It would help if you could edit my quote in your post to the parts you don't understand.
In theory, , so long as your vitamin C intake is optimal, and you are able to produce enough collagen to keep your veins and arteries strong, there is no reason to worry about lowering Lp(a) and losing its "surrogate" function. (Nobody really knows because no one is studying this as far as I know)
There are a couple of other secondary deficiencies that could lead to atherosclerosis (e.g. vitamin B6 and a copper deficiency) because these deficiencies impair the production of collagen. Usually the lack of vitamin C is the primary factor. (This is another good reason to cover all nutritional bases by following Linus Pauling's basic nutritional regimen in his 1986 book HOW TO LIVE LONGER AND FEEL BETTER.)
Lets say a person is not getting optimal vitamin C (i.e. most people) then the argument is that their arteries are being held together by the Lp(a) induced glue we call atherosclerosis.
I provided 3 methods for gauging whether vitamin C intake is optimal - because many people have such low bowel tolerances (we did not evolve to eat our vitamin C, at least until very recently). In your case, if total cholesterol is close to 180 mg/dl - that indicates that the fire has been extinguished, but if it is high, say over 240 mg/dl - that you are not taking enough vitamin C. The key is C.