Dextroversion and Noncompaction

نویسندگان

  • Josef Finsterer
  • Claudia Stöllberger
  • Fernanda Maria Silveira Souto
  • Joselina Luzia Menezes Oliveira
  • Antônio Carlos Sobral Sousa
چکیده

DOI: 10.5935/abc.20140028 Dear Editor, With interest we read the article by Gonçalves et al1 about a patient with dextrocardia and left-ventricular hypertrabeculation/noncompaction (LVHT)1. We have the following comments and concerns. Dextrocardia in association with LVHT has been repeatedly reported2. The exact pathomechanism of LVHT has not been discovered. Though the failing compaction process may play a role, there are also patients in whom LVHT developed during lifetime (acquired LVHT). Which was the cause of collapses and presyncope? Did the patient undergo cerebral magnetic resonance imaging (MRI) to rule out cardioembolic stroke originating from the inter-trabecular spaces, a complication repeatedly reported in LVHT? Which were the results of carotid ultrasound investigations? The patient required implantation of an implantable cardioverter defibrillator (ICD) because of inducible ventricular fibrillation. Did the ICD ever discharge during follow-up? LVHT is frequently associated with neuromuscular disorders (NMDs). Was the patient ever seen by a myologist to rule out a NMD? Neuromuscular disorders, such as periodic paralysis or Marden-Walker syndrome, were associated with dextrocardia. LVHT is frequently familial. Were other family members investigated for LVHT? Was LVHT found in any of the firstdegree relatives? Did any of the family members develop cardiac symptoms? The patient received gadolinium for cardiac MRI. Did radiologists observe late enhancement, which may indicate myocardial fibrosis? Myocardial late enhancement can be typically found in dystrophic NMD patients with myocardial affection3.

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عنوان ژورنال:

دوره 102  شماره 

صفحات  -

تاریخ انتشار 2014