Why the study?
Is lysyl oxidase deficiency associated with spontaneous coronary artery dissection?
Is lysyl oxidase deficiency associated with spontaneous coronary artery dissection?
Lysyl oxidase deficiency may be a novel genetic mechanism underlying spontaneous coronary artery dissection due to impaired elastin or collagen cross-linking.
May link LOX deficiency to SCAD; hypothesis-generating and should not change practice.
Spontaneous coronary artery dissection is a rare cause of myocardial ischaemia. The underlying mechanism is unknown but some dissections are associated with extracellular matrix disorganisation of genetic origin. A deficiency in extracellular matrix protein cross links has rarely been studied. A single clinical case of spontaneous coronary artery dissection is reported. Lysyl oxidase (LOX) and extracellular matrix organisation were investigated by skin immunohistology and polymerase chain reaction of LOX expression. Both approaches found a dramatic LOX decrease. LOX deficiency has a major role in human arterial wall organisation during development. The suspected mechanism is an elastin or collagen polymer cross linking deficiency.
No takes yet. Share an insight, caveat, or question.
Igor Sibon (2005) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: