Dr Eades has a formula to take into account the increase in CAC by correlating the CAC volume. When I used his calculation my increase in CAC was not significant Update 5-24-18
Dr Eades video link
Progression of coronary artery calcification at the crossroads: sign of progression or stabilization of coronary atherosclerosis? link
Dr Eades video link
Progression of coronary artery calcification at the crossroads: sign of progression or stabilization of coronary atherosclerosis? link
“Therefore, in brief:
(I) CAC progression is an independent predictor of events;
(II) statins promote plaque regression; and
(III) statins promote CAC progression.
These paradoxical results are puzzling and warrant the conduction of further studies aimed at the pathophysiological and clinical discrimination between plaque volume progression and CAC progression.
One of the potential explanations might be that conventional reading of CAC studies does not make a distinction between spotty calcifications and dense calcium.
Future discrimination between these two completely different sources of coronary calcium might become a major breakthrough in CAC imaging, since spotty calcifications have been recognized as a marker of high risk plaques (81,82).
Regarding future alternative therapeutic approaches, the combined application of molecular imaging agents with anticalcification drugs such as bisphosphonate might potentially enable targeting at different stages of the disease (18).”
"Also consistent with our data are clinical trials of statin therapy vs placebo reporting that CAC progression using the Agatston score was greater in the statin group than in the placebo group.9,10 Statins appear to have their salutary effects on CVD risk by reducing the lipid core in unstable plaque,11 and statin therapy may increase calcium density in such plaques, along with a more favorable prognosis. Similarly, a recent report from MESA showed that favorable changes in LDL-C were correlated with a significant increase in CAC progression.24 A recent report of 4425 referred patients evaluated with both CT for CAC and CT angiography showed that 1021 had only calcified plaque, 183 had only noncalcified plaque, and 685 had both calcified and noncalcified plaque. The incidence of CVD events after a median follow-up of 3 years in these 3 groups was 5.5%, 22.7%, and 37.7%, respectively.8 These results suggest that higher calcium density of plaques may be protective."
"Also consistent with our data are clinical trials of statin therapy vs placebo reporting that CAC progression using the Agatston score was greater in the statin group than in the placebo group.9,10 Statins appear to have their salutary effects on CVD risk by reducing the lipid core in unstable plaque,11 and statin therapy may increase calcium density in such plaques, along with a more favorable prognosis. Similarly, a recent report from MESA showed that favorable changes in LDL-C were correlated with a significant increase in CAC progression.24 A recent report of 4425 referred patients evaluated with both CT for CAC and CT angiography showed that 1021 had only calcified plaque, 183 had only noncalcified plaque, and 685 had both calcified and noncalcified plaque. The incidence of CVD events after a median follow-up of 3 years in these 3 groups was 5.5%, 22.7%, and 37.7%, respectively.8 These results suggest that higher calcium density of plaques may be protective."
Update on my CIMT scores
Average CCA Mean Average CCA Max Region
12-17-09 0.599 mm 0.741 mm
12-8-11 0.563 mm (.036 less) 0.661 mm (.08 less)
12-20-12 0.566 mm (.003 more) 0.676 mm (.015 more)
12-19-13 0.583 mm (.017 more) 0.709 mm (.033 more)
11-20-14 0.575 mm (.012 less) 0.679 mm (.030 less)
12-03-15 0.555 mm (.020 less) 0.675 mm (.004 less)
12-08-16 0.611 mm (0.55 more) 0.744 mm (0.99 more)
12-14-17 0.570 mm (0.41 less) 0.671 mm (0.73 less)
CAC reports below over 10 years:
Calcium score Calcium volume
2-6-01 8.93 8.02
1-10-06 20.5 57.5
12-9-11 7.9 5.9
7-21-16 144 126
My CIMT scores do not correlate with my CAC increase.
If my increase in CAC (calcium scoring) reflects true increase in risk, why did it happen?
Perhaps the best answer is insulin resistance?
My LDLp has been good.
However perhaps if my LDLp was consistently under 750 I would have had a better CAC number?
I finally have a better handle on the weight and the Hgb A1c.
Weight 220
Hgb A1c 6.8
My systolic BP is usually 120 or less on ramipril.
Recently I went off Niacin (endur-acin) for a short period and it made a difference in my LDLp.
I will continue the Endur-acin 1,000 mg a day rather than increase the atorvastatin 10 mg.
While on Atorvastatin 10 mg, Endur-acin 1,000 mg I have had very low LDLp's.
Since 12-06-11 I have gone over 800 once while on LCHF.
While on Atorvastatin 10 mg, Endur-acin 1,000 mg I have had very low LDLp's.
Since 12-06-11 I have gone over 800 once while on LCHF.
I hope to slowly get my weight down to 200 pounds with improved insulin resistance with time with LCHF.
My LCHF is pretty tight as I run nutritional ketosis above 0.5 serum usually.
I drink 2 oz ETOH most days.
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