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Query: UMLS:C0033036 (APC)
 10,214 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Atrial premature beats seldom require an antiarrhythmic treatment; reassurance and suppression of coffee, alcohol, and tobacco generally suffice. Acute atrial fibrillation is best treated by electrical cardioversion if it induces acute cardiovascular decompensation. If it is not poorly tolerated, the arrhythmia may be treated with digitalis at doses sufficient to keep the ventricular response rate at 70-90/min. This therapy may restore sinus rhythm, but conversion to sinus rhythm often requires the combined use of digitalis with a beta-blocker or class I antiarrhythmic drug (quinidine, disopyramide, procainamide, propafenone, or flecainide). Digitalis must be avoided in the presence of a preexcitation, and class IA agents, which facilitate atrioventricular (AV) nodal transport, must never be used without digitalis. Chemical cardioversion may also be achieved by i.v. amiodarone. Long-term prevention of recurrences after cardioversion or in the presence of recurrent paroxysmal atrial fibrillation requires digitalis combined with a class I agent, or a beta-blocker, preferably sotalol. Amiodarone is also very efficacious. Special mention should be made of atrial fibrillations of vagal or sympathetic origin, which are best treated by amiodarone, or beta-blockade (nadolol), respectively. In the presence of chronic established atrial fibrillation, digitalis in combination with a beta-blocking agent or a calcium antagonist, such as verapamil or diltiazem, may be useful to slow the ventricular response rate. If successful control cannot be obtained, catheter ablation of the AV node with implantation of a rate-responsive pacemaker must be contemplated. The therapeutic approach in patients with chronic atrial fibrillation, whether or not associated, is similar to atrial flutter.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Antiarrhythmic treatment of atrial arrhythmias. 172 15

To evaluate the relationship between the extent of left ventricular hypertrophy and ventricular or atrial arrhythmias, 77 patients with hypertrophic cardiomyopathy underwent two-dimensional echocardiography and 24-hour Holter monitoring. Antiarrhythmic treatment was discontinued before the study. Hypertrophy was septal in 33 patients, "extensive" (i.e., involving the septum and free wall) in 38 patients, and predominantly apical in six patients. Lown grade I and II ventricular arrhythmias were detected in 37% of patients, grade III in 21%, and grade IV in 29%. Atrial extrasystoles were seen in 52% of patients and chronic atrial fibrillation in 13%. More serious ventricular arrhythmias (Lown grades III and IV) occurred significantly more frequently in patients with extensive than in those with only septal hypertrophy (22/38 vs 11/33; p less than 0.001); similarly, chronic atrial fibrillation occurred more commonly in those with extensive hypertrophy (9/38 vs 1/33; p less than 0.01). During a mean follow-up period of 2.6 years, three patients died. All had a pattern of extensive hypertrophy. Two of them had ventricular tachycardia and the third had chronic atrial fibrillation. Results of this study suggest that an echocardiographic finding of extensive hypertrophy represents a useful marker for detecting patients at increased risk for serious ventricular and atrial arrhythmias.
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PMID:Severity of arrhythmias and extent of hypertrophy in hypertrophic cardiomyopathy. 252 48