Recognizing and Managing Asymptomatic Left Ventricular Dysfunction: After Myocardial Infarction

Transcription

Recognizing and Managing Asymptomatic Left Ventricular Dysfunction: After
Myocardial Infarction
Nancy M. Albert and Connie Lewis
Crit Care Nurse 2008, 28:20-37.
© 2008 American Association of Critical-Care Nurses
Published online http://www.cconline.org
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Cover Article
Recognizing and
Managing
Asymptomatic
Left Ventricular
Dysfunction
After Myocardial Infarction
PRIME POINTS
Nancy M. Albert, PhD, CCNS, CCRN, CNA
Connie Lewis, MSN, ACNP, ANP, CCRN
• MI survivors should
be assessed for asymptomatic LVSD.
• Patients with asymptomatic LVSD after MI
have worse outcomes
than do patients without this dysfunction.
A
pproximately 865 000
myocardial infarctions occur each year
in the United States;
of these, approximately 565 000 are new cases.1
Despite advances in treatment, disabling heart failure develops in 46%
of women and 22% of men within 6
• Improve survival and
quality of life in these
patients by recognizing
the problem and promoting prompt use of
evidence-based treatments.
• Teach patients how to
provide self-care before
they leave the hospital.
CEContinuing Education
This article has been designated for CE credit. A
closed-book, multiple-choice examination follows this article, which tests your knowledge of
the following objectives:
1. Identify the definitive measurement for the
diagnosis of asymptomatic left ventricular
systolic dysfunction (LVSD) after myocardial
infarction
2. Describe the pathophysiology of asymptomatic LVSD after myocardial infarction
3. Discuss the pharmacologic management
of asymptomatic LVSD after myocardial
infarction
years after myocardial infarction.2
Approximately 40% of myocardial
infarctions are accompanied by left
ventricular systolic dysfunction
(LVSD), with or without clinical (ie,
symptomatic) heart failure.3
Although current management of
myocardial infarction is improving
patients’ survival, a markedly compromised heart decreases quality
of life and functional capacity and
increases hospitalization and
mortality.
With such a high proportion of
survivors of myocardial infarction,
especially women, in whom heart
failure is likely to develop within a
few years of the acute event, detection of LVSD should be a priority.
During hospitalization, nurse clinicians should promote advocacy for
patients, coordination of care, and
20 CRITICALCARENURSE Vol 28, No. 2, APRIL 2008
http://ccn.aacnjournals.org
health-related education. Once cardiac damage due to a myocardial
infarction is detected, the risk for
clinical heart failure can be reduced
by using medications selected on the
basis of current clinical evidence.
Building on disease management
models that have been successful in
patients with chronic heart failure,
nurse clinicians should ensure that
patients who have had a myocardial
infarction receive the right medications, comprehensive self-care education to decrease the risk for new
cardiac events, and an appointment
for follow-up after discharge (eg, at a
nurse-led clinic).4 It is crucial to
organize hospital care structures to
ensure that all cases of LVSD after
myocardial infarction are detected
and managed appropriately.
Asymptomatic LVSD
Many patients may not immediately have signs and symptoms of
heart failure after myocardial infarction but may have LVSD due to
injury of cardiomyocytes. Asymptomatic LVSD is classified as a form
of structural heart disease that is
strongly associated with development of heart failure but without
signs or symptoms, also known as
pre–heart failure or stage B heart
failure5 (Figure 1). Asymptomatic
LVSD is often undiagnosed and
undertreated, even though its mortality and morbidity are high and
similar to those in patients with clinical heart failure.5 Moreover, undiagnosed impaired cardiac function
may confer an even higher risk for
poor outcomes because patients are
medically undertreated and do not
understand their role in self-care.
In this review, we discuss
patients with asymptomatic LVSD
after myocardial infarction in the
context of progressive disease, presenting data supporting an aggressive diagnostic and therapeutic
approach for this commonly overlooked and undertreated problem,
and describe the role of nurse clinicians in improving care.
Epidemiology
In the United States, coronary
artery disease is the most common
cause of LVSD leading to heart failure among whites.6 Ischemic cardiomyopathy is the etiology of heart
failure in approximately 61% of
patients with mild to severe signs
and symptoms.7 In the Survival and
Ventricular Enlargement (SAVE)
trial, asymptomatic LVSD was present in 58% of patients after myocardial infarction.8 Data on the
percentage of patients in whom
asymptomatic LVSD develops after
myocardial infarction are limited.
Authors
Nancy M. Albert is director of nursing research and innovation for the Nursing Institute
and a clinical nurse specialist at George M. and Linda H. Kaufman Center for Heart
Failure, Cleveland Clinic Foundation in Cleveland, Ohio.
Connie Lewis is a heart failure coordinator at Centennial Medical Center in Nashville,
Tennessee.
Corresponding author: Nancy M. Albert, RN, PhD, Cleveland Clinic Foundation, 9500 Euclid Ave, Mail Code
P32, Cleveland, OH 44195 (e-mail: [email protected]).
To purchase electronic or print reprints, contact The InnoVision Group, 101 Columbia, Aliso Viejo, CA 92656.
Phone, (800) 809-2273 or (949) 362-2050 (ext 532); fax, (949) 362-2049; e-mail, [email protected].
