题 收藏 收藏
    DOI:10.1097/00045391-199907000-00008 复制DOI
    作者列表:Michael JG,Wilson WR Jr,Tobias JD
    BACKGROUND & AIMS: :Junctional ectopic tachycardia (JET) occurs most frequently after operative repair of congenital heart defects. The mechanism is thought to involve direct trauma to the atrioventricular node and His bundle resulting in an ectopic focus. Several therapeutic methods have been described in the pediatric literature with varying degrees of success and complication rates. Because heart rates may exceed 200 to 300 beats per minute, there may be inadequate time for ventricular filling. Ventricular filling can be further compromised because of the asynchrony between the atria and the ventricles. These factors can lead to significant compromise of cardiovascular function in the postoperative patient. We describe our experience with amiodarone in two patients who developed postoperative JET after repair of congenital heart defects. Dosing regimens and previous experience with amiodarone in patients with JET are reviewed.
    背景与目标: : 先天性心脏缺损的手术修复后,交界性异位心动过速 (JET) 最常见。该机制被认为涉及对房室结及其束的直接创伤,导致异位灶。儿科文献中已经描述了几种治疗方法,其成功率和并发症发生率不同。因为心率可能超过每分钟200到300次,所以心室充盈的时间可能不足。由于心房和心室之间的不同步,可以进一步损害心室充盈。这些因素可能会导致术后患者的心血管功能显着受损。我们描述了两名在先天性心脏缺损修复后出现术后喷射的患者中使用胺碘酮的经验。回顾了JET患者的给药方案和以前使用胺碘酮的经验。
  • 【胺碘酮,维拉帕米和奎尼丁不影响地高辛的平衡结合。】 复制标题 收藏 收藏
    DOI:10.1097/00005344-199010000-00001 复制DOI
    作者列表:Colvin RA,Ashavaid TF,Katz AM,Messineo FC
    BACKGROUND & AIMS: :The binding of [3H]digoxin to purified canine cardiac sarcolemmal vesicles was characterized. Scatchard analysis of saturation isotherms yielded linear plots with a maximal binding capacity of 174 +/- 31.9 pmol/mg, a dissociation constant of 31.7 +/- 4.59 nM, and a Hill coefficient of 0.947 +/- 0.02 (mean +/- SEM), suggesting that [3H]digoxin bound to a single class of sites. In contrast to their marked effect on steady-state serum digoxin levels when administered in combination, quinidine, verapamil, and amiodarone were without effect on equilibrium binding of [3H]digoxin. Thus, increased steady-state serum concentrations of digoxin resulting from combination therapy with these particular drugs probably will have cardiac effects that may increase the risk of digitoxicity to the patient.
    背景与目标: : 表征了 [3H] 地高辛与纯化的犬心脏肌膜囊泡的结合。饱和等温线的Scatchard分析得出线性曲线,最大结合能力为174/- 31.9 pmol/mg,解离常数为31.7/- 4.59 nM,和0.947 +/- 0.02的希尔系数 (平均值 +/- SEM),表明 [3H] 地高辛结合到单一类别的位点。与联合给药时它们对稳态血清地高辛水平的显著影响相反,奎尼丁,维拉帕米,胺碘酮对 [3H] 地高辛的平衡结合没有影响。因此,与这些特定药物联合治疗导致地高辛的稳态血清浓度增加可能会产生心脏效应,这可能会增加患者的数字化风险。
  • 【静脉注射胺碘酮用于终止血液动力学耐受的持续性室性心动过速的药理学: 推注剂量胺碘酮是合适的一线治疗吗?】 复制标题 收藏 收藏
    DOI:10.1136/emj.2007.051086 复制DOI
    作者列表:Tomlinson DR,Cherian P,Betts TR,Bashir Y
