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Stimulant Drugs of Abuse and Cardiac Arrhythmias.
Dominic, P, Ahmad, J, Awwab, H, Bhuiyan, MS, Kevil, CG, Goeders, NE, Murnane, KS, Patterson, JC, Sandau, KE, Gopinathannair, R, et al
Circulation. Arrhythmia and electrophysiology. 2022;(1):e010273
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Abstract
Nonmedical use of prescription and nonprescription drugs is a worldwide epidemic, rapidly growing in magnitude with deaths because of overdose and chronic use. A vast majority of these drugs are stimulants that have various effects on the cardiovascular system including the cardiac rhythm. Drugs, like cocaine and methamphetamine, have measured effects on the conduction system and through several direct and indirect pathways, utilizing multiple second messenger systems, change the structural and electrical substrate of the heart, thereby promoting cardiac dysrhythmias. Substituted amphetamines and cocaine affect the expression and activation kinetics of multiple ion channels and calcium signaling proteins resulting in EKG changes, and atrial and ventricular brady and tachyarrhythmias. Preexisting conditions cause substrate changes in the heart, which decrease the threshold for such drug-induced cardiac arrhythmias. The treatment of cardiac arrhythmias in patients who take drugs of abuse may be specialized and will require an understanding of the unique underlying mechanisms and necessitates a multidisciplinary approach. The use of primary or secondary prevention defibrillators in drug abusers with chronic systolic heart failure is both sensitive and controversial. This review provides a broad overview of cardiac arrhythmias associated with stimulant substance abuse and their management.
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Cardiac Alternans: Mechanisms and Clinical Utility in Arrhythmia Prevention.
Kulkarni, K, Merchant, FM, Kassab, MB, Sana, F, Moazzami, K, Sayadi, O, Singh, JP, Heist, EK, Armoundas, AA
Journal of the American Heart Association. 2019;(21):e013750
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3.
Atrial high-rate episodes: prevalence, stroke risk, implications for management, and clinical gaps in evidence.
Bertaglia, E, Blank, B, Blomström-Lundqvist, C, Brandes, A, Cabanelas, N, Dan, GA, Dichtl, W, Goette, A, de Groot, JR, Lubinski, A, et al
Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology. 2019;(10):1459-1467
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Abstract
Self-terminating atrial arrhythmias are commonly detected on continuous rhythm monitoring, e.g. by pacemakers or defibrillators. It is unclear whether the presence of these arrhythmias has therapeutic consequences. We sought to summarize evidence on the prevalence of atrial high-rate episodes (AHREs) and their impact on risk of stroke. We performed a comprehensive, tabulated review of published literature on the prevalence of AHRE. In patients with AHRE, but without atrial fibrillation (AF), we reviewed the stroke risk and the potential risk/benefit of oral anticoagulation. Atrial high-rate episodes are found in 10-30% of AF-free patients. Presence of AHRE slightly increases stroke risk (0.8% to 1%/year) compared with patients without AHRE. Atrial high-rate episode of longer duration (e.g. those >24 h) could be associated with a higher stroke risk. Oral anticoagulation has the potential to reduce stroke risk in patients with AHRE but is associated with a rate of major bleeding of 2%/year. Oral anticoagulation is not effective in patients with heart failure or survivors of a stroke without AF. It remains unclear whether anticoagulation is effective and safe in patients with AHRE. Atrial high-rate episodes are common and confer a slight increase in stroke risk. There is true equipoise on the best way to reduce stroke risk in patients with AHRE. Two ongoing trials (NOAH-AFNET 6 and ARTESiA) will provide much-needed information on the effectiveness and safety of oral anticoagulation using non-vitamin K antagonist oral anticoagulants in patients with AHRE.
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4.
Role of inflammatory signaling in atrial fibrillation.
Scott, L, Li, N, Dobrev, D
International journal of cardiology. 2019;:195-200
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Abstract
Atrial fibrillation (AF), the most prevalent arrhythmia, is often associated with enhanced inflammatory response. Emerging evidence points to a causal role of inflammatory signaling pathways in the evolution of atrial electrical, calcium handling and structural remodeling, which create the substrate of AF development. In this review, we discuss the clinical evidence supporting the association between inflammatory indices and AF development, the molecular and cellular mechanisms of AF, which appear to involve multiple canonical inflammatory pathways, and the potential of anti-inflammatory therapeutic approaches in AF prevention/treatment.
