I'm curious if you recall the wall thickness of your left ventricle? With stenosis, the LV often enlarges and the wall thickens. If your walls have significantly thickened it is harder for sufficient blood to be distributed into the LV, which can cause angina, particularly if cardiac output is reduced from a narrowed aortic valve.What if it’s really the valve and dilated aorta causing the angina all this time?
This seems very speculative to me.But Bavaria said he thinks my calcified valve threw a clot that led to the heart attack.
I have a relatively low CAC score of 35. Not low for my age of 53, but relatively low in the heart and valve surgery world. I also passed my angiogram with flying colors and did not need CABG. Calcium score correlates very strongly with heart attack risk. My relatively low score, being under 100, puts me at a relatively low risk for heart attack. Yet, passing my angiogram and having this relatively low CAC does not put me at zero risk of a heart attack.
The evidence now suggests that it is the liquid soft plaque that causes most heart attacks as shown here:
Decent visual in this short video by the British Heart Foundation:
So, for me to have a heart attack, all that is needed is a little bit of soft plaque with a thin cap; cap bursts and soft/liquid plaque forms into a clot (thrombosis) which leads to heart attack, or possible stroke, depending on which way it goes. This can happen to me, even with a low CAC and good angiogram, although my relative risk is low for such event.
Anyway, I wonder why Bavaria would speculate that, when it is known that the vast majority of heart attacks happen from soft plaque thrombosis, which can happen to anyone who has even a little bit of plaque.