    BACKGROUND & AIMS: OBJECTIVE:To examine the efficacy of bolus dose intravenous amiodarone for the pharmacological termination of haemodynamically-tolerated sustained monomorphic ventricular tachycardia (VT). DESIGN, SETTING AND PARTICIPANTS:Retrospective case series of consecutive emergency admissions with haemodynamically-tolerated sustained monomorphic VT administered bolus dose intravenous amiodarone 300 mg, according to current UK advanced life support practice guidelines. MAIN OUTCOME MEASURES:Pharmacological termination rates within 20 min and 1 h and incidence of hypotension requiring emergency direct current cardioversion (DCCV) during this period. RESULTS:41 patients (35 men) of mean (SD) age 68 (10) years, the majority (85%) with ischaemic heart disease and impaired left ventricular function (mean (SD) ejection fraction 0.31 (0.11)), were enrolled in the study. The median VT duration was 70 min (range 15-6000), mean heart rate was 174 (34) bpm and systolic and diastolic blood pressures were 112 (22) and 73 (19) mm Hg, respectively. Pharmacological VT termination occurred within 20 min in 6/41 patients (15%; 95% CI 7% to 29%) and within 1 h in 12/41 patients (29%; 95% CI 18% to 45%). Haemodynamic deterioration requiring emergency DCCV occurred in 7/41 patients (17%; 95% CI 8% to 32%). CONCLUSIONS:Although advocated by advanced life support guidelines, bolus dose intravenous amiodarone was relatively ineffective for acutely terminating haemodynamically-tolerated sustained monomorphic VT with a significant incidence of haemodynamic destabilisation requiring emergency DCCV. Previous studies in the identical clinical setting suggest that alternative antiarrhythmic agents, particularly intravenous procainamide and sotalol, may be superior. A prospective randomised trial is required to determine the optimal drug treatment for stable sustained monomorphic VT in the emergency setting.
    背景与目标:
  • 10 [Cirrhosis caused by amiodarone]. 复制标题 收藏 收藏

    【[胺碘酮引起的肝硬化]。】 复制标题 收藏 收藏
    DOI: 复制DOI
    作者列表:Reñe JM,Buenestado J,Pais B,Piñol MC
    BACKGROUND & AIMS: A woman who had been taking amiodarone--400 mg/day--for over nine years, developed cirrhosis. Electron microscopy showed phospholipid-laden lysosomal lamellar bodies containing myelin figures. A review is made about the reported cases of amiodarone-induced cirrhosis, including detailed histological findings. We conclude that periodical clinical and biochemical monitoring must be made in patients receiving treatment with amiodarone, and that the pathophysiologic mechanism responsible for the amiodarone toxicity still remains unclear.

    背景与目标: 一名服用胺碘酮 (400毫克/天) 超过9年的妇女发展为肝硬化。电子显微镜显示载有磷脂的溶酶体层状体含有髓鞘图。对胺碘酮引起的肝硬化的报道病例进行了综述,包括详细的组织学发现。我们得出的结论是,必须对接受胺碘酮治疗的患者进行定期的临床和生化监测,并且导致胺碘酮毒性的病理生理机制仍不清楚。
  • 【胺碘酮对大鼠心肌中甲状腺素对三碘甲状腺素的5 '-脱碘作用的影响。】 复制标题 收藏 收藏
    DOI:10.1677/joe.0.1210431 复制DOI
    作者列表:Ceppi JA,Zaninovich AA
    BACKGROUND & AIMS: :The present work studied the effects of amiodarone (AMD) and iopanoic acid (IA) on the conversion of thyroxine (T4) to tri-iodothyronine (T3) by rat myocardium. In vivo: male Wistar rats weighing 200-250 g were injected i.p. with AMD (2.5 mg/100 g body weight per day for 12 days) or IA (5 mg/100 g body weight every 12 h for 72 h). Hearts were then removed and processed as in the in-vitro studies. In vitro: hearts were homogenized in Krebs-Ringer phosphate buffer (pH 7.4) and AMD (0.1 mmol/l) or IA (10 mmol/l) plus dithiothreitol (8 mmol/l) and 0.01 microCi [125I]T4 or [125I]T3 were added. After incubation for 2 h at 37 degrees C, radioactive compounds were identified by paper chromatography. Both AMD and IA given in vivo blocked T4 and T3 conversion significantly (P less than 0.005). When added in vitro, AMD failed to inhibit T4 deiodination to T3 whereas IA induced a significant (P less than 0.005) decrease in T3 generation. Deiodination of [125I]T3 by heart homogenates was not altered by AMD or IA. While the expected increase in circulating T4 (P less than 0.001) and decrease in T3 (P less than 0.001) did occur after AMD or IA treatment, plasma TSH in AMD-treated rats was decreased (P less than 0.001), while in IA-treated animals it was increased (P less than 0.001), thus indicating that AMD did not inhibit pituitary type-II 5'-monodeiodinase.(ABSTRACT TRUNCATED AT 250 WORDS)
    背景与目标: : 本工作研究了胺碘酮 (AMD) 和碘酸 (IA) 对大鼠心肌将甲状腺素 (T4) 转化为三碘甲状腺素 (T3) 的影响。体内: i.p.注射体重200-250g的雄性Wistar大鼠。用AMD (每天2.5 mg/100克体重,持续12天) 或IA (每12小时5 mg/100克体重,持续72小时)。然后像体外研究一样取出心脏并进行处理。体外: 将心脏在Krebs-Ringer磷酸盐缓冲液 (pH 7.4) 和AMD (0.1 mmol/l) 或IA (10 mmol/l) 加二硫苏糖醇 (8 mmol/l) 中匀浆,并加入0.01 microCi [125I]T4或 [125I]T3。在37度下孵育2小时后C,放射性化合物通过纸色谱法进行鉴定。AMD和IA在体内均显著阻断了T4和T3的转化 (P小于0.005)。当在体外添加时,AMD未能抑制T4脱碘至T3,而IA诱导T3代显着 (P小于0.005) 减少。心脏匀浆对 [125I]T3的脱碘作用没有被AMD或IA改变。而循环T4的预期增加 (P小于0.001) 和T3的减少 (P小于0.001) 确实发生在AMD或IA治疗后,AMD治疗的大鼠血浆TSH降低 (P小于0.001),而IA治疗的动物血浆TSH升高 (P小于0.001),因此表明AMD没有抑制垂体II型5 '-单脱碘酶。(摘要截短于250字)
  • 【胺碘酮对兔心肌细胞收缩作用的年龄依赖性变化。】 复制标题 收藏 收藏
    DOI:10.1177/107424849900400105 复制DOI
    作者列表:Chen F,Naim S,Friedman WF,Klitzner TS,Wetzel GT
    BACKGROUND & AIMS: :BACKGROUND: Intravenous amiodarone has increasingly been used to control life-threatening atrial and ventricular arrhythmias. In addition to its four antiarrhythmic properties, amiodarone may have complex effects on intracellular Ca(2+) stores and myocyte contractility. METHODS AND RESULTS: Contraction amplitude was recorded for cardiac ventricular myocytes isolated from neonatal and adult rabbits. Sarcoplasmic reticulum (SR) Ca(2+) stores were loaded to steady-state levels by a train of eight electric field stimulations. The SR Ca(2+) load was quantified by recording the contraction amplitude resulting from the complete depletion of SR Ca(2+) stores by exposing the cell to a 1-second pulse of 10 mmol/L caffeine. After the cells were exposed to 1 µmol/L amiodarone for 10 minutes, electrically stimulated contraction amplitudes significantly decreased in both adult and neonatal cells. Caffeine-induced cell contraction amplitudes were not affected by amiodarone in adult ventricular myocytes. By contrast, amiodarone markedly inhibited caffeine-induced contractions in neonatal ventricular myocytes. The inhibitory effect of amiodarone on the caffeine-induced contractions was not replicated by Ca(2+) channel blockade with diltiazem. CONCLUSIONS: Amiodarone markedly inhibits caffeine-induced contraction in neonatal myocytes but has no significant effect on adult myocytes. Ca(2+) influx through amiodarone-sensitive Ca(2+) channels may play a primary role in maintaining SR Ca(2+) stores in neonatal heart.
