Neonatal hypothyroidism after treatment by amiodarone during pregnancy

942

LETTERS

of normal women studied, compared with 14 of15men.Bonoweta15reportedasimilarlack of increasein ejection fraction in women, and both investigators noticed differences in the mechanisms by which men and women augmented their cardiac outputs in response to exercise. Bonow et al also found that the increase in ejection fraction normally associated with exercise was less apparent in older subjects regardless of gender. In light of these studies, Iskandrian’s findings may simply reflect the age- and gender-related variability present in healthy normal subjects. MVP is a common disorder. Because most patients with MVP are female, most patients with this disorder would normally be expected to have a small or no increase in ejection fraction in response to exercise. As physicians, we must be cautions in ascribing a serious disorder such as myocardial dysfunction to such a large number of otherwise healthy persons. Primum non nocere. Pamela S. Douglas, MD Philadelphia,

Pennsylvania 15 August 1986

1. Iskandrian AS, Heo J, Hakki AH, Mandler JM. Age- and gender-related changes in exercise left veritricular function in mitral valve prolapse. Am [ Cordiol 1986;58:117-128. 2. Hakki AH, DePace NL, Iskandrian AS. Effect of age on left ventricular function during exercise in patientswithcoronaryarterydisease. JACCl983;2: 645-651. 3. Hakki AH, Iskandrian AS. Effect ofgenderonleft ventricular function during exercise in patients with coronary artery disease. Am Heart 7 1986; 111543-546. 4. Higginbotham

MB, Morris KG, Coleman RE, Cobb FR. Sex-related differences in the normal cardiac response to upright exercise. Circulation 1984;70:357-386. 5. Bonow RO, Bacharach SL, Green MV, Robinson FC, Lakatos E, Cannon RO, Cutler RN, Larson SM. Left ventricular function in normal subjects: sex and age related effects at rest and during exercise (abstr]. JACC 1986;7:175A.

diol 1987;59:142-144. 2. Sanders M, Onah J, Licbstein E, Hollander G, Greengart A, Rivera M. Single catheter technique for accurate cardiac output from left ventricle. Cathet Cardiovas Diagn 1983;9:97-103. 3. Van Den Berg E Jr, Pacific0 A, Lange RA, WheeIan KR, Winniford MD, Hillis LJJ. Measurement of cardiac output without right heart catheterization: reliability, advantages, and limitations of a left-sided indicator dilution technique. CathetCardiovas Diagn 1986;12:205-208. 4. Roberts WC. American Journal of Cardiolow Editorial Board meetingll966. Am r Card151 1986;57:1209,1211.

NEONATAL NYPOTNYROlDlSM AFTERTREATMENT BY AMIODARONE DURINGPREGNANCY Administration of amiodarone during pregnancy is not always as well tolerated as in fhe case reported by Arnoux et a1.l The following case demonstrates this point. Fetal tachycardia (220 beats/min) with congestive heart’ failure(scalpedema,pericardialeffusion,ascites] was detected in a 30-year-old woman, gravida 2, para 2, during a routing echocardiographic examination in the 30th week of gestation. Fetal cardiac morphologic characteristicswerenormal. Digoxin, 1 mg/day, was administered and propranolol, 120 mg/day, was added during the 31st week. During the 32nd week fetal tachycardia persisted and the treatment was changed to digoxin, 0.50 mg/day, and amiodarone, 1,200 mg/day for 3 days and then 600 mg/day for 3 weeks. Fetal tachycardia varied intermittently from 180 to 110 beats/min and cardiac insufficiency improved somewhat. First-degree atrioventricular block (PR 0.42 second) was observed on the maternal electrocardiogram with plasma digoxin level at 2.5 pg/ml. Delivery occurred at the end of the 35th week. The ,infant weighed 2.96 kg, was 44 cm long and again manifested tachycardia of 200 beatszmin with

LEFTVENTRICULAR DERIVED CARDIAC OUTPUT,AGAlNANDAGAIN IagreewiththefindingsofFrenchetallinthe January 1,1987, issue of this Journal concerning the correlation bettieen cardiac output measured by green dye injected either into the left ventricle or pulmonary artery. I reported similar findings in 40 patients 4 years ago.2 These findings appear even more certain since our study was again repeated and uublished last vear.3 Roberts4 noints out the monumental job of reviewing the increasing number of manuscripts submitted to The American