Data from Europe indicate that only
about 60% of patients with myocardial infarction have their ventricular
function assessed.9,10 In a systematic
review of 33 studies of heart failure
after myocardial infarction between
1978 and 2000, Hellermann et al11
found that the incidence of heart
failure was reported in only a few
clinical trials, and generally, the criteria for diagnosis of heart failure
were not provided. If the Killip class
(a risk stratification system for
patients after myocardial infarction
that uses signs such as rales, S3 gallop, elevated jugular venous pressure,
pulmonary edema, and cardiogenic
shock) had been used as the classification measure, patients with asymptomatic LVSD would have been
classified as Killip class 1, reflecting
no clinical signs of heart failure.
The registry for the Trandolapril
Cardiac Evaluation (TRACE) study,12
a randomized controlled trial in
which placebo and trandolapril were
compared in patients with myocardial infarction, provides the best
database for examining the occurrence of asymptomatic LVSD after
myocardial infarction. Of 6676
patients in whom wall motion index
(the degree of motion of the left ventricular wall during systole, which
correlates with ejection fraction)
could be determined, major LVSD
developed in 2606 patients (39%).
Among those with LVSD, clinical
heart failure developed in 74%.12
TRACE researchers found that 30%
of all patients had both LVSD and
clinical heart failure and 54% of
patients had features of heart failure
but not LVSD, reflecting heart failure with preserved systolic
function.12 Overall, 64% of patients
had either heart failure or LVSD
CRITICALCARENURSE Vol 28, No. 2, APRIL 2008 21
into the natural history of
asymptomatic
LVSD. Overall,
total mortality
for patients
receiving
Stage B
placebo was
At high risk for heart failure;
25%, and
structural heart disease
but without clinical heart
approximately
failure
12% died
within 1 year.16
Further,
patients with a
Have the following available
Angiotensin-converting
large left venPatient education
enzyme-I or angiotensinmaterials/delivery
receptor blocker (stages A
tricle, measAdmitting order set
and B)
ured as a
with criteria for use
β-Blocker (stage B)
Preprinted discharge
baseline endImplantable cardioverter
instructions
defibrillator
diastolic presAlgorithm for follow-up
sure in the left
care after discharge
Reminder systems or
ventricle
checklists
exceeding 30
Monitor quality
mm Hg, had
Advocate preventive
therapies (flu shot)
significantly
higher rates of
Figure 1 Asymptomatic left ventricular systolic dysfunction: guidelines for stage A and B heart failure:
death or
recommended therapies and nursing leadership to facilitate adherence with guidelines.
severe heart
Based on Hunt et al.
failure at 4
years after
acute myocardial infarction than did
myocardial infarction, and death,
within the first few days after a
patients with a lower baseline left
including sudden death.13-15 In the
myocardial infarction.11 In populationventricular end-diastolic pressure.8
based community samples and regSAVE trial, the investigators specifiPatients with LVSD but no signs
istries, the incidence of new-onset
cally enrolled only patients with
or symptoms of heart failure after
heart failure after myocardial infarcacute myocardial infarction and
myocardial infarction who seemed
tion ranged from 22% to 48%, with a
asymptomatic LVSD and followed
16
to be recovering well were also at
mean of 37%, consistent with results
up those cases for 3.5 years. Of
high risk for sudden death. In the
of the TRACE study.11
2231 patients with an ejection fracValsartan in Acute Myocardial
tion of 40% or less, clinically signifiInfarction Trial (VALIANT), the incicant signs and symptoms of heart
Prognosis
dence and timing of sudden death in
failure occurred in 16% of surviving
Compared with patients without
14 609 patients with LVSD after
patients receiving placebo, and 16%
heart failure and LVSD after myocarmyocardial infarction were assessed.17
of all patients receiving placebo
dial infarction, patients who have
An increased early incidence of sudexperienced significant further deteheart failure and LVSD are at higher
den death was most apparent
rioration of left ventricular contracrisk for adverse outcomes, including
among patients with low ejection
tility, as indicated by a reduction of
cardiac rupture, cardiac arrest,
fraction. Of 156 sudden deaths or
9 units or more in ejection fraction.
stroke, longer hospitalizations, vencardiac arrests with resuscitation
These data provided some insight
tricular arrhythmias, recurrent
Stage A
At high risk for heart failure
but without structural heart
disease or clinical (symptomatic) heart failure
Therapy
Treat/control medical
conditions (hypertension,
lipid abnormalities,
metabolic syndrome or
obesity, diabetes mellitus,
vascular disease,
coronary artery disease,
or use of alcohol or illicit
drugs)
Nursing leadership
Develop/implement
algorithms or care
pathways to optimize
use of evidencebased therapies
Be sure admission order
sets include specialty
consultation and
treatment of medical
conditions that place
patients at high risk
for heart failure
Ensure that nurses
understand education
principles to teach
patients about self-care
5
that occurred during the first 30
days, 85 cases, equating to 54% of all
sudden deaths or cardiac arrests,
occurred among patients with an
ejection fraction of 30% or less,17
stressing the importance of early
recognition of LVSD after myocardial infarction.
necrotic tissue), or hypokinesis
(decreased motion of left ventricular
wall due to injured myocytes) after
myocardial infarction cause sustained activation of the compensatory mechanisms, secondary
damage of the left ventricle occurs,
resulting in worsening remodeling
of the left ventricle and cardiac
decompensation.18
Norepinephrine, angiotensin II,
endothelin, aldosterone, and tumor
necrosis factor have been implicated
as biologically active molecules that
contribute to heart failure; however,
adrenergic activation is thought to
play the most powerful role via βadrenergic signaling responses.
