Volume 121 Number 6. Part 1 Brief Communications 18 19

EC’S HR = 245 BPM FILTER = ON 7/20,1996 7: l&PM MFIb

Fig. 1. Upper tracing, ECG shows supraventricular tachycardia (SVT) at 245 beats/min (paper speed 25 mm/set) during initial adenosine administration. Note the SVT conversion to sinus rhythm at 75 beats/ min, which gradually increased to 140 beats/min. Lower tracing, Respiratory excursion recording during conversion.

sient complete AV block requiring pacing has been reported with high adenosine doses. 3, 5 A wide range of adenosine dosage (30 to 250 pg/kg) has been reported, with initial doses usually from 37.5 fig/kg to 100 /*g/kg. A slightly higher dose was used in this case, corresponding to 0.1 ml of drug.

Adenosine has previously been shown to be effective and safe in the short-term management of SVT in children and infants2*” However, little experience exists with the use of this agent in preterm babies and in those with severe con- gestive heart failure. Till et al2 described the efhcacy and safety of adenosine in the treatment of SVT in 28 infants. Adenosine was successful in converting the majority of AV reentry and AV nodal reentry tachycardias. Children with impaired cardiac output, including those receiving cate- cholamine infusions, did not sustain a fall in blood pressure after an intravenous administration of adenosine. The youngest infant described by Till et al. was 1 day old; how- ever, gestational age and/or weight were not reported. Overholt et a1.3 have also described the usefulness of ade- nosine in the treatment of five acutely ill neonates. Two of their patients had hydrops fetalis and moderate hypoten- sion. Neither of these infants was described as premature.

The experience reported here of the eflicacy of adenos- ine in a premature hydropic infant of 32 weeks’ gestation highlights the clearly unique features of adenosine. The lack of adverse hemodynamic or respiratory side effects in- dicates this may now be the treatment of choice, even in this extremely fragile patient population. Adenosine is clearly preferable to DC cardioversion, which may cause significant myocardial damage in a preterm heart. The po- tential damage is due to the excessive voltage that may be delivered, because the very low voltages that are needed are not possible with most defibrillators. Despite the immatu- rity of the AV node and conduction tissue, the efficacy of adenosine was demonstrated. The extremely brief half-life of 0.6 to 10 seconds makes adenosine a safer drug than digoxin or p-blockers in metabolically impaired infants with low cardiac output and decreased hepatic or renal drug clearance. Although adenosine may not affect reiniti- ation of the SVT as shown here, it has immediate short- term therapeutic efficacy, and should be considered for use in premature infants with SVT.

REFERENCES

1.

2.

3.

4.

5.

Epstein ML, Kiel EA, Victorica BE. Cardiac decompensation following verapamil therapy in infants with supraventricular tachycardia. Pediatrics 1985;75:737-40. Till J, Shinehourne EA, Rigby ML, Clarke B, Ward DE, Row- land E. Eficacy and safety of adenosine in the treatment of supraventricular tachycardia in infants and children. Br Heart ,J i989;62:204-I 1. Overholt ED. Rheuban KS. Guteesell HP. Lerman BB. Dimarco JP. Usefulness of’ ‘adenoiine for arrhythmias in infants and children. Am J Cardiol 1988;61:333-40. Case CL, Trippel DL, Gillette PC. New antiarryhythmic agents in pediatrics. Pediatr Clin North Am 1989;36:1293-320. Moak JP. Pharmacology and electrophysiology of antiar- rhythmic drugs. In: Gillette PC, Carson A Jr, eds. Pediatric arrhythmias: Electrophysiology and pacing. Philadelphia: WB Saunders Co, 1990:37-115.

Superiority of transesophageal echocardiography in detecting ruptured mitral chordae tendineae

Mohsin Alam, MD, and Irene Sun, RN, RDMS. Detroit, Mich.

Severe mitral valve regurgitation resulting from ruptured chordae tendineae usually occurs spontaneously in pa- tients with normal hearts, a myxomatous mitral valve, or it results from infective endocarditis, chest trauma, rheu- matic carditis, or left atria1 myxoma.1-3 Although M-mode and two-dimensional (2-D) echocardiography have been reported to be of value in diagnosing flail mitral leaflets due to ruptured chordae tendineae,*, 5 many patients are in fact diagnosed at the time of surgery or autopsy. In this study we evaluate the role of transesophageal echocardiography

From the Henry Ford Heart and Vascular Institute, Division of Cardiovas- cular Medicine, Henry Ford Hospital.

Reprint requests: Mohsin Alan, MD, Echo-Doppler Laboratory, Henry Ford Hospital, 2799 West Grand Blvd., Detroit MI 48202.

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1820 Brief Communications June 1991

American Heart Journal

Fig. 1. Transesophageal2-D echocardiogram of a patient with ruptured mitral chordae tendineae (arrow) with flail mitral leaflet. There are vegetations (arrowhead) on the posterior mitral leaflet. LA, Left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.

Fig. 2. Transesophageal color flow Doppler echocardiogram of a patient with severe mitral regurgitation (MR) resulting from ruptured mitral chordae tendineae. LA, Left atrium; LV, left ventricle; RA, right atrium.

and color flow Doppler echocardiography in diagnosing performed through transthoracic as well as transesoph- ruptured mitral chordae tendineae. ageal approaches. The ultrasound studies were performed

Methods. In 23 patients with clinical evidence of moder- on the same day using conventional techniques and instru- ate to severe mitral valve regurgitation, M-mode, 2-D mentations. The mitral valves were interrogated for the echocardiography, and color flow Doppler studies were presence of anatomic lesions and valve regurgitation. Mi-

Volume 121 Number 6, Part 1

tral regurgitation was graded as severe when the regur- gitant color flow Doppler jet occupied >40% of the left atria1 chamber by gross visual inspection.6 All patients had symptoms of dyspnea on mild exertion or congestive heart failure. Cardiac catheterization, angiography, and mitral valve replacement and/or repair surgery were subsequently performed in 12 of 23 patients. Four of six individuals who had ruptured mitral chordae tendineae demonstrated by the transesophageal study had mitral valve ring annulo- plasty, whereas two others had valve replacement surgery performed.

