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IL TUO CUORE SI STA SCOMPENSANDO?. Mancanza di fiato, gambe gonfie, facile affaticabilita’ senza ragione?. Chiedi consiglio al tuo medico. Consulta il sito www.heartfailurematters.org. GIORNATE EUROPEE PER LO SCOMPENSO CARDIACO. 9-11 MAGGIO 2014. 9-11 MAGGIO 2014.

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slide1

IL TUO CUORE SI STA SCOMPENSANDO?

Mancanza di fiato,

gambe gonfie, facile affaticabilita’ senza ragione?

Chiedi consiglio al tuo medico

Consulta il sito www.heartfailurematters.org

GIORNATE EUROPEE PER LO SCOMPENSO CARDIACO

9-11 MAGGIO 2014

9-11 MAGGIO 2014

slide2

Seminario di Aggiornamento ANMCO

CARDIOPATIA ISCHEMICA STABILE E SCOMPENSO CARDIACO:

DUE PRIORITA’ TRA OSPEDALE E TERRITORIO

GESTIONE CLINICA E CURA DELLA FASE ACUTA

slide5

Temporal Trends in Hospitalizations in Italy

200.000

DRG 127

200.609

150.000

100.000

127.043

50000

1996

1998

1999

2000

2001

2002

2003 2007

1997

Fonte Ministero della Salute

slide6

IN-HF Outcome

Acute HF: all-cause mortality

27.7%

24.0%

19.2%

(n. 1855)

(n. 1058)

(n. 797)

Oliva F, Mortara A, Cacciatore G et al EJHF 2012

slide7

Direct HF-relatedhealth care costs

Distribution per type of expenditure

50

Milion €

40

Hospital admissions for HF

30

Drug therapy

Cardiological outpatient care

20

10

0

0-19

20-49

50-54

55-59

60-64

65-69

70-74

75-79

80-84

85-89

90+

Age distribution, decades

De Maria R et al. G Ital Cardiol 2006

acute heart failure syndromes ahfs
Acute Heart Failure Syndromes (AHFS)

Since 2005, 4largeinternationalphase III trials ( VERITAS, SURVIVE, EVEREST, PROTECT) havefailed.

Evenfordrugsapprovedfor AHFS treatment ( milrinone and nesiretide in US and levosimendan in Europe) therehavebeenconcernsaboutsafety.

The pharmacologicarmamentariumfor AHFS islargelyunchangedfrom 1970.

slide12
Acutely Decompensated

CHF

Acute CHF

Pulmonary

edema

RV failure

Acute HFClinical Classification

It’ s not a singular entity with a unique cause

but a spectrum of complex multisystem pathologies

historically bound by a limited number of shared clinical charactheristics

Cardiogenic

shock

Hypertensive

AHF

ACS and HF

ESC Guidelines 2008

slide13

Durante un ricovero per SC acuto, valutazione clinico-strumentale e decisioni terapeutiche iniziano nel DE e procedono affiancate dinamicamente fino ( e oltre) alla fase di dimissione

European Heart Journal 2012 doi:10.1093/eurheartj/ehs104

slide15

Initial assessment of patient with suspected acute heart failure

Authors/Task Force Members et al. Eur Heart J 2012;33:1787-1847

slide17

IN-HF Outcome

Acute HF:

All-cause mortality by SBP (Quartiles)

35.9%

24.0%

20.5%

20.3%

16.9%

SBP (mmHg)

(n. 1855)

(n. 524)

(n. 469)

(n. 420)

(n. 425)

SBP is available for 1838 pts

Oliva F, Mortara A, Cacciatore G et al EJHF 2012

slide18

1. Terapia acuta in base al profilo emodinamico

Felker et al Circ Heart Fail 2010;3;314-325

unloading therapy with snp in pts 70 years
Unloading Therapy with SNP in Pts > 70 years

Cioffi G. et al Am J Cardiol 2003

pregnancy acute heart failure
Pregnancy & Acute Heart Failure
  • Relaxin has been shown to mediate these adaptations, as well as to have anti-ischemic, anti-inflammatory, anti-fibrotic effects.
  • Relaxin, and its signaling systems, are present in both men and women and is elevated up to pharmacologic levels during 9 months of pregnancy
  • Serelaxin (recombinant human relaxin-2) may produce these beneficial effects in patients with acute heart failure

Baylis, C. Am J Kid Dis 1999; Schrier, RW, et al. Am J Kid Dis 1987; Jeyebalan, A, et al. Adv Exp Med Biol 2007;Teichman SL et al. Curr Heart Fail Rep 2010;7:75–82.

