Hearth failure
Doc.Dr Emir Fazlibegović,ESC,FESC
Prof.Dr Mustafa Hadžiomerović,
ESC,FESC
5th International Congress of
cardiologysts and angyologysts of
Bosnia and Herzegovina,Sarajevo 2010.
WHAT IS HEART FAILURE?
“HF is a complex clinical syndrome that can result from any structural
or functional cardiac disorder that impairs the ability of the ventricle to
fill with or eject blood. The cardinal manifestations of HF are dyspnea
and fatigue, which may limit exercise tolerance, and fluid retention,
which may lead to pulmonary and peripheral edema.
Both abnormalities can impair the functional capacity and quality of life
of affected individuals, but they may not necessarily dominate the
clinical picture at the same time.”

Evaluation and Management of Chronic Heart Failure in the Adult
A Report of the ACC/AHA Task Force on Practice Guidelines
February 2002

Supply is less then demand

Failure of the heart as a pump
Systolic/Diastolic – does it matter?
Systolic:
heart cannot contract normally
and cannot pump enough blood
into the arteries (EF<40%)

Diastolic:
heart
cannot relax and fill
normally and cannot pump
enough blood into the arteries
(EF>40%)
Left, right, or both?
Right Heart Failure

Results in increased, systemic venous
congestion and peripheral oedema
Left Heart Failure

Results in pulmonary congestion
Different etiology – so what?

Many causes but clinical manifestations
similar
–
Coronary artery disease is the underlying cause of HF in
approximately two thirds of patients with ischemic left
ventricular systolic dysfunction.
– The remainder have nonischemic causes, e.g. hypertension,
valvular disease, myocardial toxins, or myocarditis
– or may have no discernible cause (e.g., idiopathic dilated
cardiomyopathy).
PHASE

Compensated phase
– Supply temporarily meets the altered
demand, no or very mild symtoms and
signs

Decompensated heart failure:
– new or worsening symptoms/signs of
dyspnoea, fatigue or oedema leading to
hospitalisation or unscheduled medical
care
Terminology or just semantics?
Congestive Heart Failure (CHF)

Heart failure with extra fluid in vessels and tissues
Acute heart failure (AHF)
sudden initial episode of HF, severe symptoms;
frequent pulmonary edema

Chronic heart failure (CHF) – (chronic HF)
Slow process of myocardium destruction, often
unnoticed, mild to moderate symptoms; frequent
peripheral edema, may follow acute insult

Acute exacerbation of chronic heart
failure
Immediate and massive decompensation of the
previously existing chronic heart

Current indication
Acutely Decompensated Severe Low-output Chronic
-24 hours?
-Abruptly
-Suddenly
Pre-existing
Symptomatic
NYHA III-IV
Cardiac –
-EF<40%
-CI<2.0 l/min/m2
-Cold
Congestive Heart Failure (CHF)
ONSET
Acute heart failure:
– sudden onset of symptoms or signs of
heart failure in a patient with no history
of heart failure and previously normal
cardiac function
ONSET
Exacerbation of chronic heart failure:
– patient with established diagnosis of
heart failure who develops increasing
signs or symptoms of the disease after a
period of relative stability
Conceptual differences between
acute and chronic heart failure

Chronic heart failure:
– neurohumoral disease that responds to
neurohumoral intervention
– Remodeling, RAAS, cateholamines, PDE

Acute heart failure:
– haemodynamic disease that responds to
haemodynamic interventions
Classification and causes of
heart failure

Acute de novo heart
failure
–
–
–
–
–
–
Myocardial infarction
Arrhythmias
Valve destruction
Myocarditis
Hypertensive crisis
Cardiac surgery

Decompensated
chronic heart failure
–
–
–
–
–
–
Myocardial ischaemia
Arrhythmias
Malcompliance
Infections
Salt overload
Hypertension
Pulmonary oedema
Low output heart failure (congestion)
Cardiogenic shock
Differences between acute heart failure
and decompensated Chronic HF
Haemodynamics:
AHF: RV +/- LV, normovolaemic
Decompensation of Chronic HF: both RV and LV,
increased EDV, hypervolaemic
Prognosis:
AHF: potentially reversible, stunning, sepsis
Decompensation of Chronic HF: chronic disease
DIAGNOSIS
Framingham Criteria
Major Criteria







Parox. Nocturnal
dyspnea
Orthopnea
 JVP
Pulmonary rales
Third heart sound
Cardiomegaly
Pulmonary edema
Minor Criteria







Peripheral edema
Night cough
Dyspnea on exertion
Hepatomegaly
Pleural effusion
Heart rate>120/min
Wight loss > 4.5 kg in
5 days
Classification
ONSET
ETIOLOGY
PATOPHYSIO
LOGY
LOCATION
NYHA
HEART
FAILURE
ISCHEMIC
TOXIC
I
ACUTE
INFALMATORY
SYSTOLIC
LEFT
II
CHRONIC
REUMATOID
DIASTOLIC
RIGHT
III
IV
IDIOPATIC
DIAGNOSIS
Cardiac
insufficiency
CARDIOMIO
PATHY
Cardiac
dysfunction
Treatment of Decompensated CHF
67%
20%
Decompensated
HF Patient
Edema (+)
Warm Extremities
SBP > 90 mm Hg
Decompensated
HF Patient
Edema (+)
Cold Extremities
SBP > 90 mm Hg
High output
Optimization of therapy:
•Increase ACEI doses
•IV diuretics
•Other PO or IV
vasodilators (nitroprusside)
8%
Decompensated
HF Patient
Edema (-)
Cold Extremities
SBP > 90 mm Hg
Low-output HF
Levosimendan
Inadequate response:
• Increasing BUN
• Persisting edema
• Persisting dyspnea
5%
Decompensated
HF Patient
Edema (+) or (-)
Cold Extremities
SBP < 90 mm Hg
Cardio shock
Dobutamine/
Dopamine/
Norepinephrine
Add Levo?
Calcium-Induced Conformational
Changes in Troponin Complex
Ca2+
cTnC
Myosin head
TnI
Tm
Actin
TnT
TnT
Tm
Tm
Myosin head
Actin
TnI
cTnC
TnT
Ca2+
TnI
Tm
Tm
Actin
Myosin head
Tm
Myosin head
Ca2+
Actin
TnT
TnI
cTnC
Ca2+
Myofilament length
Myofilament length
Levosimendan

