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Fulltext Metoprolol for prophylaxis of postoperative atrial fibrillation in cardiac surgery patients: systematic review and meta-analysis

Norhayati MN, Shaiful Bahari I, Zaharah S, Nik Hazlina NH, Mohammad Aimanazrul Z, Irfan M

BMJ Open, 2020 10 31;10(10):e038364.
PMID: 33130564 DOI: 10.1136/bmjopen-2020-038364

PURPOSE: Postoperative atrial fibrillation (POAF) is a potentially lethal and morbid complication after open heart surgery. This systematic review and meta-analysis aimed to investigate metoprolol compared with other treatments for prophylaxis against POAF.
METHODS: We searched CENTRAL, MEDLINE, EMBASE and trial registries for randomised controlled trials that evaluated metoprolol for preventing the occurrence of POAF after surgery against other treatments or placebo. Random-effects model was used for estimating the risk ratios (RRs) and mean differences with 95% CIs.
RESULTS: Nine trials involving 1570 patients showed metoprolol reduced POAF compared with placebo (416 patients; RR 0.46, 95% CI 0.33 to 0.66; I²=21%; risk difference (RD) -0.19, 95% CI -0.28 to -0.10). However, metoprolol increased the risk of POAF compared with carvedilol (159 patients; RR 1.59, 95% CI 1.20 to 2.12; I²=4%; RD 0.13, 95% CI 0.06 to 0.20). There was no difference when compared with sotalol or amiodarone. The occurrence of cardiovascular conditions after drugs administration or death between the groups was not different. The overall quality of evidence was moderate to high. Subgroup analysis and funnel plot were not performed.
CONCLUSIONS: Metoprolol is effective in preventing POAF compared with placebo and showed no difference with class III antiarrhythmic drugs. Death and thromboembolism are associated with open heart surgery, but not significant in relation to the use of metoprolol.
PROSPERO REGISTRATION NUMBER: CRD42019131585.

Matched MeSH terms: Anti-Arrhythmia Agents/therapeutic use
Amiodarone-induced phospholipidosis: an in vivo [14C]-acetate uptake study in rat

Sirajudeen KN, Gurumoorthy P, Devaraj H, Devaraj SN

Drug Chem Toxicol, 2002 Aug;25(3):247-54.
PMID: 12173246

Amiodarone (AD), a potent antiarrhythmic drug, is often associated with several adverse effects. It is shown to accumulate phospholipids in various tissues, and the impaired catabolism of phospholipids has been implicated in AD-induced phospholipidosis. The synthesis of phospholipids in tissues has not been dealt with. Hence, the incorporation of [14C]-acetate into phospholipids has been studied to understand the AD-induced phospholipidosis in lung and liver. A significant increase in lung and liver phospholipids was observed after 21 and 28 days of AD (175 mg/kg body weight/day) treatment. In the lung and liver, the incorporation of [14C]-acetate into all phospholipid fractions was elevated, while in the lung mitochondria phosphatidylcholine, phosphatidyl ethanolamine and the cardiolipin levels were significantly increased. The results indicate that, in addition to the impaired catabolism of phospholipid, AD treatment resulted in increased phospholipid synthesis.

Matched MeSH terms: Anti-Arrhythmia Agents/adverse effects*; Anti-Arrhythmia Agents/pharmacokinetics
Fulltext Multiple targets for flecainide action: implications for cardiac arrhythmogenesis

Salvage SC, Chandrasekharan KH, Jeevaratnam K, Dulhunty AF, Thompson AJ, Jackson AP, et al.

