Interaction Between Statin Use, Coronary Artery Disease Phenotypes, on Computed Tomography Angiography, and Cardiovascular Outcomes.

BACKGROUND

Although statins are recommended for decreasing cardiovascular risk, their efficacy across different patient phenotypes stratified by coronary artery disease (CAD) remains unclear.

OBJECTIVES

This study aims to evaluate whether statins decrease major adverse cardiac events (MACE) among CAD phenotypes according to severity, vulnerability and extent categorized by coronary computed tomography angiography (CTA).

METHODS

The authors analyzed consecutive patients who were referred for coronary CTA at a tertiary center for the assessment of chronic coronary syndrome. The primary endpoint was MACE defined as a composite of all-cause mortality, acute myocardial infarction, or revascularization for unstable angina. Statin use was defined as annualized days on statin therapy (days on statin based on redeemed prescriptions, divided by follow-up time), and analyzed for each 10% increase in statin use over the follow-up period. Interaction analysis, adjusting for risk factors was applied to define treatment benefit across CAD phenotypes.

RESULTS

Overall, 11,026 individuals (mean age: 58.6 ± 11.9 years, 54.7% male) were analyzed who underwent coronary CTA between January 1, 2013, and December 31, 2020. A 10% increase in statin use was associated with lower risk for MACE the stratified Cox-regression model in patients with CAD (adjusted HR [aHR]: 0.95 [95% CI: 0.92-0.99]; P = 0.006), but not in patients without CAD (aHR: 0.95 [95% CI: 0.84-1.07]; P = 0.370). In the total population using interaction analysis including CAD phenotypes, a 10% increase in statin use decreased the risk for MACE in the presence of obstructive CAD (aHR: 0.91 [95% CI: 0.85-0.97]; P = 0.006), high-risk plaque (aHR: 0.82 [95% CI: 0.68-0.98]; P = 0.026), calcium score of ≥400 (aHR: 0.93 [95% CI: 0.87-0.99]; P = 0.024), and segment involvement score of >4 (aHR: 0.89 [95% CI: 0.84-0.95]; P < 0.001), but not for any CAD (aHR: 0.95 [95% CI: 0.85-1.07]; P = 0.411).

CONCLUSIONS

Statin efficacy to decrease MACE depends on CAD phenotypes and increases with the extent and severity of disease and in the presence of high-risk plaques. Patients without CAD have no benefit from statin therapy regarding MACE. Coronary CTA may play a pivotal role in optimizing statin allocation for personalized treatment decisions to prevent MACE.