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JACC. Clinical Electrophysiology Jan 2022Increasing maternal mortality and incidence of arrhythmias in pregnancy have been noted over the past 2 decades in the United States. Pregnancy is associated with a... (Review)
Review
Increasing maternal mortality and incidence of arrhythmias in pregnancy have been noted over the past 2 decades in the United States. Pregnancy is associated with a greater risk of arrhythmias, and patients with a history of arrhythmias are at significant risk of arrhythmia recurrence during pregnancy. The incidence of atrial fibrillation in pregnancy is rising. This review discusses the management of tachyarrhythmias and bradyarrhythmias in pregnancy, including management of cardiac arrest. Management of fetal arrhythmias are also reviewed. For patients without structural heart disease, β-blocker therapy, especially propranolol and metoprolol, and antiarrhythmic drugs, such as flecainide and sotalol, can be safely used to treat tachyarrhythmias. As a last resort, catheter ablation with minimal fluoroscopy can be performed. Device implantation can be safely performed with minimal fluoroscopy and under echocardiographic or ultrasound guidance in patients with clear indications for devices during pregnancy. Because of rising maternal mortality in the United States, which is partly driven by increasing maternal age and comorbidities, a multidisciplinary and/or integrative approach to arrhythmia management from the prepartum to the postpartum period is needed.
Topics: Anti-Arrhythmia Agents; Atrial Fibrillation; Female; Flecainide; Humans; Pregnancy; Sotalol; Tachycardia
PubMed: 35057977
DOI: 10.1016/j.jacep.2021.10.004 -
Nature Reviews. Cardiology Jul 2019Postoperative atrial fibrillation (POAF) complicates 20-40% of cardiac surgical procedures and 10-20% of non-cardiac thoracic operations. Typical features include onset... (Review)
Review
Postoperative atrial fibrillation (POAF) complicates 20-40% of cardiac surgical procedures and 10-20% of non-cardiac thoracic operations. Typical features include onset at 2-4 days postoperatively, episodes that are often fleeting and a self-limited time course. Associated adverse consequences of POAF include haemodynamic instability, increased risk of stroke, lengthened hospital and intensive care unit stays and greater costs. Underlying mechanisms are incompletely defined but include intraoperative and postoperative phenomena, such as inflammation, sympathetic activation and cardiac ischaemia, that combine to trigger atrial fibrillation, often in the presence of pre-existing factors, making the atria vulnerable to atrial fibrillation induction and maintenance. A better understanding of the underlying mechanisms might enable the identification of new therapeutic targets. POAF can be prevented by targeting autonomic alterations and inflammation. β-Blocker prophylaxis is the best-established preventive therapy and should be started or continued before cardiac surgery, unless contraindicated. When POAF occurs, rate control usually suffices, and routine rhythm control is unnecessary; rhythm control should be reserved for patients who develop haemodynamic instability or show other indications that rate control alone will be insufficient. In this Review, we summarize the epidemiological and clinical features of POAF, the available pathophysiological evidence from clinical and experimental investigations, the results of prophylactic and therapeutic approaches and the consensus recommendations of various national and international societies.
Topics: Adrenergic beta-Antagonists; Amiodarone; Animals; Anti-Arrhythmia Agents; Atrial Fibrillation; Calcium Channel Blockers; Cardiac Pacing, Artificial; Cardiac Surgical Procedures; Heart Atria; Heart Rate; Humans; Myocardial Ischemia; Postoperative Complications; Practice Guidelines as Topic; Sotalol
PubMed: 30792496
DOI: 10.1038/s41569-019-0166-5 -
Basic & Clinical Pharmacology &... Aug 2019Beta-blocker overdose is potentially harmful due to the strong blood pressure-lowering and heart rate-lowering effects. However, conflicting data exist as to their...
