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1.
Evaluation and Management of Premature Ventricular Complexes.
Marcus, GM
Circulation. 2020;(17):1404-1418
Abstract
Premature ventricular complexes (PVCs) are extremely common, found in the majority of individuals undergoing long-term ambulatory monitoring. Increasing age, a taller height, a higher blood pressure, a history of heart disease, performance of less physical activity, and smoking each predict a greater PVC frequency. Although the fundamental causes of PVCs remain largely unknown, potential mechanisms for any given PVC include triggered activity, automaticity, and reentry. PVCs are commonly asymptomatic but can also result in palpitations, dyspnea, presyncope, and fatigue. The history, physical examination, and 12-lead ECG are each critical to the diagnosis and evaluation of a PVC. An echocardiogram is indicated in the presence of symptoms or particularly frequent PVCs, and cardiac magnetic resonance imaging is helpful when the evaluation suggests the presence of associated structural heart disease. Ambulatory monitoring is required to assess PVC frequency. The prognosis of those with PVCs is variable, with ongoing uncertainty regarding the most informative predictors of adverse outcomes. An increased PVC frequency may be a risk factor for heart failure and death, and the resolution of systolic dysfunction after successful catheter ablation of PVCs demonstrates that a causal relationship can be present. Patients with no or mild symptoms, a low PVC burden, and normal ventricular function may be best served with simple reassurance. Either medical treatment or catheter ablation are considered first-line therapies in most patients with PVCs associated with symptoms or a reduced left ventricular ejection fraction, and patient preference plays a role in determining which to try first. If medical treatment is selected, either β-blockers or nondihydropyridine calcium channel blockers are reasonable drugs in patients with normal ventricular systolic function. Other antiarrhythmic drugs should be considered if those initial drugs fail and ablation has been declined, has been unsuccessful, or has been deemed inappropriate. Catheter ablation is the most efficacious approach to eradicate PVCs but may confer increased upfront risks. Original research remains necessary to identify individuals at risk for PVC-induced cardiomyopathy and to identify preventative and therapeutic approaches targeting the root causes of PVCs to maximize effectiveness while minimizing risk.
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2.
A Compelling Case for Less Aggressive Arrhythmia Management in Patients With Chronic Heart Failure and Long-Standing Atrial Fibrillation.
Packer, M
Journal of cardiac failure. 2020;(1):85-92
Abstract
BACKGROUND AND METHODS Atrial fibrillation (AF) is common in chronic heart failure, and some have advocated intensive rate and/or rhythm control strategies for these patients. However, the loss of atrial systole and irregularity of the ventricular response has not been shown to contribute to the progression of heart failure, and the presence or rate of long-standing AF in patients with chronic heart failure does not have prognostic significance. RESULTS In randomized clinical trials, pharmacological rhythm control has not been shown to be superior to rate-control in influencing long-term outcomes, but the use of membrane-active antiarrhythmic drugs can increase the risk of both pump failure and arrhythmic deaths in patients with heart failure. Additionally, intensive efforts to slow the ventricular rate in AF can potentially cause clinically inapparent bradyarrhythmias, which can trigger rate-dependent lethal rhythm disturbances or hemodynamic abnormalities. In patients with AF, a more stringent approach to rate control (target rate <80/min) is not superior to a more lenient strategy (target rate <110/min) on the risk of major events. Little is known about the effects of catheter ablation of long-standing AF in established heart failure, particularly in patients with a preserved or a meaningfully reduced ejection fraction, but ablation can add to the fibrotic burden of the left atrium and impair its capacitance functions. CONCLUSIONS For all of these reasons, the management of heart failure and long-standing AF should be primarily directed to slowing of the progression of their underlying cardiomyopathic process rather than the treatment of the arrhythmia. In addition, patients should receive long-term oral anticoagulation with non-vitamin K-antagonist oral anticoagulants to reduce the risk of thromboembolic events. The utility of intensive rate and rhythm control interventions for long-standing AF in patients with established heart failure requires further study.
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3.
Thyroid effects of amiodarone: clinical update.
