Cardiac valve calcification and use of anticoagulants: Preliminary observation of a potentially modifiable risk factor

Aims: Direct oral anticoagulant (DOAC) has been recently introduced in the clinical practice. Rather than interfering with vitamin K-dependent posttranscriptional modification of various proteins, DOACs selectively inhibit factors involved in the coagulation cascade. In particular, in contrastwithWarfarin, Rivaroxabn does not interfere with activation of matrix Gla Protein (MGP), a potent vascular calcification Inhibitor. We herein sought to investigate the impact of Rivaroxaban and Warfarin on cardiac valve calcifications in a cohort of moderate-to advanced CKD patients. Methods and results: This is amulticenter, observational, retrospective, longitudinal study. Consecutive CKD stage 3b – 4 (according to KDIGO guidelines) patients from8 cardiologic outpatient clinicswere enrolled betweenMay 2015 and October 2017. All patients received anticoagulation (100Warfarin vs 247 Rivaroxaban) as part of their non-valvular atrial fibrillation management. Cardiac valve calcificationwas evaluated via standard trans-thoracic echocardiogram. 347 patients (mean age: 66 years;mean eGFR: 37 ml/min/1.73m2) were studied. Over a mean follow-up period of 16 months, Rivaroxaban compared toWarfarin reduced both mitral and aortic valve calcifications (p b 0.001) independently of the degree of calcifications at baseline and potential confounders. Notably, Rivaroxaban use was also associated with a significant reduction in C reactive protein (CRP) (p b 0.001) during follow-up. Conclusion: This study generates the hypothesis that the use of Rivaroxaban associateswith a reduction of cardiac valve calcification deposition and progression as compared to Warfarin, in a cohort of CKD stage 3b-4 patients. Future endeavors are needed to confirm and to establish the mechanisms responsible for these findings.