Release of myoglobin is different in myocardial damage due to inflammation respect to ischemic damage

Background: The differential diagnosis between myocarditis and acute coronary syndrome is still a challenge using first line diagnostic tests as clinical history, ECG and echocardiography data. The aim of this retrospective study was to assess any differences of myocite necrosis markers in patients with ischemic and inflammatory damage, in order to conjecture a different molecular and tissue expression of these two lesions. Methods: We retrospectively enrolled 74 patients with chest pain and elevated Troponin I. Of these, 40 patients had a Non St Elevation Myocardial Infarction (NSTEMI) and evidence of significant (stenosis >50%) coronary artery disease (CAD group) on coronary angiography, and 34 patients had a diagnosis of myocarditis detected by cardiac magnetic resonance (Myocarditis group). In each patient was obtained the determination of Troponin I, Myoglobin, CK-Mb, CPK and Troponin I/Myoglobin ratio at the first, the second, the third day and at the peak. Furthermore, enzymes were categorized in normal and abnormal according with their normal range. Results: Baseline characteristics were similar between groups, while CAD group showed an higher incidence of conventional cardiovascular risk factors. No differences were found regarding Troponin I, CK-Mb and CPK at the 1st, the 2nd, the 3rd day an at the peak. On the contrary, Myoglobin showed many significant differences between the two groups. In particular, its peak was lower in Myocarditis group (131.02±90.49) respect NSTEMI group (290.15±561.43). The percentage of patients with abnormality of Myoglobin at the 3rd day was significant lower (p=0.01) in the Myocarditis group (9%) than the CAD group (40%). Troponin I/Myoglobin ratio was higher in Myocarditis group vs CAD group both at the 2nd day (16.32±10.36 vs 9.92±11.64, p value=0.047) and at the 3rd day (14.92±17.17 vs 7.80±9.02, p value=0.036). Conclusion: Despite the clinical overlapping, which sometimes could direct to the wrong diagnosis, myocarditis and NSTEMI are two completely rent processes, from the pathophysiology to the myocardial necrosis markers’ curves. Its knowledge could add a one more rawplug in the differential diagnosis between ischemic and inflammatory damage.