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Acute Heart Failure: Management algorithms

J. ParissisJ. Parissis

Athens, Greece

ESC Guidelines for the Diagnosis and Treatment of

Acute and Chronic Heart Failure 2008

© 2008 The European Society of Cardiology

ΟΞΕΙΕΣ ΕΠΙ∆ΕΙΝΣΕΙΣ ΤΗΣ ΚΑΡ∆ΙΑΚΗΣ ΑΝΕΠΑΡΚΕΙΑΣ

ΕΠΙ∆ΕΙΝΝΟΥΝ ΤΗΝ ΚΑΡ∆ΙΑΚΗ ΛΕΙΤΟΥΡΓΙΑΕΠΙ∆ΕΙΝΝΟΥΝ ΤΗΝ ΚΑΡ∆ΙΑΚΗ ΛΕΙΤΟΥΡΓΙΑ

Discharge status and Discharge status and

chronic optimization

may prevent worsening

Ventr

icula

r fu

nction

Acute event

With each event,

hemodynamic alterations

contribute to progressive

Ventr

icula

r fu

nction

Acute eventcontribute to progressive

ventricular dysfunction

Time

Gheorghiade M, De Luca L, Fonarow G, et al. Am J Cardiol 2005.

ΣΥΝ∆ΡΟΜΑ ΟΞΕΙΑΣ ΚΑ: Η ΣΤΑΧΤΟΠΟΥΤΑ ΤΗΣ

ΚΑΡ∆ΙΑΚΗΣ ΑΝΕΠΑΡΚΕΙΑΣ

• Decompensated Chronic HF

• Pulnonary Edema• Pulnonary Edema

• Hypertensive HF

• Cardiogenic Shock• Cardiogenic Shock

• Isolated Right HF

• ACS and HF

ESC Classification, EHJ 2008.

Η ΑΛΛΕΠΙΚΑΛΥΨΗ Τ�Ν ΣΥ∆ΡΟΜ�Ν Ο∆ΗΓΕΙ ΣΕ

∆ΑΙΦΟΡΕΤΙΚΗ ΑΝΤΙΠΡΟΣ�ΠΕΥΣΗ ΤΟΥΣ ΣΤΙΣ

ΚΑΤΑΓΑΦΕΣΚΑΤΑΓΑΦΕΣ

4%7%

1%

ALARM�HFEHS HFII

3%11%

39%

7%

12%

11%

4%

16%

65%

37%

AdHF Pulmonary oedema Cardiogenic shock

Hypertensive HF Right HF High cardiac output failure

Pulmonary oedema (16% vs. 37%) and cardiogenic shock (4% vs. 12%)

were significantly different between the two studies. were significantly different between the two studies.

EHS HF II: 3,580 patients, ALARM.HF: 4,953 patients (1911 AdHF, 1820 p.oed, 581 C.shock, 365 Hyp AHF,

222 RV AHF, 54 High cardiac output)

Η ΣΥΣΤΟΛΙΚΗ ΑΡΤΗΡΙΑΚΗ ΠΙΕΣΗ ΕΙΣΟ∆ΟΥ ΕΙΝΑΙ Ο

ΙΣΧΥΡΟΤΕΡΟΣ ΠΡΟΓΝ�ΣΤΙΚΟΣ ΠΑΡΑΓΟΝΤΑΣ

EFICA Study

1.0

EFICA Study

High SBP

Surv

ival ra

te,

%

68%

0.5

Normal SBP

Cardiogenic shock

Surv

ival ra

te,

%

38%

0

Cardiogenic shock

Surv

ival ra

te,

%

17%

0

0 100 200 300 400

Number of days

Zannad F, Mebazaa A, et al. Eur J Heart Fail 2006;8:697/705.

ΤΑΞΙΝΟΜΗΣΗ ΑΝΑΛΟΓΑ ΜΕ ΤΗΝ ΑΡΧΙΚΗ

ΣΥΣΤΟΛΙΚΗ ΑΡΤΗΡΙΑΚΗ ΠΙΕΣΗ

Acute Heart Failure

SBP >140 mmHg SBP <140 mmHg

Acute Heart Failure

Hypertensive

(cardiovascular)

SBP >140 mmHg SBP <140 mmHg

Non�Hypertensive

(Cardiac)(cardiovascular) (Cardiac)

90< SBP <140 mmHg SBP ≤90 mmHg• 43"50 % of ADHF cases

• Usually elderly women

with preserved LVEF

Normotensive Hypotensive

with preserved LVEF

• In"hospital mortality: <2%

• 48"50 % of AHF cases

• Usually decompensation of

• 2"8 % of AHF cases

• Includes cardiogenic• Usually decompensation of

chronic HF with depressed

LVEF

• In"hospital mortality: 8"10%

• Includes cardiogenic

shock (CS)

• In"hospital mortality: >15%

(>30% in CS)

Triposkiadis F, Parissis J, Starling R, et al. Exp Opin Investig Drugs 2009;18:1"13.

