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Thrombolysis in the era of intervention

Thrombolysis revolutionized the treatment of acute ST - elevation myocardial infarction in the latter part of the last century and has been in use for more than two decades. Use of thrombolytic therapy is widespread owing to its safety, efficacy, ease of use, and affordability. Thrombolytic therapy has several limitations, many of which have been overcome with the adoption of percutaneous coronary intervention techniques in recent years. Primary percutaneous intervention is currently the preferred form of reperfusion therapy in the management of ST elevation myocardial infarction. However, thrombolytic therapy continues to have a role in many situations even in this era of intervention.

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  Thrombolytic Use for STEMI: What ED Clinicians Should Know

Thrombolytics can be categorized as fibrin non-selective (e.g. urokinase and streptokinase) or fibrin-selective (e.g. alteplase, tenecteplase, reteplase). Fibrin-non-selective agents degrade both fibrinogen and fibrin, which produces broad lytic action throughout the body. This widespread fibrin degradation and fibrinogen generation (fibrinogenesis) may increase the risk of hemorrhage, thrombosis, and tissue edema. Fibrin-selective agents (also referred to as tissue plasminogen activators [tPA]) convert plasminogen to plasmin more effectively in the presence of fibrin.

 Thrombolytic regimens for acute ST elevation myocardial infarction

Primary PCI should be delivered as the default therapy for patients with pain of <12 hours and ST elevation. Thrombolysis is not a preferred option but may be considered on a case-by-case basis for unstable patients with coronavirus pneumonia who develop a STEMI. Patients with significant co-morbidity to be discussed on a case-by-case basis.

 Thrombolytic Therapy Guidelines

Thrombolytic agents promote clot lysis and are administered to patients with myocardial infarction (MI) to restore coronary blood flow and limit myocardial injury and infarction. Common thrombolytic agents include: recombinant tissue plasminogen activator (t-PA, Activase, alteplase), and tenecteplase (TNKase).

 Thrombolytics – medicine class for STEMI

Prompt reperfusion improves myocardial salvage resulting in improved myocardial function, decreased arrhythmias and heart failure, and a reduction in mortality. Mortality rates can be reduced by up to 30% if fibrinolytic reperfusion therapy is administered within 6 hours of symptom onset in ST elevation myocardial infarction (STEMI) (Morse et al. 2009) i Thrombolytic agents do not differ in their effect on mortality, but do differ in harm profile, with streptokinase resulting in more major bleeds and allergic reactions, compared to alteplase which results in greater numbers of strokes, including haemorrhagic strokes. The choice of agent will depend on availability, and patient profile, weighing up the risks and benefits of potential adverse effects of the different agents/

Articles of Interest

Guard Your Heart

The ease of administration of tenecteplase may facilitate more RAPID TREATMENT in and out of hospital.

Acute ST-elevation myocardial infarction: The use of fibrinolytic therapy

For most patients with acute STEMI, we prefer primary PCI rather than fibrinolysis. However, fibrinolytic therapy should be used if timely primary PCI is not available. We prefer fibrin-specific agents over streptokinase, and we prefer the third-generation agents (eg, tenecteplase and reteplase) over alteplase based on their generally favorable benefit-to-risk profile and ease of use. The following conclusions regarding available agents have been reached from randomized trials and support our choice of tenecteplase...

Clot Busters - Discovery of Thrombolytic Therapy for Heart Attack and Stroke

The development of thrombolytics (“clot-busters”) to treat heart attack and stroke followed a complex pathway of basic research and clinical observation. Natural clot busting agents, from human blood vessels, leeches, vampire bat saliva, and bacteria all played a role in helping scientists understand how to harness the power of thrombolytics to save lives.

Clot Busters May Benefit Tardy Heart Attack Patients

Although primary PCI has emerged as the best treatment for STEMI, most patients don't receive this treatment within the early time frame when it is known to be most beneficial. Delay in presentation is one important factor. Another is that most patients don't arrive at a PCI-capable hospital and cannot be transferred fast enough to a PCI hospital.

Fibrinolytic Therapy for Patients with ST-Elevation Myocardial Infarction

t is clear that in remote or sparsely populated areas, fibrinolysis is often the only option to expedite reperfusion. Structural and unexpected interhospital transfer delays are often underestimated in urban areas as well. Once a STEMI patient is committed to be sent to a PPCI-capable center, but unanticipated delays occur, an opportunity for early reperfusion is lost. Such patients are likely to have benefited from early fibrinolysis in the absence of contraindications.

Guidance on the use of drugs for early thrombolysis in the treatment of acute myocardial infarction

NICE has also made recommendations about which drugs to use where emergency care arrangements for people having a heart attack include giving thrombolytic drugs before the patient reaches hospital – for example, this might be the setup for communities a long way from a hospital with emergency facilities.

Past, Present, and Future of Management of Acute Myocardial Infarction

Thrombolytic therapy has established its efficacy in the improvement of survival. However, it should be noted that inherently bleeding risk always exists with thrombolytic agents, even the use of t-PA, and the trade-off between ischemic and bleeding events must be considered in real-world practice. Especially, elderly patients are at risk of fatal bleeding such as intracranial hemorrhage after injection of t-PA agents. In addition, there remains a risk of re-occlusion after thrombolysis as well as slow revascularization by onset time of agents.

Thrombolysis for Acute Myocardial Infarction

Thrombolytic therapy has been a major advance in the management of acute myocardial infarction. Unfortunately, it continues to be underused or is administered later than is optimal. Thrombolytic therapy works by lysing infarct artery thrombi and achieving reperfusion, thereby reducing infarct size, preserving left ventricular function, and improving survival. The most effective thrombolytic regimens achieve angiographic epicardial infarct-artery patency in only ≈50% of patients within 90 minutes. Bleeding requiring transfusion occurs in ≈5% of patients and stroke in ≈1.8% with these regimens, which include adjunctive aspirin and intravenous heparin.

Thrombolysis in acute myocardial infarction

Currently, only a few fibrinolytic drugs are being used regularly. Streptokinase is a first-generation nonfibrin-specific fibrinolytic that indirectly activates plasminogen. Because it is produced by streptococci, patients who receive streptokinase develop antistreptococcal antibodies, precluding readministration. Nevertheless, although newer fibrin-specific fibrinolytics have theoretical advantages, streptokinase remains widely used because of its low cost.

Thrombolytic Therapy in Acute Myocardial Infarction: An Emergency Department Perspective

The use of thrombolyfic agents for acute MI is not new. Initial work with streptokinase (SK) was reported in the late 1940s.

Thrombolytics and Myocardial Infarction

In 1933, Dr. William Tillett discovered SK through sheer chance when he observed that streptococci agglutinated plasma but not serum. He inferred that fibrinogen contained in the plasma and not in the serum resulted in the agglutination of streptococci as fibrinogen gets absorbed onto the surface of streptococci. He further concluded that any plasma containing streptococci would not clot and this laid the foundation for thrombolysis in various settings

Thrombolytics Given for Major Heart Attack (STEMI)

Benefit was demonstrably greater with earlier treatment, with the most benefit apparent for treatment given within a few hours of symptom onset. Benefits were smaller and less statistically robust in the 12 to 24 hour period. Patients with ST-depressions were harmed rather than helped.