scholarly journals A New Prognostic Evaluation of Patients with Acute ST-Elevation Myocardial Infarction Undergoing Primary Angioplasty: Combined Zwolle and Syntax Score

2013 ◽  
Vol 62 (18) ◽  
pp. C237
Author(s):  
Şeref Kul ◽  
Huseyin Uyarel ◽  
Murat Turfan ◽  
Gokhan Ertas ◽  
Mehmet Akif Vatankulu ◽  
...  
2015 ◽  
Vol 198 ◽  
pp. 70-74 ◽  
Author(s):  
Teresa Giralt ◽  
Xavier Carrillo ◽  
Oriol Rodriguez-Leor ◽  
Eduard Fernandez-Nofrerias ◽  
Ferran Rueda ◽  
...  

Cardiology ◽  
2016 ◽  
Vol 136 (1) ◽  
pp. 15-20 ◽  
Author(s):  
Georgios Giannopoulos ◽  
Dimitrios A. Vrachatis ◽  
Georgios Oudatzis ◽  
Georgios Paterakis ◽  
Christos Angelidis ◽  
...  

Objectives: Red blood cell microparticles (RBCm) have potential adverse vascular effects and they have been shown to be elevated in ST elevation myocardial infarction (STEMI). The purpose of this study is to investigate their relationship with biochemical infarct size. Methods: RBCm were quantified with flow cytometry in blood drawn from 60 STEMI patients after a primary angioplasty. The creatine kinase-myocardial brain fraction (CK-MB) was measured at predefined time points and the area under the curve (AUC) was calculated. Results: RBCm count was correlated with CK-MB AUC (Spearman's ρ = 0.83, p < 0.001). The CK-MB AUC values per RBCm quartile (lower to upper) were: 3,351 (2,452-3,608), 5,005 (4,450-5,424), 5,903 (4,862-10,594), and 8,406 (6,848-12,782) ng × h/ml, respectively. From lower to upper quartiles, the maximal troponin I values were: 42.2 (23.3-49.3), 49.6 (28.8-54.1), 59.2 (41.4-77.3), and 69.1 (48.0-77.5) ng/ml (p = 0.005). In multivariable analysis, RBCm remained a significant predictor of CK-MB AUC (standardized β = 0.63, adjusted p = 0.001). Conclusions: Erythrocyte microparticles appear to be related to the total myocardial damage biomarker output. The exact pathophysiologic routes, if any, for this interaction remain to be identified. However, these results suggest that erythrocytes may be a - thus far virtually ignored - player in the pathogenesis of ischemic injury.


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