ΟΞΕΙΑ ΚΑ ΜΕ ΣΥΣΤΟΛΙΚΗ ΑΡΤΗΡΙΑΚΗ ΠΙΕΣΗ >90 mm

Hg: ∆ΥΟ ∆ΙΑΦΟΡΕΤΙΚΟΙ ΚΛΙΝΙΚΟΙ ΦΑΙΝΟΤΥΠΟΙ

Cardiovascular Failure

• High blood pressure

Cardiac Failure

• Normal blood pressure

• Rapid worsening

• Pulmonary congestion

• PCWP acutely increased

• Gradual worsening (days)

• Systemic rather than pulmonary

congestion• PCWP acutely increased

• Rales: present

• Severe radiographic congestion

• Weight gain minimal

• PCWP chronically high

• Rales: may be absent

• Radiographic congestion may • Weight gain minimal

• LVEF relatively preserved

• Response to therapy:

relatively rapid

• Radiographic congestion may

be present

• Weight gain significant (edema)

• LVEF usually lowrelatively rapid • LVEF usually low

• Response to therapy: continue

to have systemic congestion

in spite of the initial symptomatic

responseresponse

Gheorghiade M. Am J Cardiol 2005;96[suppl]:11G217G.

Clinical Assessment of Acute Heart Failure

SyndromesSyndromes

Nohria et al. Am J Cardiol 2005;96[suppl]:32G–40G

Acutely decompensated Heart Failure

High jugular venous

pressure Pulmonary congestion/pressure Pulmonary congestion/

oedema

Haemodynamic findings:Low cardiac output (C.I < 2.5 L/min)

High PCW'pressure (>16 mmHg)Peripheral

Vasoconstriction

High PCW'pressure (>16 mmHg)

High systemic vascular resistence

ΑΞΙΑ ΤΗΣ ∆ΙΑΦΟΡΙΚΗΣ ΠΙΕΣΗΣ ΣΤΗΝ ΠΡΟΒΛΕΨΗ ΤΗΣ ΑΞΙΑ ΤΗΣ ∆ΙΑΦΟΡΙΚΗΣ ΠΙΕΣΗΣ ΣΤΗΝ ΠΡΟΒΛΕΨΗ ΤΗΣ

ΚΑΡ∆ΙΑΚΗΣ ∆ΥΣΛΕΙΤΟΥΡΓΙΑΣ

• Pulse Pressure

Systolic BP� Diastolic BP

• Proportional Blood Pressure

• Systolic BP – Diastolic BP = ≤ 25%• Systolic BP – Diastolic BP = ≤ 25%

Systolic BP

= CI ≤ 2.2 = CI ≤ 2.2

L/min/M2

(JAMA 1989;261:884)(JAMA 1989;261:884)

Rapid Assessment of Hemodynamic Status

LowNO

Warm & Dry

Warm & Wet

Low

Perfusion

at Rest

O & Dry

Cold & Cold &

67%

YES

Cold & Wet

Cold & Dry

28%5%

NO YES

S28%5%

Congestion at Rest

Nohria,J Cardiac Failure 2000;6:64

Clinical assessment identifies hemodynamic profiles that predict

outcomes in patients admitted with HFoutcomes in patients admitted with HF

Nohria et al. JACC 2003;41:1797$1804

ΕΙΝΑΙ ΧΡΗΣΙΜΟΣ Ο ∆ΕΞΙΟΣ ΚΑΘΕΤΗΡΙΑΣΜΟΣ;

NO

(Stevenson, et al. JAMA 2005;294:1625(Stevenson, et al. JAMA 2005;294:1625��1633)1633)

ESC Ο∆ΗΓΙΕΣ ΓΙΑ ΤΗ ΧΡΗΣΗ ΤΟΥ ΚΑΘΕΤΗΡΑ

ΜΕΤΡΗΣΗΣ ΠΙΕΣΕ�Ν ΠΝΕΥΜΟΝΙΚΗΣ ΑΡΤΗΡΙΑΣ

• Usually unnecessary for diagnosis

• Distinguish between a cardiogenic and non,cardiogenic • Distinguish between a cardiogenic and non,cardiogenic

mechanism in complex patients with concurrent cardiac and

pulmonary disease

• In hemodynamically unstable patients not responding to • In hemodynamically unstable patients not responding to

traditional treatment,

• In patients with combination of congestion and hypoperfusion

• Level IIa, LoE C

ESC Guidelines. EHJ 2008.