Results. In 6 of the 23 patients with clinically moderate to severe mitral regurgitation, transesophageal 2-D echo- cardiography demonstrated linear echoes of loose chordae tendineae protruding in a whip-like fashion in the left atrium during systole (Fig. 1). In four of six patients there was associated thickening and prolapse of the valve leaf- lets, whereas two other patients had mitral valve regurgi- tation demonstrated by transesophageal color flow Doppler (Fig. 2). Good quality transthoracic ultrasound studies in all six patients failed to demonstrate ruptured chordae tendineae, but did demonstrate mitral valve prolapse with a thickened redundant valve in four, valve vegetation in one, and a moderate to severe degree of regurgitation in six instances. Clinically all these patients had moderate to se- vere mitral regurgitation, but the precise diagnosis of rup- tured chordae tendineae was made only after the trans- esophageal study. The diagnosis of ruptured mitral chor- dae tendineae was confirmed in all six instances at the time of mitral valve surgery. In 17 other patients with mitral re- gurgitation, transesophageal imaging demonstrated valve vegetation in four (two by transthoracic study), valve pro- lapse in five (three by transthoracic study), and mild mi- tral stenosis in three by both techniques. In five patients with dilated poorly-functioning left ventricles the mitral valve had a completely normal appearance by both echocar- diographic studies, indicating secondary mitral regurgita- tion.

Comments. Transesophageal echocardiography has been shown to be superior to transthoracic imaging in demon- strating anatomic abnormalities of the mitral valve, in- cluding ruptured chordae tendineae.4 Our study confirms the findings of these reports and indicates that this entity is more common than presently diagnosed. We believe that currently transesophageal 2-D echocardiography is the procedure of choice in diagnosing ruptured mitral chordae tendineae. All six patients in our study were not diagnosed by the transthoracic ultrasound studies, and even angiog- raphy, which demonstrated severe mitral valve regurgita- tion, failed to demonstrate actual rupture of the mitral chordae tendineae. We believe that the rupture of the chordae tendineae in four patients resulted from myxoma- tous mitral valves, whereas in two others it was secondary to infective endocarditis. In all four patients with myx- omatous mitral valves the surgeons planned successfully to do mitral valve ring annuloplasty surgery. In conclusion, transesophageal2-D echocardiography and color flow Dop-

Brief Communications 182 1

pler echocardiography are superior to transthoracic imag- ing and angiography in demonstrating ruptured mitral chordae tendineae. This entity occurs more often than it is presently diagnosed and should be considered in all pa- tients with moderate to severe mitral regurgitation.

REFERENCES

1.

2.

3.

4.

5.

6.

Sanders CA, Armstrong PW, Willerson JT, Dinsmore RE. Etiology and differential diagnosis of acute mitral regurgita- tion. Prog Cardiovasc Dis 1971;14:129-52. Wise JR. Mitral regurgitation due to rupture of chordae tendineae by calcified atria1 myxoma. Br Med J 1974;2:95-6. Goodman D, Kimbiris D, Linhart JW. Chordae tendineae rupture complicating the systolic click-late systolic murmur syndrome. Am J Cardiol 1974;33:681-4. Schluter M, Kremer P, Hanrath P. Transesophageal 2-D echocardiographic features of flail mitral leaflet due to rup- tured chordae tendineae. AM HEART J 1984;108:609-10. Joh Y, Yoshikawa J, Yoshida K, Akasaka T, Shakudo M, Ho- zumi T, Kato H. Transesophageal echocardiographic findings of mitral valve prolapse. J Cardiol 1989;19:(suppl 21):85-95. Helmcke F, Nanda NC, Hsiung MC, Soto B, Adey CK, Goyal RG, Gatewood RP. Color Doppler assessment of mitral regur- gitation with orthogonal planes. Circulation 1987;75:175-83.

Cardiac lymphangioma

Ilhan Pagaoglu, Riza Dogan, Sencan Ozme,* Giilsev Kale,* and A. Yiiksel Bozer. Ankara, Turkey

Primary neoplasms of the heart are uncommon and consti- tute one of the rare forms of cardiac disease. Approximately 70% of all primary neoplasms of the heart are benign and potentially curable by surgical treatment.l Cardiac lym- phangioma is the rarest, primary, benign tumor of the heart, first reported in 1911 by Armstrong and Miincke- berg.2, 3 Up to this time, three cases of cardiac lymphangi- oma have been reported. In this report, a new cardiac lym- phangioma is presented with its operative treatment and late follow-up.

A lo-year-old boy was admitted to our institution on March 29, 1985, with the finding of localized, soft, super- ficial subcutaneous lesions of four years’ duration. It is not known if these soft masses were present at birth, but they were manifest by the end of the sixth year of life. His past medical history revealed that in 1981 he had been hospi- talized in Germany for an infectious disease and the lesions were accepted as benign and nothing was done. He had a 2-year history of exertional pain in his left extremities. He

From the Department of Thoracic and Cardiovascular Surgery, and the Department of Child Health and Pediatrics* (Pediatric Cardiology & Pediatric Pathology Unit), Hacettepe University, Faculty of Medicine. Reprint requests: ilhan Pagaoklu, MD, Dept. of Thoracic and Cardiovascu- lar Surgery, Hacettepe University, Faculty of Medicine, 06100 Hacettepe, Ankara, Turkey. 414128836