First post from Maryland - advice and support needed!

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Chuck C

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What if it’s really the valve and dilated aorta causing the angina all this time?
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.
But Bavaria said he thinks my calcified valve threw a clot that led to the heart attack.
This seems very speculative to me.

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.
 

cldlhd

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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.

This seems very speculative to me.

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.
I was wondering how they go about calculating your CAC? I had an angio and that does show the calcified plaque but I was always under the impression that where there is calcified plaque there is usually also soft plaque. Maybe that's where he came to that conclusion?
 

Chuck C

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I was always under the impression that where there is calcified plaque there is usually also soft plaque.
Yes, absolutely. It is like where there is smoke, there is usually fire. Calcification correlates with higher risk of CVE very strongly. At the same time, the literature published in recent years suggests that it is the soft vulnerable plaque that puts us at risk, not so much the calcified stabilized plaque. But, where there is a lot of calcified plaque, there is almost always a lot of vulnerable soft plaque as well, which has not yet been stabilized by calcification.
One phenomenon, which seems paradoxical at first, is that 1) statins reduce the risk of CVE in patients at high risk but also 2) when first going on statins the CAC score usually goes up significantly during the first year of treatment.
It seems paradoxical until one realizes that the statins, among doing other beneficial things, are stabilizing the soft vulnerable plaque by causing them to calcify.

" Statin therapy modestly accelerates calcification of plaques leading to more stable, lower-risk compositions and sometimes an acceleration of Agatston CAC score progression. "

 
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Chuck C

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I was wondering how they go about calculating your CAC?
It is somewhat explained here:


As I understand it, it is a computer generated score that is generated based on the amount of calcium that is detected by the CT. It is good for telling you the overall calcium burden, but can't tell you the % of coronary blockage that this calcium is creating- for this the angiogram is needed. But, the CT scan is much less invasive. The calcium scan also can not tell you the amount of soft vulnerable plaque that you have- for this CIMT would be a better tool.
Where there is smoke, high CAC, there is generally fire, soft vulnerable plaque, but if a person has been treating their CAD with lifestyle and medication, they could have significantly reduced soft vulnerable plaque, which will not be picked up on CAC, but can be determined from CIMT.

Info on CIMT:

" The state of your carotid arteries correlates to the state of the arteries in the rest of your body, including your heart. "

 
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cldlhd

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Yes, absolutely. It is like where there is smoke, there is usually fire. Calcification correlates with higher risk of CVE very strongly. At the some time, the literature published in recent years suggests that it is the soft vulnerable plaque that puts us at risk, not so much the calcified stabilized plaque. But, where there is a lot of calcified plaque, there is almost always a lot of vulnerable soft plaque as well, which has not yet been stabilized by calcification.
One phenomenon, which seems paradoxical at first, is that 1) statins reduce the risk of CVE in patients at high risk but also 2) when first going on statins the CAC score usually goes up significantly during the first year of treatment.
It seems paradoxical until one realizes that the statins, among doing other beneficial things, are stabilizing the soft vulnerable plaque by causing them to calcify.

" Statin therapy modestly accelerates calcification of plaques leading to more stable, lower-risk compositions and sometimes an acceleration of Agatston CAC score progression. "

That was my next question- don't statins help stabilize soft plaque? Thanks for the links
 

CarolM

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Yeah he is a little bit on the extreme side I guess, not to mention a bit on the confidence side? I don't think a BAV when necessarily make you more likely to have a heart attack but I imagine anywhere where there's plaque buildup it could happen.
Bavaria was my surgeon (twice) and definitely an arrogant (or very self-confident) character.
 

cldlhd

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I’m bright and early tomorrow, 5 am arrival at the hospital. Hope to give you all updates soon. I know I’ll have some questions for the veterans in here at some point! Thanks again to everybody.
Best wishes for a successful surgery and smooth recovery. I can't speak for everyone but me personally the first few weeks after the surgery I felt like I was never going to be normal again. But now I feel perfectly fine
 
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Chuck C

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I’m bright and early tomorrow, 5 am arrival at the hospital. Hope to give you all updates soon. I know I’ll have some questions for the veterans in here at some point! Thanks again to everybody.
Best of luck Mark! Please give us an update as soon as you feel well enough.
 
