The Chapter contains information about the prevalence of heart failure (HF) among patients in outpatient practice. The causal structure of HF, the prevalence of risk factors for HF, and the occurrence of a reduced ejection fraction are described. It describes the frequency of overdiagnosis of HF, the disease most often simulating its symptoms. The difficulties associated with laboratory and instrumental diagnostics of this syndrome are discussed. A pharmacological test for differential diagnosis of the causes of dyspnea in patients with suspected HF is described. Information is provided on the incidence of depressive and anxiety among the patients with this disease.
Part of the book: Ultimate Guide to Outpatient Care
For more than 50 years, oral vitamin K antagonists were the choice of anticoagulant for the long-term treatment and prevention of arterial and venous thromboembolic events. In recent years, four direct oral anticoagulants (DOACs), dabigatran, rivaroxaban, apixaban and edoxaban have been compared with warfarin for thromboembolism prevention. These anticoagulants directly inhibit specific proteins within the coagulation cascade; in contrast, oral vitamin K antagonists inhibit the synthesis of vitamin K-dependent clotting factors. Dabigatran, a direct thrombin inhibitor, and rivaroxaban, apixaban and edoxaban, the factor Xa inhibitors, produce a more predictable, less labile anticoagulant effect. DOACs do not have limitations inherent vitamin K antagonists. DOACs have a predictable pharmacokinetic profile and are free of advers drugs reactions inherent in vitamin K antagonists. However, it is necessary to take into account the pharmacogenetic characteristics of the individual that can affect effectiveness and safety of use of DOACs. The results carried out to the present fundamental and clinical studies of DOACs studies demonstrate an undeniable the influence of genome changes on the pharmacokinetics and pharmacodynamics of DOACs. However, the studies need to be continued. There is a need to plan and conduct larger studies in various ethnic groups with the inclusion of sufficient associative genetic studies of the number of patients in each of the documented groups treatments with well-defined phenotypes.
Part of the book: Pharmacogenetics