Skip to main content
  • Editorial: Coronary Artery Disease and Amyloidosis: Can One Alter the Other?

    Despite advances in medical therapeutics, cardiac amyloidosis (CA) carries a poor prognosis [1,2]. In CA, the extracellular space of the heart is occupied with a fibrous, protein-rich material known as amyloid in two major forms: transthyretin – wild type (ATTRwt) or mutant (ATTRm) – and light chain (AL) [1]. There is significant variability in the prognosis of CA depending upon the type and degree of myocardial involvement. Rapid diagnosis and specific amyloidosis typing through biopsy followed by Congo Red staining and immunohistochemistry is key in allowing prognostication and initiation of type-specific treatments [2,3]. Advances in cardiac magnetic resonance imaging (CMRI) have resulted in increased detection of myocardial deposition with transmural late gadolinium enhancement (LGE) and right ventricular LGE seen more commonly with ATTR but noting that CMRI is unable to accurately distinguish between the amyloid types [4]. Whilst it is known that amyloid is deposited in both the myocardial extracellular space and intramural coronary vasculature, the angiographic pattern and distribution of the resulting coronary stenosis have not previously been studied [5].

This site uses cookies. By continuing to browse the site you are agreeing to our use of cookies. Review our Privacy Policy for more details