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Croooser

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Mark,

Hoping that everything went according to plan and that you have a rapid and complete recovery.
 

MarkZ

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Feeling pretty good today, 5 days after the surgery began (to the hour). Head is pretty clear, pain is very light when I’m sitting still. They’re trying to get my INR right which is slow moving. It was still only at 1.3 yesterday and they haven’t gotten the overnight result back yet surprisingly. On heparin drip in the meantime.

Bavaria’s speculation (which we talked about above a few weeks ago) was independently echoed by Svensson I think. He said the valve was actually unicuspid (not sure if he means fused or conegenital) and thatthe calcification was unusually troublesome. He said it was under the valve and like sandpaperwhatever that means, and actually said he was surprised it didn’t result in strokes which is a scary thing to hear! In fact, the first night of surgery I had transient left eye vision loss which could have been either ocular migraine or retinal artery occlusion. Fortunately my vision is fine now but that’s still very scary. They’ve done two CT scans and they’re not seeing any damage or blockages. I’m lucky so far.

But the calcification story I’m getting now seems consistent with Bavaria’s “throwing a clot” theory, which tells me I probably should have been more aggressive getting this surgery. Just moving forward and thanking my lucky stars!
 

cldlhd

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Feeling pretty good today, 5 days after the surgery began (to the hour). Head is pretty clear, pain is very light when I’m sitting still. They’re trying to get my INR right which is slow moving. It was still only at 1.3 yesterday and they haven’t gotten the overnight result back yet surprisingly. On heparin drip in the meantime.

Bavaria’s speculation (which we talked about above a few weeks ago) was independently echoed by Svensson I think. He said the valve was actually unicuspid (not sure if he means fused or conegenital) and thatthe calcification was unusually troublesome. He said it was under the valve and like sandpaperwhatever that means, and actually said he was surprised it didn’t result in strokes which is a scary thing to hear! In fact, the first night of surgery I had transient left eye vision loss which could have been either ocular migraine or retinal artery occlusion. Fortunately my vision is fine now but that’s still very scary. They’ve done two CT scans and they’re not seeing any damage or blockages. I’m lucky so far.

But the calcification story I’m getting now seems consistent with Bavaria’s “throwing a clot” theory, which tells me I probably should have been more aggressive getting this surgery. Just moving forward and thanking my lucky stars!
After reading that It sounds like it's a very good thing you got your valve replaced without any more waiting. I'm predicting that 6 months from now you'll be feeling better than 6 months ago and very happy that this is in the rear view mirror.
I guess even with all the scans they have these days it still comes down to what we say in the water utility industry -" the proof is in the digging".
 

caro

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Glad you’re feeling better. May be completely different from what you experienced since your vision impairment was after surgery, but Vasospasm from migraine can happen and cause retinal branch occlusion. It is rare but happened to me. There are some studies about it online. Have seen neuro opthamologists and retina specialists at Wilmer Eye and Katzen in Baltimore as well as Weil Cornell in NYC who have seen it before - all from people who had a migraine with aura that left some vision impairment. My neuro ophthalmologist in NY is studying it and has fellows researching it. I was getting several migraines a week at one point. Now taking supplements that have helped a lot.
 
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MarkZ

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The weird (minor?) stuff I’m dealing with today:
  • One of the three drainage sites began bleeding again today, tube was removed yesterday morning. They’re changing the gauze pad every hour or two
  • Taste is still weird at day 5. Everything tastes salty. Orange juice is the most normal tasting thing for me. Maybe water too. Everything else is gross.
  • My temperature has been mostly in range but I get hot and cold spells separated by minutes. It’s wild.

 
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