INTRODUCTION Infarct size has been shown to be a better predictor of mortality than classical predictors following a ST-segment elevation myocardial infarction (STEMI). Therefore it is increasingly used for risk stratification. Biomarker release (CK and troponins) have been shown to overall good correlate with gold standards for MI size quantification (MRI, SPECT). In clinical practice, some patients display a discordant CK and troponin release in STEMI (CK in the higher quartiles with troponin in the lower or the other way around). The cause of this discordance has not been systematically analyzed. It has been shown that myocyte hypertrophy results in an increase of contractile proteins (like troponins) with no increase in cytosolic ones (like CK). HYPOTHESIS In the current work we have tested the hypothesis that patients with left ventricular hypertrophy (LVH) who suffer a STEMI have a disproportional total CK/troponin blood concentrations compared to STEMI patients with no LV hypertrophy. METHODS Consecutive STEMI patients (n=657) admitted to our Coronary Care Unit were retrospectively studied. CK and troponin I levels were measured on admission and then every 4 hours until a fall in both enzymes occurred. Patients were classified into four categories according to standard echocardiography recommendations. All the statistical analyses were performed using the open-source statistical scripting language R Version 2.11.0 (R Development Core Team). RESULTS Distribution of patients was as follows. Normal LV wall thickness: 426 patients (64.84%); mild LVH: 140 patients (21.31%); moderate LVH: 81 patients (12.33%); and severe LVH: 10 patients (1.52%). While CK peak values were similar in all categories, troponin I peak values were significantly higher in patients with LVH: mild LVH ([1.8 to 21] % higher than no-LVH patients, p<0.02) and moderate/severe LVH ([7.8 to 35] % higher than no-LVH patients, p<0.001). CONCLUSIONS We found that STEMI patients with LV hypertrophy (35% of our cohort) have significantly higher troponin release at the same level of CK release in comparison to patients without LV hypertrophy. In the presence of LV hypertrophy, troponin-I peak value significantly overestimates infarct size.