Br J Pharmacol, 2018 Apr;175(8):1260-1278.
PMID: 28369767 DOI: 10.1111/bph.13807

Flecainide suppresses cardiac tachyarrhythmias including paroxysmal atrial fibrillation, supraventricular tachycardia and arrhythmic long QT syndromes (LQTS), as well as the Ca2+ -mediated, catecholaminergic polymorphic ventricular tachycardia (CPVT). However, flecainide can also exert pro-arrhythmic effects most notably following myocardial infarction and when used to diagnose Brugada syndrome (BrS). These divergent actions result from its physiological and pharmacological actions at multiple, interacting levels of cellular organization. These were studied in murine genetic models with modified Nav channel or intracellular ryanodine receptor (RyR2)-Ca2+ channel function. Flecainide accesses its transmembrane Nav 1.5 channel binding site during activated, open, states producing a use-dependent antagonism. Closing either activation or inactivation gates traps flecainide within the pore. An early peak INa related to activation of Nav channels followed by rapid de-activation, drives action potential (AP) upstrokes and their propagation. This is diminished in pro-arrhythmic conditions reflecting loss of function of Nav 1.5 channels, such as BrS, accordingly exacerbated by flecainide challenge. Contrastingly, pro-arrhythmic effects attributed to prolonged AP recovery by abnormal late INaL following gain-of-function modifications of Nav 1.5 channels in LQTS3 are reduced by flecainide. Anti-arrhythmic effects of flecainide that reduce triggering in CPVT models mediated by sarcoplasmic reticular Ca2+ release could arise from its primary actions on Nav channels indirectly decreasing [Ca2+ ]i through a reduced [Na+ ]i and/or direct open-state RyR2-Ca2+ channel antagonism. The consequent [Ca2+ ]i alterations could also modify AP propagation velocity and therefore arrhythmic substrate through its actions on Nav 1.5 channel function. This is consistent with the paradoxical differences between flecainide actions upon Na+ currents, AP conduction and arrhythmogenesis under circumstances of normal and increased RyR2 function.
LINKED ARTICLES: This article is part of a themed section on Spotlight on Small Molecules in Cardiovascular Diseases. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v175.8/issuetoc.

Matched MeSH terms: Anti-Arrhythmia Agents/pharmacology*; Anti-Arrhythmia Agents/therapeutic use
Evaluation of Teaching Clinical Pharmacology of Antiarrhythmic Drugs to First-Year MBBS Students Through Worksheet-Based Small-Group Discussion

Hasamnis AA, Arya A

J Pharm Bioallied Sci, 2017 Oct-Dec;9(4):282-283.
PMID: 29456381 DOI: 10.4103/jpbs.JPBS_96_17

Cardiac arrhythmias are a major cause of morbidity and mortality across the world. Learning the science behind the use of antiarrhythmic drugs is essential for all medical graduates. However, many antiarrhythmic drugs are available, and most of them have complex pharmacodynamic and pharmacokinetic profiles. We tried to improvise our teaching by conducting interactive, worksheet-based, small-group discussion on antiarrhythmic drugs with preclinical students of School of Medicine, Taylor's University, Malaysia. This survey was conducted to analyze the outcomes of worksheet-based, small-group discussion.

Matched MeSH terms: Anti-Arrhythmia Agents
Fulltext Drug-induced Brugada syndrome

Yap YG, Behr ER, Camm AJ

Europace, 2009 Aug;11(8):989-94.
PMID: 19482855 DOI: 10.1093/europace/eup114

Brugada syndrome is an inherited cardiac arrhythmia condition characterized by (i) coved ST-elevation and J point elevation of at least 2 mm in at least two of the right precordial ECG leads (V1-V3) and (ii) ventricular arrhythmias, syncope, and sudden death. Patients with Brugada syndrome or suspected mutation carriers can have normal ECG recordings at other times. In these cases, a diagnostic challenge with a sodium channel blocker such as ajmaline, flecainide, or pilsicainide may induce the full-blown type 1 ECG pattern and support the diagnosis. However, recently, many other pharmacological agents not related to class I anti-arrhythmic agents have been reported to induce Brugada ECG patterns including tricyclic antidepressants, fluoxetine, lithium, trifluoperazine, antihistamines, and cocaine. As published reports of the drug-induced Brugada sign have become increasingly prevalent, there is growing interest in the mechanisms responsible for this acquired ECG pattern and its clinical significance. It is possible that drug-induced Brugada syndrome may be due to an individual susceptibility that favours drug-induced ECG abnormalities, possibly as a result of an increase in a latent ion channel dysfunction similar to that in drug-induced long QT syndrome. However, further evidence is needed to confirm this postulation. In this paper, we will review the cases and evidence of drug-induced Brugada syndrome reported in the literature.

