Left Ventricular Hypertrophy and Outflow Tract Obstruction in a Patient With Anorexia Nervosa
A 14-year-old girl was admitted to our hospital for hypoglycemia and cardiac tamponade. In the 14 months preceding this hospitalization, she became obsessed with food intake and exercise and developed amenorrhea, disturbed body image, and an intense fear of becoming fat. She subsequently lost 31 kg body weight (decreasing from 52 to 21 kg), meeting the diagnostic criteria for anorexia nervosa. Her rate of weight loss was almost constant for the first 11 months (1.6 kg/mo) but accelerated during the last 3 months before admission (4.7 kg/mo). Chest radiography after drainage of a pericardial effusion (Figure 1A) showed that the patient had an extremely small heart, with a cardiothoracic ratio of 20%. Echocardiography taken after the drainage of the pericardial effusion revealed left ventricular (LV) outflow obstruction (pressure gradient, 88 mm Hg), with markedly increased ventricular wall thickness (posterior wall, 15 mm; septal wall, 12 mm) and decreased LV cavity volume (Figure 1B). Estimated LV mass, indexed to height to the power of 2.7, was markedly increased (139 g/m2.7). Plasma levels of atrial and brain natriuretic hormones were significantly elevated (70 and 1077 pg/mL, respectively). The patient gradually gained body weight in response to intravenous hyperalimentation, combined with psychotherapy and pharmacotherapy with an antidepressant. Concomitant with weight recovery, LV cavity volume increased, and the pressure gradient of the LV outflow decreased. At 1 month after hospitalization, the patient’s body weight had increased by 8 kg, her heart size had normalized (Figure 2A), and LV hypertrophy and intracavity pressure gradient had disappeared (Figure 2B). Atrial and brain natriuretic hormones also had normalized. Previous studies of cardiac morphology in anorexia nervosa generally have shown decreased LV size and mass. Thus, this report is the first to describe obstructive LV hypertrophy in this disease. In contrast to previous studies involving anorexia patients whose body weight had been stable for several months, our patient’s body weight decreased continuously over 14 months, with the rate of weight loss markedly accelerating during the last 3 months before the manifestation of LV outflow obstruction. When ventricular cavity size is reduced so acutely that the ventricular mass has no time to alter, ventricular wall thickness inevitably increases. This ventricular geometric change can cause an intraventricular pressure gradient, particularly when occurring in a small ventricle of an anorexic patient. The mortality rate is higher in anorexia nervosa than in other psychiatric illnesses, and cardiovascular complications contribute to the sudden death that is frequently observed in this disorder. LV outflow obstruction can cause sudden death and may represent a potential cause of mortality in patients with anorexia nervosa. LV hypertrophy and outflow obstruction should be considered serious complications of anorexia nervosa and should be evaluated, particularly when patients lose body weight within a short period of time. The present article also suggests the need to investigate the possible effects of anorexia nervosa on causative factors of cardiac hypertrophy.