Goundan, PN, Lee, SL
Current opinion in endocrinology, diabetes, and obesity. 2020;(5):329-334
Abstract
PURPOSE OF REVIEW Amiodarone-induced thyroid dysfunction is well established and commonly encountered but is associated with several diagnostic and management challenges. The present review discusses recent evidence published related to the effects of amiodarone on the thyroid gland and thyroid function. RECENT FINDINGS Retrospective studies to evaluate amiodarone-induced thyroid dysfunction in children show the occurrence of potential clinically significant changes within 2 weeks of amiodarone initiation that may not be detected if standard adult guidelines for thyroid hormone monitoring are followed. A small study evaluating beta-glucuronidase activity in amiodarone-induced thyrotoxicosis (AIT) demonstrated higher levels in patients with AIT type 2 compared to type 1. New data have suggested the incidence of agranulocytosis may be higher in patients on thionamides with AIT compared to hyperthyroidism because of other causes. In a small study, investigators demonstrated the use of a combination of intravenous and oral steroids to treat refractory AIT which needs to be evaluated in further controlled trials. Finally, recent data demonstrated a possible mortality benefit of surgery over medical therapy for AIT in patients with moderate to severe reduction in left ventricular ejection fraction. SUMMARY Recent research regarding the prevalence, diagnosis, and management of amiodarone-induced thyroid dysfunction were reviewed.
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4.
Ivabradine for chronic heart rate control in persistent atrial fibrillation. Design of the BRAKE-AF project.
Fontenla, A, López-Gil, M, Tamargo-Menéndez, J, Matía-Francés, R, Salgado-Aranda, R, Rey-Blas, JR, Miracle-Blanco, Á, Mejía-Martínez, E, Pastor-Fuentes, A, Toquero-Ramos, J, et al
Revista espanola de cardiologia (English ed.). 2020;(5):368-375
Abstract
INTRODUCTION AND OBJECTIVES Ivabradine is an inhibitor of the If channel, the main determinant of the pacemaker function of the sinus node. The drug has been approved for the treatment of angina and heart failure. There is some evidence of its role as an inhibitor of atrial-ventricular node (AVN) conduction. The aim of the BRAKE-AF project is to assess ivabradine use for rate control in atrial fibrillation (AF). METHODS A multicenter, randomized, parallel, open-label, noninferiority phase III clinical trial will be conducted to compare ivabradine vs digoxin in 232 patients with uncontrolled permanent AF despite beta-blockers or calcium channel blockers. The primary efficacy endpoint is the reduction in daytime heart rate measured by 24-hour Holter monitoring at 3 months. This clinical trial will be supported by an electrophysiological study of the effect of ivabradine on the action potential of the human AVN. To do this, an experimental model will be used with Chinese hamster ovarium cells transfected with the DNA encoding the expression of the t channels involved in this action potential and recording of the ionic currents with patch clamp techniques. RESULTS New data will be obtained on the effect of ivabradine on the human AVN and its safety and efficacy in patients with permanent AF. CONCLUSIONS The results of the BRAKE-AF project might allow inclusion of ivabradine within the limited arsenal of drugs currently available for rate control in AF. CLINICAL TRIAL REGISTRATION http://www.clinicaltrials.gov. Identifier: NCT03718273.
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5.
Heart Failure and Atrial Fibrillation, Like Fire and Fury.
Carlisle, MA, Fudim, M, DeVore, AD, Piccini, JP
JACC. Heart failure. 2019;(6):447-456
Abstract
Heart failure and atrial fibrillation are 2 common cardiovascular disorders that frequently complicate one another and exert a significant detrimental effect on cardiovascular health and well-being. Both heart failure and atrial fibrillation continue to increase in prevalence as the risk factors underlying each condition become more common. This review encompasses what is currently known about the epidemiology and pathophysiology of these comorbidities along with incorporation of landmark trials that have contributed to current guidelines. The focus is on clinically relevant considerations, including the contribution of inflammation in the pathophysiology of atrial fibrillation and heart failure. We explore the emerging role of catheter ablation relative to medical therapy in the management of heart failure with reduced ejection fraction, along with indications for biventricular pacing modalities in cardiac resynchronization therapy. We discuss current guideline-directed therapies and how practice models and national recommendations will likely change based on the most recent randomized controlled trials.
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6.
Trends Over Time in Drug Administration During Adult In-Hospital Cardiac Arrest.
