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Vitamin D levels do not predict cardiovascular events in statin-treated patients with stable coronary disease
Vera Bittner1, Nanette K Wenger, David D Waters
1University of Alabama at Birmingham, 35294-0007, USA. vbittner@uab.edu
Insights
This study found that vitamin D levels do not predict cardiovascular risk in patients taking statins. Changes in vitamin D during atorvastatin treatment also did not impact cardiovascular outcomes.
Area of Science:
- Cardiovascular Medicine
- Endocrinology
- Pharmacology
Background:
- Investigated the role of vitamin D in cardiovascular risk among patients treated with statins.
- Examined the association between vitamin D levels and cardiovascular outcomes in the TNT study population.
Purpose of the Study:
- To determine if baseline vitamin D levels predict cardiovascular risk in statin-treated patients.
- To assess if changes in vitamin D levels after atorvastatin treatment correlate with improved cardiovascular outcomes.
Main Methods:
- Post hoc nested case-control analysis of 1,509 patients from the TNT study.
- Vitamin D levels measured at baseline and 1 year; cardiovascular events analyzed using Cox proportional hazard models.
- Evaluated vitamin D as a continuous variable and change in levels as predictors, adjusting for confounders.
Main Results:
- Vitamin D deficiency or insufficiency was common; elevated levels were rare.
- No association was found between baseline vitamin D levels and cardiovascular events or mortality.
- Changes in vitamin D levels after 1 year of atorvastatin treatment did not correlate with cardiovascular outcomes.
Conclusions:
- Baseline vitamin D levels do not predict cardiovascular risk in patients with stable coronary heart disease treated with statins.
- Changes in vitamin D levels during atorvastatin therapy do not influence its efficacy regarding cardiovascular outcomes.
Background:
This post hoc nested case-control analysis of the TNT study was designed to investigate whether baseline vitamin D level is a significant predictor of cardiovascular risk among statin-treated patients and whether changes in vitamin D after treatment with atorvastatin are associated with improved cardiovascular outcomes.
Methods:
A total of 10,001 patients with stable coronary heart disease were randomized to atorvastatin 80 or 10 mg for a median of 4.9 years. This analysis included 1,509 patients (497 with a subsequent cardiovascular event and 1,012 without an event) with vitamin D levels determined at baseline and 1 year. Event rates were analyzed by Cox proportional hazard model by baseline vitamin D levels, with vitamin D as a continuous variable, and with change in vitamin D level as the predictor.
Results:
Vitamin D deficiency (<15 ng/mL) or insufficiency (15- <30 ng/mL) was present in 108 (7.2%) of 1,509 and 625 (41.4%) of 1,509 of patients, whereas 46 (3.0%) of 1,509 had elevated vitamin D. There was no relationship between baseline vitamin D levels or change in vitamin D levels and cardiovascular events or mortality. Modeling of events with vitamin D as a continuous variable similarly showed no relationship of vitamin D to events. These findings held true after adjustment for seasonal variations in vitamin D and other confounders.
Conclusion:
In statin-treated patients with stable coronary heart disease, vitamin D levels did not predict cardiovascular risk. Changes in plasma concentrations of vitamin D after 1 year of treatment made no contribution to the efficacy of atorvastatin therapy.
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