∆ΙΑΓΝ�ΣΗ ΟΞΕΙΑΣ ΚΑ ΣΕ ΑΣΘΕΝΕΙΣ ΜΕ ∆ΥΣΠΝΟΙΑ

ΒΑΣΙΣΜΕΝΗ ΣΤΑ ΕΠΙΠΕ∆Α Τ�Ν ΝΑΤΡΙΟΥΡΗΤΙΚ�Ν

ΠΕΠΤΙ∆Ι�ΝΠΕΠΤΙ∆Ι�Ν

Clinical examination,

ECG, Chest X&rayECG, Chest X&ray

Natriuretic peptidesNatriuretic peptides

BNP 100&400 pg/ml

NT&proBNP

BNP <100 pg/ml

NT&proBNP

BNP >400 pg/ml

NT&proBNPNT&proBNP

400&2000 pg/ml

NT&proBNP

<400 pg/ml

NT&proBNP

>2000 pg/ml

Uncertain diagnosisChronic HF unlikely Chronic HF likelyUncertain diagnosisChronic HF unlikely Chronic HF likely

ESC Guidelines. EHJ 2008.

ΕΚΤΙΜΗΣΗ ΝΑΤΡΙΟΥΡΗΤΙΚ�Ν ΠΕΠΤΙ∆Ι�Ν ΣΤΑ

∆ΙΑΦΟΡΕΤΙΚΑ ΚΛΙΝΙΚΑ ΣΕΝΑΡΙΑ ΤΗΣ ΟΞΕΙΑΣ ΚΑ

No congestion Congestion

Warm and dry Warm and wet

>600 pg/ml for BNP

>6000 pg/ml for NT*proBNP

>600 pg/ml for BNP

>6000 pg/ml for NT*proBNP Adequate perfusion at rest

Warm and dry

BNP 100�400

Warm and wet

BNP ≥600

Cool and dry Cool and wet

>6000 pg/ml for NT*proBNP >6000 pg/ml for NT*proBNP

Low perfusion at restCool and dry

BNP 400�1000

Cool and wet

BNP ≥1000ΥΨΗΛΕΣ ΤΕΛΟ∆ΙΑΣΤΟΛΙΚΕΣ ΠΙΕΣΕΙΣ ΑΡ ΚΟΙΛΙΑΣΥΨΗΛΕΣ ΤΕΛΟ∆ΙΑΣΤΟΛΙΚΕΣ ΠΙΕΣΕΙΣ ΑΡ ΚΟΙΛΙΑΣ

Omland T. Crit Care Med 2008;36:S17.

BACH TRIAL

2.8

AHFMR�proANP adds

additional information on AHF

MR

pro

AN

P

2.4

2.6

AHF

Arrhythmia ACS

additional information on

standard of care in the

diagnosis of acute

AHF

proANP

10 M

Rp

roA

NP

2.0

2.2Pneumonia

OtherCOPD

Pulm. Emb.

Arrhythmia ACS diagnosis of acute

congestive heart failure.

The use of MR�proANP

pneumonia

MR�proANP

Log

10

1.8

Chest Pain

Bronchitis

Influenza

The use of MR�proANP

together with PCT

supports the differential

diagnosis of pneumonia

Log10MR

1.4 1.2 1.0 0.8 0.6 0.4

1.4

1.6Asthma diagnosis of pneumonia

and congestive heart

failure.Log10 PCT

failure.Log10PCT

Future diagnostic algorithm

Patient suspected to have LVDPatient suspected to have LVDPatient suspected to have LVDPatient suspected to have LVD

LVD LVD BNPBNPNormal Normal

LVD LVD

unlikelyunlikely

IncreasedIncreased

Grey Zone Grey Zone

Low MRLow MR"" IncreasedIncreasedLow MRLow MR""

proANP proANP

LVD LVD

High MRHigh MR""

proANPproANP

EchocardiogramEchocardiogramLVD LVD

unlikelyunlikely

ΣΗΜΑΝΤΙΚΟΤΕΡΟΙ ΠΡΟΓΝ�ΣΤΙΚΟΙ

∆ΕΙΚΤΕΣ ΣΤΗΝ ΟΞΕΙΑ ΚΑ∆ΕΙΚΤΕΣ ΣΤΗΝ ΟΞΕΙΑ ΚΑ

• Advanced age

• Low blood pressure

• Low LVEF

• Low sodium and • Low sodium and

• High urea and creatinine serum levels

• High Troponin • High Troponin

• High levels of natriuretic peptides

are adverse prognostic factors in AHF. are adverse prognostic factors in AHF.

