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SUMMARY
Background: Heart failure is one of the most common diseases of adults in
Europe, with an overall prevalence of 12%. Among persons aged 60 and
above, its prevalence is above 10% in men and 8% in women. Acute heart
failure has a poor prognosis; it is associated with a high rate of rehospitalization
and a 1-year mortality of 2030%.
Methods: This review is based on pertinent literature, including guidelines,
retrieved by a selective search in PubMed.
Results: There are different types of acute heart failure; the basic diagnostic
assessment is performed at once and consists of ECG, echocardiography, and
the measurement of N-terminal pro-brain natriuretic peptide (NTproBNP) and
troponin levels. The most common causes of decompensation are arrhythmia,
valvular dysfunction, and acute cardiac ischemia, each of which accounts for
30% of cases. The potential indication for immediate revascularization should
be carefully considered in cases where acute heart failure is due to coronary
heart disease. The basic treatment of acute heart failure is symptomatic, with
the administration of oxygen, diuretics, and vasodilators. Ino-tropic agents,
vasopressors, and temporary mechanical support for the circulatory system are
only used to treat cardiogenic shock.
Conclusion: The treatment of acute heart failure is markedly less evidence-based
than that of chronic heart failure. Newer treatment approaches that are
intended to improve outcomes still need to be tested in multicenter trials.
Cite this as:
Hummel A, Empen K, Drr M, Felix SB: De novo acute heart failure and acutely
decompensated chronic heart failure. Dtsch Arztebl Int 2015; 112: 298310.
DOI: 10.3238/arztebl.2015.0298
298
Learning objectives
This article should enable readers to:
know the epidemiology and pathogenesis of acute
heart failure
know, and apply knowledge of, the main
symptoms and signs of acute heart failure, and the
relevant diagnostic tests
be familiar with the treatments of acute and
acutely decompensated chronic heart failure.
Prevalence
Heart failure is one of the most common
diseases of adults in Europe, with a prevalence
of 12%.
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Methods
This review is based on pertinent literature retrieved by
a selective search in PubMed up to October 2014,
including the guidelines of the European Society of
Cardiology and the German Cardiac Society.
FIGURE 1
All types
Mortality
ADCHF
De novo acute heart failure
Pathogenesis
The subtype of heart failure known as heart failure
with reduced ejection fraction (HF-REF) is characterized by left-ventricular dilatation (ventricular remodeling) and a reduction of the left-ventricular ejection
fraction (LVEF) below 40%. In contrast, heart failure
with preserved ejection fraction (HF-PEF, diastolic
heart failure) is characterized by normal left-ventricular
volume and ejection fraction (LVEF >50%), although
the thickness of the ventricular wall and the ratio of
left-ventricular mass to end-diastolic volume is increased, as is the stiffness of the myocardium. Despite
the structural and functional differences between
HF-REF and HF-PEF, decompensated heart failure of
either type displays the same pathophysiologic
mechanisms, i,e., rising cardiac filling pressures and
diminished intrinsic contractility of cardiac myocytes
(3). Often, about two weeks before acute decompensation, backward failure of the left ventricle arises,
resulting in pulmonary congestion (Figure 2) (8, 9).
Sodium and fluid retention are major components of
the clinical picture of heart failure, causing shortness of
breath and peripheral edema. Cardiac and renal
Mortality
Acute heart failure carries a high in-hospital
mortality and a poor prognosis at 1 year with
respect to recurrent hospitalization and mortality.
10
20
30
40
In-hospital mortality as a function of the past history and clinical presentation of acute
heart failure (from [5]). ADCHF, acutely decompensated chronic heart failure
Pathophysiological definition
Heart failure is defined pathophysiologically as
the inability of the heart to supply the bodys
tissues with an adequate amount of blood under
conditions of normal cardiac filling pressure.
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veins. Further typical findings include pleural effusions, a third heart sound, tachycardia, and congested
neck veins (e8). The patients past medical history
should be carefully considered, including the chronology of the onset of symptoms, any already diag-
Clinical manifestations
Acute heart faiulure is characterized by a rise in
cardiac filling pressures, with dyspnea as the
main symptom.
Diagnostic evaluation
Echocardiography is the main imaging study
and a standard test in all patients with
suspected acute heart failure.
