Atrial Flutter ; diagnosis ; drug therapy ; physiopathology ; Female ; Humans ; Infant, Newborn ; Male

The most frequent perioperative cardiovascular event is cardiac dysrhythmia, defined as an abnormality of cardiac rate, rhythm or conduction. Although the occurrence of arrhythmia during the perioperative period is not uncommon, a case of newly developed perioperative atrial flutter which spontaneously converts to atrial fibrillation is rare. We report a case of atrial flutter that developed immediately after induction of general anesthesia, in a 70-year-old male patient who previously had a normal sinus rhythm. Atrial flutter changed spontaneously to atrial fibrillation after discharge to the recovery room. Dysrhythmia was unresponsive to drug therapy, and the atrial fibrillation disappeared after electric cardioversion.
Aged ; Anesthesia, General* ; Arrhythmias, Cardiac ; Atrial Fibrillation* ; Atrial Flutter* ; Drug Therapy ; Electric Countershock ; Humans ; Male ; Perioperative Period ; Recovery Room

OBJECTIVETo observe the electrophysiological effects of ibutilide on canine and to explore the potential mechanisms of ibutilide on terminating atrial flutter.

METHODSEighteen mongrel dogs were anesthetized and intubated. The heart was exposed through thoracotomy for electrodes implantation. The electrophysiologic variables (heart rate, the conduction of intraatrium and interatrium, the conduction ratio of isthmus, the effective refractory period) were measured in the absence or presence of ibutilide (10 minute infusion with 0.10 mg/kg ibutilide, 30 minutes later with a maintaining dose of 0.01 mg/min).

RESULTSIbutilide significant suppressed sinus atrial node function, the peak effect was observed at 20 - 30 min post drug infusion and heart rate returned to normal at 2 hours post infusion. Post ibutilide infusion, 1 canine developed sinus pause for 5 seconds and 2:1 atrioventricular conduction block was evidenced in another canine. The atrial, ventricular and pulmonary vein effective refractory periods were all significant prolonged (all P < 0.05) post ibutilide infusion. However, conduction of intraatrium, interatrium and isthmus remained unchanged post ibutilide infusion (all P > 0.05).

CONCLUSIONSIbutilide could suppress sinus atrial node and the atrioventricular node function. The mechanism of ibutilide on rapidly terminating atrial flutter might be related to the prolongation of the refractory periods which might then result in the reduction of the whole excitable gap of the reentrant circuit and induce proceed inability of reentrant wavefront.

Animals ; Anti-Arrhythmia Agents ; pharmacology ; Atrial Flutter ; drug therapy ; physiopathology ; Dogs ; Heart Rate ; drug effects ; Male ; Sulfonamides ; pharmacology

OBJECTIVETo investigate the efficacy and safety of intravenous ibutilide for conversion of atrial fibrillation (AF) and flutter (AFL) to sinus rhythm.

METHODSNinety-nine consecutive patients aged 18-75 y with AF/AFL were included. The duration of arrhythmia was <90 d (1 h-90 d) and ventricular rate was >60 beats/min. Patients were assigned randomly into two groups: 49 patients in ibutilide group received ibutilide 1 mg, then repeated if AF/AFL was not converted after 10 min; 50 patients in propafenone group received propafenone 70 mg, then repeated if AF/AFL persisted after 10 min. Two drugs were diluted by 50 ml of 5% glucose and injected intravenously within 10 min.

RESULTSVentricular rates were decreased in both groups. AF/AFL were converted in 34 of 49 patients (69.4 % ) in ibutilide group and in 22 of 50 patients (44.0 %) in propafenone group (P <0.05). The converting time of ibutilide was significantly shorter than that of propafenone [(16.79 ± 12.31) min compared with (36.92 ± 11.38)min, P <0.01]. The most serious adverse effect of ibutilide was non-sustained monomorphic ventricular tachycardia (3/49,6.12 %). Transient hypotension and heart pause were the main adverse events in patients who received propafenone, acute left heart failure occurred in one patient of propafenone group.

CONCLUSIONIntravenous ibutilide is a safe and effective agent for cardioversion of recent-onset AF/AFL. Furthermore,strict processing under electrocardio-monitoring is important.

Adolescent ; Adult ; Aged ; Atrial Fibrillation ; drug therapy ; Atrial Flutter ; drug therapy ; Female ; Humans ; Male ; Middle Aged ; Propafenone ; therapeutic use ; Sulfonamides ; therapeutic use ; Treatment Outcome ; Young Adult

Administration, Oral ; Adult ; Atrial Flutter ; drug therapy ; physiopathology ; Digoxin ; therapeutic use ; Echocardiography ; Female ; Fetal Diseases ; drug therapy ; physiopathology ; Humans ; Hydrops Fetalis ; drug therapy ; physiopathology ; Infant, Newborn ; Male ; Pregnancy

Although Atrial flutter (AFL) in newborn infant with normal cardiac anatomy has benign clinical course, an intractable AFL is associated with an increased risk of development of heart failure and sudden death, and is still difficult to manage. It requires multiple external electrical cardioversions, and it shows a poor response to antiarrhythmic drug therapy. We report a case of a premature infant with an intractable AFL, which we successfully treated with oral flecainide and propranolol in spite of recurred AFL. A 1-month-old, 34-week gestation, premature baby presented with an irregular heart beat and irritability. An AFL with 2:1 atrioventricular conduction was documented. Because of the intractable AFL, repeated electrical cardioversion and amiodarone were continued for 14 days. However, amiodarone was discontinued in favour of flecainide and propranolol because of the recurrent AFL and newly developed transient hypothyroidism. During 1-year follow-up period, in which oral flecainide and propranolol were continued, no AFL was observed.
Amiodarone ; Atrial Flutter* ; Death, Sudden ; Drug Therapy ; Electric Countershock ; Flecainide* ; Follow-Up Studies ; Heart ; Heart Failure ; Humans ; Hypothyroidism ; Infant, Newborn ; Infant, Premature* ; Pregnancy ; Propranolol*

Antiarrhythmic agents may increase capture threshold, but this is rarely of clinical significance. Flecainide acetate, a class IC agent, is reported to have a significant effect on the myocardial capture threshold. In this presentation, we report the case of a 72-year-old male, with a previously implanted VVI pacemaker due to sick sinus syndrome, who was treated with flecainide acetate for paroxysmal atrial arrhythmia control. During the fifteenth day of treatment, an abrupt rise in the ventricular capture threshold with ventricular pacing failure was noted. The capture threshold decreased two days after discontinuation of flecainide acetate.
Ventricular Function/*drug effects ; *Pacemaker, Artificial ; Male ; Humans ; Flecainide/*adverse effects/therapeutic use ; Electrocardiography ; Atrial Flutter/drug therapy ; Anti-Arrhythmia Agents/*adverse effects/therapeutic use ; Aged ; Action Potentials/*drug effects