If you want a thought to make you DIZZY.
I've always thought that a physical microscopic attack by some agent, heretofore unknown, is responsible for that first tiny lesion on a blood vessel that decades later becaome a plaque. I've let my mind run riot on the huge number of possibilities about what that agent might be. Strep, influenza, rhinitis of a particualr strain, chicken pox, DDT, fungus, a spirochete, staph, food reaction. Of course, the attack would have gone unnoticed in regards the coronary artery but the stage would be set.
Such a cause would likely NEVER be found except by serendipity.
Like aspirin causing fewer heart attacks. Nobody believed it possible but in the 30's 40's and 50's people with arthritis and taking 10-16 aspirin a day didn't get heart disease.
It was spelled out as a platelet thing...but 10 aspirin a day is MIGHTILY anti-inflammatory. But if it weren't for the serendipity of the arthritiics aspirin would still be used only for aches and pains. Will science luck out in the same way with the plaque initiator?
(Just letting my thoughts run free here...no conclusions!

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