Anorexia Nervosa and the Heart

Basics

Description

Anorexia nervosa is a psychiatric illness characterized by an obsessive fear of gaining weight and severe distortion of body image, often resulting in low body weight that can be fatal. Patients with anorexia nervosa typically control their body weight through means of voluntary starvation in conjunction with excessive exercise or other weight control measures such as diet pills, laxatives or diuretic drugs.
Diagnostic criteria for anorexia nervosa include:
- Refusal to maintain body weight at or above a minimally normal weight for age and height
- Excessive fear of gaining weight or becoming fat, even though underweight
- Profound distortion of one's body weight, shape and image
- Denial of the seriousness of the current low body weight
- Amenorrhea in postmenarchal females
Serious cardiovascular complications of anorexia nervosa include ventricular arrhythmias, heart failure, and sudden cardiac death.

Epidemiology

Anorexia nervosa occurs in 0.2-1.3% of the general population and affects ~1% of predominantly adolescent and young adult women.
Socioeconomically, the disorder typically affects white, middle- to upper-class females, although the incidence is rising in males and other ethnic groups.
Increased incidence of MVP (range, 13-74%) compared to the general population (range, 6-22%)

Pathophysiology

Mechanism of EKG abnormalities:
- Electrolyte imbalances
- Metabolic disturbances
Mechanisms of heart failure:
- Underlying myofibrillar destruction from protein-calorie malnutrition leads to reduced LV mass and resultant systolic and diastolic dysfunction
- Hyperalimentation may potentiate starvation-induced hypophosphatemia, which may induce clinical heart failure.
Mechanism of mitral valve prolapse:
- Myocardial atrophy and intravascular volume depletion may lead to a disproportionate effect on the mitral valve leaflets compared to the subvalvular apparatus, resulting in a functional appearance of mitral valve prolapse without myxomatous degeneration or chordal excess. These functional changes would be expected to reverse with refeeding.
Mechanism for sudden cardiac death:
- Prolonged QT with presumed polymorphic VT
- Structural LV abnormalities coupled with electrolyte imbalance
- Autonomic dysfunction
Mechanism of refeeding syndrome:
- Upon refeeding, protein-calorie and sodium repletion may result in acute volume expansion that may be poorly tolerated in the setting of underlying systolic and diastolic dysfunction.
- Cardiovascular collapse occurs as a result of impaired contractility in the setting of volume repletion. Impaired contractility results from significant hypophosphatemia which causes depletion of intracellular ATP and reduced levels of 2,3-DPG. Anorexic patients have significant reduced intracellular phosphate stores at baseline. Severe hypophosphatemia may ensue from the increased phosphate requirements necessary for glycolysis, which occurs with the shift from fat to carbohydrate metabolism during refeeding.
- Cardiac arrhythmias may occur from hypokalemia and hypomagnesemia

Etiology

Anorexia nervosa is a complex condition involving neurobiological, psychological, and sociological factors that is associated with high mortality in severe cases. Many factors have been identified in the etiology of this condition:

Genetic
Neurobiologic:
- May be linked to a disturbed serotonin system
- Other hypotheses: Autoimmune response to melanocortin peptide
Nutritional:
- Zinc deficiency
Psychological factors:
- Anorexia nervosa is associated with certain personality and emotional traits including perfectionism, compulsivity, low self-esteem, high self-expectations, ambivalence about dependence/independence, stress caused by multiple responsibilities, familial stress and distorted body image.

Diagnosis

Physical Exam

Emaciation
Dry skin with excessive growth of lanugo hair
Skin may be yellowish due to carotenodermia
Brittle nails
Thinned scalp hair
Dental caries
Osteopenia or osteoporosis
Bradycardia and hypotension are common.
Peripheral edema may be present.
MV midsystolic click may indicate MV prolapse

Tests

Lab

No specific test for anorexia
Metabolic findings related to starvation:
- Leukopenia, thrombocytopenia, anemia, reduced ESR, reduced complement levels, low CD4/CD8 counts
- Metabolic alkalosis, hypocalcemia, hypokalemia, hypomagnesemia, hypophosphatemia, hypercholesterolemia
- Endocrine abnormalities: Decreased FSH, luteinizing hormone, thyroxine (T4), triiodothyronine (T3), and estrogens; increased cortisol and growth hormone; flat glucose tolerance curve
- Diminished BUN, creatinine clearance:
EKG:
- Most common: Low voltage QRS, T-wave inversions, nonspecific ST-segment depression
- Rare: Prolonged QT interval:
  - Conflicting data regarding incidence
  - Inconsistencies reflect differences in methods used for measurements
  - QT intervals normalize upon refeeding
- Sinus bradycardia
- Sinus tachycardia
- Low voltage P waves and QRS complexes
- Rightward QRS axis
- Nonspecific T wave abnormalities
- U waves
- ST-segment depression
- Conduction abnormalities:
  - Usually 1st- or 2nd-degree AV block
  - Advanced conduction block rare

