Fibrinolytic therapy
Fibrinolytic (thrombolytic) therapy uses a plasminogen activator to dissolve an occlusive thrombus and restore flow in ST-elevation myocardial infarction, high-risk pulmonary embolism, and acute ischemic stroke when timely mechanical reperfusion is unavailable, most often with alteplase or tenecteplase.
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What this article covers
- Overview
What it is: intravenous administration of a plasminogen activator, most often alteplase, tenecteplase, or reteplase, to convert plasminogen into plasmin and dissolve an occlusive fibrin clot.
- Epidemiology
Typical STEMI candidate: presentation to a non-PCI-capable or rural facility where transfer to a catheterization laboratory cannot occur within 120 minutes.
- Risk factors
Disease risk factors: hypertension, diabetes, smoking, and dyslipidemia for STEMI; immobility, malignancy, surgery, and thrombophilia for PE; atrial fibrillation and large-vessel atherosclerosis for ischemic stroke.
- Pathophysiology
Target system: the endogenous fibrinolytic system balances clot formation and dissolution; fibrinolytic drugs are exogenous plasminogen activators that tip this balance toward clot breakdown.
- Clinical features
Alteplase (tPA): fibrin-selective; weight-based bolus followed by a tiered infusion, with distinct regimens for STEMI, massive PE, and acute ischemic stroke.
- Differential diagnosis
Primary PCI: the preferred STEMI strategy when deliverable within 120 minutes, unlike fibrinolysis, because it achieves normal (TIMI grade 3) coronary flow in about 90% of patients versus 65% to 70%…
- Diagnosis
What establishes eligibility: ST elevation of at least 1 mm in two contiguous leads (or new left bundle branch block) with a compatible history for STEMI, hemodynamic instability or shock from a…
- Management
First action: confirm the diagnosis and time window, weigh the patient, place two large-bore intravenous lines, and screen the absolute contraindications (prior intracranial hemorrhage, structural…
- Complications
Intracranial hemorrhage: about 1% of treated patients across indications, and often catastrophic; risk is greater with age, hypertension, and delayed treatment.
- Prognosis
Reperfusion success: primary PCI achieves normal coronary flow in about 90% of patients versus 65% to 70% with fibrinolysis, but fibrinolysis remains life-saving when timely PCI is unavailable.
- Prevention
Systems-level delay reduction: a door-to-needle goal of 30 minutes and a door-to-balloon (first medical contact to device) goal under 120 minutes for transferred primary PCI patients guide systems planning.
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Related articles
- ST-elevation myocardial infarction (STEMI)
ST-elevation myocardial infarction is acute transmural myocardial ischemia from complete coronary occlusion, diagnosed by ischemic symptoms with diagnostic ST-segment elevation and a rising troponin. It is a time-critical emergency in which immediate reperfusion, primary PCI within 90 minutes or fibrinolysis when PCI is unavailable, plus antiplatelet and anticoagulant therapy, determines survival.
- Non-ST-elevation myocardial infarction (NSTEMI)
Non-ST-elevation myocardial infarction is acute myocardial injury from partial or intermittent coronary occlusion, diagnosed by ischemic symptoms and a rising troponin without diagnostic ST elevation. Management is antiplatelet and anticoagulant therapy with risk stratification (TIMI or GRACE) guiding the timing of an invasive coronary strategy.
- Pulmonary embolism
Pulmonary embolism is thrombus, usually from a lower-extremity deep vein thrombosis, obstructing the pulmonary arterial circulation and causing V/Q mismatch, right ventricular strain, and hypoxemia. Diagnosis follows Wells criteria (with PERC in low-risk patients) to sequence D-dimer, CT pulmonary angiography, and V/Q scanning, and management is risk-stratified anticoagulation escalating to thrombolysis or embolectomy for hemodynamic instability.
- Ischemic stroke
Ischemic stroke is sudden focal neurologic deficit from arterial occlusion confirmed by infarction on neuroimaging. Diagnosis relies on urgent noncontrast head CT to exclude hemorrhage; treatment is IV alteplase within 4.5 hours and mechanical thrombectomy for large-vessel occlusion within an extended window, followed by antiplatelet therapy and risk-factor control.
- Intracerebral hemorrhage
Spontaneous bleeding into brain parenchyma, most often from chronic hypertension affecting deep penetrating vessels or from cerebral amyloid angiopathy in lobar locations, diagnosed by noncontrast CT and managed with acute blood pressure lowering, reversal of anticoagulation, and surgical evacuation for select cerebellar or deteriorating hemorrhages.
- Anticoagulants
Anticoagulants are drugs that block steps in the coagulation cascade to prevent or treat venous thromboembolism, cardioembolic stroke, and valve thrombosis. Direct oral anticoagulants are first-line for most nonvalvular indications, while warfarin, titrated to an INR of 2 to 3, remains required for mechanical valves and high-risk antiphospholipid syndrome; parenteral heparins bridge and cover renal failure or urgent reversal needs.
- Antiplatelet agents
Antiplatelet agents block platelet activation and aggregation to prevent arterial thrombosis. Aspirin irreversibly inhibits cyclooxygenase-1, and P2Y12 inhibitors such as clopidogrel, ticagrelor, and prasugrel block adenosine diphosphate-driven platelet activation. Aspirin 81 mg daily anchors secondary prevention, and dual antiplatelet therapy with aspirin plus a P2Y12 inhibitor is first-line after acute coronary syndrome or coronary stenting.