Helal I, et al. Nature Reviews 2012;293-300.

inclusion and exclusion criteria
Key Inclusion Criteria

Hospitalized for AHF

Dyspnea at rest or with minimal exertion

Pulmonary congestion on chest radiograph

BNP ≥350 pg/mL or NT-pro-BNP ≥1400 pg/mL

Received ≥40 mg IV furosemide (or equivalent) at any time between admission to emergency services (either ambulance or hospital, including the ED) and the start of screening for the study

Systolic blood pressure >125 mmHg

Impaired renal function on admission (sMDRD eGFR 30-75 mL/min/1·73 m2)

Randomized within 16 hours from presentation

Age ≥18 years of age

Body weight <160 kg

Key Exclusion Criteria

Current or planned treatment with any IV therapies [i.e. other vasodilators, (nesiritide), positive inotropic agents and vasopressors] or mechanical circulatory, renal, or ventilatory support, with the exception of IV furosemide (or equivalent), or of IV nitrates if patient has screening SBP >150 mmHg

AHF and/or dyspnea from arrhythmias or non-cardiac causes, such as lung disease, anemia, or severe obesity

Infection or sepsis requiring IV antibiotics

Pregnant or breast-feeding

Stroke within 60d; ACS within 45d; major surgery within 30d

Presence of acute myocarditis, significant valvular heart disease, hypertrophic/ restrictive/ constrictive cardiomyopathy

Inclusion and Exclusion Criteria
1 endpoint dyspnea relief vas auc
1°Endpoint: Dyspnea Relief(VAS AUC)

Placebo

19.4% increase in AUC with serelaxin

from baseline through day 5 (Mean difference of 448 mm-hr)

Serelaxin

Change from baseline (mm)

AUC with placebo, 2308 ± 3082

AUC with serelaxin, 2756 ± 2588

p=0.0075

12 hrs

6

Days

Teerlink … Metra. Lancet 2013; 381: 29-39

2 endpoint cv death or hf rf re hospitalization through day 60
2°Endpoint: CV Death or HF/RF Re-hospitalization through Day 60

Composite event components (%)

K-M estimate for time to first CV Death or HF/RF re-hosp (%)

CV death: (% subjects)

HF/RF re-hospitalization

(% subjects)

Serelaxin

14

HR 1.02 ( 0.74, 1.41)

p=0.89

HR=1.2

p=0.32

HR=0.7

p=0.23

12

10

Placebo

8

6

4

2

60

n=27

n=19

n=50

n=60

0

Days

0

14

30

45

580

559

539

522

501

581

563

531

514

498

p value by log rank test

HR estimate by Cox model

cv death through day 180
CV Death through Day 180

K-M estimate for CV Death ITT (%)

14

Number ofEvents, n (KM%)*

12

HR 0.63 (0.41, 0.96); p=0.028

Placebo (N=580)

10

55 (9.6%)

NNT = 29

8

35 (6.1%)

6

Serelaxin (N=581)

4

2

0

Days

0

14

30

60

90

120

150

180

580 567 559 547 535 523 514 444 Placebo

581 573 563 555 546 542 536 463 Serelaxin

Teerlink … Metra. Lancet 2013; 381: 29-39

all cause death through day 180
All-cause Death through Day 180

K-M estimate for All-cause Death ITT (%)

14

Number ofEvents, n (KM%)

12

65 (11.3%)

Placebo (N=580)

HR 0.63 (CI 0.43, 0.93); p=0.020

10

NNT = 25

8

42 (7.3%)

6

Serelaxin (N=581)

4

2

0

Days

0

14

30

60

90

120

150

180

580 567 559 547 535 523 514 444 Placebo

581 573 563 555 546 542 536 463 Serelaxin

Teerlink … Metra. Lancet 2013; 381: 29-39

prognostic value of a 30 nt probnp decrease from baseline at day 2 and effects of serelaxin
Prognostic value of a >30% NT-proBNP decrease from baseline at Day 2 and effects of serelaxin

p = 0.0002

Metra M … Teerlink JR J Am Coll Cardiol. 2013 Jan 15;61(2):196-206.

prognostic value of a 20 hs ctnt increase from baseline and effects of serelaxin
Prognostic value of a >20% hs-cTnT increase from baseline and effects of serelaxin

p = 0.0001

Metra M … Teerlink JR J Am Coll Cardiol. 2013 Jan 15;61(2):196-206.

slide31

2.Terapia acuta in base al profilo emodinamico

Felker et al. Circ Heart Fail 2010;3;314-325

slide33

Algorithm for management of acute pulmonary oedema/congestion

European Heart Journal 2012 doi:10.1093/eurheartj/ehs104

mean change in creatinine level
Mean Change in Creatinine Level

Composite End Point of Death, Rehospitalization, or ED visit.

