November 1992 Am.J Obstet Gynecol

Villar et al.

18.

19.

20.

21.

22.

23.

lems of Nutrition in the World Annual Report. Lausanne, Switzerland: Nestle Foundation, 1986; 113-45. Malcom G, Bhattacharyya A, Velez-Duran M, Guzman M, Oalmann M, Strong J. Fatty acid composition of adipose tissue in humans: differences between subcutaneous sites. Am] Clin Nutr 1989;50;288-91. Rebuffe-Scrive M, Enk L, Crona N, et al. Fat cell metabolism in different regions in women: effect of menstrual cycle, pregnancy and lactation. ] Clin Invest 1985; 75: 1973-6. Lechtig A, Martorell R, Delgado H, et al. Food supplementation during pregnancy, maternal anthropometry and birth weight in a Guatemalan rural population. Trop Pediatr Environ Child Health 1978;24:217-22. Van Raaij ]MA, Peek MEM, Vermaat-Miedema SH, et al. New equations for estimating body fat mass in pregnancy from body density or total body water. Am] Clin Nutr 1988;48;24-9. Duerenberg P, Westrate ]A, Hautvast ]GAG. Changes in fat-free mass during weight loss measured by bioelectrical impedance and by densitometry. Am ] Clin Nutr 1989;49;33-6. Haugel S, Leturque A, Gilbert M, et al. Glucose utilization

24.

25. 26. 27. 28.

by the placenta and fetal tissues in fed and fasted pregnant rabbits. Pediatr Res 1988;23:480-3. Institute of Medicine. Subcommittee on Nutritional Status and Weight Gain during pregnancy. Nutrition during pregnancy. Part I. Weight gain. Part II. Nutrient suppliments. Washington, D.C.: National Academy Press, 1990:121-36. Pipe NG], Smith T, Halliday D, et al. Changes in fat, fatfree mass and body water in human normal pregnancy. Br] Obstet Gynaecol 1979;86:929-40. Hytten FE, Thomson AM, Taggart N. Total body water in normal pregnancy. ] Obstet Gynaecol Br Commonw 1966;73:553-61. Seitchik], Alper C, Szutka A. Changes in body composition during pregnancy. Ann N Y Acad Sci 1963; 110: 821-9. Van Raaij ]MA, Schonk CM, Vermaat-Miedema SH, Peek M, Hautvast J. Body fat mass and basal metabolic rate in Dutch women before, during and after pregnancy: a reappraisal of energy cost of pregnancy. Am ] Clin Nutr 1989;49:765-72.

A complete list of references is available from the authors on request.

Maternal ventricular tachycardia associated with hypomagnesemia Maurice E. Varon, MD, David M. Sherer, MD, Jacques S. Abramowicz, MD, and Toshio Akiyama, MD Rochester, New York We present a rare case of recurrent sustained maternal ventricular tachycardia associated with hypomagnesemia. The frequency of this arrhythmia was markedly reduced with magnesium sulfate therapy. Both maternal and fetal outcomes were good. To the best of our knowledge this is the first description of maternal ventricular tachycardia that was associated with hypomagnesemia and did not require treatment with conventional antiarrhythmic medications. We discuss the possible underlying pathophysiologic causes of this condition. (AM J OasTET GVNECOL 1992;167:1352-5.)

Key words: Maternal ventricular tachycardia, hypomagnesemia Paroxysmal monomorphic ventricular tachycardia is commonly encountered in patients with underlying ischemic or structural heart disease. Monomorphic ventricular tachycardia, however, may also occur in the From the Division of Maternal-Fetal Medicine, Department of Obstetrics and Gynecology, and the Cardiology Unit, Department of Medicine Strong MemOlial Hospital, The University of Rochester School of Medicine and Dentistry. Received for publication May 13, 1992; accepted May 29, 1992. Reprint requests: David M. Sherer, MD, Division of Maternal-Fetal Medicine, De/mrtment of Obstetrics and Gynecology, Strong Memorial Hospital, The University of Rochester School of Medicine and Dentistry, 601 Elmwood Ave., Box 8668, Rochester, NY 14642-8668. 611139720

1352

absence of structural heart disease. The underlying mechanism is presumed to be elevated adrenergic tone. Several patients with sustained (lasting >30 seconds) and nonsustained ventricular tachycardia occurring during pregnancy have been described. I Because of the rarity of ventricular tachycardia in association with pregnancy, a paucity of data exists regarding indications for and the efficacy of treatment of this condition. We describe an unusual case in which recurrent sustained maternal ventricular tachycardia was associated with hypomagnesemia and was effectively treated with magnesium supplementation and no conventional antiarrhythmic medications.

