Statins increase coronary calcification

[NHE]

Statin use is associated with increased coronary artery calcification. The risk increases significantly with longer duration of use.

Long-term statin therapy is associated with severe coronary artery calcification
PLoS One. 2023 Jul 27;18(7):e0289111.

Background: Atherosclerosis and consequent risk of cardiovascular events or mortality can be accurately assessed by quantifying coronary artery calcium score (CACS) derived from computed tomography. HMG-CoA-reductase inhibitors (statins) are the primary pharmacotherapy used to reduce cardiovascular events, yet there is growing data that support statin use may increase coronary calcification. We set out to determine the likelihood of severe CACS in the context of chronic statin therapy.

Methods: We established a retrospective, case-control study of 1,181 U.S. veterans without coronary artery disease (CAD) from a single site, the Providence VA Medical Center. Duration of statin therapy for primary prevention was divided into 5-year categorical increments. The primary outcome was CACS derived from low-dose lung cancer screening computed tomography (LCSCT), stratified by CACs severity (none = 0; mild = 1-99; moderate = 100-399; and severe ≥400 AU). Statin duration of zero served as the referent control. Ordinal logistic regression analysis determined the association between duration of statin use and CACS categories. Proportional odds assumption was tested using likelihood ratio test. Atherosclerotic cardiovascular disease (ASCVD) risk score, body mass index, and CKD (glomerular filtration rate of <60 ml/min/1.73 m2) were included in the adjustment models.

Results: The mean age of the study population was 64.7±7.2 years, and 706 (60%) patients were prescribed a statin at baseline. Duration of statin therapy was associated with greater odds of having increased CACS (>0-5 years, OR: 1.71 [CI: 1.34-2.18], p<0.001; >5-10 years, OR: 2.80 [CI: 2.01-3.90], p<0.001; >10 years, OR: 5.30 [CI: 3.23-8.70], p<0.001), and the relationship between statin duration and CACS remained significant after multivariate adjustment (>0-5 years, OR: 1.49 [CI: 1.16-1.92], p = 0.002; >5-10 years, OR: 2.38 [CI: 1.7-3.35], p<0.001; >10 years, OR: 4.48 [CI: 2.7-7.43], p<0.001).

Conclusions: Long-term use of statins is associated with increased likelihood of severe CACS in patients with significant smoking history. The use of CACS to interpret cardiovascular event risk may require adjustment in the context of chronic statin therapy.

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[ElliotB]

An interesting fact about cholesterol is that it is thought to repair damaged Mylin. Ultimately there is apparently no correlation between cholesterol and heart issues although many old school doctors believe there is. Which is not a surprise, but there is a lot of new information based on recent clinicial trials that substantiates the lack of correlation between the two. So, the decision to lower cholesterol for someone with MS and Mylin damage, can be a difficult one.

Additionally, coronary calcification is thought to be controllable through supplementation with vitamin K. BUT not all K supplements are the same. There are actually 4 forms of vitamin K, and you want a 'complex' version that has all 4. Here is a sample which happens to be the K supplement I take which contains vitamin K1, vitamin K2 mk-7, vitamin K2 mk-4. FWIW, about 4 years ago I had an echocardiogram which showed and had almost no calcification. In spite of being on an extremely high fat diet, extremely high in good GOOD (omega 3) fat diet, my echocardiogram did not show any change. I did take this K supplement throughout that the time in between the tests

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