Familial Spontaneous Coronary Artery Dissection and the SMAD-3 Mutation.
- Resource Type
- Academic Journal
- Authors
- Solomonica A; Western University, London Health Sciences Centre London, Ontario, Canada; Department of Medicine, London Health Sciences Centre London, Ontario, Canada.; Bagur R; Western University, London Health Sciences Centre London, Ontario, Canada; Department of Medicine, London Health Sciences Centre London, Ontario, Canada.; Choudhury T; Western University, London Health Sciences Centre London, Ontario, Canada; Department of Medicine, London Health Sciences Centre London, Ontario, Canada.; Lavi S; Western University, London Health Sciences Centre London, Ontario, Canada; Department of Medicine, London Health Sciences Centre London, Ontario, Canada. Electronic address: Shahar.Lavi@lhsc.on.ca.
- Source
- Publisher: Excerpta Medica Country of Publication: United States NLM ID: 0207277 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1879-1913 (Electronic) Linking ISSN: 00029149 NLM ISO Abbreviation: Am J Cardiol Subsets: MEDLINE
- Subject
- Language
- English
Spontaneous coronary artery dissection (SCAD) is a cause of about 4% of acute coronary syndrome. The pathophysiology of SCAD is not yet fully understood. Loeys-Dietz syndrome is a connective tissue disorder characterized by aortic aneurysms, arterial tortuosity, and aortic dissections. It is caused by mutations in the genes affecting the transforming growth factor β pathway. We describe a family with a SMAD3 gene mutation and Loeys-Dietz syndrome presenting with recurrent SCAD episodes.
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