In patients with minimal or no significant structural heart disease, any antifibrillatory agent can be employed. A specific agent should be selected by its side-effect profile. Class IC agents such as propafenone and flecainide have an extremely low incidence of ventricular proarrhythmia in normal hearts, and are generally well-tolerated. Sotalol and class IA agents such as disopyramide and procainamide can be used safely in this setting if careful attention is given to the dose-dependent QT-prolonging effects of these drugs. Quinidine is the exception, because it has both a dose-dependent and an idiosyncratic QT-prolonging effect in certain individuals. Periodic complete blood counts should be performed on patients who are taking either procainamide or quinidine because of the rare occurrence of blood dyscrasias. Disopyramide is well-tolerated in younger patients, but because of its significant anticholinegic effects, caution should be used in men with symptoms of an enlarged prostate in whom urinary retention may occur. Pyridostigmine, an acetylcholinesterase inhibitor (90-91), can be given in conjunction with disopyramide to mitigate the anticholinergic effects. Patients who are taking these medications should be advised to contact their physician for dosage adjustments during any acute gastrointestinal illness (diarrhea or vomiting), which can alter serum concentrations of potassium or magnesium and thus promote proarrhythmia. Both disopyramide and propafenone exhibit nonlinear pharmacokinetics, in which small increments in dosages can lead to significantly higher serum concentrations. Therefore, dosage increases should be undertaken after the patient has had time to achieve a steady state. Finally, drug selection also depends on pharmacologic interactions with other medications that the patient is taking as well as drug metabolism in patients with underlying renal or hepatic disease. Sotalol, flecainide, and dofetilide need dosage adjustment in patients with renal insufficiency. Quinidine, propafenone, ibutilide, and amiodarone are all metabolized by the liver. Dosage adjustments or complete avoidance of these drugs in patients with hepatic dysfunction is essential. With procainamide and disopyramide, both renal and hepatic metabolism, and elimination occur, and caution should be used in patients with either renal or hepatic dysfunction.
In patients with ventricular hypertrophy and normal left ventricular function, drugs that prolong the QT interval should be used with caution. Class IC agents such as propafenone are safe in this group of patients because there is no prolongation of the QT interval. Amiodarone is also acceptable. Flecainide can be used to suppress atrial arrhythmias in structurally normal hearts. Whether flecainide is safe in patients with minimal LVH vs those patients with severe LVH has yet to be determined (Table 3).
It has been our practice to initiate QT-prolonging drugs while the patient is in the hospital on telemetry. Even in patients with structurally normal hearts, there is a small risk of ventricular proarrhythmia. We are now learning that certain individuals may have a "channelopathy"—they demonstrate abnormalities in sodium or potassium channels that only become manifest when challenged with certain drugs. In patients with structural heart disease or those who may be prone to sinus-node dysfunction or atrioventricular conduction disturbances, in-hospital drug initiation is mandatory. In this manner, prompt drug discontinuation, defibrillation, or pacing can be undertaken if proarrhythmia occurs.
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