Adrenergic receptors have both beneficial and harmful biological
Pathophysiology
responses. They create a positive
inotropic and chronotropic response
and vasodilatation, but activation
also leads to growth of cardiac
myocytes, further muscle damage,
vasoconstriction, and other harmful
responses.18 In addition to activation
of harmful signaling mechanisms,
progression of disease in the left ventricle could be related to loss of beneficial effects of endogenous
vasodilators such as nitric oxide,
natriuretic peptides, and others if
the vasodilators cannot counteract
peripheral vasoconstrictor properties of norepinephrine and
angiotensin II18 (Figure 2). The biological and physiological processes
of heart failure are complex and
beyond the scope of this article, but
In asymptomatic LVSD after
myocardial infarction, the myocardial infarction is the event that initiates a decline in pumping capacity,
which leads to a reduction in ejection fraction. In order to compensate, mechanisms are activated in
the adrenergic nervous system,
renin-angiotensin aldosterone system, and cytokine system.18 The
changes lead
to restoration
of cardiac
Acute myocardial infarction
function, and
the patient
Activation of
remains
Adrenergic nervous system
Renin-angiotensin-aldosterone system
asymptoCytokine system
matic. If
changes in left
ventricular
Negative prolonged adrenergic activation:
Positive acute responses of adrenergic stimulation
systolic and
Cardiac myocyte growth
Positive inotropy
diastolic perCardiac muscle damage
Positive chronotrophy
Vasoconstriction and other harmful responses
Vasodilatation
formance
from akinesis
(lack of
Left ventricular disease progression
Maintain
motion of left
leading to remodeling
asymptomatic left ventricular
(dilatation and hypertrophy)
ventricular
dysfunction status
wall due to tissue cell
Hemodynamic effects
death), dyski↑ Left ventricular end-diastolic stress
nesis (abnor(afterload)
↑ Systolic left ventricular work
mal motion of
↓ Cardiac output
left ventricular
↓ Ejection fraction
wall due to
Figure 2 The complex pathophysiology of asymptomatic left ventricular systolic dysfunction after myocardial
aneurysm forinfarction.
mation at
Based on Mann and Bristow and Philippides.
injured or
18
19
these processes lead to deterioration
in left ventricular performance
through progressive remodeling of
the left ventricle, and such remodeling may independently lead to progression of heart failure.18
Similar to biological and physiological responses, the mechanical
responses created by remodeling of
the left ventricle are also complex
and involve alterations in the biology of cardiac myocytes, the
myocardium, and/or the left ventricle itself.18 As left ventricular size
increases and geometry changes
from an elliptical to a spherical
shape, the end-diastolic wall stress
(afterload) in the left ventricle
tion, and functional deterioration.
Alternatively, neurohormonal antagonism acts in asymptomatic LVSD
by blocking the remodeling process
responsible for the progressive
dilatation of the left ventricle and
declining systolic function that occurs
after a myocardial infarction.19-21
Numerous clinical trials16,19,22,23
have drawn attention to the clinical
importance of progressive remodeling of the left ventricle, and trial
results suggest that clinical development of heart failure may be connected to the development of left
ventricular dilatation and may occur
years after the initial ischemic injury.
Certain patient-specific factors
patients of therapies that can prevent the progression of heart failure
and reduce the risk of arrhythmias,
reinfarction, and sudden death.
Measurement of ejection fraction
after myocardial infarction is
extremely important because of the
large increase in risk for LVSD associated with myocardial infarction.
Asymptomatic LVSD should be suspected in any patient who has
recently had a myocardial infarction
and does not have symptoms of
heart failure, especially patients with
signs of heart failure such as elevated
jugular venous pressure, positive
hepatojugular reflux, and an S3 gallop. Early diagnosis of asymptomatic
Compared with patients without heart failure and LVSD
after myocardial infarction, patients who have heart
failure and LVSD are at higher risk for adverse outcomes,
including cardiac rupture, cardiac arrest, stroke, longer
hospitalizations, ventricular arrhythmias, recurrent
myocardial infarction, and death, including sudden death.
