Indications for Anticoagulation in Cardiac Amyloidosis

In cardiac amyloidosis, amyloid infiltrate at the atrial level promotes atrial dilation and contractile dysfunction as well as a higher prevalence of atrial fibrillation which, when associated with ventricular diastolic and systolic dysfunction, favors blood stasis and the consequent development of intracardiac thrombosis (ICT) and cardioembolic events. In a study of 116 autopsies of patients with cardiac amyloidosis, conducted at the Mayo Clinic, the presence of ICT was demonstrated in 33% of hearts, with a significantly higher prevalence in patients with the AL form of amyloidosis than in those with other forms (56% versus 16%, p < 0.001).1 When evaluating 324 patients with cardiac amyloidosis using cardiac magnetic resonance, we found an ICT prevalence of 6.2%, with 90% located in the atrial appendage. Among the patients, 70% had atrial fibrillation, and 30% had sinus rhythm, with a similar prevalence of ICT in the AL (5.2%) and ATTR forms (7.2%).2,3 Morphological and functional changes caused by atrial amyloid infiltrate favor the development of atrial fibrillation, with a prevalence ranging from 29% to 60%, depending on the population, and it is more prevalent in the ATTR form, given that it affects an older population. The presence of atrial fibrillation poses a high risk for the development of ICT and stroke, especially in patients with AL amyloidosis.4 Approximately 20% to 30% of patients who have ICT, as well as 27% of patients with cerebral ischemic events are in sinus rhythm.3,5 The probable mechanism respons ib le for the development of thrombotic events and thromboembolism in patients in sinus rhythm would be the presence of atrial myopathy due to amyloid infiltrate and high ventricular filling pressures, which induce atrial contractile dysfunction and favor blood stasis and ICT formation.5-7 By means of logistic regression analysis, several factors have been ident i f ied that are re lated to greater predisposition to ICT and thromboembolic