Felker et al. N Engl J Med 2011;364:797-805

slide35

IN-HF Outcome

Acute HF: acute treatment(n. 1868 pts)

Oliva F, Mortara A, Cacciatore G et al EJHF 2012

slide36

Renal Vasodilatory Action of Dopamine

Elkayam, U. et al. Circulation 2008;117:200-205

Low-Dose Dopamine on Survival in 324 Pts WithRenal Dysfunction

European Heart Journal 2012 doi:10.1093/eurheartj/ehs104

ANZICS Clinical Trials Group. Lancet 2000

escape trial
ESCAPE Trial

Weight Loss as a Function

of Maximum

In-hospital Diuretic Dose

Relation between

dose of diuretics and outcomes in HF

Hasselblad V Eur J Heart Failure 2007

resistenza ai diuretici e aumento di mortalit

Effetto dell’Insufficienza renale e dello SC sulla curva di dose-risposta della Furosemide

Resistenza ai diuretici e aumento di mortalità

Neuberg Am Heart J 2002

Ellison DH, Cardiology 2001;96:132-143

cardio renal syndrome
Cardio-Renal Syndrome

Increased Morbidity

And Mortality

Neurohormonal

Activation

Diminished

Blood Flow

Impaired Renal

Function

Decreased Renal

Perfusion

slide41

Congestione venosa e disfunzione renale

L’aumento della pressione veosa centrale riduce il gradiente netto di filtrazione glomerulare da 14 a 4 mmHg

M Jessup, MR Costanzo JACC 2009

W Mullens et al J Am Coll Cardiol 2009;53:589–96

fluid removal by ultrafiltration
Fluid Removal by Ultrafiltration

Ultrafiltration removes fluid from the blood at the same rate that the fluid can be naturally recruited from the tissue.

This “balanced diuresis” maintains sufficient intravascular volume during the restoration of the body’s fluid balance, decreasing the risk of hypotension.

In addition, the electrolyte composition of blood and ultrafiltrate remains in balance, resulting in removal of excess fluid

slide44

Snodi critici:

  • Quando iniziare la RRT in ICU
  • Scelta del tipo di RRT (cont/interm)
  • Accessi vascolari (rischio trombosi/stenosi)
  • Impatto emodinamico (ipotensione)
  • Anticoagulanti

Giornale Italiano di Nefrologia / Anno 21, S-28 2004/pp. S1-S10

slide46

Changes in serum creatinine and weight at 96 hours In 188 CHF patients with WRF

(within 12 weeks before or 10 days after index admission for heart failure)

The primary end point was the change in creatinine levels and in weight In the first 96 hours.

Bart BA et al. (CARESS-HF investigators). NEJM 2012

slide47

P=0.03

Bart BA et al. for the CARESS-HF investigators. NEJM 2012

slide48

Ultrafiltration

  • Major gaps in knowledge remain and include: short- and long-term safety, patient impact, cost-effectiveness of this approach compared with diuretic management
  • In particular issues related to venous access, systemic anticoagulation and bleeding risks, and acute kidney injury need to be explored in larger patient cohorts.

Givertz J Cardiac Fail 2013

slide49

Patients admitted with evidence of significant fluid overload should initially be treated with loop diuretics…..

  • ……When a patient with congestion fails to respond to initial doses of intravenous diuretics, several options may be considered:
    • right heart catheterization
    • a thiazide or spironolactone can be added
    • continuous infusion of the loops diuretic may be considered
  • ….. If all diuretic strategies are unsuccessful, ultrafiltration or another renal replacement strategy may be reasonable.