BOX 1
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FIGURE 2
Abnormal systolic and/or diastolic left-ventricular function
S
Y
M
P
T
O
M
S
Mitral insufficiency
Interstital
pulmonary edema
Pathophysiology
of congestion
(from [8]).
LVEDP,
left-ventricular enddiastolic pressure;
PCWP, pulmonary
capillary wedge
pressure;
DNV, distended
neck veins;
LA pressure,
left-atrial pressure
Treatment strategies
The goals of treating acute heart failure are
to improve symptoms,
to achieve hemodynamic stability,
Biomarkers
In patients with acute heart failure, elevated
biomarker levels signify a worse prognosis.
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The frequency of
clinical subtypes
of acute heart
failure (from [5])
FIGURE 3
3.2%
11.4%
3.9%
Acute decompensation of
chronic heart failure
Pulmonary edema
Cardiogenic shock
16.2%
The Shock Trial led to the finding that rapid revascularization in cases of cardiogenic shock was associated
with a 67% (relative) reduction in mortality that
persisted over six years (14). It is currently being
investigated whether the revascularization of all highgrade coronary artery stenoses in patients with cardiogenic shock confers an advantage with respect to survival compared to the revascularization only of the
vessel responsible for the infarct (CULPRIT-SHOCK,
NCT 01927549). Patients who undergo coronary
angiography and (if indicated) revascularization during
their first hospitalization for de novo acute heart failure
have a significantly lower mortality and rehospitalization rate (15).
302
Right-heart failure
Diuretics are commonly given to patients in heart failure and have a beneficial effect on symptoms (grade I
recommendation, level B evidence); their clinically
evident utility is pathophysiologically explicable by the
reduction of pulmonary congestion, but a putative improvement in outcome through the use of diuretics has
not yet been well documented in prospective trials (17).
In particular, the optimal dose, mechanism of action,
and mode of administration (oral, intravenous bolus, or
continuous infusion) remain unclear. Intravenous loop
diuretics should be given to treat acute decompensation
because of their faster effect and the independence of
their uptake from gastrointestinal resorption, which is
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FIGURE 4
Suspected acute heart failure
History and physical examination, blood pressure, respiratory frequency,
chest x-ray, ECG,
echocardiography and/or NT-proBNP, blood-gas analysis,
laboratory tests (including troponin, complete blood count, electrolytes, renal parameters,
TSH, albumin, blood glucose)
Initial
assessment
Simultaneous
specific
assessment
Hypoxemia
Hyperventilation
Hypoventilation
Life-threatening
arrhythmia or
bradycardia
Blood pressure
<85 mm Hg
or shock
Acute
treatment
Oxygen;
non-invasive
or invasive
ventilation
Electric
cardioversion,
external
pacemaker
Inotropic agents,
vasopressors,
mechanical
circulatory support
Acute coronary
syndrome
Coronary
reperfusion,
antiplatelet agents,
anticoagulation
Acute mechanical
cause/
severe valvular
disease
Cardiac surgery,
pericardial
puncture,
interventional
treatment
Diuretics
Diuretics have a beneficial effect on symptoms;
their utility is pathophysiologically explicable by
the reduction of pulmonary congestion, but
prospective trials have not yet shown that they
improve the outcome of acute heart failure.
Diagnostic
assessment of
patients with suspected acute heart
failure (based on
the guidelines of
the European Society of Cardiology
[7])
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BOX 2
Vasodilators
Vasodilators lower the systolic blood pressure and
should therefore only be used in normotensive patients
(systolic blood pressure above 110 mm Hg). In
particular, nitroglycerin and sodium nitroprusside can
be used to treat pulmonary edema in the presence of
hypertension (grade IIa, resp. IIb recommendation,
level B evidence). Nitroglycerin lowers pulmonary
capillary pressure by lessening cardiac preload. It is
relatively contraindicated in patients with severe
aortic or mitral stenosis. Sodium nitroprusside lowers
cardiac preload and afterload; the dose should be
304
Vasodilators
Because they lower the systolic blood pressure,
vasodilators should only be used in normotensive
patients (systolic blood pressure >110 mm Hg).