increases, leading to an increase in
left ventricular work during systole
that contributes to a decrease in cardiac output18 (Figure 2). Higher filling pressures (higher end-diastolic
pressure in the left ventricle) in
are associated with lower ejection
fraction and are a significant predictor of death or clinical heart failure.8
Thus, neurohormonal activation
leads to further loss of cardiomyocytes and worsening systolic
dysfunction, promoting further
remodeling, neurohormonal activa-
contribute to progression from
asymptomatic LVSD to symptomatic heart failure. Older age, diabetes, and hypertension contribute
to the progression of underlying systolic and diastolic myocardial dysfunction and the atherosclerotic
process.19
Importance of Diagnosis or
Recognition
The absence of signs or symptoms of heart failure after myocardial infarction may result in
unrecognized LVSD, depriving
LVSD is important, as suggested by
clinical trials in which mortality,
reinfarction, and other cardiovascular events were prevented when neurohormonal inhibitor therapy was
implemented.16,24,25
Left ventricular function should
be quantitatively measured by
means of echocardiography, angiography, or radionuclide imaging in
all patients after myocardial infarction. Although not a substitute for
quantitative assessment of left ventricular function, measurement of
the plasma level of brain natriuretic
peptide is useful in detecting heart
failure and requires only a single,
rapidly performed blood test. In 2
studies,26,27 measurement of the level
of brain natriuretic peptide was
helpful in predicting LVSD and
remodeling after myocardial infarction. Plasma levels of brain natriuretic peptide had an 84% sensitivity
in identifying the presence of asymptomatic LVSD in 75 patients without
symptomatic heart failure after
myocardial infarction.28
Further, some clinical features
are associated with LVSD in acute
myocardial infarction, and when
present, these features should suggest LVSD in asymptomatic
patients11,15,26,28-30 (Table 1). An algorithm that reflects the presence of
new anterior Q-wave infarction, clinical signs of heart failure, or 2 or
more previous myocardial infarctions plus an increase in level of cre-
atine phosphokinase greater than
1000 U/L in patients who had not
received thrombolytic agents had a
91% sensitivity and a 78% specificity
for detecting an ejection fraction of
40% or less in patients with acute
myocardial infarction.31
The value of early diagnosis of
LVSD after myocardial infarction
while the patient is still in the hospital should not be overlooked. The
hospital in general, and a coronary
care unit specifically, provides a
structured setting within an acute
environment with integrated care
pathways or care plans; access to
physicians, pharmacists, and specialty nurses who work in partnership; and the capacity to monitor
serum levels of hormones and
enzymes, cardiac hemodynamic
parameters, and medication tolerance. Nurse clinicians can create a
link between the acute myocardial
Table 1 Diagnostic cues of left ventricular systolic dysfunction in the
absence of symptomsa
Type of cue
Cue
Definitive
In hospital: echocardiography, ventriculography, or
radionuclide imaging results of wall motion
abnormality and left ventricular ejection fraction
≤40%
After discharge: echocardiographic results of
increased end-diastolic volume include increase
in left ventricular mass and increased wall motion
score index
Adjunctive (but not definitive)
Brain natriuretic peptide level >100 pg/dL
Clinical features associated
with left ventricular systolic
dysfunction (does not imply
causality; not definitive)
Killip class II: rales, S3 gallop, and elevated jugular
venous pressure
Presence of hepatojugular reflux
Early heart failure (shortly after admission for
myocardial infarction): older age, history of
symptomatic cardiac disease or diabetes mellitus
Late heart failure (4 days or more after myocardial
infarction): history of hypertension, male sex,
tachycardia, higher peak level of creatine
phosphokinase
Early or late myocardial infarction: myocardial
infarction of anterior wall
a Based on Hellermann et al,11 Wu et al,15 Crilley and Farmer,26 Choy et al,28 Cowie et al,29 and Papadopoulos
et al.30
infarction and the need for longterm treatment by ensuring an
echocardiogram is obtained, assessing the level of brain natriuretic peptide (when obtained), and tracking
clinical features known to be associated with LVSD after myocardial
infarction.
Underuse of Therapies for
Myocardial Infarction
Patients with LVSD after
myocardial infarction account for a
large proportion of patients treated
in hospitals. These patients are at a
high risk for adverse outcomes, and
thus therapy initiated in the hospital
must be optimized. Recent developments in pharmacological and
device therapy, as well as initiatives
to increase the use of standard
orders and promote in-hospital
communication, have improved the
care of patients who have had a
myocardial infarction.
Data from registries indicate that
care of patients with LVSD after
myocardial infarction is surprisingly
poor, despite the wealth of clinical
trial data that show benefits of treatment with numerous agents.
Researchers analyzing data from the
National Registry of Myocardial
Infarction (NRMI) of 606 500
patients with acute myocardial
infarction found that patients who
had heart failure at the time of hospitalization or in whom heart failure
developed later, were less likely to be
treated with evidence-based cardiac
therapies than were patients without
heart failure after myocardial infarction. Specifically, patients with heart
failure were much less likely to be
treated with aspirin and β-blockers
in the first 24 hours than were
patients without heart failure.33 The
Nurses must work collaboratively
with other healthcare providers and
use a team approach with nurse
peers to test all patients who have
had a myocardial infarction for the
presence of asymptomatic LVSD;
develop processes and systems that
promote use of evidence-based practices; promote education of patients
throughout the hospital stay, not
just before discharge; and implement performance-improvement
initiatives based on process and outcome measures of importance in this
population of patients (Figure 1).
Additionally, advance practice
nurses and nurse educators can provide education to increase the
understanding of nurse clinicians of
pathophysiological changes after
myocardial infarction that lead to
heart failure, optimal treatment
strategies, timing of treatment
strategies, and expectations for
teaching of patients so that care
1992-1993
1994-1995
1996-1997
2000-2001
2002-2003
80
70
60
50
40
30
20
10
0
β-Blocker
Applying a
Multidisciplinary Approach
1998-1999
90
Aspirin
Nurse clinicians, using a multidisciplinary approach, can help
overcome obstacles associated with
underuse of cardiac therapies.
delivery is coordinated and synchronized to improve patients’ outcomes.
Hospitalization should serve as a
teaching opportunity for patients
and their healthcare providers about
the importance of delivering optimal
therapy during hospitalization to
ensure cardiovascular health after
discharge. Patients who do not start
treatment with a lifesaving cardiovascular agent in the hospital are
also less likely to receive that therapy
after discharge.35 Programs that used
a multidisciplinary care approach to
promote optimization of evidencebased therapies during hospitalization were tremendously successful.35,36
The Cardiac Hospitalization Atherosclerosis Management Program
(CHAMP) was a multidisciplinary
hospital initiative that involved
nurses, physicians, medication
advice, dietary advice, and exercise
counseling after myocardial infarction.35 The multimodal intervention
100
% of patients
CRUSADE (Can Rapid Risk Stratification of Unstable Angina Patients
Suppress Adverse Outcomes with
Early Implementation of the American College of Cardiology/American
Heart Association Guidelines) registry investigators examined discharge therapy of 45 744 patients
with non–ST-elevation myocardial
infarction and heart failure. At the
time of hospitalization, 10 398
patients (22.7%) had signs of heart
failure and another 1664 (3.6%) had
clinical (symptomatic) heart failure.
