Release Kinetics of Circulating Muscle-Enriched MicroRNAs in Patients Undergoing Transcoronary Ablation of Septal Hypertrophy

Liebetrau, Christoph; Möllmann, Helge; Dörr, Oliver; Szardien, Sebastian; Troidl, Christian; Willmer, Matthias; Voss, Sandra; Gaede, Luise; Rixe, Johannes; Rolf, Andreas; Hamm, Christian W.; Nef, Holger

doi:10.1016/j.jacc.2013.05.025

Cited by 83 publications

(56 citation statements)

References 34 publications

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“…24,25 One of the most important findings of our study is that blood levels of the inflammatory cytokine IL-6 and the signaling product CRP increased throughout the prespecified time points. Our study clearly shows that CRP release, as assessed by the hs assay, can be measured within 4 to 8 hours after MI and remains increased until 24 hours.…”

Section: Discussionmentioning

confidence: 75%

“…24,25 All TASH procedures were performed in a single-session procedure using a single septal branch occlusion. During the procedure, the mean (SD) volume of ethanol administered was 1.77 (0.59) mL.…”

Section: Resultsmentioning

confidence: 99%

“…Pre-and postprocedural management of the patients has been published recently. 24,25 In brief, clinical history, physical examination, 12-lead ECG, laboratory tests, echocardiography, and coronary angiography for all patients were assessed. The final diagnosis of hypertrophic obstructive cardiomyopathy was made according to the current guidelines based on severe symptoms during physical activity, asymmetrical septal hypertrophy >15 mm, systolic movement of the anterior mitral valve leaflet, and an intraventricular pressure gradient of 30 mm Hg at rest and >50 mm Hg after provocation by the Valsalva maneuver.…”

Section: Methodsmentioning

confidence: 99%

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

Liebetrau

Hoffmann

Dörr

et al. 2015

Circulation Research

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In this context, high-sensitivity (hs) assays for CRP have been developed that provide both diagnostic and prognostic information. 14,15,17 Studies have shown that hs assays detect CRP concentrations with the required precision even in patients Rationale: Inflammation in the setting of acute myocardial infarction (MI) has been linked to risk stratification; however, the release kinetics of inflammatory biomarkers in patients with acute MI has been difficult to establish.Objective: The aim of this study was to determine the kinetics of changes in the levels of several biomarkers specifically linked to inflammation after transcoronary ablation of septal hypertrophy, a procedure that mimics acute MI. Methods and Results:We analyzed release kinetics of C-reactive protein, high-sensitivity C-reactive protein,

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Section: Discussionmentioning

confidence: 75%

Section: Resultsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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

Liebetrau

Hoffmann

Dörr

et al. 2015

Circulation Research

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“…After stroke and myocardial infarction, circulating miRNA increase as early as 15 min after acute tissue injury [10] and can exhibit relatively rapid changes over time [11]. Thus, miRNA have the potential of being early markers after neonatal HI and their dynamic nature warrant characterization of their temporal profile.…”

Section: Introductionmentioning

confidence: 99%

Temporal Profile of Circulating microRNAs after Global Hypoxia-Ischemia in Newborn Piglets

Garberg¹,

Huun²,

Baumbusch³

et al. 2016

Neonatology

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Background: There is a lack of reliable biomarkers that can identify and grade acute hypoxic-ischemic encephalopathy in newborns. MicroRNAs (miRNA) are short, non-coding strands of RNA that are released into the circulation in response to tissue stress and injury. Some miRNAs are highly tissue specific and thus may potentially be non-invasive biomarkers of neonatal hypoxic-ischemic brain injury. Objective: The aim of this study was to characterize the temporal expression of selected circulating miRNAs in a clinically relevant piglet model of neonatal hypoxia-ischemia (HI). Methods: A total of 13 anesthetized newborn piglets were randomized to either a control group (n = 5) or transient global HI group (n = 8). HI was achieved by ventilation with 8% oxygen until the point of severe acidosis (arterial base excess ≤-20 mmol/l) and/or hypotension (mean arterial blood pressure ≤20 mm Hg) was reached. Plasma was sampled at baseline, at the end of HI and 0.5, 3.5 and 9.5 h after HI. MiRNA expression was measured by qRT-PCR. Results: Compared to baseline, miR-374a increased during HI (p = 0.01), remained elevated at 0.5 h after HI (p = 0.02) and was downregulated at 9.5 h after HI (p = 0.02). MiR-210 increased during HI (p = 0.02) and rapidly normalized by 0.5 h after HI. MiR-124 and miR-125b did not exhibit significant alterations. Correlations were observed between miR-374a, arterial pH, base excess and lactate levels, and between miR-210 and pO₂ (p < 0.05). Conclusions: Our data suggest that miR-374a and miR-210 are important regulators in neonatal HI and might have a place as biomarkers in this setting.

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“…[4][5][6][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][5][6][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?…”

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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Release Kinetics of Circulating Muscle-Enriched MicroRNAs in Patients Undergoing Transcoronary Ablation of Septal Hypertrophy

Cited by 83 publications

References 34 publications

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

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

Temporal Profile of Circulating microRNAs after Global Hypoxia-Ischemia in Newborn Piglets

Myocardial Infarction and Inflammation

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