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TABLE
Treatment approaches in acute heart failure
Substance
Mechanism of action
Effects
Reduction of
mortality
References
Istaroxime
Calcium-ATPase activator
Lowers PCWP
Improves ventricular filling in diastole
No data
(32)
Rolofylline
Adenosine-receptor antagonist
Seizures
No
(33)
Nesiritide
Natriuretic peptide
Improves dyspnea
Hypotension
No
(34)
Tesozentan
Hypotension
No
(35)
Tolvaptan
Vasopressin antagonist
Improves dyspnea
Increases diuresis
Improves hyponatremia
No
(36)
Omecamtiv
mercarbil
No data
Atomic AHF,
ESC 2013
presentation*
Serelaxin
Improves dyspnea
Acts as a vasodilator
Improves renal failure
Hypotension
(37)
Cinaciguat
Lowers PCWP
Severe hypotension
No data
(38)
Urodilatin
Natriuretic peptide
Improves dyspnea
Lowers PCWP
Hypotension
No data
(39)
Inotropic agents
Patients with refractory hypotension (cardiogenic
shock) can be treated with inotropic agents such
as dobutamine.
Vasopressors
If inotropic agents are ineffective, vasopressors
are recommended, above all norepinephrine.
Increased left-ventricular afterload is a
common side effect.
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FIGURE 5
Hypoxemia
Oxygen
No
Yes
Anxiety/agitation
IV opioids
No
Blood pressure
Systolic BP <85 mm Hg
or shock
Systolic
BP >110 mm Hg
Systolic BP 85110 mm Hg
Inotropic agents
ICU level III according to ESICM
Vasodilators
Monitor further course
ICU level I/II
according to ESICM
Yes
Treatment successful
Continue
treatment
No
Clinical re-evaluation
Systolic BP <85 mm Hg
or shock
No
No
SpO2 <90%
Yes
Stop vasodilators
In shock, stop beta-blockers
Inotropic agents and/or vasopressors
Mechanical circulatory support
ICU level III according to ESICM
Yes
yes
Oxygen
Noninvasive ventilation
Invasive ventilation
ICU level I/II
or III according to ESICM
Foley catheter
Increase diuretic dose,
by continuous infusion if necessary
Right-heart catheter
Ultrafiltration
ICU level I/II according to ESICM
Treatment algorithm for acute heart failure [from 7] ESICM, European Society of Intensive Care Medicine; ICU, intensive care unit; SpO2, blood oxygen saturation
drugs and vasopressors, and if it is considered to be potentially reversible, a reasonable treatment option is
transient mechanical support of the circulatory system
(hours to 30 days) with a microaxial pump in the left
ventricle or a minimalized heart-lung machine (extracorporeal membrane oxygenation, ECMO). Such
temporary measures serve as a bridge to recovery
Levosimendan
The REVIVE-I and REVIVE-II trials revealed a
rapid improvement of symptoms with persistent
lowering of natriuretic peptide levels, but with
a tendency toward symptomatic hypotension
and cardiac arrhythmia.
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New treatments
Various new treatment approaches have been proposed
in recent years with the aim of improving the outcome
of patients with acute heart failure, but a better outcome
has not been documented in any of the clinical trials
carried out to date (Table), nor did any of the treatments
lessen the rehospitalization rate.
The only recent trial of a drug for acute heart failure
that revealed a benefit of any kind was the RELAX
trial, in which the administration of serelaxin
(recombinant human relaxin-2, a peptide of pregnancy)
was found to result in more rapid relief of symptoms,
but did not lower the rate of rehospitalization (37). The
hemodynamic effect of serelaxin is to lower both the
pulmonary capillary and pulmonary arterial pressure
and the pulmonary and systemic vascular resistance,
without raising the cardiac index (40). Hypotension
was found to be more common under treatment with
serelaxin than with placebo (ca. 46 mm Hg). The
RELAX trial was an acute trial involving a 48-hour
infusion of serelaxin starting on admission to the
hospital. Interestingly, the 180-day mortality of
patients treated with serelaxin was 37% lower than
that of those who were given a placebo (4% absolute
risk reduction); although 180-day mortality was not a
predefined secondary endpoint, this was found in a
protocol-specified additional efficacy analysis. The
finding is now being followed up in a trial on over
6000 patients, which ought to have sufficient power to
document improved survival if this is, in fact, the case
(RELAX-AHF-2, NCT01870778).
