Structural heart disease

Ventricular extrasystoles are treated only if they may degenerate into life-threatening arrhythmia. In milder forms the proarrhythmic risk of the diugs overshadows their benefits. In such cases (3-adrenoceptor antagonists may be attempted. For the treatment of ventricular extrasystoles, such as series or runs of extrasystoles, amiodarone or sotalol are used. In the absence of structural heart disease, class I anti-arrhythmic diugs can be considered an alternative. However, they may not be administered during the post-infarction period. 

N/A A Patients at high risk for heart failure but without structural heart disease or symptoms of heart failure. 

Patients with structural heart disease and current or previous symptoms... 

Most types of structural heart disease resulting in turbulence of blood flow will increase the risk for IE. Some of the most important risk factors include / Presence of a prosthetic valve (highest risk)... 

Immediate-release (IR)-To prolong the time to recurrence of paroxysmal atrial fibrillation/flutter associated with disabling symptoms in patients without structural heart disease. 

Atrial fibrillation For the prevention of paroxysmal atrial fibrillation/flutter (PAF) associated with disabling symptoms and paroxysmal supraventricular tachycardias (PSVT), including atrioventricular nodal reentrant tachycardia, atrioventricular reentrant tachycardia, and other supraventricular tachycardias of unspecified mechanism associated with disabling symptoms in patients without structural heart disease. 

At high risk for HF Structural heart Structural heart disease Refractory HF... 

Approved indications for propafenone include treatment of supraventricular arrhythmias and life-threatening ventricular arrhythmias in the absence of structural heart disease. Propafenone has been shown to increase mortality in patients with structural heart disease, and so extreme caution must be used in this subset of patients. As with flecainide, the patient should be hospitalized for initiation of therapy. 

Increased mortality and cardiac arrest recurrence when structural heart disease (51). 

AF is quite heterogeneous in its clinical presentation [19], sometimes associated with structural heart disease, and other times without any associated medical conditions. Recently, an international consensus has been reached re-... 

When the QT interval is prolonged, there is an increased risk of ventricular tachyarrhythmia, including Torsade de Pointes (TdP), particularly when combined with other risk factors (e.g., hypokalemia, structural heart disease, bradycardia), see Figure 1. 

Flecainide slows conduction in all cardiac cells including the anomalous pathways responsible for the Wolff-Parkinson-White (WPW) syndrome. Together with encainide and moricizine, it underwent clinical trials to establish if suppression of asymptomatic premature beats with antiarrhythmic drugs would reduce the risk of death from arrhythmia after myocardial infarction. The study was terminated after preliminary analysis of 1727 patients revealed that mortality in the groups treated with flecainide or encainide was 7.7% compared with 3.0% in controls. The most likely explanation for the result was the induction of lethal ventricular arrhythmias possibly due to ischaemia by flecainide and encainide, i.e. a proarrhythmic effect. In the light of these findings the indications for flecainide are restricted to patients with no evidence of structural heart disease. The most common indication, indeed where it is the drug of choice, is atrioventricular re-entrant tachycardia, such as AV nodal tachycardia or in the tachycardias associated with the WPW syndrome or similar conditions with anomalous pathways. This should be as a prelude to definitive treatment with radiofrequency ablation. Flecainide may also be useful in patients with paroxysmal atrial fibrillation. 

Poor perfusion and/or known structural heart disease ... 

The risk of death in patients with supraventricular dysrhythmias taking dofetilide has been studied in a systematic review of randomized controlled trials (59). After adjusting for the effects of dysrhjdhmia diagnosis, age, sex, and structural heart disease, the hazard ratio was 1.1 (Cl = 0.3, 4.3). 

In a retrospective study of 85 patients with recurrent atrial fibrillation (mean left atrial size 46 mm, mean left ventricular ejection fraction 0.51), 69 of whom had structural heart disease, moricizine (mean dose 609 mg/day) was withdrawn because of unacceptable adverse effects in six patients frequent ventricular extra beats and short runs of non-sustained ventricular tachycardia n — 2) significant widening of the QRS complex (n — 1) first-degree heart block (n = 1) a significant rise in liver enzymes (n = 1) and a severe rash (n = 1) (4). Six patients developed transient adverse effects that resolved spontaneously without withdrawal brief self-limiting episodes of atrial flutter (n = 2) a small increase in blood pressure (n = 1) generalized weakness and tremor n = 2) and reduced appetite (n = 1). 

In patients taking long-term propafenone for supraventricular dysrhythmias adverse effects were more common and have been reported in 14-60% of cases. Cardiac adverse effects were more common in patients with structural heart disease. The non-cardiac effects were either gastrointestinal (nausea, vomiting, taste disturbances) or neurological (dizziness). Adverse effects are dose-related. In one large study there was no difference between propafenone and placebo in the risk of death. 

The safety of oral propafenone in the treatment of dysrhythmias has been studied retrospectively in infants and children (40). There were significant electrophysiolo-gical adverse effects and prodysrhythmia in 15 of 772 patients (1.9%). These included sinus node dysfunction in four, complete atrioventricular block in two, aggravation of supraventricular tachycardia in two, acceleration of ventricular rate during atrial flutter in one, ventricular prodysrhythmia in five, and unexplained sjmcope in one. Cardiac arrest or sudden death occurred in five patients (0.6%) two had a supraventricular tachycardia due to Wolff-Parkinson-White syndrome the other three had structural heart disease. Adverse cardiac events were more common in the presence of structural heart disease and there was no difference between patients with supraventricular and ventricular dysrhythmias. 

Clinical uses PVC, paroxysmal atrial tachycardia, AF, VT Documented life-threatening ventricular arrhythmias. Flecainide also may be used for AF and supraventricular tachycardias in patients without structural heart disease. Propafenone is also indicated for paroxysmal AF. 

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