Inflammatory markers and cardiac function in acute coronary syndrome: Difference in ST-segment elevation myocardial infarction (STEMI) and in non-STEMI models

Stefano, Rossella Di; Bello, Vitantonio Di; Barsotti, Maria Chiara; Grigoratos, Chrysanthos; Armani, Chiara; Dell’Omodarme, M.; Carpi, Angelo; Balbarini, Alberto

doi:10.1016/j.biopha.2009.06.004

Cited by 66 publications

(61 citation statements)

References 34 publications

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“…This is reinforced by data on some cardiovascular biomarkers assuming distinct patterns of release in each MI type [5][6][7]. It is also noteworthy that plaque disruption, thrombosis, coronary artery occlusion and myocardial necrosis heavily differ greatly in persistence, degree and presence in STEMI and NSTEMI [18].…”

Section: Discussionmentioning

confidence: 92%

“…It is also noteworthy that plaque disruption, thrombosis, coronary artery occlusion and myocardial necrosis heavily differ greatly in persistence, degree and presence in STEMI and NSTEMI [18]. Although suggestive preliminary data on the different behaviors of inflammatory markers, necrosis markers and neurohormonal biomarkers are available, strong evidence about specific biochemical substrates characterizing STEMI and NSTEMI is still lacking [5][6][7]19].…”

Section: Discussionmentioning

confidence: 99%

“…Reports have suggested that STEMI and NSTEMI have different patterns of release of inflammatory and neurohormonal markers [5,6]. Inflammatory markers show a remarkable prognostic value in NSTEMI whereas cardiac troponins (cTns) are associated with better risk prediction for STEMI [7].…”

Section: Introductionmentioning

confidence: 99%

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New insights in the pathophysiology of acute myocardial infarction detectable by a contemporary troponin assay

Ferraro

Biganzoli

Marano

et al. 2013

Clinical Biochemistry

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Objectives: ST-elevation and non-ST-elevation myocardial infarction (STEMI, NSTEMI) are considered two distinct pathophysiologic entities. We evaluated cardiac troponin I (cTnI) release in STEMI and NSTEMI using a "contemporary" (CV > 10 to 20% at the 99th percentile concentration) cTnI assay for patients undergoing early percutaneous coronary intervention (PCI).Design and methods: 856 patients with suspected acute coronary syndrome consecutively admitted to the Emergency Department of the Maggiore Hospital of Novara (225 STEMI and 135 NSTEMI) were selected according to: 1) early (≤4 h from admission) and successful PCI; and 2) cTnI measurements at ED presentation and within 24 h. The influence of the MI type on cTnI concentrations at baseline and after PCI as well as the velocity of cTnI [cTnI V = absolute increase (after log conversion of cTnI measurements) / delay between the two measurements] was studied by multiple regression analysis, adjusting for patient parameters.Results: A statistically significant interaction between MI type and time from symptoms was reported on cTnI concentrations (p b 0.0001): STEMI and NSTEMI differed for cTnI releases at admission and after revascularization. Higher cTnI V in STEMI was detectable in patients admitted within 6 h from symptoms. Baseline cTnI concentrations were lower in patients with a history of coronary artery disease (CAD) and increased with aging (p b 0.0001). In the elderly (>75 years), the cTnI V was significantly increased.Conclusion: STEMI and NSTEMI patients have different patterns and dynamics of cTnI release influenced by the interaction with time from symptoms, by aging and history of CAD.

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Section: Discussionmentioning

confidence: 92%

Section: Discussionmentioning

confidence: 99%

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New insights in the pathophysiology of acute myocardial infarction detectable by a contemporary troponin assay

Ferraro

Biganzoli

Marano

et al. 2013

Clinical Biochemistry

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“…Yapılan çalışmalarda STEMI olgularında inflamatuar sitokin düzeylerinin NSTEMI hastalarına kıyasla anlamlı olarak daha yüksek düzeylerde olduğu ve artmış sitokin düzeylerinin koroner arter hastalığı ciddiyeti ile pozitif bir korelasyonunun olduğu gösterilmiştir [20,21]. Bununla beraber inflamatuar sitokinlerin platelet boyutunda artış ve daha aktif platelet üretimi ile ilişkili olabileceği de gösterilmiştir [22].…”

Section: Discussionunclassified

The neutrophile to lymphocyte ratio and mean platelet volume with Gensini score in patients with acute myocardial infarction

Çoşkun¹,

Sucu²,

Aksoy³

et al. 2015

Gaziantep Med J

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The aim of the present study was to investigate the relationship between the coronary artery severity and neutrophile to lymphocyte ratio (N/L) and also mean platelet volume (MPV) in patients with myocardial infarction (MI). 203 MI with ST elevation (STEMI) patients and 62 MI without ST elevation (NSTEMI) patients were included and retrospectively analyzed in the study. The severity of the coronary artery disease was assessed according to the Gensini score. Neutrophil counts were 12.5±4.1 and 11.3±3.1 in the STEMI and NSTEMI groups respectively(p=0.045). N/L ratio was 5.1±6.0 and 5.2±6.0 respectively (p=0.85) and MPV was 8.6±1.2 and 8.4±1.0 respectively (p=0.44). Mean Gensini score was 36.8±16.1 in the STEMI group and 29.7±13.9 in the NSTEMI group (p<0.002). MPV was significantly correlated with Gensini score but there was no significant correlation between the N/L ratio and Gensini score in the STEMI group(r=0.07, p=0.27 and r=0.17, p=0.01 respectively). In the NSTEMI group, correlation of neither N/L ratio nor MPV with Gensini score was not detected (r=0.12, p=0.33 and r=0.08, p=0.53 respectively). MPV is a valuable parameter to predict coronary artery severity assessed based on the Gensini score in the STEMI patients.

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“…It has been observed that inflammatory markers including IL-6 and TGF-β are elevated following myocardial infarction [14]. In addition, IL-6 has been shown to stimulate osteoclastic bone resorption in vitro [15].…”

Section: Acsmentioning

confidence: 99%

Type I collagen degradation during tissue repair: Comparison of mechanisms following fracture and acute coronary syndromes

Stansfield

Gossiel

Morton

et al. 2014

Bone

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Inflammatory markers and cardiac function in acute coronary syndrome: Difference in ST-segment elevation myocardial infarction (STEMI) and in non-STEMI models

Cited by 66 publications

References 34 publications

New insights in the pathophysiology of acute myocardial infarction detectable by a contemporary troponin assay

New insights in the pathophysiology of acute myocardial infarction detectable by a contemporary troponin assay

The neutrophile to lymphocyte ratio and mean platelet volume with Gensini score in patients with acute myocardial infarction

Type I collagen degradation during tissue repair: Comparison of mechanisms following fracture and acute coronary syndromes

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