For patients with acute cerebral infarction, they can be recanalized quickly and effectively if thrombolytics such as urokinase and streptokinase are used within 3 hours, which is medically called RT-PA therapy. But no matter what method is used to treat cerebral infarction, the incidence of recurrent cerebral infarction is still very high. In the first 30 days, the incidence is about 30%. The first reinfarction after treatment generally occurs within 7-10 days after treatment. The risk of death and sequela after reinfarction is much high than the first infarct (about 80%). How cerebral infarction patients avoid recurrent cerebral infarction has become a real challenge for both neurosurgeons and patients.
There are two methods in use:
1. Extend the use of thrombolytic enzymes for about 10 days. One of the risks of overuse of thrombolytic enzymes is that they may cause cerebral hemorrhage, because many patients with cerebral infarction are suffering from atrial fibrillation, hypertension, and atherosclerosis, and their blood vessels are very weak.
2. Use some anti-platelet aggregation drugs such as aspirin, dipyridamole, etc., but long time use of these drugs may cause damage to coagulation dysfunction.
However, a recent study from the United States has given a new method: taking a large dose of natural astaxanthin 20-24mg/day (5-6 capsules / day) can be very effective in preventing cerebral reinfarction which will not affect the coagulation function of body and avoids the risk of cerebral hemorrhage. Hypertensive patients can also use natural astaxanthin for a long time as a drug for cerebral infarction prevention. Current evidence indicates that oxidative stress and its resulting inflammatory response are the mechanisms responsible for abnormal thrombosis, whereas natural astaxanthin has potent antioxidant and anti-inflammatory properties and therefore can effectively inhibit “oxidative stress”. The process can also control the inflammatory response during thrombosis to a certain extent. Therefore, it can effectively inhibit the formation of arterial thrombosis, greatly reduce the risk of reinfarction.
At the same time, X-ray diffraction technology clearly demonstrated that natural astaxanthin can maintain the structure of cell membrane with superior antioxidant activity, while β-carotene interferes with the normal structure of cell membrane and shows extremely low antioxidant activity in cell membrane, which can easily explain why non-polar antioxidants such as beta-carotene, vitamin E, and vitamin C have not been successful clinically.
The above methods were also supported by our clinic. Patients with cerebral infarction started to use natural astaxanthin (20-24 mg/day) from the third day after thrombolytic treatment for a period of 2 months, meanwhile anticoagulant drugs were discontinued. After 2 months the intake was reduced to 12 mg/day. This method may be effective in preventing recurrence in patients with cerebral infarction.
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