    背景与目标: 背景: 静脉注射胺碘酮已越来越多地用于控制危及生命的心房和室性心律失常。除了具有四种抗心律失常特性外,胺碘酮还可能对细胞内Ca(2) 存储和心肌细胞收缩能力具有复杂的作用。方法和结果: 记录从新生和成年兔分离的心室肌细胞的收缩幅度。通过八次电场刺激将肌浆网 (SR) Ca(2) 存储加载到稳态水平。通过将细胞暴露于10 mmol/L咖啡因的1秒脉冲来记录SR Ca(2) 存储完全耗尽所产生的收缩幅度,从而量化SR Ca(2) 负载。将细胞暴露于1 µ mol/L胺碘酮10分钟后,成年和新生细胞的电刺激收缩幅度均显着降低。成年心室肌细胞中咖啡因诱导的细胞收缩幅度不受胺碘酮的影响。相比之下,胺碘酮可显着抑制咖啡因诱导的新生儿心室肌细胞收缩。胺碘酮对咖啡因诱导的收缩的抑制作用未通过地尔硫卓的Ca(2) 通道阻断来复制。结论: 胺碘酮可明显抑制咖啡因诱导的新生肌细胞收缩,但对成年肌细胞无明显影响。Ca(2) 通过胺碘酮敏感的Ca(2) 通道流入可能在维持新生儿心脏中的SR Ca(2) 存储中起主要作用。
  • 【与胺碘酮相比,1C类抗心律失常药 (普罗帕酮) 治疗感染性休克室上性心律失常的疗效和安全性: 一项前瞻性随机双盲研究的方案。】 复制标题 收藏 收藏
    DOI:10.1136/bmjopen-2019-031678 复制DOI
    作者列表:Balik M,Waldauf P,Maly M,Matousek V,Brozek T,Rulisek J,Porizka M,Sachl R,Otahal M,Brestovansky P,Svobodova E,Flaksa M,Stach Z,Pazout J,Duska F,Smid O,Stritesky M
    BACKGROUND & AIMS: INTRODUCTION:Supraventricular arrhythmias contribute to haemodynamic compromise in septic shock. A retrospective study generated the hypothesis that propafenone could be more effective than amiodarone in achieving and maintaining sinus rhythm (SR). Certain echocardiographic parameters may predict a successful cardioversion and help in the decision on rhythm or rate control strategy. METHODS AND ANALYSIS:The trial includes septic shock patients with new-onset arrhythmia, but without severe impairment of the left ventricular ejection fraction. After baseline echocardiography, the patient is randomised to receive a bolus and maintenance dose of either amiodarone or propafenone. The primary outcome is the proportion of patients that have achieved rhythm control at 24 hours after the start of the infusion. The secondary outcomes are the percentages of patients that needed rescue treatments (DC cardioversion or unblinding and crossover of the antiarrhythmics), the recurrence of arrhythmias, intensive care unit mortality, 28-day and 1-year mortality. In the posthoc analysis, we separately assess subgroups of patients with pulmonary hypertension and right ventricular dysfunction. In the exploratory part of the study, we assess whether the presence of a transmitral diastolic A wave and its higher velocity-time integral is predictive for the sustainability of mechanical SR and whether the indexed left atrial endsystolic volume is predictive of recurrent arrhythmia. Considering that the restoration of SR within 24 hours occurred in 74% of the amiodarone-treated patients and in 89% of the patients treated with propafenone, we plan to include 200 patients to have an 80% chance to demonstrate the superiority of propafenone at p=0.05. ETHICS AND DISSEMINATION:The trial is recruiting patients according to its second protocol version approved by the University Hospital Ethical Board on the 6 October 2017 (No. 1691/16S-IV). The results will be disseminated through peer reviewed publications and conference presentations. TRIAL REGISTRATION NUMBER:NCT03029169.
