High-Intensity Statin Therapy and Vitamin D Supplementation in Coronary Artery Disease

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Significantly decreased platelet reactivity occurred in patients who were given a new statin or an increased dose of a previous statin.
Significantly decreased platelet reactivity occurred in patients who were given a new statin or an increased dose of a previous statin.

High-intensity statin treatment has been linked to significant increases in vitamin D levels in patients with coronary artery disease, according to research published in Thrombosis Research.

Giuseppe De Luca, MD, PhD, from the Department of Cardiology at the Eastern Piedmont University in Novara, Italy, and colleagues conducted a cross-sectional study to assess vitamin D levels in patients undergoing dual antiplatelet therapy with high-intensity statins after acute coronary syndrome or elective percutaneous intervention.

The researchers included 246 patients in the study. Of those, 142 were discharged with either new statin therapy or an increase in previous statin therapy dose (Inc-S); 104 continued to take the same high-dose statin they had been taking previously (Eq-S). Within the Inc-S group, 69.8% of patients took atorvastatin and 30.2% took rosuvastatin; in the Eq-S group, 52.9% of patients took atorvastatin, 43.3% took rosuvastatin, and 2.8% took simvastatin.

Overall, patients in the Inc-S group were younger (63.9 ± 11.6 years vs 67.2 ± 8.8 years) and were more likely to be active smokers (36% vs 14.2%). The Inc-S group also had a history of less hypertension (69.8% vs 82.3%) and diabetes (39.5% vs 52.2%). The majority of patients in both groups were men (75.9% vs 85%).

During a median follow-up of 75.5 days, study investigators found that platelet reactivity was "significantly lower" among Inc-S patients across various stimuli (arachidonic acid, P =.02; collagen, P =.004; thrombin-activating peptide, P =.07; adenosine diphosphate, P =.002). The Inc-S group also experienced a significant reduction in low-density lipoprotein (LDL) cholesterol (−33.5% ± 29.8% vs −1.8% ± 41%; P <.001).

Vitamin D levels were also increased in the Inc-S group (delta-25-OHD: 2.08 ± 6.6 vs 0.26 ± 7.5 ng/mL; P =.048); similar results were found when the researchers assessed the variation in 25-OHD percentage (23.2% ± 20.5% vs 3.1% ± 4.7%; P =.003).

"Our main finding is a significant elevation, when considering the variation from baseline, of circulating 25-OHD," the researchers noted. "[L]ower levels of 25-OHD have been inversely associated with vascular calcifications, arterial stiffness, major cardiovascular risk factors and with the extent of coronary artery disease."

"[T]he exact mechanism of such pharmacological interaction still needs to be elucidated in more dedicated studies, as far as a potential role of vitamin D supplementation in achieving the same cardioprotective effects with a lower dose of statins, improving tolerance and adherence to [these] drugs" they concluded.

Study Limitations

  • The cross-sectional design of the study resulted in a "certain degree" of heterogeneity in patient characteristics and type of statin therapy.
  • Sample size did not allow the researchers to perform subgroup analyses or propensity score matching.
  • Data were not collected for long-term follow-up.

Reference

Verdoia M, Pergolini P, Rolla R, et al; on behalf of the Novara Atherosclerosis Study Group (NAS). Impact of high-dose statins on vitamin D levels and platelet function in patients with coronary artery disease. Thromb Res. 2017;150:90-95. doi: 10.1016/j.thromres.2016.12.019 

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