Transcript Acute Heart Failure and Atrial Fibrillation

Acute Heart Failure and
Atrial Fibrillation
M.Birhan YILMAZ, MD, FESC
Associate Professor of Cardiology,
Cumhuriyet University School of Medicine
Department of Cardiology
Sivas, TURKEY
SECOND ITALIAN GREAT NETWORK CONGRESS
October 18-21 2011
Aula Urbani, Ospedale Sant’Andrea - Roma, Italy
Atrial fibrillation (AF) is a common
rhythm in patients with acute heart
failure (AHF).
 Registry and trial data indicate that
20% to 35% of patients with AHF who
are admitted to the hospital will be in
AF at presentation.
 In about one third of these patients,
the AF will be of recent onset.

Asirvatham and Friedman. From: Shivkumar, Weiss, Fonarow,
and Narula; eds. Braunwald’s Atlas of EP in HF. 2005.
Types of AF
Triggers
ectopic foci
Paroxysmal AF
Persistent AF
Electrophysiologic
Remodeling
Chronic Substrate
fibrosis
Permanent AF
Nattel et al. Circulation 1999;100:87-95
AF-HF interaction
Loss of atrial kick
Atrial
stretch
Rapid rate
remodelling
İrregular
beat
Sympathetic
tone
SOLVD Investigators: J Am Coll Cardiol. 1998;32:695-703.
Key Questions to Consider Before Starting
Therapy
Does the patient have an ICD or pacemaker
in place?
 Does the patient have preserved or reduced
systolic function at their baseline?
 What is the duration of the AF episode?
 Is the patient already on drugs for rhythm or
rate control and anticoagulation?
 What concomitant disorders are present?

Types of AF in AHF
1-Acute symptomatic AF
 2-Incessant AF
 3-Acute on chronic AF

Acute symptomatic de novo AF
Either the AF episode itself has rapidly
precipitated heart failure in a previously stable
patient or worsening heart failure has
triggered an acute episode of AF.
 In these patients, the potential for successful
early restoration of sinus rhythm is high if the
heart failure symptoms can be controlled

Atrial Fibrillation and Tachycardia
Induced Cardiomyopathy
Cardiomyopathy can be caused by any
tachycardia (>110 bpm) that occurs as little
as 10-15% of day
 Severity related to rate and duration of  HR
 Maximal improvement after rate control may
require up to 8 months
 After improvement susceptibility to rapid
deterioration remains if tachycardia recurs

Olshansky et al Circulation 2004, Fenelon et al PACE 1996;19:95-106,
Shinbane J et al. JACC 1997;29: 709-715
Incessant AF
May be subacute or acute
 Depending on caardiac reserve,
patients become symptomatic
 During the ensuing days and weeks, the
patient gradually slips into ADHF and
then presents with severe symptoms.
 These patients will probably not convert
spontaneously but may be candidates
for a later cardioversion attempt.

Acute on chronic AF
Some patients with permanent AF that is
usually well rate controlled will develop
progressive heart failure and then
present emergently with rapid ventricular
rates due to the stress of the episode
 Unlikely to control the rhythm

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Patients with AF and signs of acute heart failure require
urgent rate control and often cardioversion.
An urgent echocardiogram should be performed in
haemodynamically compromised patients to assess LV
and valvular function and right ventricular pressure.
The Atrial Fibrillation and Congestive Heart Failure (AFCHF) trial observed no difference in cardiovascular
mortality (primary outcome) between patients with an
LVEF ≤35%, symptoms of congestive heart failure, and
a history of AF randomized to rate or rhythm control, or
in the secondary outcomes including death from any
cause and worsening of heart failure


In the general population of patients with atrial
fibrillation (AF), the main goals of therapy are the
control of symptoms and the prevention of arterial
embolism, particularly stroke. These goals are also
true for the relatively large subset of AF patients
with heart failure (HF).
In such patients, the adverse hemodynamic
consequences of AF can quickly lead to a
decrease in exercise capacity and a worsening of
symptoms, both of which may be difficult to
manage
In an analysis from the Framingham Heart Study, of 708
patients with heart failure (HF) who were in sinus rhythm,
159 (22 percent) developed atrial fibrillation (AF) at an
average of 4.2 years of follow-up.
The prevalence of AF in patients with
chronic HF varies from <10 to 50 %,
depending in part upon the severity of
HF and New York Heart Association
class
 There is also an association between
left ventricular diastolic dysfunction and
AF
 It should also be kept in mind that each
(AF and HF) may predispose or
promote the other’s persistent nature

Although the optimal resting heart
rate during AF is between 60 and 100
bpm, rates below 100 bpm may not
be achievable during AHDF until
volume overload and hypoxia have
been corrected.
 A more realistic target is to achieve a
heart rate below 120 bpm during the
first hours of treatment