Beta-blocker overdose is potentially harmful due to the strong blood pressure-lowering and heart rate-lowering effects. However, conflicting data exist as to their differential toxicity, single-substance exposures and the effect of co-exposure with additional antihypertensive medication. For this, a 10-year retrospective, explorative analysis of the Mainz Poison Center/Germany database with regard to circumstances of beta-blocker exposure, doses, symptoms and treatment was carried out. Analyses were restricted to adult patients with single-substance exposures and co-exposures with one additional antihypertensive substance. Written follow-up information was obtained in half the cases. A total of 2967 cases were analysed, of which 697 were single-substance exposures. Metoprolol was most frequently reported followed by bisoprolol, atenolol, propranolol and sotalol. Metoprolol showed a linear dose-symptom relationship, whereas propranolol and sotalol seemed to have a threshold dose beyond which symptoms aggravated. Symptoms did not differ substantially, except for more seizures being reported with propranolol, and more CNS depression/vomiting with sotalol. Activated charcoal was used in 38%, gastric lavage in 11%, temporary pacemaker in 3%, glucagon in 1%, intubation for respiratory insufficiency and cardiopulmonary resuscitation in 1% and 0.5%. All patients recovered. In 174 co-exposure cases, the distribution of poisoning severity and rate of worsening of symptoms was comparable with single-substance exposures except one patient deceased after bisoprolol and verapamil co-exposure. In adults with beta-blocker overdose, no significant differences in poisoning severity among beta-blockers were detected, and no fatalities were observed with single-substance exposures. Co-exposures with other antihypertensives, sedatives or alcohol should be carefully attended to as fatalities might occur.
Topics: Adrenergic beta-Antagonists; Adult; Aged; Charcoal; Dose-Response Relationship, Drug; Drug Overdose; Female; Gastric Lavage; Germany; Humans; Male; Middle Aged; Poison Control Centers; Retrospective Studies; Severity of Illness Index; Treatment Outcome
PubMed: 30916882
DOI: 10.1111/bcpt.13231 -
Current Clinical Pharmacology 2017The most common acquired cause of Long QT syndrome (LQTS) is drug induced QT interval prolongation. It is an electrophysiological entity, which is characterized by an... (Review)
Review
BACKGROUND
The most common acquired cause of Long QT syndrome (LQTS) is drug induced QT interval prolongation. It is an electrophysiological entity, which is characterized by an extended duration of the ventricular repolarization. Reflected as a prolonged QT interval in a surface ECG, this syndrome increases the risk for polymorphic ventricular tachycardia (Torsade de Pointes) and sudden death.
METHOD
Bibliographic databases as MEDLINE and EMBASE, reports and drug alerts from several regulatory agencies (FDA, EMEA, ANMAT) and drug safety guides (ICH S7B, ICH E14) were consulted to prepare this article. The keywords used were: polymorphic ventricular tachycardia, adverse drug events, prolonged QT, arrhythmias, intensive care unit and Torsade de Pointes. Such research involved materials produced up to December 2017.
RESULTS
Because of their mechanism of action, antiarrhythmic drugs such as amiodarone, sotalol, quinidine, procainamide, verapamil and diltiazem are associated to the prolongation of the QTc interval. For this reason, they require constant monitoring when administered. Other noncardiovascular drugs that are widely used in the Intensive Care Unit (ICU), such as ondansetron, macrolide and fluoroquinolone antibiotics, typical and atypical antipsychotics agents such as haloperidol, thioridazine, and sertindole are also frequently associated with the prolongation of the QTc interval. As a consequence, critical patients should be closely followed and evaluated.
CONCLUSION
ICU patients are particularly prone to experience a QTc interval prolongation mainly for two reasons. In the first place, they are exposed to certain drugs that can prolong the repolarization phase, either by their mechanism of action or through the interaction with other drugs. In the second place, the risk factors for TdP are prevalent clinical conditions among critically ill patients. As a consequence, the attending physician is expected to perform preventive monitoring and ECG checks to control the QTc interval.
Topics: Anti-Arrhythmia Agents; Antipsychotic Agents; Critical Illness; Death, Sudden, Cardiac; Drug-Related Side Effects and Adverse Reactions; Humans; Intensive Care Units; Long QT Syndrome; Risk Factors; Torsades de Pointes
PubMed: 29473523
DOI: 10.2174/1574884713666180223123947 -
Best Practice & Research. Clinical... Jul 2019Fetal dysrhythmias are common abnormalities, usually manifesting as irregular rhythms. Although most irregularities are benign and caused by isolated atrial ectopics, in... (Review)
Review
Fetal dysrhythmias are common abnormalities, usually manifesting as irregular rhythms. Although most irregularities are benign and caused by isolated atrial ectopics, in a few cases, rhythm irregularity may indicate partial atrioventricular block, which has different etiological and prognostic implications. We provide a flowchart for the initial management of irregular rhythm to help select cases requiring urgent specialist referral. Tachycardias and bradycardias are less frequent, can lead to hemodynamic compromise, and may require in utero therapy. Pharmacological treatment of tachycardia depends on the type (supraventricular tachycardia or atrial flutter) and presence of hydrops, with digoxin, flecainide, and sotalol being commonly used. An ongoing randomized trial may best inform about their efficacy. Bradycardia due to blocked bigeminy normally resolves spontaneously, but if it is due to established complete heart block, there is no effective treatment. Ongoing research suggests hydroxychloroquine may reduce the risk of autoimmune atrioventricular block. Sinus bradycardia (rate <3rd centile) may be a prenatal marker for long-QT syndrome.
