"All were put on treatment." Cummings and Gerber left out
the treatment was statins.
In 2004 it was not well known that statins increased CAC score with reduced risk with reaching goal of lower LDLc.
Now we know if you adjust the higher calcium score with the calcium volume we find statins did not make the plaque worse.
"in subjects receiving compared to those not receiving statin therapy (HR)
were 0.29 (95% CI 0.13 to 0.56, p = 0.001)"
Am J Cardiol. 2013 Feb 1;111(3):356-61. doi: 10.1016/j.amjcard.2012.09.033. Epub 2012 Dec 1.
Impact of coronary artery calcium progression and statin therapy on clinical outcome in subjects with and without diabetes mellitus.
Abstract
Coronary artery calcium (CAC) is a marker of atherosclerosis, and CAC progression is independently associated with all-cause mortality in the general population but not convincingly in subjects with diabetes mellitus (DM).
The aim of this study was to ascertain the differences in the
1- rates of CAC progression,
2- the effect of statin therapy, and
3-all-cause mortality in subjects with and without DM.
The study group consisted of 296 asymptomatic subjects with type 2 DM and 300 controls (mean age 59 ± 6 years, 29% women) who underwent baseline and follow-up CAC scans within a 2-year interval.
Absolute annual CAC score change, percentage annual CAC progression(change in CAC%), event-free survival, and the effect of statin therapy on survival were all assessed. The mean follow-up duration was 56 ± 11 months.
Absolute annual CAC score change was 81 ± 10 in subjects with DM and 34 ± 5 in controls (p = 0.0001).
Percentage annual CAC progression was 29 ± 9% in subjects with DM and 10 ± 7% in controls (p = 0.0001).
The hazard ratios of death in 3 groups of subjects with DM compared to controls without DM were 1.88 (95% confidence interval [CI] 1.51 to 2.36, p = 0.0001) for change of CAC of 10% to 20%, 2.29 (95% CI 1.56 to 3.38, p = 0.0001) for change of CAC of 21% to 30%, and 6.95 (95% CI 2.23 to 11.53, p = 0.0001) for change of CAC greater than 30%, all compared to change of CAC less than 10%.
The adjusted hazard ratios of all-cause mortality:
1-in subjects receiving compared to those not receiving statin therapy were 0.29 (95% CI 0.13 to 0.56, p = 0.001)
2-in those without DM and without CAC progression, 0.51 (95% CI 0.21 to 0.73, p = 0.001)
3-in those with DM and without CAC progression 0.71 (95% CI 0.25 to 0.91, p = 0.003)
with all 3 groups compared to 1.0 (reference) in those with DM, with CAC progression and without statin therapy.
In conclusion:
CAC progression was greater and event-free survival lower in patients with DM compared to controls in proportion to the extent of CAC progression. These results suggest that CAC progression is an independent predictor of all-cause mortality in patients with DM.
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