Treatment patterns and in-hospital
outcomes in both sets of patients
were compared with those of patients
without signs of heart failure.34 The
results indicated that patients with
signs of heart failure were treated
less often with medications and
invasive cardiac procedures in the
first 24 hours after presentation.
These studies suggest significant
underuse of important cardiac therapies for patients with signs of heart
failure or clinical heart failure during the early course of hospital care
after myocardial infarction.
Although no one has specifically
measured treatment patterns in
after myocardial infarction, these
patients likely also do not receive the
best evidence-based care. Possible
causes are lack of recognition of
LVSD when symptoms are not present or unwarranted fear of prescribing vasoactive cardiovascular
therapy to patients with LVSD.
Angiotensinconverting enzyme
inhibitor
Drugs prescribed
Statin
Figure 3 Sustained impact of the Cardiac Hospitalization Atherosclerosis
Management Program.
Reprinted from Fonarow,37 with permission.
resulted in a dramatic increase in the
prescription of angiotensin-converting enzyme (ACE) inhibitors, βblockers, statins, and aspirin in the
year after its implementation37 (Figure 3) and a reduction in new
myocardial infarction, heart failure,
hospitalizations, and total mortality
events.35 Increased predischarge prescription rates in patients hospitalized after myocardial infarction were
sustained for 10 years.37
A hospital-based multidisciplinary care approach can prompt
early and continued use of lifesaving
agents. Researchers from the Initiation Management Predischarge:
Process for Assessment of Carvedilol
Therapy in Heart Failure (IMPACTHF) trial showed that patients with
heart failure in whom treatment
with a β-blocker was started in the
hospital were more likely to maintain treatment at 60 days after discharge than were patients who were
discharged without a β-blocker with
a plan to start taking it in an outpatient setting. At 60 days after hospital discharge, 91% of patients who
started treatment in the hospital
were still taking treatment, compared with 73% of patients who
started treatment after discharge
(P < .001).38 Investigators from multidisciplinary programs who followed
up many patients over time found
that when therapy for acute coronary syndrome was started in the
hospital, patients were more likely
to adhere to therapies long term.39
Many hospital discharge education and disease management programs and postdischarge disease
management programs are disease
specific; care processes (documentation of education delivered or laboratory testing) and drug therapies
Table 2 American College of Cardiology/American Heart Association guidelines for patients with ST-elevation myocardial infarction: class I recommendations for education at dischargea
Time
Education on and planning for adherence
Before hospital discharge
For patients
Lifestyle changes
Drug therapies important for secondary prevention of
cardiovascular disease
At discharge
For patients and their families (to ensure early evaluation and treatment if signs or
symptoms recur)
Recognizing acute cardiac signs and symptoms
Appropriate actions to take in response to signs or
symptoms
Calling 911 if symptoms are
Unimproved or worsen after 5 minutes of onset
Unimproved or worsen 5 minutes after 1 dose of
sublingual nitroglycerin
Automated external defibrillators
Cardiopulmonary resuscitation, including referral to a
training program (training programs with a social
support component for high-risk patients preferred)
Need for follow-up appointment to assess for left
ventricular function and need for implantable
cardioverter defibrillator (if ejection fraction <35%
after optimal medical therapies)
For patients’ families
a Based on Antman et al.40
are based on disease-specific standards of care, nationally developed
performance measures, and consensus guidelines derived from
multicenter, randomized controlled studies. Although in disease
management programs, patients
generally are taught about self-care,
receive treatment related to the disease process, are monitored for
adherence to medical therapy, and
receive risk reduction testing and
therapies, management is usually
specific to the primary discharge
diagnosis. Thus, care and discharge
instructions of patients after
myocardial infarction may not
include material about chronic
heart failure. Principles for managing stage B heart failure and education of patients with asymptomatic
might be even less likely, because
patients do not have clinical (symptomatic or stage C) heart failure.
Care and discharge education for
after myocardial infarction must be
integrated into emerging multidisciplinary management programs.
In-hospital emphasis on and predischarge education about preventive and self-care measures are as
important as ensuring patients
receive proper medications. Patients
who continue to smoke, not exercise, and eat poorly are at high risk
for a secondary cardiac event,
including a new myocardial infarction. Educating patients while they
are in the hospital is a class I recommendation from the American College of Cardiology/American Heart
Association (ACC/AHA) guidelines40
for myocardial infarction with STsegment elevation to maximize
adherence to treatments and
evidence-based medications after
the event. Education should begin
early during hospitalization, be
delivered intensively at discharge
(Table 2), and continue at follow-up
during visits with providers, cardiac
rehabilitation, and interactions with
community support groups.40 Individualized teaching programs led by
cardiac nurses that can be tailored to
suit the needs of different patients
are clearly needed.41 Cardiovascular
nurse clinicians are invaluable in
bridging the gap between primary
and secondary care. Education of
patients should be viewed as a continuous process that is a part of
every encounter with a patient,
including each encounter during
hospitalization.
