any doctors, etc want to break this down in English? It seems like the same treatments previously discussed would help as ACE2 is still involved.

Imagine your blood vessel as a pipe. And along this pipe you have boxes lining the inside of the pipe (endothelial cells) with fail safe mechanisms that release material (vWF, clotting factors) to clog up the pipe if it gets damage to prevent from losing all the liquid in the pipe (preventing bleeding out). Normally these fail safes only activate when the pipe is damaged (like a cut or laceration) and having a big leak (bleeding).

Now imagine some rats (the rona) got loose in your pipes, and made holes in your pipe (leaky endothelial cells) and starting chewing on the wires that connected the control box for the failsafes (pericytes) to the actual failsafes (endothelial cells) causing the failsafes to activate prematurely. This causes the pipe to clog when it doesn't need to. Physiologically, this leads to downstream clotting events from the pipes which manifest as strokes, pulmonary embolisms etc...

Diabetics have leakier, more brittle pipes for the rats to chew through this making them more susceptible.

Coronary artery disease patients usually have disease not just in their coronary arteries (arteries that supply blood to heart) but in all of their arteries which is equivalent to gunk buildup in pipes over the years.

Lovenox and heparin are anticlotting agents that help combat all of the new clotting factors that are being released.

Hope this helps. .

Did my PhD at the medical school and focused heavily on endo -pericyte interactions, specifically related to how the cells interact during stabilization or regression of new capillary networks. Not surprised to see this implicated in the viral pathophys.