Journal

of Cardiology

each

year

and the outstanding work of their reviewers. Might not the burden of the editors, reviewers and readers be lightened by reducing the number

of confirmatow

for publication?

studies

submitted

-

mild

heart

failure,

which

was

treated

successfully initially through administration of digoxin and furosemide with subsequent addition of propranolol. Hypothyroidism was diagnosed inhis case duet6 the presence of a goiter with biologic abnormalities: thvraid-stimulating ho&one >240 mU/lit& (normal

range

in the neonate

530 mu/liter);

serumfreethyroxineO.5pg/ml(normalrange 21.5 pg/ml); and total thyroxine 48 pg/ml [normal 70 to 180). Treatment consisted of the administration of 10 wg/dayof thyroxineup to the age of 3 months. At fhat time, his cardiac and thyroid condition was considered normal and a recent review of his case at 15 months showed him to be both clinically and bioloaicallv normal. Therefore. we believe that it’is important of hypothyroidism

to point

out the possibility

due to administration of amiodarone to the mother even if the coexistence of a congenital goiter cannot be ruled out.

New Brunswick, New Jeksey 2 February 1987

Marcel Laurent Pierre Betremieux Vves Biron Main Lellelloco

1. French WJ, Haskell RJ, Knouse RW, Criley JM. Left ventricular derived cardiac output. Am r Car-

Rennes, France 4 April 1987

Michael Sanders. MD

1.AmouxP.SevralP.LlurensM,DiianeP,PotierA, Unal D. Cano Jb, Serradimigni A, fiouault F. Amiodarone and digoxin for refractory fetal tachycardia. Am J Cardiol 1987;59:166-167.

AICDDETECTION FAILURE:PERSPECTIVES OFTHEDETECTIVE The report by Bardy et all speculates that the mechanismfor AID-B@(whichusesheartrate and probability density function of the transcardiac signal as tachycardia detection criteria] detection failure was, due to automatic gain control failure to track fluctuationsin the amplitude of the rate counting signals. They do not specify the filter settings with which the signalsin Figure 1 were recorded, and the amplitude of the transcardiac signal appears extraordinarily low and is nearly isoelectric in the top recording. Several areas in the record appear to contain relatively high frequency signals that may be artifacts. This raises 2 additional possibilities for detection failure. The first is that fhe higher frequency signals present in the transcardiac signal caused fhe morphologic (probability density function [PDF])circuitto“lockout”thesignal when it contained frequencies exceeding 40 Hz.2 The second is that the transcardiac signal amplitude was so diminuitive and/or isoelectric that the transcardiac signal morphologic .criterion (PDF] for tachyarrhythmia detection was not met. The presence of relatively high frequency components in the patch-patch signal in conjunction with lowamplitude transcardiac potentials during ventricular fibrillation should at least raise consideration of signal generation and/ or attenuation due to some extrinsic factor. Bardy et al do not comment regarding this possibility or whether any additional recording or stimulating equipment was connected to the AICD leads. Considering the other possible alternatives, it is unclear why they concluded that detection failure in this instance was due solely to inability of automatic gain control to adjust rapidly enough to detect low-amplitude ventricular fibrillation signals, leading to such marked signal dropout as to fail to exceed the rate cutoff. Signal dropout has been shown without failure of detection of ventricular tachycardia or ventricular fibrillation,3 although the rate cutoffs in that study (140 to 180 beats/min) were less than that (195 beats/min)-of the device reported by the authors. It seems reasonable to assume that such signal dropout might assume greater importance at higher tachyarrhythmia detection rate cutoffs. Although they comment that the RR interval of the nondetected polymorphous arrhythmia was “adequate,” it is not stated whether the rate of the arrhythmia exceeded the AICD rate cutoff by 30 beats/min or more as recommended by the manufacturer.2 Failure to satisfy either rate or PDF criteria will result in failure of arrhythmia detection by an AID-B device. Had the device implanted bekn an AID-B [which uses rate criteria alone for tachyarrhythmia detection], with fhe caveats mentioned in the previous paragraph, the authors’ conclusions would be