EVIDENCE EVIDENCE

BASED BASED

MEDICINEMEDICINE

Typical patient in HF trials

Young ~ 65 years old

Typical patient in HF trials

Young ~ 65 years old

70�80% men70�80% men

With Systolic dysfunction

w/o comorbiditiesw/o comorbidities

• Woman 75 years old

• Obese

• Hypertensive

• Diabetic

• Creatinine 2.1 mg/dl

• Chronic atrial fibrillation

• Mild COPD

• EF 40'45%

EMOTION EMOTION

BASED BASED

MEDICINEMEDICINE

Therapeutic targets in AHF syndromes

Goals of Treatment in AHF

Immediate (ED/ICU/CCU)

Improve symptoms

Restore oxygenation

Improve organ perfusion and haemodynamics

Limit cardiac/renal damage

Minimize ICU length of stay

Intermediate (in hospital)

Stabilize patient and optimize treatment strategy

Initiate appropriate (life%saving) pharmacological therapyInitiate appropriate (life%saving) pharmacological therapy

Consider device therapy in appropriate patients

Minimize hospital length of stay

Long�term and predischarge management

Plan follow%up strategy

Educate and initiate appropriate lifestyle adjustments

Provide adequate secondary prophylaxis

Prevent early readmission

Improve quality of life and survival

ESC Guidelines 2008.

Improve quality of life and survival

Goals for Treatment of Acutely Decompensated Heart Failure

ClinicalHemodynamic

SBP > 80 mm Hg

No orthopnea

SBP > 80 mm Hg

PCWP < 15 mm Hg

ClinicalHemodynamic

No orthopnea

No peripheral edema

No hepatomegaly/ascites

JVP < 8 cm

PCWP < 15 mm Hg

RAP < 8 mm Hg

SVR < 1200 dyne%s%cm%5

JVP < 8 cm

Warm extremities

JVP = jugular venous pressure.

Management of pulmonary congestion

A) Hypertensive HF

• Vasodilators are recommended with close monitoring and • Vasodilators are recommended with close monitoring and

low�dose diuretic treatment in patients with volume overload

or pulmonary oedema

B) Pulmonary oedemaB) Pulmonary oedema

• NIV

• Vasodilators are recommended when BP is normal or high, • Vasodilators are recommended when BP is normal or high,

and diuretics in patients with volume overload or fluid

retention

• Morphine is usually indicated, especially when dyspnoea is • Morphine is usually indicated, especially when dyspnoea is

accompanied by pain and anxiety

• Intubation and mechanical ventilation may be required to


achieve adequate oxygenation

Vasodilators or Diuretics Driven Treatment

in Acute Hypetensive HFin Acute Hypetensive HF

• 110 AHF pts, O2 10 l/min, Morphine 3mg

• Group A: Furosemide 40mg �ISDN 3mg iv every 3min

• Group B: Furosemide 80mg every 15min, ISDN 1mg/h,+1mg every 15min, ISDN 1mg/h,+1mg every 10min

• Treated until SpO2 >96% or MAP�30% or MAP <90 mmHg

• Results: • Results:

• Mechanical ventilation needed in 13/40%

• AMI 17/37%• AMI 17/37%

• Mortality 1/3

• Composite primary end point 25%/46%end point 25%/46%

Cotter et al, Lancet 1998

Indications and dosing of vasodilators

Vasodilator Indication Dosing Main side effects Other

Glyceryl

trinitrate,

Acute heart

failure, when

Start 20 �g/min,

increase to

Hypotension,

headache

Tolerance on

continuous trinitrate,

5"

mononitrate

failure, when

blood pressure is

adequate

increase to

200 �g/min

headache continuous

use

Isosorbide

dinitrate

Acute heart

failure, when

Start with

1 mg/h, increase

Hypotension,

headache

Tolerance on

continuous ESC recommendation class I, Level of evidence B dinitrate failure, when

blood pressure is

adequate

1 mg/h, increase

to 10 mg/h

headache continuous

use

Nitroprusside Hypertensive

crisis, cardiogenic

0.3"5 �g/kg/min Hypotension,

isocyanate toxicity

Drug is light

sensitive

ESC recommendation class I, Level of evidence B

crisis, cardiogenic

shock combined

with intoropes

isocyanate toxicity sensitive

Nesiritidea Acute

decompensated

heart failure

Bolus 2 �g/kg |

infusion 0.015"

0.03 �g/kg/min

Hypotension

heart failure 0.03 �g/kg/min

ESC Guidelines on AHF 2008.

a Limited sales approval in ESC countries.