Topics: Arrhythmias, Cardiac; Echocardiography; Female; Fetal Diseases; Fetal Therapies; Heart Block; Heart Rate, Fetal; Humans; Pregnancy; Risk Assessment; Ultrasonography, Doppler; Ultrasonography, Prenatal
PubMed: 30738635
DOI: 10.1016/j.bpobgyn.2019.01.002 -
Cardiac Electrophysiology Clinics Jun 2016Sotalol is effective for treating atrial fibrillation (AF), ventricular tachycardia, premature ventricular contractions, and supraventricular tachycardia. Racemic (DL)... (Review)
Review
Sotalol is effective for treating atrial fibrillation (AF), ventricular tachycardia, premature ventricular contractions, and supraventricular tachycardia. Racemic (DL) sotalol inhibits the rapid component of the delayed rectifier potassium current. There is a near linear relationship between sotalol dosage and QT interval prolongation. However, in dose ranging trials in patients with AF, low-dose sotalol was not more effective than placebo. Orally administered sotalol has a bioavailability of nearly 100%. The only significant drug interactions are the need to avoid or limit use of concomitant drugs that cause QT prolongation, bradycardia, and/or hypotension.
Topics: Action Potentials; Anti-Arrhythmia Agents; Arrhythmias, Cardiac; Humans; Sotalol
PubMed: 27261833
DOI: 10.1016/j.ccep.2016.02.007 -
The Cochrane Database of Systematic... Sep 2019Atrial fibrillation is the most frequent sustained arrhythmia. Atrial fibrillation often recurs after restoration of normal sinus rhythm. Antiarrhythmic drugs have been...
BACKGROUND
Atrial fibrillation is the most frequent sustained arrhythmia. Atrial fibrillation often recurs after restoration of normal sinus rhythm. Antiarrhythmic drugs have been widely used to prevent recurrence. This is an update of a review previously published in 2006, 2012 and 2015.
OBJECTIVES
To determine the effects of long-term treatment with antiarrhythmic drugs on death, stroke, drug adverse effects and recurrence of atrial fibrillation in people who had recovered sinus rhythm after having atrial fibrillation.
SEARCH METHODS
We updated the searches of CENTRAL, MEDLINE and Embase in January 2019, and ClinicalTrials.gov and WHO ICTRP in February 2019. We checked the reference lists of retrieved articles, recent reviews and meta-analyses.
SELECTION CRITERIA
Two authors independently selected randomised controlled trials (RCTs) comparing any antiarrhythmic drug with a control (no treatment, placebo, drugs for rate control) or with another antiarrhythmic drug in adults who had atrial fibrillation and in whom sinus rhythm was restored, spontaneously or by any intervention. We excluded postoperative atrial fibrillation.
DATA COLLECTION AND ANALYSIS
Two authors independently assessed quality and extracted data. We pooled studies, if appropriate, using Mantel-Haenszel risk ratios (RR), with 95% confidence intervals (CI). All results were calculated at one year of follow-up or the nearest time point.