Matched MeSH terms: Anti-Arrhythmia Agents/adverse effects*
Impact of first-line cryoablation for atrial fibrillation on healthcare utilization, arrhythmia disease burden and efficacy outcomes: real-world evidence from the Cryo Global Registry

Zucchelli G, Chun KRJ, Khelae SK, Földesi C, Kueffer FJ, van Bragt KA, et al.

J Interv Card Electrophysiol, 2023 Apr;66(3):711-722.
PMID: 36331681 DOI: 10.1007/s10840-022-01388-6

BACKGROUND: Cryoballoon ablation (CBA) is an effective first-line treatment for symptomatic atrial fibrillation (AF), as recently demonstrated by three randomized trials. This sub-analysis of the Cryo Global Registry aims to examine current clinical practices of first-line CBA.
METHODS: AF patients treated with first-line CBA were compared to CBA in antiarrhythmic drug (AAD)-refractory patients at 12 months. Efficacy was examined using time-to-first atrial arrhythmia recurrence following a 90-day blanking period. Healthcare utilization was evaluated by repeat ablations and hospitalizations. Disease burden was examined by assessing quality of life (QOL) and patients' reporting of symptoms.
RESULTS: Of 1394 patients, 433 (31.1%) were treated with first-line CBA, which was more frequent in high-volume centers. Serious procedure-related adverse event rates were similar. Efficacy at 12 months was higher in the first-line group (87.8 vs. 81.6%, HRunadj 0.64 (95% CI 0.47-0.88); p

Matched MeSH terms: Anti-Arrhythmia Agents/therapeutic use
The relevance of CYP2D6 genetic polymorphism on chronic metoprolol therapy in cardiovascular patients

Ismail R, Teh LK

J Clin Pharm Ther, 2006 Feb;31(1):99-109.
PMID: 16476126

CYP2D6 polymorphisms are well described in normal populations but there are few data on its clinical significance. We therefore investigated the influence of CYP2D6 polymorphism on steady-state plasma concentrations and apparent oral clearance of metoprolol in patients with cardiovascular diseases.

Matched MeSH terms: Anti-Arrhythmia Agents/blood; Anti-Arrhythmia Agents/pharmacokinetics; Anti-Arrhythmia Agents/therapeutic use
Fulltext Intrauterine management of fetal supraventricular tachycardia (SVT) with cardiac failure

Muniswaran G, Japaraj RP, Asri Ranga AR, Cheong HK

Med J Malaysia, 2015 Dec;70(6):371-2.
PMID: 26988216 MyJurnal

Fetal arrhythmias are not uncommon in pregnancy. The diagnosis can be established on routine ultrasound scan. Fetal supraventricular tachycardia (SVT) is the most common cause of fetal tachycardia. If left undiagnosed and untreated, these fetuses may develop cardiac failure, hydrops fetalis and eventually death. We report two fetuses diagnosed antenatally to have fetal SVT. Both fetuses were in cardiac failure and were successfully treated with maternal administration of antiarrhythmic medications. Digoxin, and in severe instances, a combination with flecanaide significantly improved fetal outcomes and prevented fetal mortality. The long term prognosis of such patients are good.

Matched MeSH terms: Anti-Arrhythmia Agents
Fulltext Fetal supraventricular tachycardia--a case report

Soh EBS, Raman S, Chia PMK

Med J Malaysia, 1998 Sep;53(3):280-3.
PMID: 10968167

A gravid patient with fetal supraventricular tachycardia is presented. A review of this rare condition and the present recommended mode of therapy are discussed.

Matched MeSH terms: Anti-Arrhythmia Agents/therapeutic use
Thyrotoxic periodic paralysis and intravenous propranolol in the emergency setting

Birkhahn RH, Gaeta TJ, Melniker L

J Emerg Med, 2000 Feb;18(2):199-202.
PMID: 10699522

A 27-year-old male of Malaysian descent presented to the Emergency Department (ED) with rapidly progressive flaccid paralysis that quickly compromised his respiratory effort. The patient was found to have a serum potassium of 1.9 meq/L, and was diagnosed as having an acute paralytic episode secondary to thyrotoxic periodic paralysis. The paralytic attack was aborted with a combination of potassium replacement and parenteral propranolol in large doses. We report the use of a rarely described, yet possibly more effective, therapy for an acute attack of thyrotoxic periodic paralysis.

