Inflammation in heart failure: How to evaluate and intervene? · TRUE-AHF: TRial of Ularitide’s...

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Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών Ιατρική Σχολή Ά Καρδιολογική Κλινική Διευθυντής: Καθηγητής Δημήτρης Τούσουλης Role of imaging in Heart Failure Inflammation in heart failure: How to evaluate and intervene?

Transcript of Inflammation in heart failure: How to evaluate and intervene? · TRUE-AHF: TRial of Ularitide’s...

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Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών Ιατρική Σχολή

Ά Καρδιολογική Κλινική

Διευθυντής: Καθηγητής Δημήτρης Τούσουλης

Role of imaging in Heart Failure

Inflammation in heart failure: How to evaluate andintervene?

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Conflicts of Interest Statement

There are no conflicts of interest for this presentation

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Inflammation represents a physiologic response intended to provide protection and promote healing

in the setting of injury.

Φλεγμονή

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Φλεγμονή και ΚΑ

Αρχικά Δεδομένα

TNF-a

Levine B,…..Elevated circulating levels of tumor necrosis factor

in severe chronic heart failure. N Engl J Med. 1990; 323: 236-241

Circulating levels of TNF are increased in

patients with chronic heart failure and this elevation is associated with the marked

activation of the renin angiotensin system seen in

patients with end-stage cardiac disease

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The cytokine hypothesis of HF

Hemodynamic model and Neuro-humoral activation

Abnormal Ca+ handling

Cardiorenal HypothesisExtracellular Matrix Remodelling

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The cytokine hypothesis of HF

Many aspects of heart failure can be explained by the known biological effects of stress activated proinflammatory cytokines

E. Oikonomou, D. Tousoulis….Hellenic J Cardiol 2011; 52: 30-40

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The cytokine hypothesis of HF

CRP in HF prognosis

Circulation. 2005;112:1428-1434

Kaplan-Meier curves for mortality and first morbid event by quartiles of baseline plasma CRP.

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The cytokine hypothesis of HF

ICAM1 & VCAM1 in HF status

Tousoulis et al. Am Heart J 2001;141:277-80.

ICMCNTL

ICMCNTL

IIIII

IV

II III

IV

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Τ1 W imagesΠερικαρδιακό υγρό: Μαύρο

Τ1 W imagesΛίπος: Άσπρο

Τ1 W imagesΜυοκάρδιο: Γκρι

Tissue characterization

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MapsTissue characterization

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MI prognosis

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T2 imaging in ACSEdema Imaging

Int J Cardiol. 2018 May 15;259:43-46.

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Myocardial infarction with non-obstructive coronary arteries

A sizeable proportion of MIs, ranging between 1–

14%, occur in the absence of obstructive (>50%

stenosis) CAD.

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Tako-tsubo

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Myocarditis

Myocarditis: Inflammatory disease of the myocardium diagnosed by established histological*, immunological and immunohistochemicalcriteria**.

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Myocarditis

Treatment

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Myocarditis

Cardiovascular magnetic resonance imaging provides non-invasive tissue characterization of the myocardium and can support the diagnosis of myocarditis

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Heart Transplantation

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Pericarditis

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Cine

T2 STIR

T1

LGd

Pericardial diseasesPericarditis

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Systemic diseases

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FDG-PET CT

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ARVC

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Conclusions

➢The relationship between heart failure and inflammation is well documented

➢The underlying mechanisms of inflammation is less well established

➢Modern imaging modalities can help in the identification of inflammation in myocardium and in diagnosis (MI, Myocarditis, Tako-tsubo, Systemic diseases etc.)

➢ Specific anti-inflammatory treatments are not established in patients with HF

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Diagnosis and Guide treatment

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Diagnosis and Guide treatment

hsCRP

McMurray et al. Circulation 2009;120:2188–2196.

CRP>2mg/L CRP<2mg/L

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HF treatment

Specific Anti-inflammatory treatments

❑ Recombinant human soluble TNF Receptor (etanercept)

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HF treatment

Specific Anti-inflammatory treatments

❑Monoclonal antibody to TNFα (infliximab)

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Heart failure accounts for up to 4% of hospital admissions as a primary diagnosis

Africa (1 country)

0.7%

Middle East (1 country)

1.3%

Asia (3 countries)

0.8–1.2%

Australasia (2 countries)

1.4–1.5%

Latin America (3 countries)

1.6–2.1%

North America (2 countries)

1.8–3.0%

Europe (22 countries)

0.3–3.7%

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Definition of heart failure

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Διαστολική Δυσλειτουργία

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Ορολογία Καρδιακής Ανεπάρκεια

1) Κατάταξη ΚΑ σύμφωνα με τη Συστολική λειτουργία της Αριστεράς Κοιλίας και το ΚΕ