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New concepts in the therapy of atrial fibrillation.
Cocco, G, Jerie, P
Cardiology journal. 2016;(1):3-11
Abstract
Atrial fibrillation is a frequent arrhythmia with increasing prevalence. The paper reviews the most important present aspects and paradigms in the treatment of the arrhythmia. The main aim of treatment is directed to improve the quality of life while reducing morbidity and mortality. A large experience derived from epidemiological registers and clinical research, impressive advances in interventional electrophysiological therapies and the introduction of non-vitamin K antagonists had a dramatic impact on the medical approach. Recommended steps to classify and treat atrial fibrillation are presented and discussed.
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A Literature Review of the Use of Sodium Bicarbonate for the Treatment of QRS Widening.
Bruccoleri, RE, Burns, MM
Journal of medical toxicology : official journal of the American College of Medical Toxicology. 2016;(1):121-9
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Abstract
Sodium bicarbonate is a well-known antidote for tricyclic antidepressant (TCA) poisoning. It has been used for over half a century to treat toxin-induced sodium channel blockade as evidenced by QRS widening on the electrocardiogram (ECG). The purpose of this review is to describe the literature regarding electrophysiological mechanisms and clinical use of this antidote after poisoning by tricyclic antidepressants and other agents. This article will also address the literature supporting an increased serum sodium concentration, alkalemia, or the combination of both as the responsible mechanism(s) for sodium bicarbonate's antidotal properties. While sodium bicarbonate has been used as a treatment for cardiac sodium channel blockade for multiple other agents including citalopram, cocaine, flecainide, diphenhydramine, propoxyphene, and lamotrigine, it has uncertain efficacy with bupropion, propranolol, and taxine-containing plants.
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Resting heart rate and risk of incident heart failure: three prospective cohort studies and a systematic meta-analysis.
Khan, H, Kunutsor, S, Kalogeropoulos, AP, Georgiopoulou, VV, Newman, AB, Harris, TB, Bibbins-Domingo, K, Kauhanen, J, Gheorghiade, M, Fonarow, GC, et al
Journal of the American Heart Association. 2015;(1):e001364
Abstract
BACKGROUND The relationship between resting heart rate (RHR) and incident heart failure (HF) has been questioned. METHODS AND RESULTS RHR was assessed at baseline in 7073 participants in 3 prospective cohorts (Cardiovascular Health Study, Health ABC study and Kuopio Ischemic Heart Disease Study) that recorded 1189 incident HF outcomes during 92 702 person-years of follow-up. Mean age of participants was 67 (9.9) years and mean RHR was 64.6 (11.1) bpm. Baseline RHR correlated (P<0.001) positively with body mass index (r=0.10), fasting glucose (r=0.18), and C-reactive protein (r=0.20); and inversely with serum creatinine (r=-0.05) and albumin (r=-0.05). Baseline RHR was non-linearly associated with HF risk. The age and sex-adjusted hazard ratio for HF comparing the top (>72 bpm) versus the bottom (<57 bpm) quartile of baseline RHR was 1.48 (95% confidence interval [CI] 1.26 to 1.74) and was modestly attenuated (1.30, 95% CI 1.10 to 1.53) with further adjustment for body mass index, history of diabetes, hypertension, smoking status, serum creatinine, and left ventricular hypertrophy. These findings remained consistent in analyses accounting for incident coronary heart disease, excluding individuals with prior cardiovascular events, or those taking beta-blockers; and in subgroups defined by several individual participant characteristics. In a pooled random effects meta-analysis of 7 population-based studies (43 051 participants and 3476 HF events), the overall hazard ratio comparing top versus bottom fourth of RHR was 1.40 (95% CI: 1.19 to 1.64). CONCLUSIONS There is a non-linear association between RHR and incident HF. Further research is needed to understand the physiologic foundations of this association.
