Rythmol SR: New Treatment Option for Atrial Fibrillation

Salwa Beheiry, RN, CCRN Director, Electrophysiology Services
Salwa Beheiry, RN, CCRN Director, Electrophysiology Services
In the past, AF was considered just a nuisance. Patients were advised to learn how to live with it. Digoxin, and later beta blockers, were the drugs of choice to achieve rate control. We now know that AF is not just a nuisance. In fact, it is a serious problem with major and devastating complications. Although AF is commonly known to be an affliction of growing old, there are almost 100,000 people in the US who are 40 years of age or younger suffering from this arrhythmia. In this group of patients, AF can have negative and debilitating effects on their quality of life. People with AF have a 2-5% yearly chance of having a stroke than those who do not have AF. This percentage increases with age, to about 10% in those who are 65 or above. In the US, it is estimated that mortality caused by AF is approximately 10,000 per year, mainly from stroke. In AF, since the atria quiver rather than contract, blood may pool, causing a thrombus to form and a stroke to happen. Anticoagulation has become a standard therapy for AF to minimize the risk of stroke. However, anticoagulation does not entirely eliminate that risk. It is believed that even when people do not suffer from stroke or TIA while in AF, micro-embolic events can occur causing subtle memory changes and dementia. Classification of AF (Figure 2) Each of the options presented in Figure 3 aims at reducing or eliminating the patient s symptoms and the risks associated with AF, mainly stroke and cardiomyopathy. The options adopted vary from one practice to the other, and treatment may include one or more of these options combined. In this article, we will focus on the option of rhythm control with anti-arrhythmics (AA) mainly, the new generation of class 1C agents. Class 1C AA (Figure 5) The class 1C AA are a relatively new group of agents; they act by blocking the sodium channel (prolonging QRS), and have little effect on repolarization (no effect on QT interval). However, because of their negative inotropic effect, they are not recommended for patients with structural heart disease. In the landmark study CAST (Cardiac Arrhythmia Suppression Trial), it was shown that patients with coronary artery disease and poor left ventricular function (EF Rythmol and Rythmol SR In addition, the study showed that Rythmol SR did not appear to increase the recurrence of regular supraventricular tachycardia as atrial flutter (something which was widely reported when class 1C was initially introduced). Rythmol SR also did not appear to increase the occurrence of asymptomatic AF as evident by Holter monitoring. Rythmol SR Dosing Rythmol SR comes in three strengths: 225, 325, and 425 mg. Dosage should be titrated according to patient s response and tolerance. It is usually started at 225 mg every 12 hours. If the therapeutic effect is not achieved (e.g. occurrence of daily AF episodes), the dose can be increased to 325 mg every 12 hours at a minimum of five days after the initial dose of 225 mg. The same pattern is repeated if the higher dose of 425 mg is needed. Adverse Effects of Rythmol SR The adverse effects of Rythmol SR are dose related. In the RAFT study, the most common adverse effects were reported to be: dizziness, fatigue, palpitations, taste disturbance, nausea, GI upset and constipation. These symptoms commonly occur in the first 7-14 days after initiation of therapy. Other severe adverse effects are less common and may include: severe bradycardia, especially if used in combination with beta blockers or calcium channel blockers, and also hypotension, heart block or proarrhythmia. Since Rythmol SR is highly metabolized by the liver, it should be used with caution in patients with liver impairment. Rythmol SR and other class 1C antiarrhythmics are contraindicated in patients with congestive heart failure, ischemic heart disease and those with poor left ventricular function. Conclusion