Jessup M. et al. Circulation 2009

slide50

IN-HF Outcome

Acute HF: diagnostic test performed

during hospitalization (2)

Oliva F, Mortara A, Cacciatore G et al EJHF 2012

slide52

IN-HF Outcome

Acute HF: baseline characteristics

(n. 1868 pts)

Oliva F, Mortara A, Cacciatore G et al EJHF 2012

slide53

IN-HF Outcome

Acute HF: physical examination

(n. 1868 pts)

Oliva F, Mortara A, Cacciatore G et al EJHF 2012

slide54

IN-HF Outcome

Acute HF: acute treatment

(n. 1868 pts)

snp in low co state
SNP in “Low CO state”

Mullens W et al J Am Coll Cardiol 2008

adhere use of inotropic agents resulted in higher mortality
ADHERE: Use of Inotropic Agents Resulted in Higher Mortality

Abraham WT, et al. J Am Coll Cardiol. 2005;46:57-64.

escape use of inotropic agents resulted in higher mortality
ESCAPE: Use of Inotropic Agents Resulted in Higher Mortality

Elkayam U et al. Am Heart J. 2007 Jan;153(1):98-104

slide61

IN-HF Outcome

Acute HF:

Independent predictors of all-cause in-hospital death

(clinical variables and laboratory measures and treatments)

Oliva F, Mortara A, Cacciatore G et al EJHF 2012

survive survival data
SURVIVE: Survival data

1.0

Levosimendan

0.9

Dobutamine

0.8

Probability of Surviving

0.7

Overall 180-d

Mortality: 27%

0.6

0.5

0.4

0

30

60

90

120

150

180

Days Since Start of Study Drug Infusion

A Mebazaa et al. JAMA 2007; 297:1883-1891

all cause mortality in patients with without previous hf

0.5

2

All-Cause Mortality in Patients With / Without Previous HF

SURVIVE:

Favors

Levosimendan

Favors

Dobutamine

Day, Group

5Previous HF

31Previous HF

180Previous HF

HR 0.58 (0.33-1.01)

No previous HF

No Previous HF

No Previous HF

Hazard Ratio (95% CI)

effect of b blockers at baseline on mortality

Effect of b-blockers at baselineon mortality

A Mebazaa et al. HF meeting Hamburg 2007

slide65

Il Trattamento con Inotropi: revisione delle evidenze scientifiche e cliniche per i “vecchi” e “nuovi” farmaci

PAS 90-100 mmHg

Scompenso de novo Eziologia non ischemica

Scompenso cronico riacutizzato

e/o in -bloccante

Eziologia ischemica

Dobutamina

Enoximone

(Levosimendan*)

Levosimendan*

* No bolo

Congestione persistente e/o ipoperfusione,

per svezzare da Dobutamina

Giuseppe Ambrosioa , Andrea Di Lenardab ,Francesco Fedele c, Domenico Gabriellid, Marco Metrae,

Fabrizio Olivaf, Gianpiero Pernad, Michele Sennig , Renata De Mariah

omecamtiv mecarbil a cardiac myosin activator
Omecamtiv MecarbilA Cardiac Myosin Activator

Preclinical

Selective activator of cardiac myosin

Prolongs duration of systole by

Increasing entry rate of myosin into force-producing state

Thus increasing overall number of active cross-bridges

No increase in myocyte calcium

Increases stroke volume

No change in dP/dtmax

No increase in MVO2

Omecamtiv Mecarbil

(MW = 401.43)

Malik FI, et al. Science 2011

slide69

The effectsof the cardiacmyosinactivator, omecamtivmecarbil, on cardiacfunction in systolicheartfailure: a double-blindplacebo-controlled, crossover, dose-rangingphase2 trial

SET

SV

LVESV

LV EDV

John G F Cleland et Al, Lancet 2011; 378: 678-83

atomic ahf ascending dose cohort design
ATOMIC-AHF:Ascending Dose Cohort Design

Objective: Evaluate the effect of 48 hours of IV omecamtiv mecarbil compared with placebo on dyspnea

Study Population: Dyspnea at rest due to HF, hospitalized for a worsening HF and requiring IV therapy for HF, LVEF ≤ 40% and chronic HF

Endpoints: Dyspnea symptom response (Likert), death, worsening HF, PGA, NT-proBNP, safety and tolerability, PK

Cohort 1

Cmax Range

30-250 ng/mL

Cohort 2

Cmax Range

75-500 ng/mL

Cohort 3

Cmax Range

125-700 ng/mL

ClinicalTrials.gov Identifier: NCT01300013

slide74

IN-HF Outcome

Acute HF: All-cause mortality

by clinical profile at entry

38.1%

32.2%

24.0%

23.4%

22.6%

22.6%

15.8%

(n. 1855)

