Abstract
Anticoagulant treatment is extremely important and frequently encountered in the therapy of various cardiovascular diseases. Vitamin K antagonists (VKA) are in use for the prevention and treatment of arterial and venous thromboembolism, despite the introduction of new direct-acting oral anticoagulants (NOAC). The VKA still have the clear recommendation in patients with a mechanical prosthetic heart valve replacement or moderate to severe mitral stenosis of the rheumatic origin, in deep vein thrombosis associated with congenital thrombophilia, and in cases where NOAC are prohibited by social condition (financial reason) or by comorbidities (extreme weight, severe renal or liver disease). VKA dosing required to reach the targeted therapeutic range varies largely between patients (inter-individual variability). This inter-individual variability depends on multiple environmental factors such as age, mass, diet, etc. but it is also influenced by genetic determinism. About 30 genes implicated in the metabolism coumarins derivatives were identified, the most important being CYP2C9 and VKORC, each with several polymorphisms. Herein, we review the data regarding genetic alterations in general and specific populations, highlight the diagnosis options in particular cases presenting with genetic alteration causing higher sensitivity and/or resistance to VKA therapy and underline the utility of NOAC in solving such rare and difficult problems.
Highlights
Anticoagulant treatment is extremely important and frequently encountered in the therapy of various cardiovascular diseases
The risk of hemorrhagic events associated with a higher level of International Normalized Ratio (INR) is greater, with 10% to 17% occurring during the first weeks of treatment
Another group of patients who benefit from vitamin K antagonists (VKA) treatment is those suffering from recurrent thrombosis or thrombosis in atypical sites associated with major congenital thrombophilia [14]
Summary
Anticoagulant treatment is extremely important and frequently encountered in the therapy of various cardiovascular diseases. The achievement and maintenance of efficient anticoagulation with vitamin K antagonists (VKA) is difficult because of the narrow target range with the adverse effects of overdosing associated with hemorrhagic events and suboptimal dosing responsible for thromboembolic events. The risk of hemorrhagic events associated with a higher level of International Normalized Ratio (INR) is greater, with 10% to 17% occurring during the first weeks of treatment. Most of the major bleedings take place after the initiation of the therapy, with the hemorrhagic risk being 10 times higher in the first month than in the twelfth month of anticoagulant treatment [1]. Some studies showed that suboptimal anticoagulation was associated with poor clinical outcomes, a higher rate of hospitalization, and increased risk for ischemic stroke and other thromboembolic events [2]
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