New insights in the pathophysiology of acute myocardial infarction (MI) detectable by a new generation Troponin I assay

cardiovascular biomarkers measured in the acute phase of MI on case series including both patients with ST-elevation MI (STEMI) and MI with no ST-elevation at electrocardiogram (NSTEMI). This contrasts with the definition of MI, considering STEMI and NSTEMI as two distinct pathophysiologic entities. According to the advancement in the pathophysiology of myocardial injury gained by cardiac troponin I (cTnI) assays with improved sensitivity, we sough to evaluate cTnI release in STEMI and NSTEMI patients undergoing early percutaneous coronary intervention (PCI). Methods: From 856 individuals with suspected acute coronary syndrome (ACS) consecutively admitted to the ED, STEMI (n=225) and NSTEMI (n=135) patients were selected whether undergoing early (≤4 h from admission) and successful PCI, and cTnI measurements (Siemens Advia Centaur TnI-Ultra) at ED presentation and within 24 h. The influence of MI type on cTnI concentrations at baseline and after PCI and on the rate of marker increase (RMI) were studied by multiple regression analysis, adjusting for patient features. Results: A statistically significant (P <0.0001) interaction between MI type and time from symptoms was reported on cTnI concentrations: STEMI and NSTEMI differed for cTnI release at admission (after 5h from symptoms) and after revascularisation (within 24h from symptoms). A higher RMI in STEMI was detectable in patients admitted within 6h from symptoms. Baseline cTnI concentrations were lower in patients with history of ACS and increased with aging (P <0.0001). In the elderly (>75 years) the RMI significantly increased. Conclusions: STEMI and NSTEMI patients have different patterns and kinetics of cTnI release, influenced by the interaction with time from symptoms, aging and previous history of ACS. In STEMI a rapid cTnI increase is likely to mirror the sharp washout of necrosis markers after an early successful PCI, whereas in NSTEMI later PCI seems to cause the slow ongoing cTnI increase, even persisting for several hours. Stating different biochemical substrates, STEMI and NSTEMI should be investigated separately for reporting on cardiovascular biomarkers to avoid biased estimate of diagnostic and prognostic performances.