Key result
Non-invasive reperfusion assessment using biochemical markers in 85 AMI patients showed poor agreement and provided no significant prognostic information due to dependency on infarct size.
Why the study?
Do release kinetics of biochemical markers accurately assess reperfusion and predict 1-year outcomes in thrombolysed AMI patients?
Cohort (n=85)
Do release kinetics of biochemical markers accurately assess reperfusion and predict 1-year outcomes in thrombolysed AMI patients?
Routine use of biochemical markers for non-invasive reperfusion assessment in AMI is not justified due to their dependency on infarct size, which confounds prognostic accuracy.
Biochemical markers should not guide reperfusion assessment in AMI; challenges prior validation of release kinetics thresholds.
Background: Thrombolytic therapy often fails to obtain reperfusion in acute myocardial infarction (AMI). To allow further intervention, various methods for non-invasive reperfusion assessment, e.g. release kinetics of biochemical markers and ST segment recovery analysis on the ECG, have been proposed. Methods and Results: In 85 thrombolysed AMI patients <76 years with significant ST elevation on ECG and time delay ≤6 h, blood was drawn and ECGs recorded before and 90 min after the start of treatment. Myoglobin, creatine kinase-MB and troponin I were measured, and slopesand relative increases (RIs) of the markers were calculated. Moreover, the relative decrease in total sum of ST elevation (ST recovery₀–₉₀) on the ECG was calculated. A slope₀–₉₀ or RI₀–₉₀ below previously validated threshold values or an ST recovery <25% was considered indicative of failed reperfusion. Final infarct size was determined as cumulative release of LD1. Patients were followed for 1 year to register deaths, re-infarctions, and coronary revascularisation. The various non-invasive reperfusion indexes showed poor agreement, and no significant prognostic information was obtained. A positive correlation between increase rates and infarct size probably reflected a direct, concentration-dependent enhancement of release of biochemical markers in blood. Thereby, high-risk patients with large, non-reperfused infarcts might have been overlooked while only low-risk patients with small non-reperfused infarcts were recognised. This could readily explain the lack of correlation with long-term outcome. Conclusions: Dependency on infarct size seems to limit the usefulness of biochemical markers for reperfusion assessment. Correction for expected infarct size might improve performance in the future. At present, routine use of biochemical markers for reperfusion assessment is not justified.
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Haastrup et al. (2001) conducted a cohort in Acute Myocardial Infarction (n=85). Biochemical markers (Myoglobin, CK-MB, Troponin I) and ST segment recovery was evaluated on Agreement between reperfusion indexes and prognostic information (deaths, re-infarctions, coronary revascularisation). Non-invasive reperfusion assessment using biochemical markers in 85 AMI patients showed poor agreement and provided no significant prognostic information due to dependency on infarct size.
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