    背景与目标:
  • 【胺碘酮合并治疗perhexiline的一系列病例。】 复制标题 收藏 收藏
    DOI:10.1097/FTD.0b013e318245e5a6 复制DOI
    作者列表:Gilutz H,Frenneaux MP,Horowitz JD
    BACKGROUND & AIMS: BACKGROUND:Concomitant treatment with amiodarone and perhsexiline has been considered to be relatively contraindicated because of the hypothetical risk of potentiated adverse effects mediated by additive inhibition of carnitine palmitoyl transferase 1. AIM:To study the prevalence of adverse effects associated with the concomitant use of perhexiline and amiodarone. METHODS:A retrospective analysis of a single hospital database of patients receiving perhexiline and amiodarone between July 2009 and April 2011. Files were reviewed for short- and long-term adverse effects requiring drug cessation. Glucose concentration, gamma glutamyl transferase activity. and perhexiline blood concentrations were recorded. RESULTS:We identified 26 patients concomitantly treated with perhexiline and amiodarone, 20 on a long-term basis. In 6 cases, amiodarone was introduced on top of preceding perhexiline. In none of the cases were drugs stopped because of adverse effects. Although blood glucose concentrations fell significantly 48 hours postadmission to hospital, this seems to reflect the resolution of "admission hyperglycemia" rather than onset of hypoglycemia; the latter was rare (5 patients), mild, and clinically silent. In 4 patients, gamma glutamyl transferase approximately doubled. CONCLUSIONS:Traditionally, concomitant treatment with amiodarone and perhexiline has been considered to be relatively contraindicated on the basis of the theoretical potential for synergistic toxicity. This cohort of 26 patients received this concomitant treatment without any excess of major adverse reactions. Our findings suggest that concomitant treatment with perhexiline and amiodarone may be safe in the setting of (1) previous tolerance of either agent, and (2) titration of plasma perhexiline concentrations to guide therapy.
    背景与目标:
  • 【长期服用胺碘酮对猪缺血性心肌病模型心肌纤维化和左心室重构演变的影响。】 复制标题 收藏 收藏
    DOI:10.1186/s40064-016-3249-3 复制DOI
    作者列表:Zagorianou A,Marougkas M,Drakos SG,Diakos N,Konstantopoulos P,Perrea DN,Anastasiou-Nana M,Malliaras K
    BACKGROUND & AIMS: :Amiodarone is effective in suppressing arrhythmias in heart failure patients. We investigated the effect of long-term amiodarone administration on myocardial fibrosis and left ventricular (LV) remodeling in a porcine model of ischemic cardiomyopathy. Eighteen infarcted farm pigs were randomized to receive long-term amiodarone administration for 3 months (n = 9) or conventional follow-up (n = 9). Evolution of LV remodeling over 3 months post-myocardial infarction was examined at tissue level (myocyte size, myocardial fibrosis and vascular density assessed by whole-field digital histopathology), organ level (LV structure and function assessed by echocardiography), and systemic level (BNP and MMP-9 levels). Long-term administration of the standard anti-arrhythmic doses of amiodarone was not associated with adverse effects on myocardial fibrosis and other features of adverse cardiac remodeling. This favorable safety profile suggests that long-term anti-arrhythmic therapy with amiodarone warrants further clinical investigation in the subpopulation of heart failure patients with significantly increased burden of arrhythmias.
    背景与目标: : 胺碘酮可有效抑制心力衰竭患者的心律失常。我们研究了长期服用胺碘酮对缺血性心肌病猪模型中心肌纤维化和左心室 (LV) 重塑的影响。将18只梗塞的猪随机分配接受长期胺碘酮给药3个月 (n = 9) 或常规随访 (n = 9)。在组织水平 (通过全场数字组织病理学评估心肌细胞大小,心肌纤维化和血管密度),器官水平 (通过超声心动图评估LV结构和功能) 和全身水平 (BNP和MMP-9水平) 检查心肌梗死后3个月左室重塑的演变。长期服用标准抗心律失常剂量的胺碘酮与对心肌纤维化的不良影响和不良心脏重塑的其他特征无关。这种良好的安全性表明,胺碘酮的长期抗心律失常治疗值得在心律失常负担显着增加的心力衰竭患者亚群中进行进一步的临床研究。

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