2) Κατάταξη ΚΑ σύμφωνα με τη ΒαρύτηταΝΥΗΑStages A, B, C, DKillip Class«Προχωρημένη» (severe symptoms, recurrent decompensation and severe cardiac dysfunction)

3) Ανάλογα με το χρόνο/τρόπο εμφάνισης

Οξεία

Χρόνια

Διάγνωση

Και

Αντιμετώπιση

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Διάγνωση/Αντιμετώπιση Καρδιακής Ανεπάρκεια

1) Χρόνια Καρδιακή Ανεπάρκεια

2) Οξεία Καρδιακή Ανεπάρκεια

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Διαγνωστικός Αλγόριθμος χρόνιας ΚΑ

Εκτίμηση Πιθανότητας Ύπαρξης ΚΑ

Απουσία ενδείξεων

ΚΑ Απίθανη

≥ 1 Κριτηρίου

(-)

Αποκλεισμός

ΚΑ Απίθανη

(+)

HF(+) HF(-)

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Χρόνια Καρδιακή Ανεπάρκεια

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1)

2)

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Καρδιακή Ανεπάρκεια με Διατηρημένο κλάσμα ΕξώθησηςΘεραπεία

It is recommended to screen patients with HFpEF or HFmrEF for both cardiovascular and noncardiovascularcomorbidities, which, if present, should be treated provided safe and effective interventions exist to improve symptoms, well-being and/or prognosis.

Diuretics are recommended in congested patients with HFpEF or HFmrEF in order to alleviate symptoms and signs.

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Διάγνωση/Αντιμετώπιση Καρδιακής Ανεπάρκεια

1) Χρόνια Καρδιακή Ανεπάρκεια

2) Οξεία Καρδιακή Ανεπάρκεια

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Οξεία ΚΑ

➢ Worsening (“decompensation”) of chronic heart failure – commonly in a sub-acute or acute-on-

chronic fashion. Often not acute!

➢ “New onset” (denovo) heart failure again, may not be truly “acute”. Better to describe these two gr

oups, if admitted, as “hospitalised heart failure”?

➢ Rapid onset heart failure complicating another event such as acute myocardial infarction or an

arrhythmia.

➢ With treatment, symptoms and signs may resolve partially or completely (patient is

“compensated”).

➢ Many or all of these terms may be applied to the same patient at different times, depending on what

stage of their illness they are in

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Οξεία ΚΑΚλινική Εμφάνιση

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Κλινικοί Φαινότυποι Εμφάνισης Οξείας ΚΑ

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Οξεία ΚΑΝατριουρητικά Πεπτίδια

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Οξεία ΚΑΝατριουρητικά Πεπτίδια

Μία σειρά Από Καταστάσεις Μπορούν να Επηρεάσουν τα επίπεδα των Νατριουρητικών ΠεπτιδίωνΗλικίαHFpEF vs HFrEFΝεφρική ΛειτουργίαΠαχυσαρκίαΚολπική Μαρμαρυγή

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Οξεία ΚΑΝατριουρητικά Πεπτίδια

Διαχωριστικά Όρια

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Οξεία ΚΑΝατριουρητικά Πεπτίδια

ΝΤ-proBNP

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Acute stabilizationMechanical circulatory support: Impella / ECMO / LVAD

Ventilatory Support

Pharmacological treatment: vasopressors,vasodilators, diuretics

Renal replacement: Dialysis, Ultrafiltration

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Νεότερα Δεδομένα στην Αντιμετώπιση της Οξείας ΚΑ???

➢Vasopressin antagonists: TACTICS-HF, SECRET of HF

➢Ularitide: TRUE-AHF

➢ Serelaxin: Relax-AHF-II

➢Omecamtiv mecarbil (OM)

➢ Nitroxyl (HNO)

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Targeting acute congestion with Tolvaptan in congestive heart failure (TACTICS-HF)

Vasopressin Antagonist

257 pts within 24h of AHF admission

No LVEF entry criterion

Randomized to:

30mg of tolvaptan or placebo given at 0, 24, and 48 h in addition to fixed-dose furosemide

regimen as background therapy

Primary endpoint: Proportion of responders at 24 h

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Short-Term Effects of Tolvaptan in Patients With Acute Heart Failure and Volume Overload (SECRET of CHF)

250 pts within 36h of AHF admission, active dyspnea, and either:- eGFR <60 ml/min/1.73m2;- hyponatremia;- diuretic resistance

Randomized to tolvaptan 30 mg/day or placebo

Primary endpoint: 7-point change in selfassessed dyspnea at 8 and 16 h

Konstam MA, et al. J Am Coll Cardiol 2017;69:1409-19.

