Thrombolytic therapy

Thrombolytic agents such as rt-PA preferentially bind to fibrin and active plasminogen in close proximity to a clot to form plasmin, which dissolves clot fibrin and prevents formation of more fibrin.

Prevents fibrinogen from making fibrin, and rt-PA binding to fibrin limits fibrinolysis to the thrombus , preventing systemic activation when used in catheters.

All fibrinolytic agents work to increase plasmin, which breaks down fibrin, thus removing the fibrin cross – links in the thrombus and allowing disillusion.

Standard thrombolytic therapy consists of high doses of the human fibrinolytic tissue plasminogen activator or (tPA) alone.

Thrombolytic agents can treat catheter malfunction in both nondialysis and dialysis catheters.

Fibrinolytic agents are most effective when administered within 120 minutes of the onset of ischemia, when the thrombus is softer, with less fibrin cross – linking.

Fibrinolytic therapy is currently indicated for patients presenting with STEMI to a hospital without primary PCI capability if transfer will result in more than a hundred twenty minutes from the first medical contact to device time.

Should be given only in the first three hours after ischemic stroke onset, as after that increased bleeding risks outweigh thrombolytic benefits.

In acute myocardial infarction saves 30 lives for every 1000 patients treated.

Patients who receive fibrinolytic therapy should have angiography 3-16 hours after receiving such treatment, regardless of clinical status as part of the delayed invasive strategy of care.

In pulmonary embolism such therapy degrades clots bound to fibrinogen, results in faster clot resolution with the potential to improve pulmonary blood flow and cardiopulmonary status.

In pulmonary embolism is indicated for acute disease with cardiopulmonary compromise with systolic hypotension, carcinogenic shock or right ventricular dysfunction.

Use in pulmonary embolism associated with major hemorrhage.

Compared with percutaneous reperfusion strategies in patients with non-ST elevated-acute coronary syndromes, outcomes such as death, nonfatal MI and recurrent ischemia are worse with fibrinolysis with the added risk of increased fatal and nonfatal bleeding.

There is no role for fibrinolytic therapy in the treatment of in non-ST elevated -acute coronary syndromes.

Overall there is a one and a half percent risk of major bleeding with the use of fibrinolysis.

Fibrinolysis should not be as administered to patients receiving oral anticoagulation, intravenous glycoproteins IIb/III@ because of the risk of bleeding.

Most devastating complication is intracranial hemorrhage.

Intracranial hemorrhage reported in 2.1.% of 559 patients treated with thrombolytic therapy for pulmonary embolism (Dalen JE et al).

No consistent association exists between the use of thrombolytic therapy and mortality in pulmonary embolism, regardless of the patient’s cardiopulmonary status.

Fibrinolytic treatment in hemodynamically stable patients with acute pulmonary embolism and right ventricular dysfunction can decrease the frequency of chronic thromboembolic pulmonary hypertension (Kline JA et al).

In a randomized controlled study comparing standard anticoagulation with primary thrombolytic therapy in pulmonary embolism, there was no difference in mortality (Perlroth).

Associated with symptomatic intracerebral bleeding rates approximately 10 times higher in stroke patients than in acute myocardial infarction patients. (6% v. 0.7% at 36 hours.)

Accomplishes restoration of epicardial blood flow in only 60% of patients after myocardial infarction and 29% of patients are prone to recurrent ischemia before hospital discharge.

Door-needle time should be less than 30 minutes after arrival.

Fibrinolysis is particularly effective in patient with anterior STEMI if it ministered within 60 Minutes of onset.

Transfer of patients to facilities that perform PCI has a goal of 30 min. has been largely un-attained, suggesting a higher use of thrombolytic therapy should be considered for acute ST elevation MI.

Present thrombolytic strategies have reduced the mortality benefit of primary percutaneous coronary intervention in STEMI such that only trivial differences remain for the highest risk subgroup.

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