Reversibility of Cardiac Abnormalities in Adolescents With Anorexia Nervosa After Weight Recovery
Anorexia nervosa is a life-threatening condition, with significant risk for death due to cardiac complications. The objective of this study was to analyze the cardiac involvement in anorexia nervosa and to study the reversibility of cardiac abnormalities.
Thirty-one consecutive adolescents (aged 12 to 17 years) with a diagnosis of anorexia nervosa were evaluated from January 1998 to January 1999 at the Hospital Clínic (University of Barcelona, Catalonia, Spain). An electrocardiogram, an echocardiogram, a 24-hour Holter recording with heart rate variability, an exercise test, and a tilt test were performed at initial examination and after refeeding (3 to 18 months later).
The basal body mass index was 15.2 +/- 2 kg/m2. Sinus bradycardia was found in 35% of patients, 93% showed a decreased left ventricular mass, and 70% had a diminished thickness of cardiac walls. The Holter recordings showed nocturnal bradycardia in 60% with an increased heart rate variability. After refeeding, a significant decrease in QT interval (p <.05) and QT dispersion (p <.01) was observed. Echocardiograms showed an increase in cardiac diameters (p <.01), left ventricular mass (p <.001), and cardiac output (p <.001). There was also an improvement in the exercise capacity (p <.05) and a normalization of the heart rate and heart rate variability (p <.05).
Cardiac structural and functional abnormalities provoked by anorexia nervosa are reversible in young adolescents after refeeding.
Available from: Ignacio Jáuregui-Lobera
- "In the case of anorexia nervosa, although many of these medical manifestations improve with nutritional rehabilitation and recovery from the ED, some are potentially irreversible.4 Cardiovascular disturbances may have detrimental consequences and it seems they are present in the early stages of anorexia nervosa among adolescents.5 Refeeding syndrome can result from the use of oral, enteral, or parenteral nutrition in malnourished patients.4 "
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ABSTRACT: Eating disorders are usually associated with an increased risk of premature death with a wide range of rates and causes of mortality. "Sudden death" has been defined as the abrupt and unexpected occurrence of fatality for which no satisfactory explanation of the cause can be ascertained. In many cases of sudden death, autopsies do not clarify the main cause. Cardiovascular complications are usually involved in these deaths. The purpose of this review was to report an update of the existing literature data on the main findings with respect to sudden death in eating disorders by means of a search conducted in PubMed. The most relevant conclusion of this review seems to be that the main causes of sudden death in eating disorders are those related to cardiovascular complications. The predictive value of the increased QT interval dispersion as a marker of sudden acute ventricular arrhythmia and death has been demonstrated. Eating disorder patients with severe cardiovascular symptoms should be hospitalized. In general, with respect to sudden death in eating disorders, some findings (eg, long-term eating disorders, chronic hypokalemia, chronically low plasma albumin, and QT intervals >600 milliseconds) must be taken into account, and it must be highlighted that during refeeding, the adverse effects of hypophosphatemia include cardiac failure. Monitoring vital signs and performing electrocardiograms and serial measurements of plasma potassium are relevant during the treatment of eating disorder patients.
Available from: PubMed Central
- "Myocardial mass decreases together with body weight, and results in a reduction in LV ejection fraction and diffuse global wall motion abnormalities. Myocardial damage is reversible with a tolerable prognosis since body weight can be regained.7) "
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ABSTRACT: Stress-induced cardiomyopathy is a unique reversible cardiovascular disease precipitated by acute emotional or physical stress. It is associated with a high prevalence of chronic anxiety disorder that precedes the onset of cardiomyopathy, as well as comorbid cardiovascular risk factors that are similar to the ST segment elevation of myocardial infarction. A thirty-five-year-old woman suffering from anorexia nervosa visited our hospital complaining of severe general weakness. She was diagnosed with stress-induced cardiomyopathy and mural thrombus using a transthoracic echocardiogram. Therefore, she was given anticoagulation therapy and nutrition with immediate psychiatric interventions. After two weeks of treatment, the follow-up echocardiogram indicated a significant improvement of the left ventricular dysfunction and mural thrombus.
Available from: Eitan Gur
- "In contrast, Koschke et al.  conducted ECGs on the second day of hospitalization. It is reasonable to assume that medical treatments and weight gain may cause normalization of QT variability indexes, as was reported for QTd in hospitalized patients with AN   . Finally, all of our included patients had normal electrolytes including normal serum potassium, whereas in the cohort of Kosche et al., some patients had hypokalemia, which was significantly associated with abnormal QT dynamics . "
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ABSTRACT: Anorexia nervosa (AN) may be complicated by cardiac arrhythmias and sudden death. A single study reported an increased QT variability index (QTVI), a marker for cardiac arrhythmogenicity, in AN patients. The aim of the current study was to further evaluate repolarization dynamics in a large cohort of patients with AN without electrolyte abnormalities and to evaluate previously unreported repolarization dynamics parameters.
Forty-three AN patients and 45 age- and sex-matched controls were included in the study. Twenty-nine AN patients were hospitalized for a mean time of 1.5±1.1 months. The rest were ambulatory AN patients. Electrocardiograms were conducted under strict standards. QT variability index, normalized QT variability (QTVN) and power spectral analysis of QT dynamics were conducted with designated computer software.
None of the patients had an electrolyte imbalance. Although mean QT was higher in AN patients compared with controls, QTc results were similar following corrections for RR interval. There was no significant difference in QTVI, QTVN and power spectral analysis parameters among groups. The results of QTVI and QTVN were comparable to those previously published for healthy individuals. During 3 years of follow-up, no patient developed arrhythmias or suddenly died.
Medically treated AN patients who gained weight and had normal serum electrolytes appeared to have normal QTc and QT variability indexes, reflecting a nonincreased risk for cardiac arrhythmias. We suggest that weight normalization, medical treatment and lack of electrolyte abnormalities are responsible in part for these results. Further evaluation of the prognostic significance of QTVI and QTVN in AN is warranted.
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