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TRUE-AHF: TRial of Ularitide’s Efficacy and safetyin patients with AHFNatriuretic Peptide

Inclusion criteria: 2157 patientsHospitalization for AHF/ Worsening dyspnea at rest > 1 week- evidence of heart failure on chest radiography- NTproBNP >2000 pg/ml- Dyspnea at rest for at least 2 hours after ≥40 mg of furosemide i.v.

Primary endpoint: Clinical composite at 48hrs; all cause mortality;

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Serelaxin in AHF

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Omecamtiv Mecarbil (OM) A novel Selective Cardiac Myosin Activator

Acute Treatment with Omecamtiv Mecarbil to Increases Contractility in Acute Heart Failure

Teerlink JR, et al. J Am Coll Cardiol 2016; 67:1444–55

Admitted for AHF with history of heart failure, LVEF ≤ 40% ~ 600 patients

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Nitroxyl DonorsHNO

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ΣυμπεράσματαΕμφάνιση Οξείας Καρδιακής Ανεπάρκειας

➢ Relieve symptoms (dyspnea) and edema as rapidly as possible.

➢ Get the patient off intravenous treatment, mobilized and out of hospital as quickly as possible.

➢ Detect and treat any precipitant of worsening and co-morbidities.

➢ Optimise long-term treatments (ACE-I/ARNI, BB, MRA) before discharge.

➢ Decompensating chronic heart failure: 80% of all admissions

➢ Acute de novo heart failure (diagnosed for the first time): 15%

➢ Advanced / end-stage / refractory HF: 5%

Στόχοι Θεραπείας

➢ Most patients rapidly improve symptoms with usual treatment (mainly diuretics, RASS, Sac/VAL, BB) and go home.

➢ When added to usual treatment, short-term administration of drugs that improve haemodynamics do not have a beneficial effect

➢ Some inotropic agents may be harmful and hypotension induced by vasodilators may also be dangerous.

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Ευχαριστώ

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Natriuretic peptides in heart failure patients

Session: How to interpret laboratory tests

in acute heart failure

Presenter: M Richards (Christchurch,NZ)

http://congress365.escardio.org/Search-

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Καρδιακή ΑνεπάρκειαΤο Εύρος του

Προβλήματος

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Επιπολασμός-Νοσηρότητα-Θνητότητα-Κόστος Νοσηλείας

Κόστος Διαχείρισης/Αντιμετώπισης

Circ Heart Fail. 2013;6:606-619

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Επιπολασμός-Νοσηρότητα-Θνητότητα-Κόστος ΝοσηλείαςΈκταση του Προβλήματος

➢ Διάγνωση / Παρακολούθηση▪ Κλινική Επάρκεια

▪ Απεικόνιση

▪ Διαγνωστικές Εξετάσεις-Βιοδείκτες

➢ Αρρυθμίες / Επανασυγχρονισμός

➢ Προχωρημένη Καρδιακή Ανεπάρκεια▪Δεξιός Καθετηριασμός

▪Ενδομυοκαρδιακή Βιοψία

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Συμπεράσματα

➢ Η ΚΑ αποτελεί ένα πρόβλημα με αυξανόμενο επιπολασμό, νοσηρότητα, θνητότητα και κόστος θεραπείας

➢ Υπάρχει ανάγκη εξειδικευμένων καρδιολόγων που να μπορούν να αντιμετωπίσουν συνολικά τα προβλήματα των ασθενών με ΚΑ

o (Κλινικά, αρρυθμιολογικά, επεμβατικά)

➢ Τα τελευταία μόλις χρόνια έχει γίνει κατανοητό ο ρόλος ειδικών που θα μπορούν να αντιμετωπίσουν συνολικά τον ασθενή με ΚΑ

➢ Προς αυτό το σκοπό αναπτύσσονται εκπαιδευτικά προγράμματα και προγράμματα πιστοποίησης που βρίσκονται όμως σε αρχικό στάδιο

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Διαστολική Δυσλειτουργία

Διαστολική Δυσλειτουργία

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BNP Versus NT-proBNP

McCullough PA, Rev Cardiovasc Med. 2003.

Characteristic BNP NT-proBNP

Components BNP molecule NT fragment (1–76)

Molecular Weight 4 kilodaltons 8.5 kilodaltons

Genesis Cleavage from proBNP Cleavage from proBNP

Half-life 20 minutes 120 minutes

Clearance Mechanism Neutral endopeptidase

Clearance receptors

Renal clearance

Increases with Normal

Aging

+ ++++

Correlation With Estimated

Glomerular Filtration Rate

–0.20 –0.60

Approved cutoff(s) for CHF

Diagnosis

100 pg/mL Age < 75: 125 pg/mL

Age > 75: 450 pg/mL

Entry on U.S. Market November, 2000 December, 2002