Impact of structural heart disease on the selection of class III antiarrhythmics for the prevention of atrial fibrillation and flutter

1998 ◽  
Vol 135 (4) ◽  
pp. 551-556 ◽  
Author(s):  
James A. Reiffel
Keyword(s):  
Atrial Fibrillation ◽  
Heart Disease ◽  
Structural Heart Disease ◽  
Class Iii ◽  
Class Iii Antiarrhythmics ◽  
Atrial Fibrillation And Flutter ◽  
Selection Of

The Place of Antiarrhythmic Drugs and Rhythm Control in the Treatment of Atrial Fibrillation

2009 ◽  
Vol 5 (1) ◽  
pp. 36
Author(s):  
Philippe Chevalier ◽  
Keyword(s):  
Atrial Fibrillation ◽  
Heart Disease ◽  
Antiarrhythmic Drugs ◽  
Structural Heart Disease ◽  
Rhythm Control ◽  
Disease Course ◽  
Drug Trials ◽  
Cardiac Safety ◽  
Selection Of

Atrial fibrillation (AF) is the most common arrhythmia, with incidence increasing with age and a ranging severity of symptoms. The arrhythmia, perpetuated from electrical, functional and structural remodelling by AF itself, can ultimately lead to increased morbidity and mortality. Emerging evidence appears to support the initiation of rhythm control, particularly early on in the disease course. Antiarrhythmic drugs have proved useful in inducing and maintaining cardioversion, but treatment varies depending on the degree of structural heart disease. Drug trials and selection of therapy have historically focused largely on cardiac safety. Class Ic drugs have demonstrated safety and efficacy in patients with little to no structural heart disease, yet their use continues to be superseded by the use of other drugs, especially amiodarone, which carries significant risks of extracardiac effects and end-organ toxicities. This article discusses the role of sinus rhythm control and antiarrhythmic drugs in AF, with an emphasis on patients exhibiting no or minimal structural heart disease and the importance of selecting an appropriate antiarrhythmic drug, taking into account arrhythmia burden, presence of concurrent cardiovascular disease and severity and, most importantly, the safety of the drug therapy.

Advanced interatrial block precedes atrial fibrillation and stroke. The prospective interatrial Block And Yearly EventS (BAYES) registry

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
M Martinez-Selles ◽  
R Elosua ◽  
M Ibarrola ◽  
M De Andres ◽  
P Diez-Villanueva ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Heart Disease ◽  
Sinus Rhythm ◽  
Structural Heart Disease ◽  
P Wave ◽  
Wave Duration ◽  
P Wave Duration ◽  
Previous Diagnosis ◽  
Surface Ecg ◽  
Interatrial Block

Abstract Background Advanced interatrial block (IAB), prolonged and bimodal P waves in surface ECG inferior leads, is an unrecognized surrogate of atrial dysfunction and a trigger of atrial dysrhythmias, mainly atrial fibrillation (AF). Our aim was to prospectively assess whether advanced IAB in sinus rhythm precedes AF and stroke in elderly outpatients with structural heart disease, a group not previously studied. Methods Prospective observational registry that included outpatients aged ≥70 years with structural heart disease and no previous diagnosis of AF. Patients were divided into three groups according to P-wave characteristics. Results Among 556 individuals, 223 had normal P-wave (40.1%), 196 partial IAB (35.3%), and 137 advanced IAB (24.6%). After a median follow-up of 694 days; 93 patients (16.7%) developed AF, 30 stroke (5.4%), and 34 died (6.1%). Advanced IAB was independently associated with AF (hazard ratio [HR] 2.9, 95% confidence interval [CI] 1.7–5.1, p<0.001), stroke (HR 3.8, 95% CI 1.4–10.7, p=0.010), and AF/stroke (HR 2.6, 95% CI 1.5–4.4, p=0.001). P-wave duration (ms) was independently associated with AF (HR 1.05, 95% CI 1.03–1.07, p<0.001), AF/stroke (HR 1.04, 95% CI 1.02–1.06, p<0.001), and mortality (HR 1.04, 95% CI 1.00–1.08, p=0.021). Conclusions The presence of advanced IAB in sinus rhythm is a risk factor for AF and stroke in an elderly population with structural heart disease and no previous diagnosis of AF. P-wave duration was also associated with all-cause mortality. Figure. Age- and sex-adjusted linear and non-linear association between P-wave duration (msec) and atrial fibrillation (A), stroke (B), and atrial fibrillation or stroke (C) risk. Results of a generalized additive model with spline smoothing functions and 4 degrees of freedom. Figure 1. Kaplan-Meyer curves of survival free of atrial fibrillation (A), stroke (B) and atrial fibrillation or stroke (C) in patients with normal P-wave, partial interatrial block (IAB) and advanced IAB. Funding Acknowledgement Type of funding source: None

scholarly journals Electropathological Substrate of Long-Standing Persistent Atrial Fibrillation in Patients With Structural Heart Disease

