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  • Writer's pictureOren Zarif

The Benefits and Risks of Thrombolytic Therapy for Stroke - Oren Zarif - TPA Stroke

A new study has examined the benefits and risks of tPA treatment for stroke. Researchers analyzed data from six previous trials to calculate the likelihood of benefit and harm from the treatment. The results of the study showed that 16.9 patients would benefit and only 3.4 would be harmed by tPA treatment. While tPA isn't perfect, it still provides a significant benefit for stroke patients. Here are some of the benefits and risks of tPA stroke treatment.

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There are many risks associated with thrombolytic therapy, including narrow eligibility, significant comorbidity, and perceived lack of efficacy in high-risk subgroups. However, the study shows that tPA is effective in reducing death and dependency, a significant outcome when considering the current cost of the drug. Further, the study's authors suggest that better education is necessary to optimize tPA treatment for all stroke patients. Future research should focus on enhancing tPA's efficacy and safety through improved neuroimaging, rapid stroke diagnosis, refinement of advanced neuromarkers, and improved alternative reperfusion.

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The study results suggest that tPA is effective in restoring blood flow to the affected brain regions. However, there are limitations to the study. The study lasted about 3 to 4.5 hours. However, this short duration is not ideal. A post-hoc analysis of the study's data indicates that tPA is effective in limiting damage to brain tissues and functional impairments. But it still remains an open question, and more trials are needed to understand whether this therapy is effective for stroke patients.

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Although tPA was first studied in the 1980s, it wasn't widely used for stroke patients until the 1990s. The first studies were limited to animal models, with only a handful of heart attack patients undergoing the treatment. In the 1980s, biotechnology allowed scientists to directly express proteins in cell cultures and clone genes. This allowed companies like Genentech to produce recombinant tPA in sufficient quantities for commercialization. In 1984, the National Heart, Lung, and Blood Institute funded the first randomized clinical trial involving patients.

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A major issue with the study was that the NINDS criteria were too narrow. The analysis was confounded by the indications and patients' underlying vascular disease. The study also failed to detect a significant difference between the two groups of patients. Nonetheless, the outcomes of the two studies were similar. The rates of mortality, disability, and intracerebral hemorrhage were similar in both. In addition, the study included a post-hoc analysis of tPA stroke.

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The study results from the NINDS part II trial did not show any change in mortality after tPA administration. The data strongly suggest that tPA is best administered within three to four hours of the onset of symptoms. However, the concept of "enough time" can lead to a delay in treatment. In short, the earlier tPA is administered, the better the outcomes. The data will allow doctors to evaluate the patient's condition and recommend the treatment.

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However, a significant downside of tPA is its risk of adverse side effects. Although there is an inherent risk of the drug, it has been shown to improve 90-day outcomes for patients undergoing it. It is also associated with a higher rate of intracerebral hemorrhage and mortality. This drug may not be right for everyone. However, it has been used successfully in the treatment of stroke patients.

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Another disadvantage of tPA for stroke is its neurotoxicity. Despite its effectiveness, approximately 25 percent of stroke patients are not treated with the drug within three hours of onset. The American Stroke Association strongly recommends that tPA be given to patients with an acute ischemic stroke within three hours of onset. In addition, tPA is a neurotoxic drug and promotes leukocyte infiltration and microglial activation.

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While tPA is the only approved treatment for acute ischemic stroke, it is not without risks. Late tPA administration increases the risk of edema, HT, and ICH. Further, delayed tPA administration is associated with increased mortality and reperfusion injury. In addition, tPA activation activates matrix metalloproteases, which further disrupt the BBB. Moreover, tPA may cause further damage by activating a molecule called MMP-2.

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Among the new drugs that are available for tPA stroke, argatroban may be an additional benefit. The drug, argatroban, inhibits both free and clot-associated thrombin. It also improves the rate of reperfusion, reduces lesion volume, and decreases fibrin deposition in the ipsilateral cortical microvasculature. It is important to note that both drugs are effective in reducing the risk of reocclusive stroke.

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