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476 When prevention changes the disease: acute coronary syndrome (ACS) plaque morphology in the statin era

heartjnl · 2026-06-09 · canonical JSON source

9 visible annotations · policy: published · automated confidence ≥ 75.00%

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Introduction Statins are cornerstone therapy in cardiovascular prevention, plaque reduction and stabilisation. With the advent of injectable statin alternatives, the influence of statin intensity and exposure duration on baseline angiographic disease severity at emergency ACS presentation warrants further investigation.Methods We conducted a retrospective cohort study of ACS patients in 2024 at a tertiary centre, who underwent emergency coronary angiography and were discharged with confirmed MI or unstable angina. Patients with prior coronary artery bypass graft, non-ACS diagnosis, and in-hospital mortality were excluded. Demographics, medications, and angiographic parameters were collected from hospital and primary care records. Coronary artery disease (CAD) severity was quantified using Gensini scores and categorized as mild (<30), moderate (30-59), severe (≥ 60). We compared CAD severity between statin-exposed (SE) and statin-naive (SN) patients at the time of admission.Multivariable regression was used after adjusting for age, hypertension (HTN), diabetes mellitus (DM), prior CAD, chronic kidney disease (CKD), non-high-density lipoprotein cholesterol (non-HDL-C), and smoking. A secondary subgroup analysis was performed on SE patients to evaluate the impact of intensity and duration. Statistical significance was set at p<0.05.Results The cohort included 164 patients: 47.6% in the SE group and 52.4% in the SN group. The mean duration of pre-admission statin therapy was 5.5 years (standard deviation 5.85 years).SE group had a higher prevalence of HTN (64.1% versus 36.0%), DM (34.6% versus 7.0%), higher HbA1c (44 versus 38 mmol/mol), but lower non-HDL-C (2.5 versus 4.2 mmol/L). The distribution of CAD severity was mild 9.8%, moderate 42.7%, and severe 47.6%, with 80.5% of patients exhibiting coronary calcification.The SN group had a higher quantitative atheroma burden than the SE group, with a mean Gensini score of 63.20 [49.12-75.38] versus 55.20 [39.62-68.75], p=0.009.In adjusted multivariable regression, pre-admission statin use was associated with a lower Gensini score (coefficient -9.61, 95% confidence interval [-19.24, 0.02], p=0.05). However, no significant association was found between pre-admission statin use and angiographic calcification (p=0.56). Age was a significant positive predictor of higher Gensini scores (coefficient 0.5, p=0.003), while HTN was inversely associated (coefficient -11.35, p=0.003).Conclusions Our study showed that in patients presenting with ACS, pre-admission statin use is associated with lower overall atherosclerotic burden, but not with a reduction in coronary calcification. The results suggest statins modify plaque volume but may not limit calcification progression, warranting further investigation into plaque morphology determinants.