Pharmacological and
Device Therapies
Nurse clinicians involved in hospital management of patients who
have had a myocardial infarction
must be able to accurately determine
the timing for initiating treatment
strategies to promote optimal care
that decreases the risk for poor outcomes. Some studies42 have focused
on reestablishing coronary blood
flow as soon as possible because of a
significant mortality benefit from
thrombolytic therapy in patients
with acute myocardial infarction.
Reperfusion therapies do not halt or
slow the progression of LVSD; left
ventricular remodeling still occurs
after successful percutaneous transluminal coronary angioplasty
despite sustained patency of the
infarct-related artery and preservation of regional and global function
of the left ventricle.43 In a study30 of
55 patients who had reperfusion
after acute myocardial infarction
and treatment with antiremodeling
medications (ACE inhibitor and βblocker), 28% experienced increases
in left ventricular volume within 6
months. Similarly, 1 year after acute
myocardial infarction of the anterior
wall in 266 patients, 31% had left
Table 3 American College of Cardiology/American Heart Association guidelines for management of ST-elevation myocardial infarctiona
Acute therapies
Discharge and postdischarge therapies
Aspirin
Aspirin
Clopidogrel (if percutaneous
coronary intervention)
Clopidogrel
β-Blocker
Angiotensin-converting
enzyme inhibitor
Heparin (low-molecularweight heaprin or unfractionated heparin)
Glycoprotein IIb-IIIa
inhibitor (if percutaneous
coronary intervention)
Percutaneous coronary
intervention or primary
thrombolysis
β-Blocker
Angiotensin-converting enzyme inhibitor
Aldosterone antagonist
Statin (preferred) or other lipid-lowering therapy
Smoking cessation counseling
Cardiac rehabilitation or aerobic exercise
Weight control if obese; diet high in omega-3 fatty acids
Control of blood pressure (resting systolic blood
pressure <140 mm Hg; resting diastolic blood
pressure <90 mm Hg)
Control of diabetes (fasting blood glucose level 80-100
mg/dL)
Anticoagulants, if indicated
Placement of implantable cardioverter defibrillator
(after 40 days after myocardial infarction) if ejection
fraction remains <35% after optimal medical
therapies
a Based on Antman et al40 and Amin.45
ventricular remodeling, even though
87% underwent coronary stenting of
the infarct-related lesion and 54%
received thrombolysis therapy.44 Even
if a patient has had revascularization
or does not initially have signs or
symptoms of heart failure, LVSD may
still be present and must be appropriately and aggressively treated to
halt progression of the disease.
As recommended by the ACC/
AHA treatment guidelines for both
heart failure and myocardial infarction, management of patients with
asymptomatic LVSD after myocardial infarction should be directed at
treating neurohormonal activation
due to remodeling and progression
of coronary artery disease.5,40 The
guidelines recommend treatment of
risk factors for coronary artery disease, including hypertension, cigarette smoking, and dyslipidemia,
and the use of evidence-based therapies for left ventricular dysfunction
including, ACE inhibitors and βblockers.5 Use of neurohormonal
antagonists is strongly recommended
for acute myocardial infarction.40 A
number of other therapies are beneficial in patients with asymptomatic
and are reviewed briefly in the following sections and in Table 3. Table
4 gives the major clinical outcomes
from trials that included patients
with asymptomatic LVSD.12,16,21,46-55
ACE Inhibitors/Angiotensin
Receptor Blockers
An ACE inhibitor should be
administered orally within the first
24 hours after a myocardial infarction in patients with anterior
myocardial infarction, heart failure,
or an ejection fraction less than 40%
Table 4
Clinical trials in patients with asymptomatic left ventricular systolic dysfunction12,16,21,46-55
Risk reduction, %
Study
Average
duration,
months
Relative mortality
Sudden death
Death due to
worsening
heart failure
Population of patients (N)
Treatment
Acute myocardial infarction and
asymptomatic LVSD (2231)
Captopril vs
placebo
42
19 (P = .02)
No difference
(P = NS)
36 (P = .032)
Asymptomatic LVSD (4228)
Enalapril vs
placebo
37.4
8 (P = NS)
No difference
(P = NS)
Trandolapril vs
placebo
24-50
22 (P = .001)
24 (P = .03)
20a
(P < .001)
29b
ACE inhibitors
SAVE
SOLVD
prevention
TRACE
Myocardial infarction and
LVSD (6676; 1749 randomized); asymptomatic LVSD
(542)
(P = .003)
β-Blockers
Retrospective
analysis of
SOLVD
prevention
Asymptomatic LVSD (4228;
1015 patients taking
β-blockers)
β-Blockers vs
no β-blockers
plus enalapril
37.4
23 (P < .01)
28c (P < .05)
29 (P < .05)
Post hoc
analysis of
SAVE
Asymptomatic LVSD (2231;
789 patients taking
β-blockers )
β-Blockers vs
no β-blockers
plus captopril
42
43 (P < .001)
NR
32b
(P < .001)
Heart failure (415);
Carvedilol vs
placebo
19
36a (P = .02)
10 (P = NS)
8 (P = NS)
LVSD after acute myocardial
infarction (1959); asymptomatic LVSD (1023)
Carvedilol vs
placebo
(including ACE
inhibitor)
15.6
23 (P = .03)
26 (P = .098)
40 (P = .08)
LVSD, heart failure, or both
(14 703); asymptomatic
LVSD (4099)
Valsartan,
captopril, or both
24.7
No difference
(P = NS)
NR
No difference
(P = NS)
Acute myocardial infarction
and symptomatic heart
failure (5477);
Losartan vs
captopril
32.4
13% increase in risk
with losartan
(P = .07)
19% increase
in risk with
losartan
(P = .07)
NR
ANZ
CAPRICORN
Angiotensin-receptor blockers
VALIANT
OPTIMAAL
Implantable cardioverter defibrillators
MADIT-II
LVEF ≤30% (1232);
ICD vs CMT
20
31 (P = .02)
NR
NR
DEFINITE
Nonischemic dilated
cardiomyopathy,
LVEF <36% (458);
ICD vs CMT
29
35 (P = NS)
80d
(P = .006)
NR
Abbreviations: ACE, angiotensin-converting enzyme; CMT, conventional medical therapy; ICD, implantable cardioverter defibrillator; LVEF, left ventricular ejection
fraction; LVSD, left ventricular systolic dysfunction; NR, not reported; NS, not significant.
