Troponine als Biomarker bei Myokardschaden und Myokardinfarkt

Blankenberg, Stefan; Wittlinger, Thomas; Nowak, Bernd; Rupprecht, H J

doi:10.1007/s00059-019-4783-x

Cited by 6 publications

(3 citation statements)

References 7 publications

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“…For example, cardiac-specific troponins are peptides released from cardiac muscle cells activated during muscle contraction, while BNP is a hormone secreted by cardiomyocytes in response to stretching of the ventricles due to increased intravascular volume. Increased troponin levels are detected in cases with cardiomyocyte damage like myocardial ischemia and necrosis in acute coronary syndromes [ 2 , 46 ], and NT-proBNP is considered a classical biomarker of heart failure [ 3 , 14 ]. Several large-scale studies have demonstrated associations between elevations of hs-cTnT and NT-proBNP with increased risk of CV and all-cause deaths in the general population [ 47 – 49 ].…”

Section: Discussionmentioning

confidence: 99%

“…Several pathological mechanisms common in CKD increase the risk of developing CVD. Cardiac biomarkers are commonly used to assess various cardiovascular events, where cardiac-specific troponins (cTn) are characterized as markers of myocardial injury [ 2 ] and N-terminal pro-B-type natriuretic peptide (NT-proBNP) a marker of increased volume and cardiac load [ 3 ].…”

Section: Introductionmentioning

confidence: 99%

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Cardiac biomarkers in pediatric CKD—a prospective follow-up study

et al. 2022

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Background The N-terminal pro-B-type natriuretic peptide (NT-proBNP) and high-sensitive cardiac-specific troponin T (hs-cTnT) are associated with abnormal cardiac structure and function and an increased risk of cardiovascular death in chronic kidney disease (CKD) patients. There is limited knowledge about these cardiac markers in pediatric CKD patients. Methods Longitudinal levels of NT-proBNP and hs-cTnT were analyzed in 48 pediatric patients, 22 with CKD (GFR range 8.8–68 mL/min/1.73 m2) and 26 transplanted patients (CKD-T; GFR range 30–99 mL/min/1.73 m2). Follow-up was scheduled after 1 and 3 years. Longitudinal patterns and associations to kidney function, cardiovascular risk markers, and echocardiographic parameters were assessed. Results High NT-proBNP was present in 27% of CKD and 11% of CKD-T patients. Similarly 32% of CKD and 8% of CKD-T patients had elevated hs-cTnT levels. In longitudinal multivariate analyses, high log NT-proBNP was associated with low GFR (β = − 0.01, p = 0.01) and elevated left ventricular mass index (LVMI; β = 0.02, p = 0.05). The strong association to LVMI remained when using GFR-adjusted NT-proBNP in similar analysis. Patients with left ventricular hypertrophy (LVH) also had higher NT-proBNP (235 [146–301] ng/L) than patients without LVH (86 [11–477] ng/L), p = 0.02. High hs-cTnT over-time was also associated with low GFR (β = − 0.007, p = 0.01) and a low cc-TDI e´/a´, indicating a worse LV diastolic function (β = − 0.09, p = 0.05). This association did not persist for GFR-adjusted hs-cTnT. Conclusions NT-proBNP and hs-cTnT are elevated in pediatric CKD and CKD-T patients. GFR-adjusted NT-proBNP was associated with longitudinal levels of elevated LVMI suggesting this might be a marker for early subclinical myocardial damage. Graphical abstract A higher resolution version of the Graphical abstract is available as Supplementary information.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Cardiac biomarkers in pediatric CKD—a prospective follow-up study

et al. 2022

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“…Eine Troponinerhöhung oberhalb der 99. Perzentile einer gesunden Referenzbevölkerung ist ein etablierter Marker für myokardialen Zelluntergang und damit für die Diagnose des Myokardinfarkts[4]. Je ausgeprägter die Dynamik, desto höher ist die Wahrscheinlichkeit für einen akuten Myokardinfarkt.…”

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Biochemische Marker der Myokardschädigung bei ischämischer versus nicht ischämischer Ätiologie

Magnussen¹,

Schnabel²

2019

Aktuel Kardiol

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ZusammenfassungBiomarker sind objektiv gemessene Indikatoren physiologischer oder pathologischer biologischer Prozesse, die möglichst sensitiv, spezifisch, reproduzierbar und kosteneffektiv bestimmt werden sollten. Sie werden als Antwort auf akute myokardiale Ischämie, chronischen myokardialen Stress, Inflammation oder strukturelle Umbauprozesse freigesetzt. Die wichtigsten Biomarker in der klinischen Routine sind (hochsensitive) Troponine (akute Myokardischämie) und natriuretische Peptide (Druck-/Volumenbelastung). Strukturelle Marker (Fibrose/Remodeling) werden noch nicht routinemäßig eingesetzt.

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