Abstract
A 50-year-old woman with history of multiple pulmonary arteriovenous malformation embolisations caused by hereditary haemorrhagic telangectasia (Rendu-Osler-Weber syndrome), complained of atypical chest pain and dyspnea. Electrcardiographic (ECG) findings were normal and the bicycle stress test was equivocal. ECG-gated 64-row cardiac multidetector computed tomography (MDCT) showed no significant coronary stenosis, but a membranous ventricular septal defect (VSD) (Fig. A, B). Patient responded well to a treatment with beta-adrenergic blocker (Carvedilol 3.125 mg/day), and considering the surgical risks, no attempt to close the VSD was performed.
Highlights
A responded well to a treatment with beta-adrenergic blocker (Carvedilol 3.125 mg/day), and considering the surgical risks, no attempt to close the ventricular septal defect (VSD) was performed
A 50-year-old woman with history of multiple pulmonary arteriovenous malformation embolisations caused by hereditary haemorrhagic telangectasia (Rendu-Osler-Weber syndrome), complained of atypical chest pain and dyspnea
Congenital intracardiac defects allow communication of blood between the left and right cardiac cavities with left-to-right flow in most cases
Summary
A responded well to a treatment with beta-adrenergic blocker (Carvedilol 3.125 mg/day), and considering the surgical risks, no attempt to close the VSD was performed. A 50-year-old woman with history of multiple pulmonary arteriovenous malformation embolisations caused by hereditary haemorrhagic telangectasia (Rendu-Osler-Weber syndrome), complained of atypical chest pain and dyspnea. Electrcardiographic (ECG) findings were normal and the bicycle stress test was equivocal.
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