Calcium sensitisation through binding
to troponin C
–

increases cardiac contractility and efficiency
Opening of ATP-sensitive potassium
channels in vascular smooth muscles
–
pulmonary, coronary, systemic vasodilation
Calcium Sensitization by Levosimendan
No increase in cAMP
No increase in i/c calcium
•No increase in energy consumption
•No arrhythmogenicity
•No impairment in relaxation
•Anti-stunning effect
•No antagonism by -blockers
Heart Failure
LIDO study
– 203 patients with severe HF, levo vs. dobut
CASINO study
– 299 patients low-output HF, levo vs. dobut vs. placebo.
REVIVE-2 study
– 600 patients. Levo vs placebo. Higher early mortality, but
no difference at 90 days.
SURVIVE trial
1327 patients, levo vs. dobutamine: No mortality
difference at 180 days.
IHD and Cardiac surgery

RUSSLAN study
– 504 patients with recent MI, levo vs.
placebo. Trend to lower mortality at 180
days.

Small studies in cardiac surgery show
levosimendan increases cardiac output
and lowers SVR
Mostar study in 20
patients NYHA III-IV



aged 43-84, average 69
All patients treated with ACE inhibitors,
diuretic, beta blockers, aldosterone blockers,
statins, and cardiotonics (digoxin chronically
and dobutamin, dopamine in the shortly
crisis period).
on follow-up 1-3 day after infusion and 3
and 6 month, and 1-2-3 year after.
Levosimendan and NYHA
NYHA kl.
4
4
4
4 4 4
4
4
4
4
4
4
4
4 4 4
3,5
3
3
3 3 3 3 3 3
3
3
3 3
3 3
3
3
3 3 3
2,5
2
2 2
2
2
2
2
2
2
2
1,5
1
0,5
0
1 1 1 1 2 2 2 3 3 3 4 4 5 5 6 6 7 7 7 8 8 9 9 10 10 11 11 12 12 13 13 14 15 16 16 17 17 18 18 19 19 20 20
Levosimendan and NYHA
Mean=-1.0000
Std Dev=0.6124
P< 0.0001
EFLV in patients with
levosimendan
EF
90%
82%
80%
72%
70%
71%
69%
64%
60%
58%
55%
53%
50%
57%
59%
57%
52%
48%
45%
45%
40%
38%
45%
43%
41%
37%
35%
33%
44%
37%
32%
35%
32%
36%
39%
37%
36%
32%
30%
27%
27%
20%
20%
26%
21%
20%
17%
27%
26%
17%
10%
0%
1
1
1
1
2
2
2 3
3
3
4
4
5
5
6
6
7 7
7
8
8
9
9 10 10 11 11 12 12 13 13 14 15 16 16 17 17 18 18 19 19 20 20
Levosimendan and EFLV
Mean=15.7059
Std Dev=14.3952
P= 0.0004
Levosimendan and ENDLV
EndLV
10
9,8
9,2
9
8
7
6
5
7,3
9,2
7,9
7,7
7
6,1
5,9
5,4
5,6
5,6
5
5,5
5,9 5,7
5,2
5,8 5,9
9
8,7 8,8
8,1
7,9
6,8 6,9 6,9
5,6
8,7 8,8
7,3
6,6
6,6 6,4
6,3
6,5
5,7 5,9
6,1
5,9
5,4
4,8
4
3
2
1
0
1 1 1 1 2 2 2 3 3 3 4 4 5 5 6 6 7 7 7 8 8 9 9 10 10 11 11 12 12 13 13 14 15 16 16 17 17 18 18 19 19 20 20
Levosimendan and FS
FS
60%
51%
50%
42%
40%
40%
41%
39%
35%
32%
30%
31%
29% 28%
30%
25%
20%
17%16%
13%
18%
23%
20%
21%
22%
11%
10%
32%
31%
13%13%
23%
24%
22%
20%19%20%
18% 17%17% 17% 18%
16%
15%
12%
12%
7%
0%
0
1 1 1 1 2 2 2 3 3 3 4 4 5 5 6 6 7 7 7 8 8 9 9 10 10 11 11 12 12 13 13 14 15 16 16 17 17 18 18 19 19 20 20
Distrubtion of FS with
levosimendan
Med=0.0818
SD=0.0915
P= 0.002
Conclusion 1

Experience from our practice shows
that single dose of Levosimendan in
patients with decompensated
advanced heart failure produces
significant improvement, which reflects
in extension of life.
Conclusion 2

Use of Levosimendan seams to be
beneficial demonstrated by great
benefit in the quality of life with better
systolic function without any
arrythmogenic effect.
Conclusion 3

There are probably other benefits
masked by uknown lusitropic and
pleotropic influences of Levosimendan
in the physiology and pathophysiology
of heart and others systems of body.
Conclusion 4




Almost all cases of death are results of
co-morbidity disease, and are not
related to levosimendan effect
In the future
ICD device
Cardiac surgery
Transplantation