a Death or hospitalization for heart failure.
b Severe heart failure.
c Arrhythmic death.
d Sudden death from arrhythmia.
Reprinted from Goldberg and Jessup,55 with permission.
reflecting asymptomatic LVSD. If
tolerated, the ACE inhibitor should
be administered during convalescence and continued indefinitely
after discharge.40 Researchers in a
pivotal randomized clinical trial
(SAVE),16 specifically addressed
after myocardial infarction. Compared with placebo, use of captopril
was associated with a 19% risk
reduction in all-cause mortality
(P = .02).16 Captopril also decreased
progression to clinical heart failure
by 37% (P < .001), hospitalization
for heart failure by 22% (P = .02),
and recurrent myocardial infarction
by 25% (P = .02).16
An echocardiographic substudy56
of SAVE indicated that left ventricular remodeling can be attenuated by
ACE inhibitors. In 420 patients, 2dimensional echocardiography was
performed soon after infarction and
repeated after 1 year. The size of the
left ventricle increased both in patients
who received placebo and in patients
who received captopril; however, the
increases were significantly greater in
the placebo-treated group (P = .02 for
diastolic and for systolic).56
In VALIANT, patients with left
ventricular dysfunction after
myocardial infarction were randomized to treatment with captopril
alone (target dose: 50 mg 3 times
daily), valsartan alone (target dose:
160 mg twice daily), and combination therapy (target doses: captopril
50 mg 3 times daily, valsartan 80 mg
TIMELY
DIAGNOSIS AND
A MULTIDISCIPLINARY
APPROACH TO
PATIENT CARE
IS CRUCIAL
twice daily).51 After median followup of 24.7 months, no significant
differences in the risk of death
among the 3 groups were apparent,
although the combination group
had more drug-related adverse
events (hypotension, hyperkalemia,
renal dysfunction). VALIANT provided evidence that the angiotensinreceptor blocker valsartan was just
as effective as an ACE inhibitor in
after myocardial infarction. However, the addition of an angiotensinreceptor blocker to an ACE inhibitor
did not provide an incremental benefit and therefore is not recommended as an addition to therapy.51
Angiotensin-receptor blockers may
be used as an alternative for patients
who are intolerant of ACE inhibitors
because of cough, symptomatic
hypotension, or angioedema.
β-Adrenergic Blockers
Although the benefits of βblocker therapy in patients who
have had a myocardial infarction are
established, relative risks and benefits in patients with LVSD after
myocardial infarction are not as well
understood. Many early trials of βblocker therapy excluded patients
with heart failure or known LVSD.
• Survivors of
myocardial infarction should be
assessed for
asymptomatic left
ventricular systolic
dysfunction
(LVSD).
Investigators in the Carvedilol PostInfarct Survival Control in Left Ventricular Dysfunction (CAPRICORN)
trial specifically enrolled 1959
patients who had LVSD after
myocardial infarction (ejection fraction ≤40%), with or without signs or
symptoms of heart failure, and compared the effect of carvedilol with
that of placebo on mortality and
morbidity.21 In the CAPRICORN
study, 34% of participants had no
signs or symptoms of heart failure.
Patients received an ACE inhibitor
(97%) and aspirin (86%), and many
had thrombolysis or primary angioplasty (46%) for acute myocardial
infarction before enrollment.
Carvedilol-treated patients experienced a 23% relative risk reduction
in all-cause mortality (P = .03) and a
41% relative risk reduction in recurrent nonfatal myocardial infarction
(P = .01) during 1.3 years of followup.21 Subgroup analysis indicated
that all-cause mortality was reduced
similarly in patients treated with
carvedilol regardless of their status
relative to signs and symptoms of
heart failure.55
The improvement in clinical outcomes in the CAPRICORN trial is
consistent with a retrospective
analysis49 of patients enrolled in
• Patients who
have asymptomatic LVSD after
myocardial infarction have worse
outcomes than do
patients without
LVSD.
• Cardiac nurses are
uniquely positioned to
help improve patients’
survival and quality of life
by facilitating recognition
of LVSD and promoting
use of evidence-based
therapies early in the
course of treatment.
SAVE who concomitantly received βblockers (approximately 35% of study
participants). β-Blocker use was
associated with a 30% risk reduction
in cardiovascular death and a 21%
risk reduction in progression to
severe heart failure that were independent of concomitant use of an
ACE inhibitor or a placebo.49 In the
SOLVD Prevention trial,48 the combination of a β-blocker and an ACE
inhibitor was associated with a synergistic reduction in the risk of death in
patients with asymptomatic LVSD.