Non�invasive ventilation

Indications

• Non�invasive ventilation (NIV) refers to all modalities that• Non�invasive ventilation (NIV) refers to all modalities that

assist ventilation without the use of an endotracheal tube but

rather with a sealed face�mask

• NIV with positive endexpiratory pressure (PEEP) should be • NIV with positive endexpiratory pressure (PEEP) should be

considered as early as possible in every patient with acute

cardiogenic pulmonary oedema and hypertensive AHF as it

improves clinical parameters including respiratory distressimproves clinical parameters including respiratory distress

• Class of recommendation IIa, level of evidence B

CPAP: Beneficial effects on mortality

Meta�analysis Meta�analysis

of 12 studies

Total 160�240 /groupTotal 160�240 /group

Mortality reducedMortality reduced

from 22% to 11%

RR 0.53 RR 0.53

(95% CI 0.35�0.81)

Masip et al. JAMA 2005;294:3124�3130

3CPO Multicenter Trial: Primary end�point

Cumulative

Survival

1.0

0.9 Non�invasive

Standard

Oxygen Therapy

Ventilation

0.8

Oxygen TherapyP=0.685

0 10 20 30Days

Non�Invasive Ventilation in ACPE

Masip J, Mebazaa A, Filippatos G. N Engl J Med 2008

Inotropes in clinical practice

• Inotropic agents should be considered in patients with low• Inotropic agents should be considered in patients with low

output states, in the presence of signs of hypoperfusion or

congestion despite the use of vasodilators and/or diuretics to

improve symptomsimprove symptoms


Available inotropic agents

Dobutamine: cl IIa, Level evidence BDobutamine: cl IIa, Level evidence B

PDEIs: cl IIb, Level evidence B

Dopamine: cl IIb, Level evidence C

PDEIs: cl IIb, Level evidence B

Dopamine: cl IIb, Level evidence C

Levosimendan: cl IIa,Level evidence B Levosimendan: cl IIa,Level evidence B


Hazard Ratios for Patients With a History of CHF

Appeared to Favor Levosimendan

Day, Group

Interaction

p�value

Favors

Levosimendan

Favors

Dobutamine

5 Previous history of CHFNo previous history of CHF


0.053

No previous history of CHF

31 Previous history of CHFNo previous history of CHF 0.046



0,1 1 10

No previous history of CHF

0.5 2

88% had history of CHFHazard Ratio (95% CI)

88% had history of CHF

12% had no previous history of CHF

European Journal of Heart Failure Advance Access published January 21, 2009.

Hazard Ratio (95% CI)

Hazard Ratios for Patients on β�Blockers at Baseline

Appeared to Favor Levosimendan

Favors

LevosimendanDay, Group

Favors

Dobutamine

Interaction

p�value

5 β�blocker users*β�blocker non�users


p�value = 0.01 0.014

β�blocker non�users




0 0,5 1 1,5 2

Hazard ratio (95% CI)

β�blocker non�users

Hazard ratio (95% CI)

* Within 24 hours of study drug infusion.

European Journal of Heart Failure Advance Access published January 21, 2009.

SURVIVE: Mean Change from Baseline in BNP

0

�300

�200

�100

0

Mean c

hange f

rom

baselin

e

�500

�400

�300

Dobutamine

Levosimendan

Mean c

hange f

rom

baselin

e

�800

�700

�600

�500

Mean c

hange f

rom

baselin

e

�800

0 1 2 3 4 5 6

Days since start of study drug infusion

For comparison between treatment groups at all time points (P<0.0001).

Due to the skewness in the data, median percent change is presented versus mean percent change from baseline.

Levosimendan, Compared to Dobutamine, Reduces Enzymatic

Markers Associated with Liver Congestion And Right Heart Failure: Markers Associated with Liver Congestion And Right Heart Failure:

A SURVIVE Subanalysis

5

10

Dif

fere

nce

(L

ev

os

ime

nd

an

–

Do

bu

tam

ine

) in

Ch

an

ge

Fa

vo

rsDo

bu

tam

ine

80 75 111Baseline, ", IU/L

0.008 0.002 <0.001P)value*

80 75 11180 75 111Baseline, ", IU/L

0.008 0.002 <0.001P)value*

)10

)5

0

5

Dif

fere

nce

(L

ev

os

ime

nd

an

Do

bu

tam

ine

) in

Ch

an

ge

Fro

m B

as

eli

ne

, IU

/L† AST APALT

Fa

vo

rsDo

bu

tam

ine

Le

vo

sim

en

dan

)30

)25

)20

)15

Dif

fere

nce

(L

ev

os

ime

nd

an

Do

bu

tam

ine

) in

Ch

an

ge

Fro

m B

as

eli

ne

, IU

/L

Day 1 Day 3 Day 5Day 1 Day 3 Day 5

Le

vo

sim

en

dan

)35

)30

Dif

fere

nce

(L

ev

os

ime

nd

an

Do

bu

tam

ine

) in

Ch

an

ge

Day 1 Day 3 Day 5Day 1 Day 3 Day 5

*P)value from repeated measures ANCOVA model for treatment effect, model also included

effects for time (all were p<0.05) and treatment)by)time interaction (all were p=NS). †Point

estimates from ANCOVA model with baseline as covariate. Error bars are standard errors.

