Pediatr Cardiol 13:241-242, 1992 Pediatric Cardiology

�9 Springer-Verlag New York Inc. 1992

Heart Failure Secondary to Hypomagnesemia in Anorexia Nervosa

We would like to report a case of heart failure due to hypomagnesemia in a patient with anorexia ner- vosa.

Cardiac problems account for much of the 15- 20% mortality associated with anorexia nervosa [1, 2, 4]. Electrolyte problems are common, but iso- lated hypomagnesemia was never documented as responsible for ventricular failure.

We encountered a 15-year-old girl, with ano- rexia nervosa since age 13, who presented in heart failure, with dyspnea and orthopnea, having in- creased her weight from 27 to 37 kg (for a height of 155 cm) in 10 days. Her heart rate was 150/rain and blood pressure 150/100 mmHg. She had a gallop, a

murmur of mitral regurgitation, hepatomegaly, and lower extremity edema. The arterial blood gas, on 100% oxygen by rebreather mask, showed pH 7.52, pco2 24 mmHg, po2 48 mmHg. The chest x-ray showed cardiomegaly, central interstitial pulmo- nary edema, and bilateral pleural effusions (Fig. 1). Echocardiography showed a mildly dilated, poorly contractile, left ventricle. Ejection fraction was 10%. There was moderate mitral regurgitation. The left ventricular mass of 64 g was diminished, and the end-systolic wall stress index of 274 g/cm 2 was ele- vated. Extensive blood work revealed hypomagne- semia (0.8 mEq/L, normal 1.5-2) as the only pre- dominant biochemical abnormality. Potassium was 3.6 mEq/L. Total calcium was mildly decreased (7.7 mg/dl, normal 8.5-10.7), but serum total pro- teins were also low (5.4 g/dl, normal 6-8.2), sug-

Fig. 1, Chest x-rays on admission show mild cardiomegaly, moderate central interstitial pulmonary edema, and bilateral pleural effusions.

Fig. 2, Chest x-rays 2 days later show resolution of the cardiomegaly and pleural effusions and clearing of the lung fields.

242 Pediatric Cardiology Vol. 13, No. 4, 1992

gesting a normal ionized calcium. A drug screen was negative. Liver and thyroid function tests, se- rum vitamin, and carnitine levels were normal. Mul- tiple bacterial and viral cultures and serology titers were negative.

The patient was digitalized, started on a dobu- tamine drip at 5/xg/kg/min, and diuresed with intra- venous Lasix. Magnesium sulfate was supple- mented intravenously, and serum level was normal within i8 h. Dyspnea and hypertension disappeared 24 h after admission, and the hepatomegaly and pe- ripheral edema resolved 2 days later. Radionuclide ventriculography 36 h after admission revealed a left ventricular ejection fraction of 53%. At 48 h, chest x-ray was normal (Fig. 2) and echocardio- graphy showed normal cardiac function and no mi- tral regurgitation. Dobutamine and Lasix were dis- continued 24 h after admission. Digitalis was stopped a month later and the patient remains asymptomatic and with normal ventricular function 18 months later.

Hypomagnesemia has been reported as respon- sible for heart failure, in the presence of concomi- tant hypocalcemia and hypokalemia [1, 6, 7]. The present case is the first documentation of ventricu- lar failure with hypomagnesemia as the only pre- dominant biochemical abnormality. It is likely that this abnormality was responsible for the severe ven- tricular dysfunction. Although low-dose dobu- tamine, digitalis, and diuretic administration con- tributed to the rapid improvement, their early withdrawal was not accompanied by recurrence of symptoms or ventricular dysfunction. This rapid and lasting improvement also argues against a role for other nutritional factors (e.g., selenium) not rou- tinely measured. It is unlikely that a primary ano- rexia nervosa cardiomyopathy was present since the duration of disease and degree of nutritional defi- ciency were not great.

At least two mechanisms may be proposed as a cause for the ventricular failure. The first postulates an abnormality of mitochondrial function related to relative magnesium deficiency in a teenager who may require increased dietary magnesium [5]. The second implicates a low left ventricular mass [3] and

increased afterload manifested as elevated blood pressure, possibly related to alteration of catechol- amine and aldosterone levels in magnesium defi- ciency [5]. This would produce increased wall stress, afterload mismatch, and left ventricular dys- function with or without an intrinsic abnormality of the contractile process. Both mechanisms (but par- ticularly the second) would respond quickly to mag- nesium administration and produce the findings in our patient.

In young patients with anorexia nervosa, clini- cal heart failure, and hypertension, isolated magne- sium deficiency should be considered and, if present, treated aggressively.

References

I. Fonseca V, Havard CWH (1985) Electrolyte disturbances and cardiac failure with bypomagnesemia in anorexia nervosa. Br Med J 291:1680-1682

2. Halmi K (1974) Anorexia nervosa: Demographic and clinical features in 94 cases. Psychosom Med 36:18-26

3. Moodie DS (1987) Anorexia and the heart. Postgrad Med 81:46-61

4. Schwartz D, Thompson M (1981) Do anorectics get well? Current research and future needs. Am J Psychiatry 138:319- 323

5. Seelig M (1989) Cardiovascular consequences of magnesium deficiency and loss: Pathogenesis, prevalence and manifesta- t ions-magnesium and chloride loss in refractory potassium repletion. Am J Cardiol 63:4G-21G

6. Warren SE, Steinberrg SM (1979) Acid-base and electrolyte disturbances in anorexia nervosa, abstracted. Am J Psychia- try 136:415-418

7. Whang R, Oei TO, Aikawa J, et al. (1984) Predictors of clini- cal hypomagnesemia, hypokalemia, hypophosphatemia, hy- ponatremia, and hypocalcemia. Arch Intern Med 144:1794- 1796

Alexander Davidson Paul C. Anisman Eshagh Eshaghpour Department of Pediatric Cardiology St. Christopher's Hospital for Children Philadelphia, Pennsylvania, USA