The effects of Allopurinol on levels of cardiac troponin Following Non-ST Elevation Myocardial Infarction: A Pilot Randomized Clinical Trial

2021 ◽  
Author(s):  
Sajad Khiali ◽  
Parvin Sarbakhsh ◽  
Sina Mashayekhi ◽  
Elham Mohamadrezapour ◽  
Samaneh Dousti ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Clinical Trial ◽  
Randomized Clinical Trial ◽  
Cardiac Troponin ◽  
Myocardial Injury ◽  
Standard Treatment ◽  
Troponin I ◽  
Cardiac Troponin I ◽  
St Elevation Myocardial Infarction ◽  
St Elevation

Purpose: Given the potential anti-ischemic effects of allopurinol, we aimed to assess whether allopurinol administration may reduce myocardial injury following non-ST elevation myocardial infarction (NSTEMI). Methods: A randomized clinical trial (RCT) was conducted on 100 individuals with NSTEMI. The intervention group (n=50) received 600 mg oral allopurinol at the time of diagnosis of NSTEMI, followed by 300 mg every day for two next days and the standard treatment of NSTEMI, while the control group (n=50) received only the standard treatment. Serum concentrations of cardiac troponin I (cTnI) were measured at baseline, and 8, 16, 24, and 32 hours after the treatment. Results: The baseline demographic and clinical data of the patients were not statistically different between the intervention and control groups (all P > 0.05). The comparing estimated marginal mean ± standard error for cardiac troponin I (cTnI) levels revealed no significant difference between the study groups (2.93 ± .27, 2.25 ± .27; P=0.082). The linear mixed model results showed that the interaction of time and group was not statistically different (P=0.751). Moreover, there was a decreasing trend over time for cTnI in both groups (P=0.039). Conclusion: The present pilot RCT did not support the potential cardio-protective benefits of allopurinol administration on decreasing myocardial injury following NSTEMI.

Relation of cardiac troponin I and microvascular obstruction following ST-elevation myocardial infarction

2011 ◽  
Vol 13 (1) ◽  
pp. 48-51 ◽  
Author(s):  
Jonas Hallén ◽  
Jesper K. Jensen ◽  
Peter Buser ◽  
Allan S. Jaffe ◽  
Dan Atar
Keyword(s):  
Myocardial Infarction ◽  
Cardiac Troponin ◽  
Microvascular Obstruction ◽  
Troponin I ◽  
Cardiac Troponin I ◽  
St Elevation Myocardial Infarction ◽  
St Elevation

scholarly journals Time Course of Degradation of Cardiac Troponin I in Patients With Acute ST-Elevation Myocardial Infarction

2006 ◽  
Vol 99 (10) ◽  
pp. 1141-1147 ◽  
Author(s):  
Lene H. Madsen ◽  
Geir Christensen ◽  
Terje Lund ◽  
Victor L. Serebruany ◽  
Chris B. Granger ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Cardiac Troponin ◽  
Time Course ◽  
Troponin I ◽  
Cardiac Troponin I ◽  
St Elevation Myocardial Infarction ◽  
St Elevation

Circulating Erythrocyte Microparticles and the Biochemical Extent of Myocardial Injury in ST Elevation Myocardial Infarction

Cardiology ◽  
2016 ◽  
Vol 136 (1) ◽  
pp. 15-20 ◽  
Author(s):  
Georgios Giannopoulos ◽  
Dimitrios A. Vrachatis ◽  
Georgios Oudatzis ◽  
Georgios Paterakis ◽  
Christos Angelidis ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Myocardial Injury ◽  
Troponin I ◽  
Multivariable Analysis ◽  
Area Under The Curve ◽  
Myocardial Damage ◽  
Primary Angioplasty ◽  
St Elevation Myocardial Infarction ◽  
Vascular Effects ◽  
St Elevation

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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