Prevention of thromboembolism
During the cardiac recompensation phase, and for as
long as the patient is confined to bed, a prophylactic
drug against thromboembolism should be given, e.g., a
low-molecular-weight heparin (grade I recommendation, level A evidence). Atrial fibrillation is an indication for full anticoagulation (grade I recommendation, level A evidence).
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7. McMurray JJ, Adamopoulos S, Anker SD, et al.: ESC guidelines
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Cardiology. developed in collaboration with the Heart Failure
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compensated to acute decompensated heart failure: pathophysiological insights obtained from continuous monitoring of intracardiac pressures. Circulation 2008; 118: 143341.
New treatments
New treatments have not yet been able to
improve the prognosis of acute heart failure.
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308
25. Testani JM, Chen J, McCauley BD, Kimmel SE, Shannon RP: Potential effects of aggressive decongestion during the treatment
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the short-term clinical course of patients with acutely decompensated heart failure. J Am Coll Cardiol HF 2013; 1: 10311.
29. Mebazaa A, Nieminen MS, Packer M, et al.: Levosimendan vs
dobutamine for patients with acute decompensated heart failure: the SURVIVE randomized trial. JAMA 2007; 297: 188391.
30. Landoni G, Biondi-Zoccai G, Greco M, et al.: Effects of levosimendan on mortality and hospitalization. A meta-analysis of
randomized controlled studies. Crit Care Med 2012; 40:
63446.
31. Thiele H, Zeymer U, Neumann FJ, et al.: Intraaortic balloon support for myocardial infarction with cardiogenic shock. N Engl J
Med 2012; 367: 128796.
32. Shah SJ, Blair JEA, Filippatos GS, et al.: Effects of istaroxime on
diastolic stiffness in acute heart failure syndromes: Results from
the hemodynamic, echocardiographic, and neurohormonal effects of Istaroxime, a novel intravenous inotropic and lusitropic
agent: a Randomized controlled trial in patients hospitalized with
heart failure (HORIZON-HF) Trial. Am Heart J 2009; 157:
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33. Massie BM, OConnor CM, Metra M, et al.: Rolofylline, an
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34. OConnor CM, Starling RC, Hernandez AF, et al.: Effect of nesiritide in patients with acute decompensated heart failure. N Engl
J Med 2011; 365: 3243.
35. McMurray JJ, Teerlink, JR, Cotter G, et al.: Effects of tezosentan
on symptoms and clinical outcomes in patients with acute heart
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Prevention of thromboembolism
During the cardiac recompensation phase, and for
as long as the patient is confined to bed, a
prophylactic drug against thromboembolism
should be given, e.g., a low-molecular-weight
heparin.
Further treatment
Once the patient with acute heart failure or
acutely decompensated chronic heart failure has
become stable, the question of further treatment
of the cause of the condition should be
addressed.
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Please answer the following questions to participate in our certified Continuing Medical Education
program. Only one answer is possible per question. Please select the most appropriate answer.
Question 1
Question 6
Question 2
Question 7
Question 3
Question 8
Question 4
What diagnostic test should be performed as soon as
possible in acute heart failure, along with an ECG and a
chest x-ray?
a) Left-heart catheterization
b) Right-heart catheterization
c) Computed tomography of the heart
d) Magnetic resonance imaging of the heart
e) Echocardiography
Question 9
What is the indication for the administration of cardiac
glycosides in acute heart failure?
a) To treat hypotension
b) To treat absolute tachyarrhythmia in atrial fibrillation
c) To lower myocardial oxygen consumption
d) To bring about pharmacological cardioconversion
e) To prevent ventricular arrhythmias
Question 5
Question 10
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2003; 361: 18438.
e8. Hummel A, Empen K, Drr M, Felix SB: Diagnostik der systolischen und diastolischen Herzinsuffizienz. Internist 2014; 55:
64754.
e9. Kociol RB, Horton JR, Fonarow GC, et al.: Admission, discharge,
or change in B-Type Natriuretic Peptide and Long-Term Outcomes. Circ Heart Fail 2011; 4: 62836.
Deutsches rzteblatt International | Dtsch Arztebl Int 2015; 112 | Hummel et al.: eReferences