Acute myocardial infarction is associated with endothelial glycocalyx and cell damage and a parallel increase in circulating catecholamines

This was a prospective study of 678 consecutive STEMI-patients admitted to a single high-volume invasive heart centre for primary percutaneous coronary intervention (pPCI) from September 2006-July 2008. Blood samples were drawn immediately before pPCI. Plasma adrenaline, noradrenaline, syndecan-1 and thrombomodulin were measured retrospectively with complete data in 571 patients (84%). Median follow-up time was 28 (IQR 23-34) months. Follow-up was 99.7% complete. Outcomes were all-cause and cardiovascular mortality, re-myocardial infarction and admission due to heart failure (HF).Circulating noradrenaline and adrenaline correlated weakly but independently with syndecan-1 (rho=0.15 and rho=0.13, both p<0.01) and thrombomodulin (rho=0.11 and rho=0.17, both p<0.01), biomarkers of glycocalyx and endothelial cell damage, respectively. Considering biomarkers, patients with shock pre-pPCI had higher adrenaline and syndecan-1 and patients admitted to ICU post-pPCI had higher syndecan-1 (all p<0.05), and in the shocked patients (n=51) catecholamines correlated strongly with thrombomodulin and syndecan-1 (rho=0.31-0.42, all p<0.05). During follow-up, 78 (14%) patients died (37 cardiovascular deaths) and 65 (11%) were admitted with HF. By multivariate Cox proportional hazards analyses, one quartile higher plasma adrenaline was weakly but independently associated with both 30-day and long term mortality and HF (30-day all-cause mortality Hazard Ratio (95% CI) 1.39 (1.01-1.92), p=0.046; 30-day HF 1.65 (1.17-2.34), p=0.005; long-term cardiovascular mortality 1.49 (1.08-2.04), p=0.014). Furthermore, one quartile higher syndecan-1 was also weakly independently associated with long-term all cause mortality (1.26 (1.02-1.57), p=0.034).In STEMI-patients treated with pPCI, catecholamines correlated weakly with biomarkers of endothelial damage, with the strongest correlations and highest adrenaline and syndecan-1 levels in shocked patients. Furthermore, adrenaline and syndecan-1 were we