TPA and Stroke - Oren Zarif - TPA Stroke
The benefits of tPA therapy for stroke patients were shown in a new study conducted by the Lansberg group. Researchers used data from six previous trials to calculate the odds of benefit and harm for patients undergoing the treatment. The results showed that 16.9 patients would benefit from the drug, while only 3.4 were adversely affected. Although the results showed that tPA is not as effective as earlier treatments, the new findings demonstrate that the drug can still provide a substantial benefit for stroke patients.
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Although tPA has been approved for ischemic strokes, emergency physicians are reluctant to prescribe it to patients who have suffered a hemorrhagic stroke, which is a type of vascular disease in which there is bleeding in the brain. Because tPA has a six percent risk of hemorrhage, most ER doctors prefer to wait for a neurologist to make the final decision about treatment.
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However, most patients are not treated with tPA in time. In fact, only 27% of patients who arrive at the hospital within three hours of their onset of symptoms are treated with thrombolytic therapy. Further, 31% of patients were excluded because their symptoms were too mild or improved rapidly. This finding highlights the importance of early intervention in stroke. There are numerous reasons why patients fail to receive IV TPA. But if you want to know more about TPA and stroke, read on.
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Although tissue plasminogen activator is the only approved treatment for acute ischemic stroke, it has been linked to increased risk of ICH, HT, and edema. If tPA is given too late, the risk of ICH is even higher. Despite these risks, tPA remains the best therapy for acute stroke. However, there is a time limit for the drug to be effective. So, it is best to use it as soon as possible after the patient's stroke symptoms appear.
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The latest data regarding tPA for stroke patients are limited. The results of the study were mixed. Among those who received the drug, 44.5% achieved a good outcome and 7.4% exhibited no or minimal disability. Moreover, the tPA treatment arm had a lower proportion of good outcomes and higher mortality. In addition, patients who received tPA had more severe strokes and had higher levels of comorbidities than those who did not receive the drug.
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While the use of tPA for stroke patients is gaining widespread approval, many hospitals are not equipped to administer the drug. Therefore, most hospitals have a neurologist on hand. Moreover, there are telemedicine links between doctors and patients. This allows a stroke specialist to assess a patient's condition and assess his/her CT scan. It is important to know that the patient's situation depends on how quickly the treatment is administered.
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The combination of low-dose tPA and rA2 may be an efficient thrombolytic therapy for patients with ischemic stroke. This new combination has also been found to reduce the risk of ICH transformation. The combined low-dose tPA and rA2 therapy improves the therapeutic efficacy and safety of tPA-based thrombolytic therapy. These findings have important implications for stroke patients.
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In a mouse model, tPA and PDTC are given to rats who have suffered a transient MCAO. tPA significantly reduces the infart volume and edema. PDTC decreased the level of the enzyme MMP-2 in the cortex. tPA also promotes leukocyte infiltration, microglial activation, and the production of free radicals. Thus, it may be beneficial to administer a neuroprotectant in patients who have undergone tPA treatment.
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Despite the potential benefits of tPA for stroke patients, high rates of delivery of this drug have been difficult to sustain. A significant barrier to delivering tPA to stroke patients is late presentation. Moreover, physicians are often at risk of medical malpractice lawsuits if they refuse to use tPA when it is recommended. Although there are few systematic reviews of the relationship between malpractice and the use of thrombolytic therapy, improvements have been made in the delivery of this drug.
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In a study of tPA, delayed combination treatment improved neurological function recovery in patients with tPA-induced hemorrhage. Furthermore, tPA reduces the amount of angiostatin-associated endothelial toxicity. This may translate into improved long-term neurological outcomes. However, tPA is not a cure for stroke. But delayed treatment may be the solution. In the meantime, it may help patients whose tPA levels are too high to benefit from a tPA stroke.
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