Volume Ilii l\umber 5

Maternal ventricular tachycardia with hypomagnesemia

,--,---r-,--

-,-- r--,-- -

H 1

.n

---,...--.

,-~

VI

.-- --

T

I

ru

f\

'\

i---ftJ' III II

'\

"\1

'"

81"+-1' it7 r-tt±, , [.

i

~L

':

,

L

'

-!

I

,

~

..

If

II 11

f

II II

1\ I

\

II

\I

'\

\,

1\ 1\ 1 V L I

--

!1

l_LL~ L_L~_---1 __ Ll

i_L-L-L___i

;

I

i 't ___ L

I

r~

I i

~L-~_

7.

LLl' ' ~

v

I

I lAll

~~

j

,L

Ll

',II

1

I

LLLL

J

.I

Ll

I I I

,

l __

.~_J

r---r< ~ . iT - '--T --tl-T;V1-~~lr~, '! -r v~--+--+-"--,--+--+--+-+-l_-='Tv'S+-+-+--_H'--__l+----IT'-+'-"t-'-il-+! ! : t-*+Il--++I+--t-ttt-+++-+-Hl-+,-+-r-f-t-+~f--t-f-+--+-+-+--tI.-t-fl+lI...t--t fI.+--1-, +--+--+--ll-t--+t--t-+c+-a+l+-! I

±--+-+-+-1

i'

1353

1

lin-;

L~4H-+t+-+-~~~~'/7'-+I~ArH++~+*h~~+rTI1~~~HJ~MJ~~I~+r~~iI*--l\~H+I-+I~+mIl, r1I [ ' I :~ , I ' ! I \ II I 1\ til r 1/11 I / 'IIJIL~ f ' ii, ,II J' I!' 'i '" ,I "~ ll,l • 1 V I 1-1 I I \J, \J i i 'I I. 1 1 , -

trHr r

fI

r Ir

I

J ell/v

I t+--t++I""-i+ft-H+i'f'-t-tlc+T: tt-'H--1 ~f-t-tt--t--lfl-+-lH--tHI--tt ~+""--t!+Itf-I+ttrt-t-\Hif'-l--lHr-t-+-+t---ll-It-+-+-+

1 \

III' I ll:JV

1\

'J

~

tJ

J

'V

Fig. 1. Twelve·lead electrocardiogram demonstrating ventricular tachycardia (paper speed 25 em/sec, I mY /cm).

Case report

A 19-year-old woman, gravida 1, para 0, was evaluated in the emergency department of her community hospital at 32 weeks of gestation, 2 weeks after a syncopal episode. During the 28th week of an otherwise uncomplicated pregnancy, she began experiencing palpitations and episodic lightheadedness. She had had one syncopal episode lasting for only seconds. This occurred after standing and working at a cash register for several hours. On initial evaluation, performed during sustained ventricular tachycardia, blood pressure was 134170 mm Hg and pulse was regular at 120 beats/ min. The lungs were clear; jugular venous pressure was 6 cm H,O and cannon a waves were detected. The first heart sound varied in intensity, the second heart sound was normal, and there were no murmurs or gallops. Fundal height was appropriate for gestational age. She had trace peripheral edema. Initial electrocardiogram revealed monomorphic regular ventricular tachycardia at 125 beats/min with QRS complex of 0.16 second and atrioventricular dissociation (Fig. 1). Treatment was initiated with intravenous procainamide and acebutalol. The serum magnesium level was 1.1 mEq/L (normal 1.3 to 2.0 mEq/L), and a 2 gm bolus of intravenous magnesium sulfate was administered. She subsequently converted to normal sinus rhythm with PR interval 0.15 second, QRS complex 0.08 second, QT, 0.42 second, and QRS axis - 10 degrees. On transfer to Strong Memorial Hospital, she remained in normal sinus rhythm with frequent asymp-

