Oh my Goodness! I’ve been a silent partner on this DVT site. I do read all of the feeds, but the “psychological” part really got my attention. It has been a little over 2 years since my DVT-PE. Just a refresher for those that may not remember my story. When I finally decided I needed to go to the Dr. I had a massive clot from my belly to my foot on my left side. I had clots that had traveled to both lungs. I am on 325 aspirin daily now and have my leg ultrasounded every 6 months. Being followed up with a Vascular Surgeon who is very knowledgable in MTS. He came to Heart Hospital OKC from Dallas, Dr. Lenny Stubbs. Wonderful man. The last 6 months it has hit me, didn’t realize until reading the post, thought maybe it was Menopausal, maybe it was losing my mom not quite 5 years ago. But, after reading I’m thinking this is what it is. I was on anti-depressants and we were weaning me when I had my DVT, so we stayed on them for awhile. When I was over the hump, I was ready to come off of them. Haven’t been on anti depressants for over 2 years. My family has strongly urged me to seek help, but I hate the side effects of anti-depressants. I’m really close to seeking help, but such an emotional wreck that I think all I would do is cry. I am in constant pain in my leg, any pain that is above and beyond I think, What if?
In the arterioles blood pressure is lower than in the major arteries. This is due to bifurcations, which cause a drop in pressure. The more bifurcations, the higher the total cross-sectional area, therefore the pressure across the surface drops. This is why [ citation needed ] the arterioles have the highest pressure-drop. The pressure drop of the arterioles is the product of flow rate and resistance: ∆P=Q xresistance. The high resistance observed in the arterioles, which factor largely in the ∆ P is a result of a smaller radius of about 30 µm.  The smaller the radius of a tube, the larger the resistance to fluid flow.
A team of scientists led by Dr. Brian F. Gage at Washington University in St. Louis investigated whether genetic testing can help predict the best warfarin dose to give a patient. They compared outcomes for patients whose initial doses were based on clinical information alone to those whose initial doses were based on their genetic makeup (genotype) along with clinical factors. The trial was funded primarily by NIH’s National Heart, Lung, and Blood Institute (NHLBI). Results appeared in the Journal of the American Medical Association on September 26, 2017.