Moskowitz, A, Ross, CE, Andersen, LW, Grossestreuer, AV, Berg, KM, Donnino, MW, ,
Critical care medicine. 2019;(2):194-200
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Abstract
OBJECTIVES Clinical providers have access to a number of pharmacologic agents during in-hospital cardiac arrest. Few studies have explored medication administration patterns during in-hospital cardiac arrest. Herein, we examine trends in use of pharmacologic interventions during in-hospital cardiac arrest both over time and with respect to the American Heart Association Advanced Cardiac Life Support guideline updates. DESIGN Observational cohort study. SETTING Hospitals contributing data to the American Heart Association Get With The Guidelines-Resuscitation database between 2001 and 2016. PATIENTS Adult in-hospital cardiac arrest patients. INTERVENTIONS The percentage of patients receiving epinephrine, vasopressin, amiodarone, lidocaine, atropine, bicarbonate, calcium, magnesium, and dextrose each year were calculated in patients with shockable and nonshockable initial rhythms. Hierarchical multivariable logistic regression was used to determine the annual adjusted odds of medication administration. An interrupted time series analysis was performed to assess change in atropine use after the 2010 American Heart Association guideline update. MEASUREMENTS AND MAIN RESULTS A total of 268,031 index in-hospital cardiac arrests were included. As compared to 2001, the adjusted odds ratio of receiving each medication in 2016 were epinephrine (adjusted odds ratio, 1.5; 95% CI, 1.3-1.8), vasopressin (adjusted odds ratio, 1.5; 95% CI, 1.1-2.1), amiodarone (adjusted odds ratio, 3.4; 95% CI, 2.9-4.0), lidocaine (adjusted odds ratio, 0.2; 95% CI, 0.2-0.2), atropine (adjusted odds ratio, 0.07; 95% CI, 0.06-0.08), bicarbonate (adjusted odds ratio, 2.0; 95% CI, 1.8-2.3), calcium (adjusted odds ratio, 2.0; 95% CI, 1.7-2.3), magnesium (adjusted odds ratio, 2.2; 95% CI, 1.9-2.7; p < 0.0001), and dextrose (adjusted odds ratio, 2.8; 95% CI, 2.3-3.4). Following the 2010 American Heart Association guideline update, there was a downward step change in the intercept and slope change in atropine use (p < 0.0001). CONCLUSIONS Prescribing patterns during in-hospital cardiac arrest have changed significantly over time. Changes to American Heart Association Advanced Cardiac Life Support guidelines have had a rapid and substantial effect on the use of a number of commonly used in-hospital cardiac arrest medications.
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7.
When the Heart Is Not in It: Breastfeeding with Cardiovascular Disease.
Anderson, PO
Breastfeeding medicine : the official journal of the Academy of Breastfeeding Medicine. 2019;(2):80-82
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Pharmacotherapeutic strategies for atrial fibrillation in pregnancy.
Georgiopoulos, G, Tsiachris, D, Kordalis, A, Kontogiannis, C, Spartalis, M, Pietri, P, Magkas, N, Stefanadis, C
Expert opinion on pharmacotherapy. 2019;(13):1625-1636
Abstract
Introduction: Atrial fibrillation (AF) is rare during pregnancy but its incidence is expected to rise in parallel to increasing age of women in pregnancy and fraction of pregnant women with structural heart disease. Areas covered: The authors provide a review of the contemporary evidence on diagnostic work-up and optimal pharmacotherapeutic management of AF in pregnancy. The authors have performed a systematic search for relevant articles using MEDLINE, the COCHRANE LIBRARY, and ClinicalTrials.gov. Expert opinion: New-onset AF during pregnancy is usually an indication of underlying heart disease and should lead to hospital admission. Patients should be evaluated by an experienced cardiologist or an electrophysiologist. Direct cardioversion is highly effective and safe in pregnant women and should be prioritized over pharmacologic cardioversion with intravenous ibutilide or flecainide. Amiodarone should be avoided if possible. Digoxin and beta-blockers are the rate-control pharmaceutic agents with the widest experience of use. Catheter ablation during pregnancy should be considered in selected cases of atrial flutter refractory to medication and only performed using fluoroless techniques, preferably during the second trimester. Vitamin K antagonists (VKAs) can be used after the first trimester, while low molecular weight heparin should be accompanied by periodic evaluation of anti-Xa factor. Non-VKA oral anticoagulants should be avoided because of limited experience in pregnancy.
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9.
Low-dose Magnesium Sulfate Versus High Dose in the Early Management of Rapid Atrial Fibrillation: Randomized Controlled Double-blind Study (LOMAGHI Study).
