Assessment of Coagulation Factors in Patients with Severe Rheumatic Mitral Stenosis in Sinus Rhythm with Left Atrial Appendage Inactivity

Background: Patients with severe mitral stenosis (MS) in normal sinus rhythm (NSR), presenting with left atrial appendage (LAA) inactivity and associated left atrial spontaneous echo contrast (LASEC) are prone to left atrium (LA) or LAA thrombus formation. But unlike for atrial fi brillation, oral anticoagulants are not commonly prescribed for this patient subset. This study aimed to compare the levels of pro- coagulants and fi brinogen in both local (LA) and systemic contexts between patients with severe MS in NSR vs those in healthy control subjects. Methods: The study involved 35 patients with severe MS in NSR with LAA inactivity and LASEC who were eligible for balloon mitral valvuloplasty vs 35 healthy controls. All patients underwent transthoracic and transesophageal echocardiography to assess MS severity, LAA activity, and LASEC grade, and had blood samples analyzed for pro- coagulant levels. Results: Results showed comparable baseline characteristics between groups, with most patients in the New York Heart Association II or III functional classes, and with varying LASEC grades. Patients exhibited significantly fi cantly higher levels of prothrombin fragment 1 + 2 [patient vs control, 9017 pg/mL (6228.0-10,963.5) vs 1790 pg/mL (842.32712), P < 0.0001], thrombin-antithrombin III [patient vs control, 39 ng/mL (5.45-74.85) vs 2.80 ng/mL (1.6-6.5), P < 0.0001], plasminogen activator inhibitor-1 (patients vs controls, 26.09 + 8.18 ng/mL vs 8.05 + 3.53 ng/mL, P < 0.0001), and fi brinogen (3.48 + 0.89 g/L vs 3.01 + 0.53 g/L, P = 0.029) in the LA of patients, compared to those in control subjects. Systemic procoagulant levels also were elevated in patients, but D-dimer levels were similar between the 2 groups. Conclusions: The fi ndings suggest a hypercoagulable state in patients, similar to that in patients with atrial fi brillation. The study advocates for consideration of use of oral anticoagulants in these patients until LA and LAA function improves, to mitigate thrombus formation.