Release Kinetics of Inflammatory Biomarkers in a Clinical Model of Acute Myocardial Infarction

Liebetrau, Christoph; Hoffmann, Jedrzej; Dörr, Oliver; Gaede, Luise; Blumenstein, Johannes; Biermann, Hannes; Pyttel, Lukas; Thiele, P; Troidl, Christian; Berkowitsch, Alexander; Rolf, Andreas; Voss, Sandra; Hamm, Christian W.; Nef, Holger; Möllmann, Helge

doi:10.1161/circresaha.116.304653

Cited by 56 publications

(40 citation statements)

References 52 publications

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“…3 This model allows for precise definition of the exact time point of myocardial ischemia. By using TASH, the authors intended to screen early release kinetics of some soluble inflammatory biomarkers and leukocyte subsets within 24 hours of myocardial injury.…”

Section: Article See P 867mentioning

confidence: 99%

Myocardial Infarction and Inflammation

Hristov

Weber

2015

Circulation Research

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A therosclerosis as a persistent arterial disease is characterized by an imbalanced lipid metabolism and maladaptive immune response, resulting in subendothelial lipoprotein retention and endothelial activation with continuous migration of leukocytes and smooth muscle cells to the inflamed intima. 1,2 Over decades, this leads to the formation of stable atheromas that induce chronic tissue ischemia or of vulnerable plaques that cause acute occlusive atherothrombotic complications, such as myocardial infarction and stroke. As such, atherosclerosis and its consequences remain the leading causes of mortality and morbidity in Western countries. Acute myocardial infarction (AMI) often occurs as the first and fatal manifestation of atherosclerotic coronary artery disease. In general, AMI represents a typical sterile inflammation with release of inflammatory cytokines, platelet activation, leukocytosis, and hyperglycemia. The pathophysiological and laboratory parameters of AMI are monitored at admission after confirming the diagnosis only; however, this hampers any consideration and distinction of the very critical interval between initiation of myocardial ischemia, with the first symptoms of AMI often being imprecise or rather nontypical, and hospitalization. Numerous animal studies have provided detailed experimental data on AMI pathophysiology starting with the time of induction of ischemia by coronary artery ligation, whereas comparable data in men remain largely elusive and obscure. Article, see p 867In this issue of the journal, Liebetrau et al provide intriguing evidence in humans by taking advantage of ethanol-based transcoronary ablation of septal hypertrophy (TASH) in 21 patients with hypertrophic obstructive cardiomyopathy as a clinical model to induce AMI. 3 This model allows for precise definition of the exact time point of myocardial ischemia. By using TASH, the authors intended to screen early release kinetics of some soluble inflammatory biomarkers and leukocyte subsets within 24 hours of myocardial injury. They found a sustained elevation in interleukin (IL)-6, C-reactive protein, neutrophils and classical CD14 ++ CD16− monocytes, whereas sCD40L levels were decreased (Figure).In fact, the same group has recently published studies with identical design and on the same patient collective.4-7 Their results revealed the release kinetics of additional early ischemic biomarkers in the setting of TASH-induced AMI, such as cardiac troponin-T, NT-proBNP, s-Flt1, microRNAs, ischemia-modified albumin, and heart-type fatty acid-binding protein.4-7 A common conclusion implied that all these biomarkers may harbor a certain diagnostic value in the setting of AMI. Yet, the questions remained unanswered which of the biomarkers has a major effect and whether a single biomarker or rather the combination of >1 biomarker (eg, in a panel) are useful for routine measurement during the onset of AMI? This clearly mandates the need for more conclusive research with solid prospective data on outcome and correlation to cardiac fun...

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Section: Article See P 867mentioning

confidence: 99%

Myocardial Infarction and Inflammation

Hristov

Weber

2015

Circulation Research

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“…I read with great interest the recent article published by Liebetrau et al, 1 which described the release kinetics of several inflammatory markers (C-reactive protein, interleukin 6, troponin T, and soluble CD40 ligand) over a time course after the transcoronary ablation of septal hypertrophy as a model of induced acute myocardial infarction in humans.…”

Section: To the Editormentioning

confidence: 99%

Revisiting the Role of sCD40L as an Inflammatory Biomarker in a Clinical Model of Acute Myocardial Infarction

Lee

2015

Circulation Research

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“…Pre-and postprocedural management as well as the proof of concept of the TASH method as an equivalent for AMI have been recently published (13)(14)(15)(16)(17). In brief, a clinical history and the results of a physical examination, 12-lead electrocardiography, laboratory tests, echocardiography, and coronary angiography were assessed for all patients.…”

Section: Patients With Hypertrophic Obstructive Cardiomyopathy Undergmentioning

confidence: 99%

“…We recently reported the early release kinetics of several biomarkers, including cTnT and NT-proBNP, in patients undergoing transcoronary ablation of septal hypertrophy (TASH) as a model for patients with AMI ( [13][14][15][16][17]. There are currently no data, however, regarding the exact release kinetics of BNPsp in patients with AMI.…”

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confidence: 99%

Reference Values and Release Kinetics of B-Type Natriuretic Peptide Signal Peptide in Patients with Acute Myocardial Infarction

et al. 2015

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BACKGROUND The signal peptide for human B-type natriuretic peptide preprohormone (BNPsp), which is released from cardiomyocytes, is increased in plasma of patients with acute myocardial infarction (AMI); however, its exact release kinetics have not been defined. METHODS We measured BNPsp and high-sensitivity cardiac troponin T (hs-cTnT) in a reference group of individuals without structural heart disease (n = 285) and determined the release kinetics of these biomarkers in patients (n = 29) with hypertrophic obstructive cardiomyopathy undergoing transcoronary ablation of septal hypertrophy (TASH), a procedure allowing exact timing of onset of iatrogenic AMI. Blood samples were collected before TASH and at numerous preselected time points after TASH. RESULTS The reference median BNPsp concentration was 53.4 pmol/L [interquartile range (IQR) 47.0–61.0; 95th percentile 85.9 pmol/L; 99th percentile 116.3 pmol/L]. Baseline concentrations in patients undergoing TASH were higher than in the reference group [91.9 pmol/L (IQR 62.9–116.4); P < 0.0001]. BNPsp increased significantly, peaking at 15 min after induction of AMI [149.6 pmol/L (109.5–204.9) vs baseline; P = 0.004] and declining slowly thereafter, falling below the preprocedural value after 8 h (P = 0.014). hs-cTnT increased significantly 15 min after induction of AMI [26 ng/L (19–39) vs 18 ng/L (11–29); P = 0.001] and remained high at all later time points. CONCLUSIONS BNPsp concentrations increased immediately after AMI induction, providing early evidence of myocardial injury. The release kinetics of BNPsp differed from those of hs-cTnT. These findings provide information that should help in establishing the diagnostic value of BNPsp in the setting of early AMI.

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Release Kinetics of Inflammatory Biomarkers in a Clinical Model of Acute Myocardial Infarction

Cited by 56 publications

References 52 publications

Myocardial Infarction and Inflammation

Myocardial Infarction and Inflammation

Revisiting the Role of sCD40L as an Inflammatory Biomarker in a Clinical Model of Acute Myocardial Infarction

Reference Values and Release Kinetics of B-Type Natriuretic Peptide Signal Peptide in Patients with Acute Myocardial Infarction

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