MULTIFOCAL ATRIAL TACHYCARDIA AND IBUTILIDE THE AMERICAN JOURNAL OF GERIATRIC CARDIOLOGY 2001 VOL. 10 NO. 4 193

Multifocal atrial tachycardia is a well describedarrhythmia seen in hospitalized patients. The

electrocardiographic characteristics include an atrialrate of >100 beats/min, at least three morphological-ly distinct P waves, irregular P-P intervals, and an iso-electric baseline between P waves.1 The rhythm isusually recognized in elderly, severely ill patients andportends an ominous outcome.2–5 The mechanism ofmultifocal atrial tachycardia has been presumed to betriggered activity. This mechanism was arrived at be-cause of the causal relationship noted with theo-phylline toxicity, excessive catecholemines, hypoxia,acidemia, and electrolyte disturbances. Delayed after-potentials are caused by intracellular calcium over-load, which, in turn, is caused by catecholamineexcess,6 cardiac glycosides,6 phosphodiesterase inhi-bition,2 acidemia,2 and hypoxemia.2 Thus, the in-ferred mechanism of multifocal atrial tachycardia isdelayed afterpotentials triggering arrhythmogenic ac-tivity. This has not been demonstrated clinically orexperimentally. We report a patient with none ofthese predisposing factors who required, and re-sponded to, novel treatment of multifocal atrialtachycardia.

CASE REPORTThe patient was a 70-year-old African American fe-male who was admitted in March, 1998 after threeepisodes of syncope on the day of admission. She hadsustained a moderate laceration to the scalp. Uponadmission she complained of head pain but denied

dyspnea, palpitations, dizziness, chest pain/pressure,swelling, nausea, vomiting, or diaphoresis. Her med-ical history was significant for long-standing hyper-tension. Her medication was Procardia XL® 60 mgq.d. This was her first hospital admission.

The physical examination was remarkable for apulse of 130; supine blood pressure of 115/60 mmHg; and seated blood pressure of 95/60 mm Hg. Thehead and neck examination was normal and thelungs were clear, with good air entry. Her heartbeatwas irregular and tachycardic, with a II/VI systolicmurmur at the apex radiating to the axilla and S3.The abdomen was benign and there was no clubbing,cyanosis, or edema of the extremities.

An electrocardiogram showed multifocal atrialtachycardia, with a rate of 150–160 beats/minute,and left ventricular hypertrophy with a repolariza-tion abnormality (Fig. 1). Laboratory values were asfollows: arterial blood gases—pH, 7.53; pCO2, 29mm Hg; pO2, 87 mm Hg; O2 saturation, 98%. Elec-trolytes—Na, 139; K, 3.2; Cl, 104; and CO2, 24.Blood urea nitrogen was 16 mg/dL; creatinine, 1.4mg/dL; glucose, 85 mg/dL; Ca+2, 8.9 mg/dL; andMg+2, 1.3 mg/dL. Thyroid function: T4, 5.1 µg/dL;and TSH, 3.5 µIU/ml. Echocardiography revealed adilated left ventricle with severe systolic dysfunction,a left ventricular ejection fraction of 18%, normal left and right atria, severe mitral regurgita-tion, mild tricuspid regurgitation, and an estimatedpulmonary pressure of 38 mm Hg. Pulmonary func-tion tests indicated a FEV1 of 1.6 L, 95% predicted.

Multifocal Atrial Tachycardia and Ibutilide

Walter J. Pierce, MD; KellyAnn McGroary, BS, RNFrom the Division of Cardiology, The Brooklyn Hospital Center, New York Presbyterian Hospital Network, Brooklyn, NYAddress for correspondence/reprint requests: Walter Pierce, MD, Director of Cardiac Catheterization and Electrophysiology, The Brooklyn Hospital Center, Division of Cardiology, 121 Dekalb Avenue, Brooklyn, NY 11201Manuscript received February 4, 2000; accepted March 13, 2000

Multifocal atrial tachycardia is an electrocardiographic phenomenon seen primarily in the el-derly. The hemodynamic consequences of multifocal atrial tachycardia in an elderly womanare presented. Successful treatment with Ibutilide is demonstrated. Treatment with a class IIIantiarrhythmic agent opposes the frequently accepted mechanism of triggered activity in caus-ing this arrhythmia. (AJGC. 2001;10:193–195) ©2001 CVRR, Inc.