Adverse Hemodynamic Effects of AF



Heart rate changes. In cases where the ventricular
response is fast and maintained, a chronic tachycardia
can lead to a rate-related cardiomyopathy.
In cases where the ventricular response is exceptionally
slow, patients can develop symptomatic bradycardia and
possibly syncope.
Activation of neurohumoral vasoconstrictors such as
angiotensin II and norepinephrine, as well as other
maladaptive and procoagulant biochemical mechanisms.
Adverse Hemodynamic Effects of AF

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Beat-to-beat variations in atrial pressure (preload). The influence of
preload on left ventricular ejection (Frank-Starling mechanism) is important
in AF only when afterload is relatively low .
Beat-to-beat variations in myocardial contractility . Among patients with AF,
the preceding RR interval has a significant positive correlation with left
ventricular ejection, as a shorter RR interval (more rapid ventricular
response) reduces the LVEF . This effect is independent of end-diastolic
volume, indicating that it cannot be explained by the Frank-Starling
mechanism. In addition, the "pre-preceding" RR interval has
a negative correlation with left ventricular ejection, which has been
ascribed to postextrasystolic potentiation .
Inefficient ventricular mechanics due to abrupt changes in cycle length .
Adverse Hemodynamic Effects of AF
Irregular RR Intervals Impair Cardiac Performance
*p < 0.01
N=16
NSR AF
VVI VVI VVT
60 AVG
Clark DM. JACC 1997; 30:1039-45
VVI -AVG
VVT
Adverse Hemodynamic Effects of AF
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Atrial systole — Contraction of the left atrium injects a
volume of blood under pressure into the left ventricle,
leading to increments in ventricular diastolic volume,
end-diastolic pressure, and stroke volume .
Loss of atrial systole can therefore diminish the stroke
volume. This may be particularly important when left
ventricular compliance is reduced and in mitral stenosis.
The importance of atrial systole has been demonstrated
in patients with hypertrophic cardiomyopathy, which is
typically associated with an increased atrial contribution
to ventricular filling (31 versus 16 percent in controls in
one report)
Impact on Prognosis in Chronic HF


A three-year follow-up of 6517 patients in the SOLVD trials (patients
with asymptomatic left ventricular dysfunction or NYHA class II to III
HF) found that AF (present in 6.4 percent) was a significant predictor
of all-cause mortality (34 versus 23 percent in those without AF), even
after multivariate analysis [7].
The V-HeFT I and II trials included 1427 patients with NYHA class II to
III HF, 206 of whom (14 percent) had AF [5]. There was no significant
difference in mortality at two years in either trial (34 versus 30 percent
and 20 versus 21 percent, respectively) or in hospitalization for HF
EHFS II: A survey on hospitalized AHF patients

AF may worsen symptoms in patients
with HF and uncontrolled HF can
precipitate or speed the ventricular
response of AF
Most patients with AF will have
unacceptable symptoms attributable in part
to a rapid ventricular rate. These patients
require a slowing of the ventricular rate
prior to a decision about rhythm or rate
control as a long-term strategy to control
symptoms.
 In the general population of patients with
AF, rate control strategy for many might be
preferable.

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The AF-CHF trial was the first large, randomized trial to test the
hypothesis that long-term rhythm control is better than rate
control in patients with HF and paroxysmal AF
In this trial, 1376 patients with a left ventricular ejection fraction
<35 percent, HF symptoms, and a history of paroxysmal (or
persistent) AF were assigned to a strategy of either rhythm
control (amiodarone, sotalol, or dofetilide), or rate control (with
beta blockers). At a mean follow-up of 37 months, there was no
significant difference in the primary outcome of death from
cardiovascular causes between the rhythm and rate control
groups (27 versus 25 percent, respectively).
This finding is consistent with that in the general population.

For many patients with AF and chronic HF, a rate control is
preferred to a rhythm control strategy given the burdens of
cost, a more complicated medical regimen, and the potential
for adverse side effects of antiarrhythmic therapy. In
particular a rate control strategy is an acceptable initial
approach to patients who can easily be rate controlled, are
very unlikely to maintain sinus rhythm in the long term, and
who are not bothered by symptoms such as palpitations that
are attributable to AF. Nevertheless, certain circumstances
may warrant attempts at rhythm control depending on a
patient’s hemodynamic status, severity of symptoms, and
ability to adequately control the ventricular response rate.
AHF-AF: Possible Relationships
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Atrial fibrillation (AF) is a common arrhythmia,
particularly in patients with underlying heart
disease. Among patients with both HF and AF,
there are several possible relationships:
Acute HF can precipitate AF due to increases in
left atrial pressure and wall stress.
AF can cause acute HF, particularly if the
ventricular response is rapid.
AF may be chronic and not directly related to the
acute HF decompensation.
It is usually difficult to determine whether AF is the
cause or result of ADHF.
 A reliable history of palpitations that clearly precede the
decompensation suggests but does not prove that AF
was the cause of the pulmonary edema.
 The treatment of AF depends upon whether or not it is
associated with significant hemodynamic instability and
whether or not it is believed to be the precipitant of HF
decompensation.
 In some patients with AF and ADHF, effective treatment
of pulmonary edema results in slowing of the
ventricular rate or spontaneous reversion of the
arrhythmia. If AF persists, it is treated in the same
fashion as AF in other situations.

