Dear Peter, In my opinion, your own rheumatologist did a good job dissecting the issues in your case. Of course, I like what he wrote, by and large, because he agrees with me, (1) even if you’ve had COVID, it is still a good idea to get vaccinated, and (2) ADE is unlikely to play an important role in the genesis of severe COVID, with or without vaccine. When you told us about your recent medical history, I was struck by the fact that, were it not for your telling us you had a positive PCR test for virus in association with your acute illness, I would have doubted that you actually had a second infection, which is to say that it is not necessary to postulate that you had a second infection in order to explain your recent pulmonary emboli. For one thing, what you described are major thromboembolic phenomenon that blocked some of your major vessels. Although that probably can happen in COVID, COVID more typically causes "microthrombi" of the capillary bed that feeds pulmonary alveoli, the air sacs responsible for gas exchange in the lungs. Similarly, small clots can also form in other organs where the ACE2 receptor protein required by the virus for cell entry is expressed (heart, brain, etc), by a similar mechanism. Those are not "embolic"; they don’t come from somewhere else in the body. They are thought to be caused by direct infection of endothelial cells that line the pulmonary capillary wall. Those cells efficiently express ACE2. When they get infected, they release a clotting factor that alone can start the cascade that leads to microthrombi. Having very elevated D-dimers is not proof of COVID per se. Elevation of D-dimers in blood (and fibrin consumption) can occur in several other pathologic states. For another thing, you don’t describe much in the way of other symptoms that characterize COVID, except that you felt lousy for a few days before going to hospital. However, those who took care of you know much more about your case than I ever will, and if they say you had a second illness from COVID, I am in no position to doubt it.
I would take issue with only one point your doctor made: In COVID, absent vaccination, autoantibodies are not implicated in clotting abnormalities. See above for the accepted pathogenesis of "micro" clots in lungs and other organs. Autoantibodies are definitely implicated in the very rare cases of severe and often fatal thrombo-embolic disease in those who received either of the two vaccines that use adenovirus as a vector (AstraZeneca and J&J). The mechanism is very recently described (last week) and seems to be due to the fact that adenoviruses bind to platelets. In rare cases, this results in the generation of antibodies that recognize platelets, and that results in platelet destruction. The resulting very low platelet concentration in blood heralds the clotting problems that ensue. (It’s paradoxial that low platelets leads to clotting, but that is another story.) The incidence is very very low, probably lower than one case per million vaccine doses, but the consequences have been grave for those who contract this problem. When an adverse event is that rare, (and there is no prior basis to suspect it, because there have never been any other adeno-vectored vaccines in widespread use), there is no way to design a clinical trial to detect the problem prior to release of the vaccine. Fortunately, the recent reports also describe effective treatment regimens, if they are implemented promptly.