tomatic monomorphic ventricular tachycardia occurring at rates between 120 and 130 beats/min. With 24hour Holter monitoring performed without medications there were 76,045 ventricular ectopic beats (3168 per hour) including 3302 runs of asymptomatic sustained monomorphic ventricular tachycardia at a maximum rate of 160 beats/min lasting up to 20 minutes. The ventricular ectopic beats and the ventricular tachycardia had identical QRS morphologic features. An echocardiogram documented normal left and right heart function, chamber size, and valves. She underwent exercise testing on a modified Bruce protocol. She was in sustained ventricular tachycardia at the onset of the study and remained in this rhythm throughout the 7V~-minute test. Blood pressure increased physiologically, and the ventricular tachycardia rate increased from 130 to 160 beats/min with no variation in the morphologic characteristics. The test was stopped because of leg fatigue. The serum magnesium level Huctuated with values as low as 1.0 mEq/L. She received a 2 gm intravenous bolus injection of magnesium sulfate, followed by continuous drip at 1 gm/hr. Repeat Holter monitoring documented a marked decrease in the frequency of sustained ventricular tachycardia along with a concurrent increase in the number of unifocal ventricular ectopic beats. The serum magnesium level with this regimen was maintained at 2.2 mEq/L. On discontinuation of the magnesium sulfate, the frequency of ventricular tachycardia returned to pretreatment levels and the number of ventricular ec-

1354

Varon et al.

November 1992 Am J Obstet Gyneco1

t

BEATS

A 3 4 5 6 7 9 918Ul2A21 VEliTRIClLM TACHVCMDIA

234567891811121"12

B 3 4

5

6

3

5

6

7 8

9

18 11 12A2 1

2

3

4

S 6

7

8 9

18 11

121" 1

2

7 9

9

18

2

3

4

5 6

7

9 9

18

12P 1

2

VEHTRICl.l.M ECTOPIC - SIt«iUS

c 4

11 12A2 1

VENTRICl.l.M ECTOPIC -

11

TOT~

Fig. 2. Results of 24-hour Holter monitoring. A, Total runs of ventricular tachycardia. Large arrow, Time at which magnesium bolus was given (serum magnesium level was 1.2 mEql L before therapy) and continuous infusion was started. Small arrow, Time at which magnesium infusion was discontinued (serum magnesium level was 2.2 mEq/L). B, Hourly totals of single ventricular ectopic beats. Note inverse relationship in frequencies of ventricular tachycardia and isolated ventricular ectopy. C, Hourly totals of ventricular ectopy including single ectopic beats, pairs, and bigeminal beats.

topic beats decreased (Fig. 2). The serum magnesium level was subsequently maintained within the normal range with oral magnesium supplement. Transtelephonic monitoring revealed frequent ventricular ectopic beats and nonsustained ventricular tachycardia, At 39 weeks of gestation she was admitted to the hospital for elective induction of labor. She remained asymptomatic in sustained ventricular tachycardia throughout labor and delivery. She spontaneously converted back to normal sinus rhythm several hours after normal vaginal delivery of a healthy 3210 gm male infant with Apgar scores of 9 and 9 at 1 and 5 minutes, respectively. Within 72 hours nonsustained ventricular tachycardia recurred. She was discharged on a regimen of oral magnesium supplementation with no evidence of cardiac compromise.

Comment Ventricular tachycardia occurring during pregnancy is most likely the result of increased sensitivity to catecholamines in patients already predisposed to this con-

dition. In our patient both pregnancy and hypomagnesemia appear to have contributed to the preexisting tendency to development of ventricular tachycardia. The exact mechanism by which magnesium inhibits ventricular tachycardia is unclear. In our case magnesium effectively suppressed ventricular tachycardia but not the isolated ventricular ectopic beats (Fig. 2, B and C), both of which had the same QRS morphologic characteristics. Thus it appears that magnesium caused "use-dependent" prolongation of the effective refractory period of a ventricular reentry circuit," thereby preventing continuation of reentry after the first reentry beat (i.e., an isolated ventricular ectopic beat). While limited data exist regarding the indications for and the efficacy of antiarrhythmic drug therapy for ventricular tachycardia in pregnancy, the outcome for most patients appears to be good, especially in the absence of underlying structural heart disease. This case exemplifies the possible association of hypomagnesemia and ventricular tachycardia in pregnancy. Whether