Bouida, W, Beltaief, K, Msolli, MA, Azaiez, N, Ben Soltane, H, Sekma, A, Trabelsi, I, Boubaker, H, Grissa, MH, Methemem, M, et al
Academic emergency medicine : official journal of the Society for Academic Emergency Medicine. 2019;(2):183-191
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Abstract
OBJECTIVES We aim to determine the benefit of two different doses magnesium sulfate (MgSO4 ) compared to placebo in rate control of rapid atrial fibrillation (AF) managed in the emergency department (ED). METHODS We undertook a randomized, controlled, double-blind clinical trial in three university hospital EDs between August 2009 and December 2014. Patients > 18 years with rapid AF (>120 beats/min) were enrolled and randomized to 9 g of intravenous MgSO4 (high-dose group, n = 153), 4.5 g of intravenous MgSO4 (low-dose group, n = 148), or serum saline infusion (placebo group, n = 149), given in addition to atrioventricular (AV) nodal blocking agents. The primary outcome was the reduction of baseline ventricular rate (VR) to 90 beats/min or less or reduction of VR by 20% or greater from baseline (therapeutic response). Secondary outcome included resolution time (defined as the elapsed time from start of treatment to therapeutic response), sinus rhythm conversion rate, and adverse events within the first 24 hours. RESULTS At 4 hours, therapeutic response rate was higher in low- and high-MgSO4 groups compared to placebo group; the absolute differences were, respectively, 20.5% (risk ratio [RR] = 2.31, 95% confidence interval [CI] = 1.45-3.69) and +15.8% (RR = 1.89, 95% CI = 1.20-2.99). At 24 hours, compared to placebo group, therapeutic response difference was +14.1% (RR = 9.74, 95% CI = 2.87-17.05) with low-dose MgSO4 and +10.3% (RR = 3.22, 95% CI = 1.45-7.17) with high-dose MgSO4 . The lowest resolution time was observed in the low-dose MgSO4 group (5.2 ± 2 hours) compared to 6.1 ± 1.9 hours in the high-dose MgSO4 group and 8.4 ± 2.5 hours in the placebo group. Rhythm control rate at 24 hours was significantly higher in the low-dose MgSO4 group (22.9%) compared to the high-dose MgSO4 group (13.0%, p = 0.03) and the placebo group (10.7%). Adverse effects were minor and significantly more frequent with high-dose MgSO4 . CONCLUSIONS Intravenous MgSO4 appears to have a synergistic effect when combined with other AV nodal blockers resulting in improved rate control. Similar efficacy was observed with 4.5 and 9 g of MgSO4 but a dose of 9 g was associated with more side effects.
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Mexiletine Shortens the QT Interval in Patients With Potassium Channel-Mediated Type 2 Long QT Syndrome.
Bos, JM, Crotti, L, Rohatgi, RK, Castelletti, S, Dagradi, F, Schwartz, PJ, Ackerman, MJ
Circulation. Arrhythmia and electrophysiology. 2019;(5):e007280
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Abstract
BACKGROUND Long QT syndrome is a potentially lethal yet highly treatable cardiac channelopathy. Although β-blocker therapy is standard for most patients, concomitant therapy with sodium channel blockers, like mexiletine, is often utilized for patients with sodium channel-mediated type 3 long QT syndrome (LQT3). The potential role of sodium channel blockers in patients with potassium channel-mediated long QT syndrome (ie, LQT1 and LQT2) has not been investigated in detail. METHODS We performed a retrospective chart review on 12 patients (5 females; median age at diagnosis 14.1 years (interquartile range [IQR], 7.7-23; range, 0-59, median heart rate-corrected QT interval [QTc] at diagnosis 557 ms (IQR, 529-605) with genetically established LQT2 (10) or a combination of LQT1/LQT2 (1) or LQT2/LQT3 (1), who received mexiletine. Data were collected on symptomatic status, treatments, and breakthrough cardiac events after diagnosis and initiation of treatment. Additionally, 12-lead ECGs were collected at diagnosis, before initiation of mexiletine and following mexiletine to evaluate the drug's effect on QTc. RESULTS Before diagnosis, 6 patients were symptomatic and, before initiation of mexiletine, 4 patients experienced ≥1 breakthrough cardiac event on β-blocker. Median age at first mexiletine dose was 24.3 years (IQR, 14-32.4). After mexiletine, the median QTc decreased by 65±45 ms from 547 ms (IQR, 488-558) premexiletine to 470 ms (IQR, 409-529) postmexiletine ( P=0.0005) for all patients. In 8 patients (67%), the QTc decreased by ≥ 40 ms with a mean decrease in QTc of 91 ms ( P < 0.008). For the 11 patients maintained on mexiletine therapy, there have been no breakthrough cardiac events during follow-up. CONCLUSIONS Although commonly prescribed in patients with LQT3, mexiletine also shortens the QTc significantly in two-thirds of a small subset of patients with potassium channel-mediated LQT2. In patients with LQT2, pharmacological targeting of the physiological late sodium current may provide added therapeutic efficacy to β-blocker therapy.