(n. 239)

(n. 42)

(n. 501)

(n. 95)

(n. 164)

(n. 814)

ACS=Acute Coronary Syndrome; CS=Cardiogenic shock; PE=Pulmonary edema

severity of end stage heart failure intermacs levels
Severity of End-Stage Heart FailureINTERMACS Levels

%1-Years

Survival

100%

Advanced NYHA III

7

Exertion limited (Walking wounded)

6

Exertion intolerant (Housebound)

5

Resting symptoms home on oral therapy

50%

25%

10%

4

Stable dependent

3

Sliding fast

2

Crash & Burn

1

Dying/MOF

O%

*Does not account for arrhythmia

short term device quale
Short Term Device: quale?

Performance sovrapponibili

Esperienza del Centro

Matching Paziente/Device

slide80

SupportoMeccanicoPercutaneo

Bridge to Recovery/Decision

Vantaggi

Facilità di impianto per via percutanea

Possono dare un aumento di flusso e garantire la perfusione periferica

Possono dare un adeguato unloading del ventricolo (limitazioni nell’ECMO)

Bassa percentuale di complicanze

Obiettivi

Mantenere vivo il paziente

Stabilizzare il quadro clinico

Migliorare la perfusione periferica

Limitare i danni d’organo

slide81

Supporto Meccanico Percutaneo

Quando è indicato ?

Terapia con inotropiottimizzata

Segni di Ipoperfusione

Segni di Bassa Portata

  • Cianosi/pallore
  • Diaforesi
  • Estremità ipotermiche
  • Polsi periferici iposfigmici
  • Sensorio alterato
  • Oliguria (QU< 0,5 ml/kg/h)
  • PAS < 90 mmHg
  • ( > 30 minuti)
  • IC < 2.2 L/min/m2
  • PWP > 18 mmHg
  • SVO2 < 60%
  • Lattati > 2 mMol/lt
patients potentially eligible for implantation of a ventricular assist device
Patients potentially eligible for implantation of a ventricular assist device

ESC/HFA Guidelines 2012

Heart Failure 2012

19-22 May 2012, Belgrade - Serbia

slide83

ESC Guidelines 1012 - Recommendations for surgical implantation of LVADs in patients with systolic heart failure

  • Keyevidence
  • Ventricular assist devicesmayultimatelybecome a more general alternative to transplantation, ascurrent 2- to 3-year survivalrates in carefullyselectedpatientsreceiving the latestcontinuous flow devices are muchbetterthan with medicaltherapyonly.
  • Patientsreceivingthesedevicesalsohave a post-transplantsurvival rate similar to thosenotrequiringbridging

Heart Failure 2012

19-22 May 2012, Belgrade - Serbia

scompenso cardiaco acuto la realt
Scompenso Cardiaco AcutoLa realtà
  • Epidemiologia: prevalenza, incidenza, ospedalizzazioni, mortalità e costi aumentati negli ultimi 25 anni.
  • Mancanza di target terapeutici adeguati.
  • Mancanza di trattamenti efficaci /utilizzo non corretto dei farmaci disponibili.
  • Linee guida inadeguate ( “non linee guida”/ consensi).
scompenso cardiaco acuto cosa fare sul campo i
Scompenso Cardiaco AcutoCosa fare sul campo (I)
  • Rapido inquadramento all’ingresso
    • Profili a rischio ( markers prognostici negativi)
    • Interazione con Medicina d’urgenza
    • Ecocardiogramma
  • Tempestivo inizio dei trattamenti
    • Limiti evidenze
    • Non esiste un trattamento per tutti
scompenso cardiaco acuto cosa fare sul campo ii
Scompenso Cardiaco AcutoCosa fare sul campo (II)
  • Ricerca diagnosi eziologica.
  • ricovero = occasione per reinquadramento clinico-strumentale.
  • Attenzione alle comorbidità!
  • Dimissione: programma follow up personalizzato.
scompenso cardiaco acuto ricerca societ scientifiche decisori
Scompenso Cardiaco AcutoRicerca/Società scientifiche/Decisori
  • Ricerca osservazionale.
  • Identificare target per sottogruppi di pazienti e testare farmaci specifici.
  • Eventi formativi.
  • Rete per lo shock e lo scompenso cardiaco avanzato.
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