So it seems statins are a primary preventative after all, not just going after cholesterol which seems like going after an incidental factor in atheroscelerosis. But your doctor should know about all this, so ask for this in layperson terms.
http://www.ncbi.nlm.nih.gov/pubmed/27081016
Park SJ1,
Kang SJ2,
Ahn JM2,
Chang M2,
Yun SC3,
Roh JH2,
Lee PH2,
Park HW2,
Yoon SH2,
Park DW2,
Lee SW2,
Kim YH2,
Lee CW2,
Mintz GS4,
Han KH2,
Park SW2.
Abstract
BACKGROUND:
How statins alter the natural course of coronary atherosclerosis with compositional changes remains unclear.
OBJECTIVES:
This study aimed to determine the effect of statin therapy on modifying plaque composition.
METHODS:
The
STABLE (Statin and Atheroma Vulnerability Evaluation) prospective,
single-center, double-blind, randomized study evaluated the effect of
statins on functionally insignificant coronary stenoses. We randomly
assigned 312 patients with a virtual histology (VH) intravascular
ultrasound-defined fibroatheroma-containing index lesion to rosuvastatin
40 mg versus 10 mg (2:1 ratio). In 225 (72%) patients, grayscale- and
VH-intravascular ultrasound were completed at baseline and 12 months.
The primary endpoint was the change in VH-defined percent compositional
volume within the target segment from baseline to follow-up in the
per-protocol analysis set.
RESULTS:
Percent
necrotic core (NC) volume within the target segment significantly
decreased from 21.3 ± 6.8% to 18.0 ± 7.5% during 1-year follow-up,
whereas the percent fibrofatty volume increased (11.7 ± 5.8% vs. 14.8 ±
9.3%; all p < 0.001). Percent fibrous (59.4 ± 7.8% vs. 59.2 ± 8.6%)
and dense calcium (7.6 ± 5.1% vs. 7.8 ± 5.6%) volumes were unchanged.
Frequencies of VH (55% vs. 29%) decreased significantly. Normalized
total (202.9 ± 72.3 mm(3) vs. 188.5 ± 67.8 mm(3); p = 0.001) and percent
(51.4 ± 8.3% vs. 50.4 ± 8.8%; p = 0.018) atheroma volumes decreased.
Independent predictors of percent NC volume change were body mass index
(β = 0.37; 95% confidence interval [CI]: 0.05 to 0.70), high sensitivity
C-reactive protein (β = -3.16; 95% CI: -5.64 to -0.69), and baseline
percent NC volume (β = -0.44; 95% CI: -0.68 to -0.19; all p < 0.05).
VH-defined percent compositional volume changes in the rosuvastatin 40-
and 10-mg groups were similar.
CONCLUSIONS:
Rosuvastatin
reduced NC and plaque volume and decreased thin-cap fibroatheroma rate.
There were no significant differences between high- versus
moderate-intensity rosuvastatin. (Statin and Atheroma Vulnerability
Evaluation [STABLE];
NCT00997880).
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