BACKGROUND: Mortality in ST-elevation myocardial infarction (STEMI) patients developing cardiogenic shock (CS) during hospitalization is high. Catecholamines, ischemia, and inflammation (parameters present in CS) affect the endothelium. We hypothesized that plasma level of biomarkers reflecting endothelial damage would be associated with CS and mortality. METHODS: In 96% of 1467 consecutive patients with suspected STEMI, biomarkers reflecting endothelial cell- (soluble thrombomodulin, sTM) and glycocalyx- (syndecan-1) damage were measured on admission. Patients were stratified by CS development or not. CS-Patients were substratified by CS on admission (admission-CS), CS developed in the catheterization laboratory (cath. lab.-CS), or late CS. RESULTS: STEMI patients with admission-CS (n = 85) and cath.lab.-CS (n = 25) had higher levels of sTM and syndecan-1 compared with no-CS patients (n = 1,299). Late CS-patients (n = 58) had higher levels of sTM (median (25th; 75th percentile) 8.8 (7.0; 11.6) vs. 7.4 (6.0; 9.0) ng/mL, P = 0.0004) but not Syndecan-1 (P = 0.26) compared with no-CS patients. sTM was, however, not independently associated with late CS development (OR (95% CI) 1.07 (0.99-1.16), P = 0.09). Patients with the highest level of sTM and syndecan-1 had the highest 30-day mortality (Plogrank<0.0001). However, neither sTM nor Syndecan-1 was independently associated with 30-day mortality (HR (95% CI) sTM: 1.06 (0.996-1.12), P = 0.07; Syndecan-1: 1.04 (0.99-1.08), P = 0.12). CONCLUSION: Patients with suspected STEMI patients and admission-CS/cath.lab.-CS had elevated admission levels of sTM and Syndecan-1 compared with no CS patients. Patients developing late CS had higher sTM plasma concentration compared with patients without shock. However, the biomarker levels were not independently associated with late CS and mortality.
BACKGROUND:Mortality in ST-elevation myocardial infarction (STEMI) patients developing cardiogenic shock (CS) during hospitalization is high. Catecholamines, ischemia, and inflammation (parameters present in CS) affect the endothelium. We hypothesized that plasma level of biomarkers reflecting endothelial damage would be associated with CS and mortality. METHODS: In 96% of 1467 consecutive patients with suspected STEMI, biomarkers reflecting endothelial cell- (soluble thrombomodulin, sTM) and glycocalyx- (syndecan-1) damage were measured on admission. Patients were stratified by CS development or not. CS-Patients were substratified by CS on admission (admission-CS), CS developed in the catheterization laboratory (cath. lab.-CS), or late CS. RESULTS: STEMI patients with admission-CS (n = 85) and cath.lab.-CS (n = 25) had higher levels of sTM and syndecan-1 compared with no-CS patients (n = 1,299). Late CS-patients (n = 58) had higher levels of sTM (median (25th; 75th percentile) 8.8 (7.0; 11.6) vs. 7.4 (6.0; 9.0) ng/mL, P = 0.0004) but not Syndecan-1 (P = 0.26) compared with no-CS patients. sTM was, however, not independently associated with late CS development (OR (95% CI) 1.07 (0.99-1.16), P = 0.09). Patients with the highest level of sTM and syndecan-1 had the highest 30-day mortality (Plogrank<0.0001). However, neither sTM nor Syndecan-1 was independently associated with 30-day mortality (HR (95% CI) sTM: 1.06 (0.996-1.12), P = 0.07; Syndecan-1: 1.04 (0.99-1.08), P = 0.12). CONCLUSION:Patients with suspected STEMI patients and admission-CS/cath.lab.-CS had elevated admission levels of sTM and Syndecan-1 compared with no CS patients. Patients developing late CS had higher sTM plasma concentration compared with patients without shock. However, the biomarker levels were not independently associated with late CS and mortality.
Authors: V Bogner-Flatz; M Braunstein; L E Ocker; T Kusmenkov; J Tschoep; L Ney; W Böcker; T Annecke Journal: Mediators Inflamm Date: 2019-04-17 Impact factor: 4.711