2010 ◽  
Vol 3 (6) ◽  
pp. 606-615 ◽  
Author(s):  
Maurits A. Allessie ◽  
Natasja M.S. de Groot ◽  
Richard P.M. Houben ◽  
Ulrich Schotten ◽  
Eric Boersma ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Heart Disease ◽  
Structural Heart Disease ◽  
Persistent Atrial Fibrillation

Atrial flutter: clinical presentation

ESC CardioMed ◽  
2018 ◽  
pp. 2208-2211
Author(s):  
Bhupesh Pathik ◽  
Jonathan M. Kalman
Keyword(s):  
Atrial Fibrillation ◽  
Heart Disease ◽  
Atrial Flutter ◽  
Clinical Presentation ◽  
Three Dimensional ◽  
Structural Heart Disease ◽  
Underlying Mechanism ◽  
Clinical Presentations ◽  
Ventricular Response ◽  
Focal Atrial Tachycardia

Atrial flutter refers to an electrocardiographic (ECG) appearance of continuously undulating flutter waves without an isoelectric baseline. It represents a heterogeneous group of atrial arrhythmias characterized by a macroreentrant mechanism. However, focal atrial tachycardia, especially if rapid and in the context of underlying structural heart disease or prior atrial surgery, may also cause a similar ECG appearance. A definition based on the underlying macroreentrant mechanism is therefore preferred particularly in the current era of three-dimensional electroanatomical mapping which allows detailed anatomical delineation of the circuit location. The clinical presentations of atrial macroreentry are variable and are influenced by ventricular response rate, presence of underlying structural heart disease, prior atrial surgery, or medications. The purpose of this chapter is to describe the different clinical presentations of this arrhythmia as well as its classification according to underlying mechanism. In addition, the clinical presentation of atrial macroreentry in special clinical situations is discussed. These include (1) the relationship between atrial fibrillation and cavotricuspid isthmus-dependent atrial macroreentry, (2) the organization of atrial fibrillation into atrial macroreentry with flecainide treatment, and (3) the association between atrial macroreentry and tachycardia-induced cardiomyopathy.

Atrial premature beats

ESC CardioMed ◽  
2018 ◽  
pp. 2050-2052
Author(s):  
Tatjana Potpara
Keyword(s):  
Heart Disease ◽  
Sinus Node ◽  
Pulmonary Veins ◽  
Atrioventricular Node ◽  
Structural Heart Disease ◽  
Class Iii ◽  
P Waves ◽  
Asymptomatic Patients ◽  
Narrow Qrs Complex ◽  
Premature Beats

Atrial premature beats (APBs), also referred to as atrial or supraventricular extrasystoles, represent premature atrial depolarization occurring earlier than the next expected regular sinoatrial activation, usually from a site outside the sinus node. Premature depolarizations originating from the atrioventricular node or His bundle are termed atrioventricular junctional premature beats. In general, APBs occur in adults of any age, with or without structural heart disease. Increased atrial volume and/or pressure, or increased sympathetic tone are associated with increased frequency of APBs, while in individuals without structural heart disease APBs often originate from the pulmonary veins and may precipitate atrial fibrillation. Patients with APBs are often asymptomatic, or experience palpitations, dizziness, or even presyncope. Significant haemodynamic compromise due to APBs is uncommon. Physical examination may reveal pulse irregularity, and surface electrocardiograms (ECGs) usually show premature P waves which differ from the sinus P morphology, followed by a normal, shortened, or prolonged PR interval (depending on the APB site of origin) and narrow QRS complex. Ambulatory ECG (Holter) monitoring helps to establish the diagnosis when symptoms are sporadic or to quantify the frequency of APBs. Counselling and reassurance would suffice in most minimally symptomatic or asymptomatic patients with APBs, but any underlying cardiovascular disorder must be treated. Beta blockers or class III antiarrhythmic drugs (or class IC in patients without significant structural heart disease) can be used to attenuate symptoms or suppress the APBs facilitating other tachyarrhythmias. Catheter ablation could be considered in selected patients.

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