Nikolaou M, Parissis J, Mebazza A, presented at ESC congress Paris France 2011.

Istaroxime: a Na/K�ATPase inhibitor with positive

lusitropic properties

Sabbah et al. Am J Cardiol 2007;99:41A

Adamson et al. J Cardiovasc Pharmacol 2003;42:169

Changes in hemodynamic and other measures in the

HORIZON�HF trial, three dosages of IV istaroxime vs

placeboplacebo�g/kg/min

Parameter 0.5, n=29

1.0, n=30

1.5, n=30 Placebo, n=31 n=29 n=30 n=31

PCWPa (mm Hg) 3.2b 3.3c 4.7d 0.0

Systolic BP (mm Hg) +4.9 +8.3b +15.6d +1.3Systolic BP (mm Hg) +4.9 +8.3 +15.6 +1.3

MAP (mm Hg) +2.2 +3.3 +7.5c +0.9

LVEDV (mL) +2.9 6.4 14.1b +3.9

QTc (ms) 25.7e 38.0e 49.2e 2.4QTc (ms) 25.7e 38.0e 49.2e 2.4

a. Primary end pointb. p<0.05b. p<0.05c. p<0.01 d. p<0.001e. p=0.0001PCWP=pulmonary capillary wedge pressureMAP=mean arterial pressure

Gheorghiade M et al. J Am Coll Cardiol 2008; 51:2276�2285.

MAP=mean arterial pressureLVEDV=left ventricular end%diastolic volume; QTc=corrected QT interval

Relaxin Mechanisms of ActionRelaxin Mechanisms of Action

• Vasodilation

• NO, cGMP effectorsRelaxin • NO, cGMP effectors

• Induction of NOS II/III

• Upregulation of endothelial endothelin type B receptor, which mediates

Relaxin

type B receptor, which mediates vasodilation

• Preferential dilation of constricted vessels

• Relaxin%upregulated ETB receptors act as vasodilating ET%1 sink

• Anti�inflammatory• Anti�inflammatory

• Down%modulation of inflammatory cytokines linked to outcome in HF (TNF%α, TGF%β)

• Other: Anti�ischemic, Anti�apoptotic, Anti�fibrotic

Teichman, SL, et al. Heart Fail Rev 2009; Dschietzig, T, et al. Pharmacol Therap 2006

Rapid Dyspnea Improvement through 24 hours

(Likert Scale)(Likert Scale)

Proportion of Patients with Moderate/Marked

Improvement in Dyspnea at 6, 12 and 24 hrImprovement in Dyspnea at 6, 12 and 24 hr

40

45

50 p = 0.04

25

30

35

Pa

tie

nts

(%

)

10

15

20

25

Pa

tie

nts

(%

)

Placebo 10 30 100 2500

5

10

Relaxin (mcg/kg/d)

J Teerlink RELAX�AHF ACC 2009

ΧΕΙΡΙΣΜΟΣ ΤΝ ΑΣΘΕΝΝ ΜΕ ΟΞΕΙΑ ΚΑ ΠΟΥ

ΘΕΡΑΠΕΥΟΝΤΑΙ ΜΕ ΑΜΕΑ Η ΑΝΤ ΥΠΟ∆ΟΧΕΝ ΘΕΡΑΠΕΥΟΝΤΑΙ ΜΕ ΑΜΕΑ Η ΑΝΤ ΥΠΟ∆ΟΧΕΝ

ΑΓΓΕΙΟΤΕΝΣΙΝΗΣ

• ACEIs are not indicated in the early stabilization of patients

with AHF

• There is no consensus on the ideal timing for initiation of • There is no consensus on the ideal timing for initiation of

ACEI/ARB therapy in AHF. In general, it is recommended that

treatment with these agents should be initiated before

discharge from hospitaldischarge from hospital

• Patients on ACEIs/ARBs admitted with worsening HF should

be continued on this treatment whenever possible

• Class of recommendation I, level of evidence A

Use of betablockers during acute exacerbation of HF

• The dose of βblocker may need to be reduced temporarily

or omitted, although generally treatment should not be

stopped, unless the patient is clinically unstable with signs stopped, unless the patient is clinically unstable with signs

of low output

• Treatment may be interrupted or reduced in the presence of• Treatment may be interrupted or reduced in the presence of

complications (bradycardia, advanced AV block,

bronchospasm, or cardiogenic shock) or in cases of severe

AHF and an inadequate response to initial therapy



ΕΠΙ∆ΡΑΣΗ ΤΗΣ ΣΥΝΕΧΙΣΗΣ Η ΑΠΟΣΥΡΣΗΣ ΤΟΥ Β�

ΑΝΑΣΤΟΛΕΑ ΣΤΗ ΕΠΙΒΙ�ΣΗ ΤΗΣ ΟΞΕΙΑΣ ΚΑ

Findings from the OPTIMIZE�HF Program

Fonarow, et al. JACC 2008;52:190.