Rate control is often the preferred initial
strategy for the following reasons:
Because acute HF can precipitate AF,
cardioversion prior to the resolution of acute HF
will often be followed by early recurrence of AF.
 AF is often a chronic condition that is not
contributing to the acute decompensation.



However, if a rate control strategy is selected, the
negative inotropic effects of beta-blockers and
nondihydropyridine calcium channel blockers can
be problematic in patients with systolic dysfunction.
For this reason, short-acting IV formulations of such
drugs (eg, esmolol or diltiazem) are often used. In
addition, digoxin is also potentially useful in this
setting, although its use has lessened considerably
due to toxicity issues and slow onset of action.
Amiodarone can be considered.
Restoration of sinus rhythm should be
considered in the following settings:
 If AF is associated with hypotension or
evidence of cardiogenic shock
 If AF is clearly the cause for pulmonary edema
 If the response to effective therapy of
pulmonary edema is slow or suboptimal
 Heparin should be started prior to
cardioversion, whenever possible.


ALARM-HF
database
AF in ALARM-HF
Mortality (p=0.33)
12.0
10.0
8.0
6.0
Mortality
4.0
2.0
0.0
no AF
Acute AF Acute on
chronic
AF
chronic
AF
HFSA
Rate and rhythm control of
AF
aClass
of recommendation. bLevel of evidence.
AF = atrial fibrillation; EHRA = European Heart Rhythm Association.
CHA2DS2VASc score
Rate control of atrial
fibrillation
The choice of drugs depends on life style and underlying disease
Acute rate control in
AF
aClass
of recommendation. bLevel of evidence.
AF = atrial fibrillation; i.v. = intravenous.
Beta-blocker therapy in treatment of atrial fibrillation
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Randomized studies have confirmed the superiority of
beta-blockers in controlling the ventricular response,
especially with exercise.
First, a small population of patients experience recurrent
AF in association with stress or anxiety; these patients with
adrenergically mediated AF may respond well to betablockade
Second, and more common, is the use of beta-blockers for
prevention of AF in patients following cardiothoracic
surgery (post-op AHF) , in which AF occurs in approx. 30%
of patients.
The efficacy of beta-blockers in this circumstance likely
relates to the elevated sympathetic tone present
postoperatively.
Long-term rate control in
AF
aClass
of recommendation. bLevel of evidence.
AF = atrial fibrillation; bmp = beats per minute; LV = left ventricular; NYHA = New York Heart Association.
AV node ablation in AF
patients
aClass
of recommendation. bLevel of evidence.
AF = atrial fibrillation; AV = atrioventricular; CRT = cardiac resynchronization therapy; LV = left ventricular;
LVEF = left ventricular ejection fraction; NYHA = New York Heart Association.
Choice of an antiarrhythmic
drug
for AF control
aClass
of recommendation. bLevel of evidence.
AF = atrial fibrillation; AV = atrioventricular; LoE = level of evidence; NYHA = New York Heart Association.
Surgical ablation of
AF
aClass
of recommendation.
bLevel of evidence.
AF = atrial fibrillation.
AF
with “upstream”
therapy
aClass
of recommendation.
bLevel of evidence.
ACEI = angiotensin-converting enzyme inhibitor; AF = atrial fibrillation; ARB = angiotensin receptor blocker.
Secondary prevention of
AF
with “upstream” therapy
aClass
bLevel
of recommendation.
of evidence.
ACEI = angiotensin-converting enzyme inhibitor; AF = atrial fibrillation; ARB = angiotensin receptor blocker.
Rate control during AF with heart
failure
aClass
bLevel
of recommendation.
of evidence.
AF = atrial fibrillation; AP = accessory pathway; LVEF = left ventricular ejection fraction.
Rate control during AF with heart
failure
aClass
of recommendation.
bLevel
of evidence.
AF = atrial fibrillation; AV = atrioventricular; CRT = cardiac resynchronization therapy;
LVEF = left ventricular ejection fraction; NYHA = New York Heart Association.
Rhythm control of AF in heart
failure
aClass
of recommendation. bLevel of evidence.
AF = atrial fibrillation; DCC = direct current cardioversion; NYHA = New York Heart Association.
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Atrial Fibrillation in Heart Failure
Background
 Pathophysiology
 Influence on disease state and
progression
 Clinical approach – Management

