The influence of thrombolytic therapy on C-reactive protein in ST-segment elevation acute myocardial infarction.
BACKGROUND
Inflammation plays a crucial role in atherosclerotic processes and in acute coronary syndromes (ACS). Strong evidence of this is the elevation of C-reactive protein (CRP) serum levels during an ACS and its short- and long-term prognostic potency. The present study aimed to assess the relation between CRP serum levels and the elevation of cardiac markers in patients with ST elevation acute myocardial infarction (STEMI) as well as the effect of intravenous thrombolysis on a time series of CRP values.


METHODS
Thirty-six patients with STEMI were enrolled in the study. Twenty-eight of them received intravenous thrombolysis successfully and 8 did not receive thrombolysis. We measured serum concentrations of CRP, troponin I, creatine kinase, creatine kinase isoenzyme and lactate dehydrogenase in all patients on admission, 24 and 48 hours later. CRP serum values were obtained using the turbidimetric method. Coronary angiography was performed in all patients to estimate disease severity and culprit vessel flow after treatment.


RESULTS
Patients who were thrombolysed had lower CRP values on admission (p < 0.05), at 24 hours (p < 0.001) and 48 hours later (p < 0.05), compared to those without thrombolysis. CRP values on admission had a positive correlation with markers of cardiac myocyte necrosis and a negative correlation with TIMI flow.


CONCLUSIONS
Thrombolytic therapy in patients with STEMI is associated with a less pronounced response of CRP during the first 48 hours. The close relation of CRP with cardiac enzymes and troponin I on admission adds to the proven value of this inflammatory marker and suggests directions for further research.
Tsakiris
Alexandros K
AK
1st Cardiology Department, Hellenic Red Cross Hospital-Korgialeneio-Benakeio, Athens, Greece.
Marnelos
Panagiotis G
PG
Nearchou
Nearchos S
NS
Papadakis
John E
JE
Karatzis
Emmanouil N
EN
Skoufas
Panagiotis D
PD
D000368:Aged; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000187:drug effects* / Q000378:metabolism*; D017023:Coronary Angiography; D003402:Creatine Kinase / Q000097:blood / Q000187:drug effects; D052279:Creatine Kinase, MB Form / Q000097:blood / Q000187:drug effects; D004562:Electrocardiography; D005260:Female; D005343:Fibrinolytic Agents / Q000627:therapeutic use*; D006329:Heart Conduction System / Q000503:physiopathology; D006801:Humans; D007770:L-Lactate Dehydrogenase / Q000097:blood / Q000187:drug effects; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood* / Q000188:drug therapy* / Q000201:enzymology / Q000503:physiopathology; D010343:Patient Admission; D011994:Recombinant Proteins / Q000627:therapeutic use; D012720:Severity of Illness Index; D013318:Stroke Volume / Q000187:drug effects; D000077785:Tenecteplase; D015912:Thrombolytic Therapy; D010959:Tissue Plasminogen Activator / Q000627:therapeutic use; D016896:Treatment Outcome; D019210:Troponin I / Q000097:blood / Q000187:drug effects
D015415:Biomarkers; D005343:Fibrinolytic Agents; D011994:Recombinant Proteins; D019210:Troponin I; D002097:C-Reactive Protein; C087896:reteplase; D007770:L-Lactate Dehydrogenase; D003402:Creatine Kinase; D052279:Creatine Kinase, MB Form; D010959:Tissue Plasminogen Activator; D000077785:Tenecteplase