Cardiac markers ZDEŇKA ČERMÁKOVÁ KLM LF MU BRNO OKB FN BRNO Cardiac markers •ISCHEMIA, NECROSIS •VOLUME OVERLOAD •MECHANICAL DAMAGE •TOXIC EFFECTS • •Markers of acute coronary syndrom •Markers of chronic heart failure •Regulation: GDF-15,galektin3 • •Diagnosis Treatment Prognosis • • Výsledek obrázku pro anatomie srdce 2 Tropomyosin complex troponin1 tn_myo_komplex ØStrukture of TnT a TnI ØCardiac-specific isoforms ØImunochemical assay Ø ØTnC - no cardiac specificity 3 Possible causes of increased hypersensitive troponins 4 From: Fourth universal definition of myocardial infarction (2018) Eur Heart J. Published online August 25, 2018. doi:10.1093/eurheartj/ehy462 Eur Heart J | This article has been co-published in European Heart Journal, Journal of the American College of Cardiology, Circulation, and Nature Reviews Cardiology. All rights reserved. © 2018 European Society of Cardiology, American College of Cardiology, American Heart Association, and World Heart Foundation. The articles are identical except for minor stylistic and spelling differences in keeping with each journal’s style. Any citation can be used when citing this article.This article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://academic.oup.com/journals/pages/open_access/funder_policies/chorus/standard_publication_mo del) Cover 5 Figure 7 Illustration of early cardiac troponin kinetics in patients after acute myocardial injury including acute myocardial infarction. The timing of biomarker release into the circulation is dependent on blood flow and how soon after the onset of symptoms samples are obtained. Thus, the ability to consider small changes as diagnostic can be problematic. In addition, many comorbidities increase cTn values and, in particular, hs-cTn values, so that elevations can be present at baseline even in those with myocardial infarction who present early after the onset of symptoms. Changes in cTn values or deltas can be used to define acute compared with chronic events, and the ability to detect these is indicated in the figure. Increased cTn values can often be detected for days after an acute event. cTn = cardiac troponin; URL = upper reference limit. Troponin in the blood-mixture of intact molecules and grafts Time-Dependent Degradation Pattern of Cardiac Troponin T Following Myocardial Infarction Eline P.M. Cardinaels, Alma M.A. Mingels, Tom van Rooij, Paul O. Collinson, Frits W. Prinzen, Marja P. van Dieijen-Visser DOI: 10.1373/clinchem.2012.200543 Published June 2013 6 Diagnosis of AMI Výsledek obrázku pro EKG infarkt History ECG Laboratory cTn • •cTn >cut off •dynamics 7 Advantages of TnI, TnT in MI diagnostics §High specifity §Myocardial isoforms § §High sensitivity §Very small MI lesions § §Dynamics of Tn concentration changes §Multiple increase Tn level after MI § §Increased Tn level continues 1-2 weeks §Delayed dignostics of MI 8 Clinical application of hs troponin T •First specimen at the time of first contact •Repeat specimen (to review the change) in 3 hours (1-2 hours) • •99.percentil application • •Application of the "delta" principle •Absolute - 10ng / l •Relative 20% (above 50ng / l) • 50% 99(below 50ng/l) • Prognosis 9 Time course of cardiac markers 1000 100 10 1 0 Hours from the onset of stenocardia The upper limit of the reference values 10 Casuistry 1 •Men, 64 years old, brought by emergency medical service at 12:30 •Strong retrosternal pain, spreading to the neck, sweating • (at 5 o´clock in the morning) •Duration about 20 minutes, relief after vomiting • •In last 2 weeks occasional feeling of pressure on the chest during exercise (duration of about 10 minutes) • • 11 PCI: prox. RIA +DES stent • •EKG: Q V1-5,elevation ST 0,5mm, negative T V1-V5 •Dg: subacute transmural MI 12 Casuistry 2 •Men, 44 years old •Retrosternal pains for about one year, spreading to the neck, troubles in the rest and also during excercise • •Dg: IHD dg.VI/2018, sy AP, SKG - PCI ACS+DES,prox. RIA 30%,RC 40% • •About 3 weeks after revascularization he was completely trouble-free, then it started to return • • 13 EKG : SR, TF 67/min re SKG VIII/2018: complete revascularization Ischemic heart disease without signs of ACS 14 Casuistry 3 • •Women 83 years old •Retrosternal pain, spreading do the neck and head • Now she feels uncomfortable, weakness, doesnt feel sure when walking 15 NSTEMI Therapy: dual antiagregation (ASA+clopidogrel) EKG: SR, TF 79/min ,ST depression to 2 mm V3-V5 16 Casuistry 5 •Men 77 years old •Retrosternal pressure pain, duration about 30 minutes •Last few days same difficulties without dependence on exercise • •EMS: supraventricular tachyarhrythmia 170/min, hypertensin 17 18 NSTEMI, supraventricular tachyarhythmia Natriuretic peptides Ø ØProtein (peptide) hormones ØSynthesis: myocard ØEndothelium, kidney ØProtect KV system against volume and pressure overload ØDiuretic, natriuretic and hypotensive effects 19 Mechanism of NP function ØKidney: ØInhibit Na reabsorption = natriuresis, diuresis د blood volume د renin secretion د aldosteron Ø ØBlood vessels ØVasodilatation ØCNS د sympathetic bnp_fce 21 Synthesis of BNP: pro BNP ØProBNP - cleaved into 2 fragments: BNP, NT ProBNP ØBNP: biological active polypeptide (32 AA) ØNT-proBNP: biological inactive (76 amino acid, N-terminal) ØCo-secreted with BNP ØHalf-life: ØBNP: 18 min ØNT-ProBNP: 2 h. bnp_pre_pro 22 Clinical evaluation of NT-proBNP •Dg. of heart failure •Diff. dg. of dyspnoe • •Cut-off levels for excluding heart failure (rule-out) •Chronic heart failure NT-proBNP < 125 pg/ml •Acute heart failure NT-proBNP < 300 pg/ml 23 Acute heart failure – age dependance (NTpro BNP) • •< 50 years cut-off 450 pg/ml •50-75 years cut-off 900 pg/ml •> 75 years cut-off 1800 pg/ml • Illustration of a person with heart failure 24 25 Casuistry 5 •Woman,77 years old • •Previously amputation of the lower limb for ischemic disease, atrial fibrillation • •Symptoms: dyspnoe, febrilia, sweat 26 Atrial fibrillation with rapid ventricular response, heart failure 27 Kasuistika 6 •Woman, 77 years old •Repeatedly hospitalized for chronic heart failure •Syndrom of angina pectoris, PCI -3x DES •NSTEMI (2008,2012) •Since the evening day before, shortness of breath, in the morning retrosternal pain (5:30). During the last week worsening of swelling of lower limbs. 28 Obj: breathlessness, BP 170/60 SF 65 irreg ECG atrial fibrillation 70/min , RTG: S+P – fluidothorax bilat. Závěr: acute heart failure 29