Items in AFP with MESH term: Anti-Arrhythmia Agents
Management of Newly Detected Atrial Fibrillation - Editorials
Pharmacologic Cardioversion for Atrial Fibrillation and Flutter - Cochrane for Clinicians
ABSTRACT: In approximately 5 percent of sudden cardiac deaths, no demonstrable anatomic abnormality is found. Some cases are caused by sudden arrhythmia death syndrome. A prolonged QT interval is a common thread among the various entities associated with sudden arrhythmia death syndrome. A number of drugs are known to cause QT prolongation (e.g., terfenadine), as are hypokalemia, hypomagnesemia, myocarditis, and endocrine and nutritional disorders. Recently, attention has focused on a group of inherited gene mutations in cardiac ion channels that cause long QT syndrome and carry an increased risk for sudden death. Some of the highest rates of inherited long QT syndrome occur in Southeast Asian and Pacific Rim countries. The median age of persons who die of long QT syndrome is 32 years; men are predominately affected. In addition to a prolonged QT interval, which occurs in some but not all persons with long QT syndrome, another characteristic electrocardiographic abnormality is the so-called Brugada sign (an upward deflection of the terminal portion of the QRS complex). Most cardiac events are precipitated by vigorous exercise or emotional stress, but they also can occur during sleep. Torsades de pointes and ventricular fibrillation are the usual fatal arrhythmias. Long QT syndrome should be suspected in patients with recurrent syncope during exertion and those with family histories of sudden, unexpected death. Unfortunately, not all persons with long QT syndrome have premonitory symptoms or identifiable electrocardiographic abnormalities, and they may first present with sudden death. Beta blockers, potassium supplements, and implantable defibrillators have been used for treatment of long QT syndrome. Identifying the specific gene mutation in a given patient with long QT syndrome can help guide prophylactic therapy.
ABSTRACT: Amiodarone is a potent antiarrhythmic agent that is used to treat ventricular arrhythmias and atrial fibrillation. The drug prevents the recurrence of life-threatening ventricular arrhythmias and produces a modest reduction of sudden deaths in high-risk patients. Amiodarone is more effective than sotalol or propafenone in preventing recurrent atrial fibrillation in patients for whom a rhythm-control strategy is chosen. When long-term amiodarone therapy is used, potential drug toxicity and interactions must be considered. The dosage of amiodarone should be kept at the lowest effective level. In patients who also are taking digoxin and warfarin, physicians must pay close attention to digoxin levels and prothrombin time, keeping in mind that the effects of interaction with amiodarone do not peak until seven weeks after the initiation of concomitant therapy. Laboratory studies to assess liver and thyroid function should be performed at least every six months.
ABSTRACT: In patients without established cardiac disease, the occurrence of premature ventricular complexes without sustained ventricular tachycardia is more an annoyance than a medical risk, and treatment is not required. In contrast, patients with established heart disease and premature ventricular complexes have a higher likelihood of developing ventricular tachycardia or fibrillation. These patients should be treated with a beta blocker or class I antiarrhythmic drug. Treatment of arrhythmias in pregnant women is rarely needed. When treatment is required, amiodarone should be avoided, and beta blockers should be used with caution, because these agents have been associated with fetal growth retardation. The most important rhythm abnormality in athletes is ventricular tachycardia associated with hypertrophic cardiomyopathy. If the presence of the disease is confirmed by echocardiography, beta-blocker therapy is necessary, and these patients should be limited to participation in nonstrenuous sports. Acute arrhythmias in children with Wolff-Parkinson-White syndrome can be treated with adenosine. Radiofrequency ablation of the accessory pathway can provide long-term control.
ABSTRACT: Family physicians frequently encounter patients with symptoms that could be related to cardiac arrhythmias, most commonly atrial fibrillation or supraventricular tachycardias. The initial management of atrial fibrillation includes ventricular rate control to provide adequate cardiac output. In patients with severely depressed cardiac output and recent-onset atrial fibrillation, immediate electrical cardioversion is the treatment of choice. Hemodynamically stable patients with atrial fibrillation for more than two days or for an unknown period should be assessed for the presence of atrial thrombi. If thrombi are detected on transesophageal echocardiography, anticoagulation with warfarin for a minimum of 21 days is recommended before electrical cardioversion is attempted. Patients with other supraventricular arrhythmias may be treated with adenosine, a calcium channel blocker, or a short-acting beta blocker to disrupt reentrant pathways. When initial medications are ineffective, radiofrequency ablation of ectopic sites is an increasingly popular treatment option.
Facial Hyperpigmentation - Photo Quiz
Blue-Gray Centrofacial Hyperpigmentation - Photo Quiz
Adenosine vs. Calcium Channel Blockers for Supraventricular Tachycardia - Cochrane for Clinicians