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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)
12-18 0.567 mm (0.03 less) 0.643 mm (0.28 less) 1-20. 0.552 mm (0.015 less). 0.685 mm (0.042 more)
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 LDLp 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 LDLp 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.
Do Statins Promote Coronary Calcification? Study Says Yes, and It Might Be a Good Thing
"CLEVELAND, OH – The results of a new study suggest that there is a paradoxical relationship between
1-calcification of the coronary artery and
2-atheroma volume
among individuals treated with statin therapy.
In the analysis, statins, specifically high-intensity statin therapy, actually promoted coronary calcification despite regressing the volume of coronary atheroma[1].
"The question of calcium is very relevant because we have people doing calcium scans as a means to determine the burden of disease," senior investigator Dr Steven Nissen (Cleveland Clinic, OH) told heartwire.
"What we were struck by in this analysis was that the most aggressively treated patients—the high-intensity statin patient—if anything, developed more calcification. So if we're going to use coronary calcification as a measure of disease burden, you really have to know if the patient has received a lot of statins or not."
The study, led by Dr Rishi Puri (Cleveland Clinic) and published March 30, 2015 in the Journal of the American College of Cardiology, is a
post hoc analysis of eight intravascular ultrasound (IVUS) studies
that assessed the effect of medical therapies, including statins, on serial changes in coronary atheroma burden. The studies, among them REVERSAL, SATURN, ILLUSTRATE, and ASTEROID, included 1545 individuals who received high-intensity statin therapy, 1726 who received low-intensity statin therapy, and 224 who didn't receive a statin.
Individuals treated with a high-intensity statin, such as
1-atorvastatin 80 mg (Lipitor)
2-rosuvastatin 40 mg (Crestor, AstraZeneca),
had regression of percent atheroma volume measured by IVUS.
In these patients, percent atheroma volume declined 0.6% from baseline,
whereas percent atheroma volume increased 0.8% and 1.0%, respectively, among those who received a low-intensity statin and those not treated with a statin.
Regarding the change in the IVUS-derived
calcium index—a measure of coronary calcification—
all three study arms showed an increase in coronary calcification from baseline.
In a model that adjusted for the change in percent atheroma volume,
the increase in coronary calcium was greater among the
1-low-intensity statin vs no-statin arm (P=0.03) and the
2-high-intensity statin vs no-statin arm (P=0.007).
There was no significant difference in the change in coronary calcification among high- and low-intensity statin-treated patients, although there was a numerical difference with more calcification in the high-intensity arm.
The researchers observed no correlation between the change in the calcium index and on-treatment levels of LDL cholesterol or C-reactive protein (CRP).
"It wasn't correlated with the lipid changes," said Nissen. "You can't attribute this just to LDL alterations. It looks like it's related to something that statins do.
We know the drugs have complex biological effects, and some of those effects have not been worked out scientifically."
"In the first study[1], which was led by Dr Khurram Nasir (Baptist Health South Florida, Miami), investigators found that 50% of 4758 MESA participants would be recommended for moderate- or high-intensity statin therapy based on the 2013 American College of Cardiology/American Heart Association (ACC/AHA) clinical guidelines. Moreover, another 12% of patients could be "considered" for statin therapy based on their 10-year 5% to 7.5% risk of atherosclerotic cardiovascular disease (ASCVD)."
"Taken together,
the researchers say that nearly two-thirds (62%) of the MESA cohort would be recommended or considered for statin therapy.
Yet among those recommended statins—this included
1-patients w an LDL-cholesterol level greater190 mg/dL,
1-patients w an LDL-cholesterol level greater190 mg/dL,
2-DM patients w an LDL-c level 70–189 mg/dL, and
3- nonDM patients w an LDLc level 70–189 mg/dL
4-and an estimated 10-year ASCVD risk greater than7.5%
—more than 40% of these individuals had CAC of zero and an ASCVD event rate of 5.2 per 1000 person-years of follow-up.
Among those who could B considered 4 statin therapy, 57% of these individuals had a CAC score of zero and an ASCVD event rate of 1.5 per 1000 person-years of follow-up.
Of the entire group eligible for statins, either recommended or considered,
44% of 2966 pts had CAC score of zero at baseline
and a 10-year ASCVD event rate of 4.2 per 1000 person-years."
"Overall, our results showed that nearly 50% of individuals who are statin candidates, if they undergo a test that costs between $75 and $100, would have a calcium score of zero, and their 10-year risk would be below the threshold in which the guidelines recommend statins," Nasir told heartwirefrom Medscape. "This is most important for the patients in the middle, those who have a 10-year risk of 5% to 20%."
"In contrast, 56% of patients considered statin eligible based on the guidelines had coronary calcification identified on the noncontrast computed tomography (CT) scan (CAC>0) and had an ASCVD event rate of 11.2 events per 1000 person-years."
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