Heart Failure in the USA
Prevalence: 5 million patients
 Annual new diagnoses: 550,000 per year
 Mortality: 54,000 per year
 Consumption of medical resources:

 12 to 15 million office visits / year
 6.5 million hospital days / year

Predicted steady increase
ACC / AHA Guidelines 2006
Atrial fibrillation:
prevalence increases with severity of heart failure
0,6
% Patients with Atrial Fibrillation
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Class III - IV
Atrial Fibrillation is Increasing
Age-specific prevalence (per 10.000 population) of hospitalizations for
atrial fib- among adults aged 35 yrs or older by year, 1985 to 1999
Concomitant Heart Failure: 13 % age 35 – 64 yrs
21 % age > 65 yrs
Wattigney, W. A. et al. Circulation 2003;108:711-716
Development of AF is Associated with Clinical
Deterioration in Heart Failure
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prospective follow-up of 344 patients with CHF and sinus
rhythm for 19 ± 12 months.
28 patients developed AF which became chronic in 18 pts
When AF occurred
 NYHA class worsened (from 2.4 ± 0.5 to 2.9 ± 0.6, p = 0.0001),
 peak exercise O2 consumption declined
 (from 16 ± 5 to 11 ± 5 ml/kg per min, p = 0.002),
 cardiac index decreased (from 2.2 ± 0.4 to 1.8 ± 0.4, p =
0.0008),
 mitral and tricuspid regurgitation increased
thromboembolism occurred in 3 of the 18 patients with AF.
9 of 18 patients died after AF
occurrence of AF was a predictor of major cardiac events.
Pozolli et al, JACC 1999
Atrial Fibrillation is Associated with
Increased Mortality in Chronic HF
Atrial Fib- Sinus
p
n
419
6098
Mortality
34%
23%
<0.0001
Heart Failure Death 17%
9%
<0.0001
Arrhythmic Death
6%
NS
7%
RR 1.34 (1.11 - 1.61) adjusted for severity, medication
Dries et al, SOLVD, JACC 1998
A) Impact of Treatment of Heart Failure on Atrial
Fibrillation - RAAS
Targeting atrial-specific ion channels and developing
antiarrhythmic drugs with selected channel-blocking profiles
are very attractive approaches.
 Success in preventing components of AF pathophysiology,
including the prevention of AF-promoting structural
remodelling by suppressing renin–angiotensin activation,
has been achieved in animal experiments.
 Clinical trials indicate the value of inhibiting
angiotensin-converting enzyme or blocking
angiotensin type-1 receptors in preventing AF
recurrence (RAAS).


Antiarrhythmic drugs for atrial fibrillation: Do we need better use, better drugs or a randomized
trial of ablation as primary therapy? Stanley Nattel, Montreal Heart Institute Research Center,
CMAJ 2004 ; 171 (7).
Prevention of Atrial Fib With Angiotensin-Converting Enzyme
Inhibitors and Angiotensin Receptor Blockers:
A Meta-Analysis
11 studies with 56,308 patients
Overall, ACEIs and ARBs reduced the relative risk of
AF by 28% (95% C] 15% to 40%
 Benefit is similar for ACE-inhibitors and AII blockers
 Reduction in AF was greatest in patients with heart
failure (relative risk reduction 44%, p = 0.007).


Healey, et al JACC 2005;45:1832
A) Impact of Treatment of Heart Failure on Atrial Fibrillation RAAS
Aldosterone has a wide range of both genomic and
non-genomic actions and is a potent stimulus for
cardiac fibrosis. In addition, aldosterone may produce
direct electrophysiological changes.
 AF increases serum aldosterone concentrations,
whereas restoration of sinus rhythm returns
aldosterone concentrations to normal.
 Aldosterone production is enhanced by the renin–
angiotensin activation occurring in CHF, and it would
not be surprising if the resulting mineralocorticoid
receptor stimulation contributed to the atrial fibrosis
that is an important component of the AF substrate
associated with CHF.



Stanley Nattel . Aldosterone antagonism and atrial fibrillation: time for clinical assessment? European Heart Journal 2005 26(20):20792080
Milliez P, DeAngelis N, Rucker-Martin C, Leenhardt A, Vicaut E, Robidel E, Beaufils P, Delcayre C, Hatem SN, Spironolactone reduces
fibrosis of dilated atria during heart failure in rats with myocardial infarction. Eur Heart J 2005;26:2193–2199. First published on
September 1, 2005
Atrial Fibrillation and Heart Failure
Prevention – the best medicine
Neurohormonal antagonists
Aggressive therapy of initial AF episodes?
Anticoagulation
Statins?
Targeting heart failure
Thanks for your attention