MULTIFOCAL ATRIAL TACHYCARDIA AND IBUTILIDE194 THE AMERICAN JOURNAL OF GERIATRIC CARDIOLOGY 2001 VOL. 10 NO. 4

Initial therapy included intravenous hydrationwith normal saline and intravenous diltiazem. Theheart rate decreased to 90–100 beats/minute, but re-mained irregular, with multiple P wave morpholo-gies. Because of the hemodynamic intolerance of thetachycardia, antiarrhythmic therapy was considered.We were hesitant to increase the diltiazem or substi-tute a ß blocking agent in light of the severe left ven-tricular dysfunction. Thus, ibutilide was infused at 1mg/50 ml over 10 minutes, and the infusion was re-peated after a 10-minute period of monitoring. Dur-ing the second infusion the patient’s rhythmconverted from multifocal atrial tachycardia to sinusrhythm (Fig. 2). Her rhythm was monitored, and 6hours after the completion of the infusion therhythm reverted to multifocal atrial tachycardia.Oral amiodarone, 800 mg b.i.d., was initiated. Afterthe second dose, the patient again converted to sinusrhythm. After a loading period, the patient was dis-charged to home, in sinus rhythm, on oral amio-darone 200 mg q.d.

DISCUSSIONThe usual approach to multifocal atrial tachycar-dia is to treat the underlying disease process.Here we describe a patient with neither pul-monary nor systemic disease processes. There

are reported cases of treatment of multifocalatrial tachycardia with amiodarone7 and intra-venous flecainide.8 We chose ibutilide for initialtherapy, since it was not clear if the patient hada paroxysmal arrhythmia. Ibutilide offers rapidadministration and has a relatively short t1/2.The spontaneous reversion to multifocal atrialtachycardia after approximately 6 hours demon-strated that the rhythm was responsive to theclass III antiarrhythmic, and it was non-paroxys-mal, since ibutilide’s effect was lost after approx-imately two half-lives.

The response of this patient’s multifocal atrial tachycardia to ibutilide and the reported responses to flecainide8 are inconsistent withtriggered activity. Triggered activity, as themechanism of multifocal atrial tachycardia, hasbeen inferred from the milieu in which it usuallypresents. Here we describe a patient who pre-sented outside of that classic milieu and re-sponded to a therapy that also does not supportthe triggered mechanism. It may be that theelectrocardiographic characteristics of multifocalatrial tachycardia are an epiphenomenon andno single mechanism should be inferred. We doknow that it appears to be a process prevalent inthe elderly. Elucidation of the mechanism would

Figure 1. The patient’s 12-lead electrocardiogram demonstrating multiple P wave morphologies (arrows) at a rategreater than 100 beats per minute. Note the irregularly irregular pattern and variable atrioventricular conduction, includ-ing completer block. This is multifocal atrial tachardia prior to any antiarrhythmic therapy.

MULTIFOCAL ATRIAL TACHYCARDIA AND IBUTILIDE THE AMERICAN JOURNAL OF GERIATRIC CARDIOLOGY 2001 VOL. 10 NO. 4

allow tailored therapy for elderly patients, in whom diastolic and systolic dysfunction isalso prevalent. This may help to avoid the he-modynamic consequences of multifocal atrialtachycardia.

REFERENCES

1 Shine KI, Kastor JA, Yurchak PM. Multifocal atrialtachycardia: Clinical and electrocardiographic featuresin 32 patients. N Engl J Med. 1968;279:344–349.

2 McCord J, Brosak S. Multifocal atrial tachycardia.Chest. 1998;113:203–209.

3 Wang K, Goldfarb BL, Gobel FL. Multifocal atrialtachycardia. A clinical analysis in 41 cases. Arch In-tern Med. 1977;137:161–164.

4 Lin CI, Chung IN, Cheng KK. Arrhythmogenic effects of theophylline in human atrial tissue. IntJ Cardiol. 1987;17:289–297.

5 Bittar G, Friedman HS. The arrhythmogenicity oftheophylline. Chest. 1991;99:1415–1420.

6 Wit AL. Cellular electrophysiologic mechanisms of car-diac arrhythmias. Cardiol Clin. 1990;8:393–409.

7 Kavaras G, Cokkinos DV, Rodriguez J. The effec-tive treatment of multifocal atrial tachycardia withamiodarone. Jpn Heart J. 1989;30:301–312.

8 Barranco F, Sanchez M, Halal G. Efficacy of flecainidein patients with supraventricular arrhythmias and res-piratory insufficiency. Intensive Care Med.1994;20:42–44.

195

Figure 2. The patient’s 12-lead electrocardiogramdemonstrating uniform P wave morphology and regulari-ty, including fixed atrioventricular conduction. This issinus rhythm after ibutilide infusion.