Key result
Impaired coronary vasodilation independently predicts progression to lipid-rich plaque at 12–18 months.
Why the study?
Although coronary endothelial function and atherosclerotic plaque progression are both associated with adverse cardiovascular events, their relationship with the lipid burden and natural history of lipid-rich coronary plaque remained unknown.
Does impaired baseline coronary endothelial function predict subsequent progression of lipid-rich plaque and atheroma volume in patients with stable angina or ACS?
Cohort (n=33)
Does impaired baseline coronary endothelial function predict subsequent progression of lipid-rich plaque and atheroma volume in patients with stable angina or ACS?
Impaired baseline coronary endothelial-dependent and endothelial-independent vasodilator function independently predicts subsequent progression of lipid core and atheroma volume, respectively, over 12–18 months.
Answers are grounded in this paper and cite their sources.
Impaired vasodilator responses should not yet alter risk stratification in stable angina; leaves open whether endothelial testing refines lipid-rich plaque prediction beyond imaging.
Background: Coronary endothelial function and atherosclerotic plaque progression have both been shown to be associated with adverse cardiovascular events. However, the relationship between these factors and the lipid burden of coronary plaque remains unknown. Purpose: To investigate the relationship between impaired coronary endothelial function and the natural history of lipid rich plaque (LRP). Methods: 33 patients with stable angina or ACS underwent serial assessment of coronary endothelial function and plaque imaging by dual modality intravascular ultrasound and near infrared spectroscopy. Salbutamol and glyceryl trinitrate (GTN) were used as the endothelium dependent and independent vasoreactive stimulus respectively. Coronary segmental macrovascular response [% change segmental lumen volume (ΔSLV)], plaque burden [per cent atheroma volume (PAV)], and lipid core [LRP and lipid core burden index (LCBI)] were measured at baseline and after an interval of 12–18 months (N=520 consecutive 2-mm coronary segments). Results: Coronary segments which progress into LRP demonstrated greater reduction in vasodilator response to salbutamol (-0.24±2.96 vs 5.60±1.47%, p=0.04) and GTN (13.91±4.45 vs 21.19±3.19%, p=0.036), at baseline. By multivariate analysis, increase in lipid core was independently predicted by reduced baseline coronary endothelium dependent vasodilator function (table), whereas increase in atheroma volume was predicted by baseline coronary endothelial independent function (β coefficient: 0.21, 95% CI (0.09 to 0.33), p=0.0005). In the secondary analysis, serial changes in coronary endothelial independent function was associated with changes in plaque volume (β coefficient: -0.06, 95% CI (-0.09 to -0.02), p=0.001). There is poor correlation between atheroma volume growth and plaque compositional change (β coefficient -0.35, p=0.721).
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Sidharta et al. (2017) conducted a cohort in Stable angina or acute coronary syndrome (ACS) (n=33). Impaired baseline coronary endothelial function (assessed via salbutamol and glyceryl trinitrate vasoreactivity) vs. Preserved coronary endothelial vasodilator response / non-progressing coronary segments was evaluated on Progression into lipid rich plaque (LRP) and change in per cent atheroma volume (PAV) (beta coefficient 0.21 (for baseline endothelial-independent function predicting atheroma volume increase), 95% CI 0.09-0.33, p=0.04). Impaired baseline coronary vasodilator response to salbutamol (-0.24% vs 5.60%, p=0.04) and GTN (13.91% vs 21.19%, p=0.036) predicted progression into lipid-rich plaque at 12-18 months.
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