Imaging

CXR:
- Cardiothoracic ratio <0.40
Echo:
- Reduction in LV mass
- Decreased end-systolic and end-diastolic dimensions
- Preserved LV ejection fraction
- Impaired diastolic relaxation in laboratory models
- Abnormal motion of mitral valve without frank prolapse (62%)
- Definite mitral valve prolapse (19%)
- Mitral regurgitation is usually mild

Differential Diagnosis

Depression with loss of appetite
Inanition due to physical disorder
Schizophrenia
Conversion disorder
Endocrine disorder (hypo- or hyperthyroidism, Addison disease, DM, panhypopituitarism)
GI disorders (celiac disease, Crohn disease, parasitosis)
Infectious disease (AIDS, TB, chronic infection)
Cardiovascular disease (other causes of cardiomyopathy)
Malignancy

Treatment

Medication

Conventional treatment for CHF due to volume overload (ACE inhibitors, diuretics, and vasodilators).

Additional Treatment

General Measures

Multidisciplinary approach (psychological, medical, and nutritional)
Gradual weight gain (1-3 lb/wk) to avoid precipitating CHF
Identification and management of patients at risk for refeeding syndrome (chronically malnourished or no minimal oral intake for antecedent 7 days):
- Measurement and correction of serum electrolytes before refeeding
- Obtain serum chemistry values every other day for the 1st 7-10 days, then weekly during remainder of refeeding.
- Slowly increase daily caloric intake every 3-4 days.
- Cautious repletion of salt and volume
- Close monitoring for the development of shortness of breath, tachycardia, edema, or other symptoms of heart failure
- Cautious ECG monitoring during refeeding, especially in patients with prolonged QT interval

Ongoing Care

Patient Education

Anorexia Nervosa & Related Eating Disorders, P.O. Box 5102, Eugene, OR 97405, (503) 344-1144;
National Association of Anorexia Nervosa and Associated Disorders (ANAD), P.O. Box 7, Highland Park, IL 60035, (708) 831-3438.

Prognosis

Recovery:
- 20%: Achieve full recovery
- 20%: Remain chronically ill
- 60%: Suffer from relapses
Mortality:
- Significant (0.56% per year) assessed among patients referred to eating disorders centers
- 10-fold increase in mortality compared to age-matched controls
Causes of death:
- Complications of eating disorder (cardiovascular, starvation, etc.) (54%)
- Suicide (27%)

Complications

CHF:
- Risk of clinical heart failure is greatest within the 1st 2 wk of refeeding
Refeeding syndrome:
- Potentially fatal condition resulting from rapid changes in volume and electrolyte status when extremely malnourished patients are given oral, enteral or parenteral feedings
- Cardiovascular collapse due to CHF and arrhythmias, rhabdomyolysis, seizures and delirium
- Risk factors:
  - Severe weight loss (<75% of ideal body weight)
  - Risk is greatest within the 1st 2-3 wk of refeeding
  - Prolonged weight loss
Sudden cardiac death

Additional Reading

1
Cook RA, Chambers JB, Singh R. QT interval in anorexia nervosa. Br Heart J. 1994;72:69-73. 2
de Simone G, Scalfi L, Galderisi M, et al.
Cardiac abnormalities in your women with anorexia nervosa. Br Heart J. 1994;71:287-292. [View Abstract] 3
Herzog DB, Greenwood DN, Dorer A. Mortality in eating disorders: A descriptive study. Intern J Eating Dis. 2000;28(1):20-26. [View Abstract] 4
Hoeck HW.
Incidence, prevalence and mortality of anorexia nervosa and other eating disorders. Curr Opin Psychiatry. 2006;19(4):389-394. 5
Heymsfield SB, Bethel RA, Ansley JD. Cardiac abnormalities in cachectic patients before and during nutritional repletion. Am Heart J. 1978;95:584-594. [View Abstract] 6
Isner JM, Roberts WC, Heysmfield SB. Anorexia nervosaand sudden death. Ann Intern Med. 1985;102:49-52. [View Abstract] 7
Meyers DG. Mitral valve prolapse in anorexia nervosa. Ann Int Med. 1986;105:384-386. [View Abstract] 8
Nilsson EW, Gillberg C, Gillberg IC. Ten-year follow-up of adolescent-onset anorexia nervosa: Personality disorders. J Amer Acad Child Adolesc Psychiatry. 1996;39(11):1389-1395. www.ncbi.nlm.nih.gov/pubmed/10560225. Retrived 2009-09-23.

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