Post�discharge survival by beta�blocker treatment groups

Degree of Renal Damage in Patients Admitted for Decompensated HF

50

35

40

45

50

Males

20

25

30

35Males

Females

5

10

15

20

0

5

Nml GFR Moderate Renal

Failure

Mild SevereKidney

Damage100,000

Admissions>90 60$89eGFR 30$59 15$29 >15

Admissions

ADHERE

What is the evidence for ‘renal impairment’ in the ALARM�HF

patient population?patient population?

Renal status in all AHF patients vs ADCHF vs De Novo

43%50%

20%25%

10%

37%43%

27%

15% 16% 14%20%

30%

40%

50%

10%15% 14%

0%

10%

20%

History of CRDHistory of CRD

Initial serum creatinine >1.5mg/dL

Renal failure complicationRenal failure complication

Sample = All AHF patients (4,953) vs ADCHF (3,161) vs De Novo AHF patients (1,792)

J Parissis on behalf of Steering Committee

“HOT” POINTS INDICATE A RISK FOR

ACUTE RENAL FAILURE IN CHFACUTE RENAL FAILURE IN CHF

• Persistently low urinary sodium

• Concomitant increase of hepatic enzymes and BUN (Risk of hepatonephric syndrome) (Risk of hepatonephric syndrome)

• Increased plasma urea/creatinine ratio and uric acid (discontinuation of ACEi?)

• Mean arterial pressure <80 mmHg

• Hyponatremia (max neurohormonal activation)

• Changes in effective circulating volume (fever, blood • Changes in effective circulating volume (fever, blood loss, decrease in dietary salt, etc.)

• Other: angiogaphic contrast, older age, diabetes, major surgery, use of NSADs surgery, use of NSADs

Optimizing treatment of renal dysfunction according

to BUN/CRE Ratio

CO BUN/CRE

to BUN/CRE Ratio

CO BUN/CRE

VasodilatorsCorrect volume

Stop ACEi

Vasodilators

Inotropes

hemofiltration

DRY WET

PCWP Wt (kg)

DRY WET

PCWP Wt (kg)

Cardiorenal syndromeCardiorenal syndrome�� Overcoming the resistance Overcoming the resistance

to diureticsto diureticsto diureticsto diuretics

1.1. Increase furosemide dose Increase furosemide dose 1.1. Increase furosemide dose Increase furosemide dose

2.2. Stop ACEiStop ACEi

3.3. Use continuous iv furosemideUse continuous iv furosemide

4.4. Add metolazoneAdd metolazone4.4. Add metolazoneAdd metolazone

5.5. Add dopamine at 2Add dopamine at 2��3 mcg/kg3 mcg/kg

6.6. Add vasodilators or inotropes according to SBPAdd vasodilators or inotropes according to SBP6.6. Add vasodilators or inotropes according to SBPAdd vasodilators or inotropes according to SBP

7.7. Start ultrafiltrationStart ultrafiltration

8.8. Insert IABPInsert IABP

9.9. Insert another deviceInsert another device9.9. Insert another deviceInsert another device

The role of CVP in renal worsening in ADHF patients

Mullens, et al. J Am Coll Cardiol 2009;53:589�96.

Ultrafiltration (UF) Versus Usual Care (UC)

for Patients with AHF: RAPID�CHF Trialfor Patients with AHF: RAPID�CHF Trial

• The early application • The early application

of UF for patients with

CHF was feasible, well�

tolerated, and resultedtolerated, and resulted

in significant weight loss

and fluid removal

• A larger trial is underway

UF UC

• A larger trial is underway

to determine the relative

efficacy of UF versus

standard care in ADHF

p=0.001

p=0.01

n=40n=40

Bart et al. JACC 2005;46:2043

UNLOAD: Freedom From Rehospitalization UNLOAD: Freedom From Rehospitalization

for HF

100 �

Pe

rce

nta

ge o

f P

ati

en

ts

Fre

e F

rom

Re

ho

sp

ita

lizati

on Ultrafiltration Arm (16 Events)

80 �

60 �

40 �

Pe

rce

nta

ge o

f P

ati

en

ts

Fre

e F

rom

Re

ho

sp

ita

lizati

on

Standard Care Arm (28 Events)

40 �

20 �

10 20 30 40 50 60 70 80 90

Pe

rce

nta

ge o

f P

ati

en

ts

Fre

e F

rom

Re

ho

sp

ita

lizati

on

P=.037

0 10 20 30 40 50 60 70 80 90

Days

No. Patients at Risk

Ultrafiltration Arm 88 85 80 77 75 72 70 66 64 45

0

Standard Care Arm 86 83 77 74 66 63 59 58 52 41

Costanzo MR et al. J Am Coll Cardiol. 2007;49:675�683.

