Soluble ST2 levels are not associated with secondary cardiovascular events and vulnerable plaque phenotype in patients with carotid artery stenosis

- Soluble ST2 (sST2) has developed as a biomarker in ischemic heart disease.
- Here, sST2 plasma levels were assessed in patients with carotid artery disease.
- We report no predictive value of sST2 for future cardiovascular events.
- No association was found between sST2 levels and vulnerable plaque characteristics.

ObjectiveSoluble ST2 (sST2), a novel biomarker predictive for heart disease, has recently been shown associated with the progression of atherosclerotic disease in a mouse model. The present study was designed to assess sST2 plasma levels in patients scheduled for carotid endarterectomy and relate it with the occurrence of adverse cardiovascular events during follow-up. In addition, sST2 levels were associated to patient clinical data and atherosclerotic plaque characteristics.Methods and resultsPlasma sST2 levels were measured in 391 patients who underwent carotid endarterectomy and were subsequently followed for 3 years. Primary composite endpoint was the occurrence of an adverse cardiovascular event.At baseline, no differences were observed in sST2 levels between asymptomatic (n = 75) and symptomatic (n = 316) patients (85 [49-122] versus 90 [58-137] pg/ml, p = 0.263). Soluble ST2 plasma levels did not differ between patients who experienced a secondary manifestation of cardiovascular disease and patients who remained free of symptoms (90 [60-129] versus 88 [46-140] pg/ml, p = 0.519). There was no association between sST2 levels and any of the following plaque characteristics: size of a lipid core, degree of calcification, number of macrophages or smooth muscle cells, amount of collagen and number of microvessels.ConclusionsSoluble ST2 plasma levels have no predictive value for future cardiovascular events in patients with significant carotid artery stenosis. In addition, we did not observe an association between plasma sST2 levels and the histopathological features of a rupture prone plaque. This study does not provide supportive evidence that sST2 reflects a progressive state of advanced atherosclerotic disease.