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[Hypertrophic cardiomyopathy during ACTH treatment]
Insights
Adrenocorticotropic hormone (ACTH) treatment in infants with infantile myoclonic seizures may lead to hypertrophic cardiomyopathy (HCM). Regular cardiac monitoring is recommended during ACTH therapy to detect potential heart issues.
Area of Science:
- Pediatric Neurology
- Cardiology
- Endocrinology
Background:
- Infantile myoclonic seizures are a severe form of epilepsy in infants.
- Adrenocorticotropic hormone (ACTH) therapy is used for certain pediatric conditions.
- Hypertrophic cardiomyopathy (HCM) is a condition characterized by thickening of the heart muscle.
Observation:
- Two infants receiving ACTH (Tetracosactid) for infantile myoclonic seizures developed signs of HCM.
- Diagnosis was confirmed via echocardiography.
- One infant experienced cardiac insufficiency, treated successfully with propranolol, leading to symptom resolution and reduced myocardial thickness.
Findings:
- A correlation between ACTH treatment and the development of cardiomyopathy was observed.
- Hypothetical mechanisms include glycogen deposition, enhanced protein synthesis, myocardial edema, and hypertension.
- One patient showed complete reversal of cardiac changes after treatment.
Implications:
- ACTH treatment may pose a risk for developing hypertrophic cardiomyopathy in infants.
- Regular echocardiographic and physical examinations are crucial for early detection of cardiac involvement during ACTH therapy.
- Further research is needed to elucidate the exact mechanisms linking ACTH and cardiomyopathy.
Abstract:
We report on two infants (two and six month old) with infantile myoclonic seizures, who developed signs of hypertrophic cardiomyopathy (HCM), while receiving ACTH treatment (Tetracosactid=Synacthen Depot). The diagnosis of HCM was established by echocardiography. The first patient (R.M. female). showed signs of cardiac insufficiency and was treated with a beta-blocking agent (Propranolol=Dociton). This led to resolution of the clinical symptoms and reversal of myocardial muscle thickness as determined by echocardiography. The second patient (R.S. female) did not develop cardiac symptoms. A correlation between cardiomyopathy and ACTH treatment is discussed. Based on the various biological effects of ACTH different hypothetical explanations for this correlation are proposed: increased deposition of glycogen, enhanced protein synthesis, oedema of the myocardial tissue and systemic hypertension. Because of the correlation observed between ACTH treatment and the development of cardiomyopathy we recommend regular physical and echocardiographic examinations to detect cardiac involvement during treatment with ACTH.