Prognostic value of C-reactive protein and cardiac troponin I in primary percutaneous interventions for ST-elevation myocardial infarction

Admission Levels of C-Reactive Protein and Plasminogen Activator Inhibitor-1 in Patients With Acute Myocardial Infarction With and Without Cardiogenic Shock or Heart Failure on Admission

“…However, somewhat in contrast to the above observations, several studies have reported that there is no 4,34) or an adverse 40) relationship between CRP levels on admission and LVEF and enzymatic measures of myocardial infarct size. The authors have explained these results by the time lag of 6 hours in the hepatic synthesis of CRP, 4) by the association of CRP elevation with preinfarction unstable angina pectoris accompanied by silent myocardial ischemia, which acts as ischemic preconditioning, and by the inductive effect of inflammation on expression of angiogenic growth factors associated with reduced infarct size and on endogenous production of nitrous oxide, which protects myocardium from reperfusion injury.…”

“…Nevertheless, to the best of our knowledge there are no studies examining the relationship between CRP levels and LVD when both of these factors were assessed on admission. Concerning the issue of the association between CRP and LVD after AMI, it has been demonstrated that the presence of a larger enzymatic infarct size and angiographically multiple complex lesions, both of which reflect the severity of the ongoing disease process, are associated with both the occurrence of HF and/ or CS [31][32][33] and increased levels of CRP 30,33,34) during the early phase of AMI. Of interest, several other factors related to a pre-existing medical condition, such as diabetes, hypertension, previous coronary heart disease (CHD), and MVD at angiography have also been shown to be associated with the occurrence of HF or CS after AMI, [35][36][37] but none of these factors are associated with increased CRP levels in this clinical setting.…”

Cardiac troponin I for prediction of clinical outcomes and cardiac function through 3-month follow-up after primary percutaneous coronary intervention for ST-segment elevation myocardial infarction

“…These results are in harmony with previous smaller studies applying post-PCI sampling with other cTn assays to predict clinical outcomes. 4,6,7,21,22 In addition, we showed that cTnI provided incremental discriminative information, which is a biologically plausible finding because injured myocardium is a significant driver of these events.…”

“…[3][4][5] These findings support the use of cTn as a risk stratification tool in STEMI patients, but knowledge on the value of cTnI for prediction of other outcome measures than infarct size and left ventricular function is limited. [6][7][8] Further studies investigating the relationship between the amount of cTnI release and clinical events or biochemical measures of global cardiac function at follow-up are thus critically important to better define the clinical utility.…”

Predictive Factors and Impact of No Reflow After Primary Percutaneous Coronary Intervention in Patients With Acute Myocardial Infarction

“…One mechanism by which higher levels of C-reactive protein promote development of no reflow may involve suggestion that elevated level of C-reactive protein may increase infarct size 21,22 by activating the complement cascade in the ischemic/necrotic tissue. 23 Additionally, elevated level of C-reactive protein or other inflammatory molecules may promote microvascular obstruction through an array of mechanisms.…”