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Resting heart rate and outcomes in patients with cardiovascular disease: where do we currently stand?
Menown, IB, Davies, S, Gupta, S, Kalra, PR, Lang, CC, Morley, C, Padmanabhan, S
Cardiovascular therapeutics. 2013;(4):215-23
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Abstract
BACKGROUND Data from large epidemiological studies suggest that elevated heart rate is independently associated with cardiovascular and all-cause mortality in patients with hypertension and in those with established cardiovascular disease. Clinical trial findings also suggest that the favorable effects of beta-blockers and other heart rate-lowering agents in patients with acute myocardial infarction and congestive heart failure may be, at least in part, due to their heart rate-lowering effects. Contemporary clinical outcome prediction models such as the Global Registry of Acute Coronary Events (GRACE) score include admission heart rate as an independent risk factor. AIMS This article critically reviews the key epidemiology concerning heart rate and cardiovascular risk, potential mechanisms through which an elevated resting heart rate may be disadvantageous and evaluates clinical trial outcomes associated with pharmacological reduction in resting heart rate. CONCLUSIONS Prospective randomised data from patients with significant coronary heart disease or heart failure suggest that intervention to reduce heart rate in those with a resting heart rate >70 bpm may reduce cardiovascular risk. Given the established observational data and randomised trial evidence, it now appears appropriate to include reduction of elevated resting heart rate by lifestyle +/- pharmacological therapy as part of a secondary prevention strategy in patients with cardiovascular disease.
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Cardiac effects of muscarinic receptor antagonists used for voiding dysfunction.
Andersson, KE, Campeau, L, Olshansky, B
British journal of clinical pharmacology. 2011;(2):186-96
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Abstract
Antimuscarinic agents are the main drugs used to treat patients with the overactive bladder (OAB) syndrome, defined as urgency, with or without urgency incontinence, usually with increased daytime frequency and nocturia. Since the treatment is not curative and since OAB is a chronic disease, treatment may be life-long. Antimuscarinics are generally considered to be ‘safe’ drugs, but among the more serious concerns related to their use is the risk of cardiac adverse effects, particularly increases in heart rate (HR) and QT prolongation and induction of polymorphic ventricular tachycardia (torsade de pointes). An elevated resting HR has been linked to overall increased morbidity and mortality, particularly in patients with cardiovascular diseases. QT prolongation and its consequences are not related to blockade of muscarinic receptors, but rather linked to inhibition of the hERG potassium channel in the heart. However, experience with terodiline, an antimuscarinic drug causing torsade de pointes in patients, has placed the whole drug class under scrutiny. The potential of the different antimuscarinic agents to increase HR and/or prolong the QT time has not been extensively explored for all agents in clinical use. Differences between drugs cannot be excluded, but risk assessments based on available evidence are not possible.
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Methadone-induced mortality in the treatment of chronic pain: role of QT prolongation.
Andrews, CM, Krantz, MJ, Wedam, EF, Marcuson, MJ, Capacchione, JF, Haigney, MC
Cardiology journal. 2009;(3):210-7
Abstract
Methadone is increasingly prescribed for chronic pain, yet the associated mortality appears to be rising disproportionately relative to other opioid analgesics. We review the available evidence on methadone-associated mortality, and explore potential pharmacokinetic and pharmacodynamic explanations for its greater apparent lethality. While methadone shares properties of central nervous system and respiratory depression with other opioids, methadone is unique as a potent blocker of the delayed rectifier potassium ion channel (IKr). This results in QT-prolongation and torsade de pointes (TdP) in susceptible individuals. In some individuals with low serum protein binding of methadone, the extent of blockade is roughly comparable to that of sotalol, a potent QT-prolonging drug. Predicting an individual's propensity for methadone-induced TdP is difficult at present given the inherent limitations of the QT interval as a risk-stratifier combined with the multifactorial nature of the arrhythmia. Consensus recommendations have recently been published to mitigate the risk of TdP until further studies better define the arrhythmia risk factors for methadone. Studies are needed to provide insights into the clinical covariates most likely to result in methadone-associated arrhythmia and to assess the feasibility of current risk mitigation strategies.