Long-term oral anticoagulant treatment was associated with significantly (2-fold) larger aortic valve calcifications compared to matched non-treated patients.
Observational
Does long-term oral anticoagulant treatment induce aortic valve calcification in patients with cardiovascular disease?
Long-term use of vitamin K antagonist oral anticoagulants is associated with a 2-fold increase in aortic valve calcification, highlighting a potential adverse effect of this antithrombotic therapy.
Effect estimate: 2-fold larger
Calcification is a common complication in cardiovascular disease and may affect both arteries and heart valves. Matrix gamma-carboxyglutamic acid (Gla) protein (MGP) is a potent inhibitor of vascular calcification, the activity of which is regulated by vitamin K. In animal models, vitamin K antagonists (oral anticoagulants OACs) were shown to induce arterial calcification. To investigate whether long-term OAC treatment may induce calcification in humans also, we have measured the grade of aortic valve calcification in patients with and without preoperative OAC treatment. OAC-treated subjects were matched with nontreated ones for age, sex, and disease. Calcifications in patients receiving preoperative OAC treatment were significantly (2-fold) larger than in nontreated patients. These observations suggest that OACs, which are widely used for antithrombotic therapy, may induce cardiovascular calcifications as an adverse side effect.
Schurgers et al. (Wed,) conducted a observational in Cardiovascular disease. Oral anticoagulants (OACs) vs. No OAC treatment was evaluated on Grade of aortic valve calcification (2-fold larger). Long-term oral anticoagulant treatment was associated with significantly (2-fold) larger aortic valve calcifications compared to matched non-treated patients.