MAIN RESULTS
This update included one new study (100 participants) and excluded one previously included study because of double publication. Finally, we included 59 RCTs comprising 20,981 participants studying quinidine, disopyramide, propafenone, flecainide, metoprolol, amiodarone, dofetilide, dronedarone and sotalol. Overall, mean follow-up was 10.2 months.All-cause mortalityHigh-certainty evidence from five RCTs indicated that treatment with sotalol was associated with a higher all-cause mortality rate compared with placebo or no treatment (RR 2.23, 95% CI 1.03 to 4.81; participants = 1882). The number need to treat for an additional harmful outcome (NNTH) for sotalol was 102 participants treated for one year to have one additional death. Low-certainty evidence from six RCTs suggested that risk of mortality may be higher in people taking quinidine (RR 2.01, 95% CI 0.84 to 4.77; participants = 1646). Moderate-certainty evidence showed increased RR for mortality but with very wide CIs for metoprolol (RR 2.02, 95% CI 0.37 to 11.05, 2 RCTs, participants = 562) and amiodarone (RR 1.66, 95% CI 0.55 to 4.99, 2 RCTs, participants = 444), compared with placebo.We found little or no difference in mortality with dofetilide (RR 0.98, 95% CI 0.76 to 1.27; moderate-certainty evidence) or dronedarone (RR 0.86, 95% CI 0.68 to 1.09; high-certainty evidence) compared to placebo/no treatment. There were few data on mortality for disopyramide, flecainide and propafenone, making impossible a reliable estimation for those drugs.Withdrawals due to adverse eventsAll analysed drugs increased withdrawals due to adverse effects compared to placebo or no treatment (quinidine: RR 1.56, 95% CI 0.87 to 2.78; disopyramide: RR 3.68, 95% CI 0.95 to 14.24; propafenone: RR 1.62, 95% CI 1.07 to 2.46; flecainide: RR 15.41, 95% CI 0.91 to 260.19; metoprolol: RR 3.47, 95% CI 1.48 to 8.15; amiodarone: RR 6.70, 95% CI 1.91 to 23.45; dofetilide: RR 1.77, 95% CI 0.75 to 4.18; dronedarone: RR 1.58, 95% CI 1.34 to 1.85; sotalol: RR 1.95, 95% CI 1.23 to 3.11). Certainty of the evidence for this outcome was low for disopyramide, amiodarone, dofetilide and flecainide; moderate to high for the remaining drugs.ProarrhythmiaVirtually all studied antiarrhythmics showed increased proarrhythmic effects (counting both tachyarrhythmias and bradyarrhythmias attributable to treatment) (quinidine: RR 2.05, 95% CI 0.95 to 4.41; disopyramide: no data; flecainide: RR 4.80, 95% CI 1.30 to 17.77; metoprolol: RR 18.14, 95% CI 2.42 to 135.66; amiodarone: RR 2.22, 95% CI 0.71 to 6.96; dofetilide: RR 5.50, 95% CI 1.33 to 22.76; dronedarone: RR 1.95, 95% CI 0.77 to 4.98; sotalol: RR 3.55, 95% CI 2.16 to 5.83); with the exception of propafenone (RR 1.32, 95% CI 0.39 to 4.47) for which the certainty of evidence was very low and we were uncertain about the effect. Certainty of the evidence for this outcome for the other drugs was moderate to high.StrokeEleven studies reported stroke outcomes with quinidine, disopyramide, flecainide, amiodarone, dronedarone and sotalol. High-certainty evidence from two RCTs suggested that dronedarone may be associated with reduced risk of stroke (RR 0.66, 95% CI 0.47 to 0.95; participants = 5872). This result is attributed to one study dominating the meta-analysis and has yet to be reproduced in other studies. There was no apparent effect on stroke rates with the other antiarrhythmics.Recurrence of atrial fibrillationModerate- to high-certainty evidence, with the exception of disopyramide which was low-certainty evidence, showed that all analysed drugs, including metoprolol, reduced recurrence of atrial fibrillation (quinidine: RR 0.83, 95% CI 0.78 to 0.88; disopyramide: RR 0.77, 95% CI 0.59 to 1.01; propafenone: RR 0.67, 95% CI 0.61 to 0.74; flecainide: RR 0.65, 95% CI 0.55 to 0.77; metoprolol: RR 0.83 95% CI 0.68 to 1.02; amiodarone: RR 0.52, 95% CI 0.46 to 0.58; dofetilide: RR 0.72, 95% CI 0.61 to 0.85; dronedarone: RR 0.85, 95% CI 0.80 to 0.91; sotalol: RR 0.83, 95% CI 0.80 to 0.87). Despite this reduction, atrial fibrillation still recurred in 43% to 67% of people treated with antiarrhythmics.
AUTHORS' CONCLUSIONS
There is high-certainty evidence of increased mortality associated with sotalol treatment, and low-certainty evidence suggesting increased mortality with quinidine, when used for maintaining sinus rhythm in people with atrial fibrillation. We found few data on mortality in people taking disopyramide, flecainide and propafenone, so it was not possible to make a reliable estimation of the mortality risk for these drugs. However, we did find moderate-certainty evidence of marked increases in proarrhythmia and adverse effects with flecainide.Overall, there is evidence showing that antiarrhythmic drugs increase adverse events, increase proarrhythmic events and some antiarrhythmics may increase mortality. Conversely, although they reduce recurrences of atrial fibrillation, there is no evidence of any benefit on other clinical outcomes, compared with placebo or no treatment.
Topics: Anti-Arrhythmia Agents; Atrial Fibrillation; Electric Countershock; Humans; Randomized Controlled Trials as Topic; Recurrence; Secondary Prevention
PubMed: 31483500
DOI: 10.1002/14651858.CD005049.pub5