(67) Effect of Statins on Coronary Artery Calcification: A Systematic Review and Meta-Analysis of Randomized Controlled Trials

Saturday, August 27, 2022

8:00 AM – 6:00 PM CEST

Location: Hall C

Publication Number: 741

Presenting Author(s)

Mitra Nekouei Shahraki
– erasmusmc, Rotterdam, Zuid-Holland, Netherlands

Co-Author(s)

Soroush Mohammadi Jouabadi, PharmD, MSc
– erasmusmc, Rotterdam, Zuid-Holland, Netherlands
Daniel Bos
– Associate Professor, Department of Radiology & Nuclear Medicine, Erasmus University Medical Center, Rotterdam, The Netherlands, Netherlands
Bruno H. Stricker
– Professor of Pharmacoepidemiology, Epidemiology department, Erasmus Medical Center, Rotterdam, The Netherlands, Rotterdam, Netherlands
Fariba Ahmadizar
– Assistant Professor, Molecular (Pharmaco) Epidemiology, Julius Center, UMC Utrecht, the Netherlands, Netherlands

Background: Coronary artery calcification (CAC) measured by computed tomography (CT) is a surrogate marker of atherosclerosis and vascular aging. Although increasing evidence points toward the pleiotropic effects of statins on CAC, controversy remains about whether statins accelerate the progression of CAC or slow it down.

Objectives: The main objective of this study is to provide a systematic review and meta-analysis (SR&M-A) of Randomized Control Trials (RCTs) on the effect of statins on CAC. We also studied whether different methods of CAC quantification could influence the results.

Methods: This SR&M-A was registered in the PROSPERO database (CRD42021254187) and conducted according to the PRISMA statement. We formulated a search strategy and searched Embase, Medline, Web of Science, and Cochrane for RCTs from inception to January 2022. RCTs were included if CAC was measured before and after statin-use by CT scan. RCTs were excluded if they did not recruit a control group or assessed statins in combination with other medications. RCTs were categorized according to the method of quantifying CAC, either using Agatston score (AS) or volume (mm3). Mean change and corresponding standard deviation of each arm were used to obtain standardized mean difference (SMD). SMDs were pooled by fixed- or random-effect models in the case of low (I2 < 50%) or high heterogeneity (I2 >50%). Publication bias was assessed by visually detecting funnel plots and the Egger test. Meta-regression was performed for mean age, the proportion of men, and prevalent cardiovascular disease at the study level.

Results: In total, 706 records were screened, and 12 RCTs were included with a mean follow-up of 1.3 years (range, 1-2). The pooled SMD of CAC in 12 RCTs was -0.02 (95%CI, -0.22 to 0.17). The pooled SMD of CAC quantified in AS in 10 RCTs was -0.07 (95%CI, -0.33 to 0.19). The pooled SMD of CAC quantified in volume in six RCTs was 0.26 (95%CI, -0.03 to 0.55). There was no statistically significant difference between the pooled SMDs of the two groups (95%CI = -0.69 to 0.03).

Conclusions: The pooled results in 12 RCTs suggest no substantial effect of statins on CAC. Given that the CAC is quantified as AS or volume, the results could differ, albeit marginally insignificant. Further studies are warranted to quantify various aspects of the effect of statins on subclinical measurements of atherosclerosis.