Matched MeSH terms: Anti-Arrhythmia Agents/administration & dosage*
Fulltext Cardiac Potassium Channels: Physiological Insights for Targeted Therapy

Jeevaratnam K, Chadda KR, Huang CL, Camm AJ

J Cardiovasc Pharmacol Ther, 2018 03;23(2):119-129.
PMID: 28946759 DOI: 10.1177/1074248417729880

The development of novel drugs specifically directed at the ion channels underlying particular features of cardiac action potential (AP) initiation, recovery, and refractoriness would contribute to an optimized approach to antiarrhythmic therapy that minimizes potential cardiac and extracardiac toxicity. Of these, K+ channels contribute numerous and diverse currents with specific actions on different phases in the time course of AP repolarization. These features and their site-specific distribution make particular K+ channel types attractive therapeutic targets for the development of pharmacological agents attempting antiarrhythmic therapy in conditions such as atrial fibrillation. However, progress in the development of such temporally and spatially selective antiarrhythmic drugs against particular ion channels has been relatively limited, particularly in view of our incomplete understanding of the complex physiological roles and interactions of the various ionic currents. This review summarizes the physiological properties of the main cardiac potassium channels and the way in which they modulate cardiac electrical activity and then critiques a number of available potential antiarrhythmic drugs directed at them.

Matched MeSH terms: Anti-Arrhythmia Agents/therapeutic use
Evaluation of a technique to measure heart rate variability in anaesthetised cats

Khor KH, Shiels IA, Campbell FE, Greer RM, Rose A, Mills PC

Vet J, 2014 Feb;199(2):229-35.
PMID: 24321367 DOI: 10.1016/j.tvjl.2013.11.006

Analysis of heart rate (HR) and heart rate variability (HRV) are powerful tools to investigate cardiac diseases, but current methods, including 24-h Holter monitoring, can be cumbersome and may be compromised by movement artefact. A commercially available data capture and analysis system was used in anaesthetised healthy cats to measure HR and HRV during pharmacological manipulation of HR. Seven healthy cats were subjected to a randomised crossover study design with a 7 day washout period between two treatment groups, placebo and atenolol (1mg/kg, IV), with the efficacy of atenolol to inhibit β1 adrenoreceptors challenged by epinephrine. Statistical significance for the epinephrine challenge was set at P<0.0027 (Holm-Bonferroni correction), whereas a level of significance of P<0.05 was set for other variables. Analysis of the continuous electrocardiography (ECG) recordings showed that epinephrine challenge increased HR in the placebo group (P=0.0003) but not in the atenolol group. The change in HR was greater in the placebo group than in the atenolol group (P=0.0004). Therefore, compared to cats pre-treated with placebo, pre-treatment with atenolol significantly antagonised the tachycardia while not significantly affecting HRV. The increased HR in the placebo group following epinephrine challenge was consistent with a shift of the sympathovagal balance towards a predominantly sympathetic tone. However, the small (but not significant at the critical value) decrease in the normalised high-frequency component (HFnorm) in both groups of cats suggested that epinephrine induced a parasympathetic withdrawal in addition to sympathetic enhancement (increased normalised low frequency component or LFnorm). In conclusion, this model is a highly sensitive and repeatable model to investigate HRV in anaesthetised cats that would be useful in the laboratory setting for short-term investigation of cardiovascular disease and subtle responses to pharmacological agents in this species.

Matched MeSH terms: Anti-Arrhythmia Agents/pharmacology
Hypokalemic periodic paralysis due to Graves disease

Drakaki A, Habib M, Sweeney AT

Am J Med, 2009 Dec;122(12):e5-6.
PMID: 19958876 DOI: 10.1016/j.amjmed.2009.06.016

Hypokalemic thyrotoxic periodic paralysis is a potentially life-threatening complication of hyperthyroidism, defined by 3 characteristic features: thyrotoxicosis, hypokalemia, and acute painless muscle weakness. In this case, a 25-year-old Malaysian man presented with acute, painless lower extremity weakness immediately after a meal. His associated symptoms included palpitations, tremor, and anxiety. He also reported a 30-pound unintentional weight loss over the previous 18 months, dyspnea on exertion, and insomnia.

Matched MeSH terms: Anti-Arrhythmia Agents/therapeutic use

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