Peripheral Ultrafiltration

• Ultrafiltration should be considered to reduce fluid overload

(pulmonary and/or peripheral oedema) in selected patients

and correct hyponatraemia in symptomatic patients

refractory to diuretics.

• Class of recommendation IIa, level of evidence B• Class of recommendation IIa, level of evidence B

Key evidence

• Although earlier studies suggested only temporary benefit,• Although earlier studies suggested only temporary benefit,

more recent trials have demonstrated sustained effects.

The most appropriate selection criteria have not been

established. However, technological advances facilitate established. However, technological advances facilitate

ultrafiltration and will probably increase experience in this

population.

Therapeutic Algorithm (I)

Hypertensive AHF (SBP>140 mmHg)

• A) Restoration of low oxygen saturation (>95% in patients without COPD • A) Restoration of low oxygen saturation (>95% in patients without COPD or >90% in patients with COPD ) using oxygen supply or CPAP/BiPAP or mechanical ventilation.

• B) Alleviation of patient anxiety and pain using iv analgesics (e.g. morphine).

• C) Improvement of pulmonary congestion using high doses of iv vasodilators and low doses of iv diuretics.

• D) Restoration of sinus rhythm or achievement of a satisfactory heart rate control in the co-existence of atrial fibrillation (or other supra-ventricular tachycardias) using electroversion or anti-arrhythmics (e.g. digoxin, tachycardias) using electroversion or anti-arrhythmics (e.g. digoxin, amiodarone).

Filippatos, Parissis. Acute Heart Failure. OXFORD Handbook 2010

Treatment algorithm (II)

Normotensive AHF (140>SBP>90 mmHg)

• A) Improvement of fluid overload using high doses of iv diuretics (consider combination of different classes of diuretics in resistant (consider combination of different classes of diuretics in resistant cases)

• B) Reduction of elevated cardiac filling pressures and afteload (if • B) Reduction of elevated cardiac filling pressures and afteload (if SBP>100 mmHg) using low doses of iv vasodilators (e.g. nitrates) with a parallel close monitoring of SBP.

• C) Improvement of peripheral organ hypoperfusion using iv inotropes (e.g. levosimendan, dobutamine) in cases resistant to the above therapies or as initial approach in the cases with low output symptoms and 120>SBP>90 mmHg.symptoms and 120>SBP>90 mmHg.

• D) Mechanical improvement of fluid status using devices of peripheral hemofiltration in patients with worsening of renal function under the recommended iv medications.recommended iv medications.


Treatment Algorithm (III)

Hypotensive AHF (SBP <90 mmHg) *Hypotensive AHF (SBP <90 mmHg) *

• A) Evaluation of fluid status using pulmonary artery catheter (exclusion of hypovolemia).

• B) Restoration of SBP and peripheral hypoperfusion using iv vassopressors (e.g high doses of dopamine and/or dobutamine, norepinephrine).

• C) Improvement of coronary and peripheral perfusion using mechanical support (implantation of intra+aortic balloon counterpulsation or other portable devices).

• D) Improvement of oliguria/anouria using portable devices of peripheral hemofiltration in resistant cases to the above strategies.

* Revasc and IABP in ACS


What is hot in new ESC guidelines?

• Combination of AHF and CHF guidelines • Combination of AHF and CHF guidelines

• The role of ACS in classification

• The role of biomarkers in diagnosis (cut off values for • The role of biomarkers in diagnosis (cut off values for

rule out)

• The short and long term management

• Guidelines for the use new devices and machines• Guidelines for the use new devices and machines

• Guidelines for the background treatment of AHF

(ACEi/ARBs, beta blockers)(ACEi/ARBs, beta blockers)

What is not?

• Overlapping of 6 conditions in ESC classification (reconsider • Overlapping of 6 conditions in ESC classification (reconsider

a new one based on SBP)

• Absence of cut"off values of biomarkers according to

different clinical scenarios and their role as therapeutic different clinical scenarios and their role as therapeutic

targets – The role of multi"marker strategy ?

• No specific guidelines for the use of iv inotropes in AHF

patients with special conditions or co"morbidities (renal patients with special conditions or co"morbidities (renal

dysfunction, ACS, high BNP, on beta"blocker therapy)

• Absence of Class I therapies for AHF (in contrast to CHF)• Absence of Class I therapies for AHF (in contrast to CHF)

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