Assessing Safety of Thrombolytic Therapy

Abstract

Thrombolytic therapy involves thrombolytic agents administered to patients suffering from venous or arterial thrombosis. The therapy induces systemic effects interrelated with the thrombolytic agent used. Bleeding is a prominent complication of thrombolytic therapy. Exhaustion of coagulation factors, generation of excessive amounts of fibrin degradation products (FDPs), therapy-induced activation of coagulation, therapy-induced anticoagulation, and formation of new fibrin all illustrate the complexity of effects of the treatment and challenges the hemostatic balance in the patients. The therapy-induced effects can be modulated by parallel administration of anticoagulants. Risk assessment is mandatory prior to thrombolytic therapy. Anticoagulated and unconscious patients represent particular safety concerns, and should be fully evaluated. Several guidelines describe the choice of tests and their safety limits in relation to pretreatment evaluation of anticoagulated patients. Fibrinogen depletion and FDPs during treatment may be promising markers for the evaluation of bleeding risk posttreatment. Future risk assessment measures should focus on the dynamics of the hemostatic balance. Here, thromboelastography may be considered a tool addressing clot formation, fibrin structure, and fibrinolytic resistance in parallel. Suitable laboratory analysis performed shortly after treatment may help to recognize severe treatment-induced systemic effects that can be counteracted by rational treatment, thereby reducing bleeding risk.

Fibrinolytic drugs induced hemorrhage: mechanisms and solutions

“…Currently, antithrombotic drugs used clinically for thrombotic diseases are divided into three categories: anticoagulant drugs, antiplatelet aggregation drugs, and thrombolytic drugs [2]. Anticoagulant drugs, such as heparin, fondaparinux, idraparinux, warfarin, and rivaroxaban, inhibit the specific factors of coagulation cascade [3]. Antiplatelet aggregation drugs, such as aspirin, prasugrel, and ticagrelor, reduce the risk of platelet aggregation [4].…”

Biophysical Mechanisms Mediating Fibrin Fiber Lysis

“…However, it is expected that a deeper understanding of how the mechanical properties of fibrin mediate fibrinolysis could have clinical relevance. Lytic strategies for treating acute myocardial infarctions often see recanalization rates of only 80%–90%, while the mechanical breakdown of blood clots often achieves higher patency [4]. This suggests the need for a further examination of the fibrinolytic determinants and highlights the importance of understanding fibrinolysis in light of fibrin's biophysical characteristics.…”