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2-020 Complex coronary lesions in HMG-CoA reductase inhibitor (statin) pre-treated patients presenting with acute coronary syndrome despite lower lipid levels: too late or too little?

heartjnl · 2025-08-13 · canonical JSON source

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

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Introduction Current NICE guidelines advise statin therapy following acute coronary syndrome (ACS). Long-term pre-treatment with statins has traditionally reduced coronary events, however, the impact on the complexity of coronary artery disease (CAD) in those presenting with ACS is still unclear. We aimed to assess if patients presenting with ACS and pre-treated with statins had less complex CAD lesions compared to those who were statin naïve.Methods Our study is a prospective analysis of retrospectively collected data of 100 consecutive patients presenting with ACS in a large volume tertiary cardiac centre. Percutaneous coronary intervention (PCI) complexity was used as a surrogate marker of CAD lesion severity in statin-naïve and statin-pre-treated individuals. Patients who died during hospitalisation and those on end-of-life care were excluded. Patient demographics, including age, sex, conventional cardiovascular risk factors and previous lipid lowering therapies were analysed. Angiographic parameters of lesion complexity were chosen to be the number of vessels involved, and the number, length and location of lesions treated with stents. Complex PCI was defined by the presence of at least one of the following: stent to the left main stem, more than one vessel treated, stent length ≥ 28 mm, stent placement at a bifurcation, or stent to a degenerated vein graft. Statistical comparisons were performed using appropriate parametric and non-parametric tests, with significance set at p < 0.05.Results We compared 53 patients in the statin-pre-treated group to 47 in the statin-naïve group. As anticipated, the statin-pre-treated group was older (in years, 73 ± 10.1 vs 66 ± 15.6, p < 0.01) and exhibited a higher prevalence of type 2 diabetes, hypertension, and prior cardiovascular disease. Complexity of lesions treated by PCI was similar between the groups and the difference persisted on multivariable analysis. Procedural complexity, as reflected by the number of stents (1.6 ± 1.06 vs 1.5 ± 0.77, p=0.83) and lesion length (in mm, 28.8 ± 5.41 vs 28.3 ± 4.98, p=0.85) was similar between the statin-pre-treated and statin-naïve group, despite the former achieving lower levels of LDL cholesterol (in mmol/l, 2.0 ± 0.59 vs 3.5 ± 1.05), total cholesterol, and non-HDL cholesterol (p < 0.01 for all comparisons). Among those treated with statins, the timing of initiation (early versus late, p=0.11) and intensity of statin therapy (high versus middle-low, p=0.94) did not affect coronary lesion complexity.Conclusion Our finding that prior statin exposure did not reduce the severity of CAD in patients presenting with ACS despite good lipid control is novel and needs to be confirmed in prospective large-scale multi-centre studies. When combined with other aggressive risk factor modifications, statin therapy may result in less complex CAD lesions in view of multifactorial pathophysiology in CAD. It remains to be seen if statin therapy alone may be too little and too late to those at high risk for cardiovascular events.