Thrombus

The Mechanism Behind Thrombus

Blood clots (or thrombi) form when strands of protein called fibrin accumulate in a blood vessel. In the heart, blood clots cause blockage of blood flow to muscle tissue. If blood flow is blocked, the oxygen supply to that tissue is cut off and it eventually dies. This can result in angina and heart attacks. Clots in chambers of the heart can mobilize to the brain. In the brain, blood clots also block blood and oxygen from reaching necessary areas, which can result in senility and/or stroke.¹

Thrombolytic enzymes are normally generated in the endothelial cells of the blood vessels. As the body ages, production of these enzymes begins to decline, making blood more prone to coagulation. This mechanism can lead to cardiac or cerebral infarction, as well as other conditions. Since endothelial cells exist throughout the body, such as in the arteries, veins and lymphatic system, poor production of thrombolytic enzymes can lead to the development of thrombotic conditions virtually anywhere in the body.⁷

It has recently been revealed that thrombotic clogging of the cerebral blood vessels may be a cause of dementia. It has been estimated that sixty percent of senile dementia patients in Japan is caused by thrombus. Thrombotic diseases typically include cerebral hemorrhage, cerebral infarction, cardiac infarction and angina pectoris, and also include diseases caused by blood vessels with lowered flexibility, including senile dementia and diabetes (caused by pancreatic dysfunction). Hemorrhoids are considered a local thrombotic condition. If chronic diseases of the capillaries are also considered, then the number of thrombus related conditions may be much higher. Cardiac infarction patients may have an inherent imbalance in that their thrombolytic enzymes are weaker than their coagulant enzymes. Nattokinase holds great promise to support patients with such inherent weaknesses in a convenient and consistent manner, without side effects.^1,6,7 Nattokinase is capable of directly and potently decomposing fibrin as well as activating pro-urokinase (endogenous).

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