Measuring and Imaging the Arterial Platelet Thrombus in Heart Attack and Stroke
: Saving Lives by Rapid Intervention with Drugs, Devices and Genetics
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I was thinking about writing a medical story book with a lot of visual arts on the most challenging human diseases, the heart- or brain-attack and the presumed vascular culprit: the platelet thrombus from its initiation, rapid maturation, migration, lodging in the critical, narrowing arteries of heart or brain, choking these hard-working organs to death by blocking the blood supply of vital oxygen and other nutrients. When they are healthy, the proteins, the cells of blood and the composite structure of artery do a great job in maintaining the vascular sanity, called homeostasis. For a variety...
I was thinking about writing a medical story book with a lot of visual arts on the most challenging human diseases, the heart- or brain-attack and the presumed vascular culprit: the platelet thrombus from its initiation, rapid maturation, migration, lodging in the critical, narrowing arteries of heart or brain, choking these hard-working organs to death by blocking the blood supply of vital oxygen and other nutrients. When they are healthy, the proteins, the cells of blood and the composite structure of artery do a great job in maintaining the vascular sanity, called homeostasis. For a variety of reasons from our inherent genetics and our unhealthy lifestyles, the endothelial cells of the inner wall of artery become unhappy, inflamed and become sticky to the white cells of blood, called the monocytes. They open their tightly interlocked junctions and invite the monocytes and let them stay put. However, these monocytes have their own plan and imbibe more protein-cholesterol particles, called low-density lipoprotein-cholesterol (LDL-C) and turned into monsters called macrophages, the big eaters. They also release the protein-fiber cutting enzymes, called matrix metalloproteases (MMPs), where they cut the collagen fibers synthesized by the smooth muscle cells (SMCs) of media.
