Role of Myeloperoxidase as Predictor of Systemic Inflammatory Response Syndrome in Patients With ST-Segment Elevation Myocardial Infarction After Primary Percutaneous Coronary Intervention
“…A literature review performed with PubMed, using the keywords ‘systemic inflammatory response syndrome (SIRS)’ and ‘ST-elevation acute myocardial infarction (STEMI)’, identified few reports in the English language literature between 1990 and 2013. In contrast to our case, two published reports by Samimi-Fard et al 3 and van Diepen et al 4 found that patients with STEMI may present with SIRS after primary percutaneous coronary intervention (PPCI). Conversely, our case showed that SIRS may cause STEMI, which is an extraordinary finding, given the absence of relevant coronary stenosis.…”
Systemic inflammatory response syndrome (SIRS) complicated with ST-elevation myocardial infarction has rarely been reported, and the precise mechanisms of myocardial injury remain unclear. Here, we present a case involving a 45-year-old man who developed SIRS secondary to diabetesinduced infection, and who ultimately developed ST-elevation myocardial infarction with acute heart failure, fulminant diabetes, acute liver dysfunction, acute kidney dysfunction and rhabdomyolysis. The patient eventually recovered due to early detection, correct diagnosis and powerful treatment. Clinicians should be aware of this new type of myocardial infarction, which is induced by inflammatory injury, but is not due to a primary coronary event such as plaque erosion and/or rupture, fissuring or dissection.
“…A literature review performed with PubMed, using the keywords ‘systemic inflammatory response syndrome (SIRS)’ and ‘ST-elevation acute myocardial infarction (STEMI)’, identified few reports in the English language literature between 1990 and 2013. In contrast to our case, two published reports by Samimi-Fard et al 3 and van Diepen et al 4 found that patients with STEMI may present with SIRS after primary percutaneous coronary intervention (PPCI). Conversely, our case showed that SIRS may cause STEMI, which is an extraordinary finding, given the absence of relevant coronary stenosis.…”
Systemic inflammatory response syndrome (SIRS) complicated with ST-elevation myocardial infarction has rarely been reported, and the precise mechanisms of myocardial injury remain unclear. Here, we present a case involving a 45-year-old man who developed SIRS secondary to diabetesinduced infection, and who ultimately developed ST-elevation myocardial infarction with acute heart failure, fulminant diabetes, acute liver dysfunction, acute kidney dysfunction and rhabdomyolysis. The patient eventually recovered due to early detection, correct diagnosis and powerful treatment. Clinicians should be aware of this new type of myocardial infarction, which is induced by inflammatory injury, but is not due to a primary coronary event such as plaque erosion and/or rupture, fissuring or dissection.
“…Systemic inflammatory response syndrome was defined as ^ 2 of 1 ) heart rate > 90 beats/ min, 2) respiratory rate > 20 breaths/min, 3) body temperature > 38 or < 36°C, or 4) leukocyte count > 12 or < 4 x 10=/L. SIRS has been reported in 11-19% of patients presenting with ST-elevation myocardial infarction (STEMI); however, studies reporting associated outcomes have been limited to small case series with conflicting associations with mortality (8)(9)(10). Coronary plaque rupture in the setting of myocardial infarctions is associated with a systemic biochemical inflammatory response, but considerable less is known about the clinical inflammatory response (6,7).…”
The diagnosis of systemic inflammatory response syndrome and the cumulative number of systemic inflammatory response syndrome criteria were independently associated with 90-day clinical outcomes in a population of patients with ST-elevation myocardial infarction. The independent association of this simple composite measure of the inflammatory response with outcomes underscores the importance of the clinical inflammatory response in ST-elevation myocardial infarction.
“…In our study, we used serum collection tubes as they had been used in a previous large observational study enrolling patients with acute coronary syndromes where MPO levels were found to predict the clinical outcome. 4 Similar studies have also reported an association between serum MPO levels and myocardial reperfusion after thrombolysis 5 and systemic inflammation after a primary percutaneous coronary intervention, 6 thus indicating that MPO measured in serum is clinically meaningful. Finally, the findings in our clinical study are consistent with those in our postmortem tissues from sudden coronary deaths that showed a higher density of MPO-positive cells in thrombi overlying eroded lesions relative to plaque rupture.…”
We thank Dr Schindhelm for his constructive comments and interest in our study. 1 In a further analysis using a multiple linear regression model where plaque erosion and smoking status were entered as independent variables and the myeloperoxidase (MPO) level was entered as the dependent variable, with the assumptions of normality of residuals, absence of heteroscedasticity, and presence of linearity all met, plaque erosion (coefficient 1195. Dr Schindhelm's second comment addresses the experience that MPO concentrations in EDTA-plasma are lower than those in serum, where the latter suggests uncontrolled ex vivo release of MPO from leukocytes during and after sample collection. 2 A more recent study by Wendland et al, 3 however, reports the opposite findings, concluding that the collection of MPO in tubes containing EDTA "alters in expressive way the results." In our study, we used serum collection tubes as they had been used in a previous large observational study enrolling patients with acute coronary syndromes where MPO levels were found to predict the clinical outcome. 4 Similar studies have also reported an association between serum MPO levels and myocardial reperfusion after thrombolysis 5 and systemic inflammation after a primary percutaneous coronary intervention, 6 thus indicating that MPO measured in serum is clinically meaningful. Finally, the findings in our clinical study are consistent with those in our postmortem tissues from sudden coronary deaths that showed a higher density of MPO-positive cells in thrombi overlying eroded lesions relative to plaque rupture.
DisclosuresNone.
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