Volume 167 Number 5

antiarrhythmic drug therapy is indicated during pregnancy with recurrent ventricular tachycardia should be decided after detailed clinical assessment. This should include evaluation of symptoms and hemodynamic status during spontaneous episodes of ventricular tachycardia and with exercise stress testing. Furthermore, the presence or absence of ominous electrocardiographic features (rapid ventricular tachycardia rate, multiform or polymorphic ventricular tachycardia, and frequent ectopy) must be considered.

Maternal ventricular tachycardia with hypomagnesemia

REFERENCES I. WiderhornJ, Rahimtoola SH, Elkayam U. Cardiac rhythm disorders. In: Gleicher N, ed. Principles of practice ofmedical therapy in pregnancy. Norwalk, Connecticut: Appleton & Lange, 1992:830-1. 2. Allen BJ, Brodsky MA, Capparelli EV, Luckett CR, Iseri LT. Magnesium sulfate therapy for sustained monomorphic ventricular tachycardia. Am J Cardiol 1989; 64:1202-4.

Maternal floor infarction: Relationship to X cells, major basic protein, and adverse perinatal outcome Karen K. Vernof, MD,.· b Kurt Benirschke, MD/ Gail M. Kephart, BS: Terri L. Wasmoen, PhD: and GeraldJ. Gleich, MDb.c Rochester, Minnesota, and San Diego, California OBJECTIVE: Maternal floor infarction of the placenta is characterized by gross placental abnormalities and histologic evidence of X-cell proliferation. Previously, pregnancy-associated major basic protein has been localized to the placental X cell and identified at elevated levels in serum and amniotic fluid in all normal pregnancies. Here we test the hypothesis that pregnancy-associated major basic protein is localized to the X cells in maternal floor infarction and that it contributes to the pathophysiologic features of pregnancies complicated by maternal floor infarction. STUDY DESIGN: Seven patients with eight pregnancies complicated by maternal floor infarction were evaluated. We analyzed placental tissue, serum, amniotic fluid, and placental cyst fluid for pregnancy-associated major basic protein. RESULTS: Placental tissue from pregnancies complicated by maternal floor infarction had increased numbers of X cells and fibrinoid material that occupied or surrounded degenerating villi and that stained intensely for pregnancy-associated major basic protein. Serum pregnancy-associated major basic protein levels were variable and likely cannot be used to predict the occurrence of maternal floor infarction. CONCLUSION: Pregnancy-associated major basic protein, a potent cytotoxin, is localized to X cells and is deposited in close proximity to chorionic villi in maternal floor infarction and may contribute to the pathophysiology of this disorder. (AM J OSSTET GVNECOl 1992;167:1355-63.)

Key words: Placenta, intrauterine growth retardation, major basic protein Maternal floor infarction is an uncommon and poorly recognized disorder of pregnancy. ,:I It is characterized by massive fibrinoid deposition in the placenta at the maternal floor or basal plate. Fibrinoid virtually fills the From the Departments of Obstetrics and Gynecology," Immunology,' and Internal Medicine,' Maro Clinic and Mavo Foundation, and the Department of Pathology, University of California, San Diego. d Supported in part by National Imtitutes of Health grants HD 22924, AI 15231, and AI 07047, and the Mara Foundation. Received for publication August 27. j 991; revised December 16. 1991; accepted Decembel' 30.1991. Reprint requests: Gerald J. Gleich. MD, Department of Immunolog)" Mayo Clinic, 200 First St. SW, Rochester, MN 55905. 6/]/35993

intervillous space encasing the chorionic villi, which become avascular and atrophy. Exchange of gases and nutrients cannot occur across the affected villi, and the fetus is compromised by the increasing placental insufficiency. Occasionally, the deposition of fibrinoid is not confined to the basal plate but extends throughout the placenta, giving it a firm texture because of the diffuse streaking of fibrinoid in the placental substance. In the German literature this has been referred to as Gitterinfarct or netlike infarct.' No clear-cut distinctions between the two entities can be made, and the two are thus considered as one and the same condition. The

1355