An echocardiographic substudy57
of 127 patients from the CAPRICORN trial indicated that β-blocker
treatment was associated with reversal of left ventricular remodeling at 6
months. Although carvedilol treatment did not significantly alter enddiastolic volume, end-systolic
volume decreased 4.8 mL with
carvedilol and increased 4.5 mL with
placebo (P = .02). Left ventricular
ejection fraction also increased in
the carvedilol group by 5% after 6
months of treatment; no change was
observed with placebo.57
blocker) reduced the risk of mortality in patients with LVSD after
myocardial infarction and symptomatic heart failure in the Eplerenone
Post-Acute Myocardial Infarction
Heart Failure Efficacy and Survival
Study (EPHESUS).20 Aldosterone
antagonists have not been investigated in patients with asymptomatic
LVSD. In EPHESUS, 6642 patients
with LVSD after myocardial infarction were randomized to treatment
with eplerenone or placebo.
Eplerenone treatment was associated with a relative risk reduction in
all-cause mortality (15%; P = .008),
sudden death (21%; P = .03), and
hospitalization for heart failure (15%;
P = .03).20 Aldosterone blockade with
eplerenone also had early benefits.
In an analysis58 of all-cause mortality
and sudden cardiac death in the
EPHESUS trial after 30 days of treatment, researchers found a 31% risk
reduction in all-cause mortality and
a 37% risk reduction in sudden cardiac death compared with placebo.
Statins
Statins (hydroxymethylglutarylCoA reductase inhibitors) are indicated in the management of patients
after myocardial infarction and
Use of an aldosterone antagonist
should be considered in patients
(added to an ACE inhibitor and a βwith
asymptomatic
• A multidisciplinary
• Cardiac nurses can
LVSD
after
approach to care of
reduce risks and enhance
myocarpatients with asymptopatients’ adherence to
dial
matic LVSD after myocarmedical therapies by
infarcdial infarction prompts
ensuring that each
tion. Repatient understands what evidence-based treatment
searchers
he or she is taught before and may help patients
in 2 lipidcontinue with therapies.
hospital discharge.
lowering
studies59,60
Aldosterone Receptor
Antagonists
specifically enrolled survivors of
myocardial infarction without heart
failure. Researchers of the Scandinavian Simvastatin Survival Study59
found that simvastatin reduced the
relative risk of new nonfatal myocardial infarction by 38% and the overall risk of heart failure by 21% in
4444 randomized patients with a
history of myocardial infarction. In
the Cholesterol and Recurrent
Events (CARE) trial60 4159 survivors
of myocardial infarction without evidence of heart failure were randomized to treatment with pravastatin or
placebo.60 Compared with placebo,
pravastatin reduced the relative risk
of myocardial infarction by 25%. In a
CARE trial subgroup of patients
with LVSD (706 with ejection fraction between 25% and 40%), pravastatin provided a significant 28%
reduction in risk for myocardial
infarction.60
Implantable Cardioverter
Defibrillators
Although the ACC/AHA guidelines stress the importance of preventing the progression of LVSD
from an asymptomatic state to
symptomatic heart failure, patients
who have had a myocardial infarction, especially those with LVSD, die
suddenly and unexpectedly of lethal
arrhythmias.16,21,61 The role of treatment with an implantable cardioverter defibrillator (ICD) was
compared with drug therapy for
patients with LVSD after myocardial
infarction in several trials. Investigators in the Multicenter Unsustained
Tachycardia Trial (MUSTT) enrolled
2202 patients with unsustained ventricular tachycardia, left ventricular
ejection fraction less than 40%, and
coronary artery disease.62 Rates of
arrhythmic death and overall mortality were lower in the patients who
had an ICD.62
In the second Multicenter Automatic Defibrillator Implantation
Trial (MADIT II), 1232 patients with
a left ventricular ejection fraction of
30% or less and a history of prior
myocardial infarction were randomized to receive preventive placement
of an ICD or conventional medical
therapy after myocardial infarction.
Patients who received an ICD had
a myocardial infarction include
implantation of an ICD if ejection
fraction criteria are met 40 days
after myocardial infarction.
Care Pathways
Risk-stratification tools are available for patients with acute coronary
syndromes.65-70 These clinical prediction models can facilitate optimization of patients’ management and
were integrated into national guidelines to help enhance patients’ out-
vide resources and processes that
match pathway actions.
A number of tools, including
preprinted orders,45,73 care maps,73,74
discharge forms,45,73,74 physician/nursing education plans,45,73,74
and treatment utilization reports,73,74
have been developed to encourage
the initiation of as many lifesaving
therapies as possible before patients
are discharged. Tools are designed to
specify guideline-recommended
treatments and encourage proper
Nurse clinicians can create a link between the acute
myocardial infarction and the need for long-term
treatment by ensuring an echocardiogram is obtained,
assessing the level of brain natriuretic peptide (when
obtained), and tracking clinical features known to be
associated with LVSD after myocardial infarction.
significantly better survival after 20
months.53 In the Defibrillator in
Acute Myocardial Infarction Trial
(DINAMIT), patients with a left ventricular ejection fraction of 35% or
less and decreased heart rate variability were randomized to receive
an ICD between 6 and 40 days after
myocardial infarction.63,64 Overall
mortality was not improved by early
implantation of an ICD because the
reduction in arrhythmic death was
offset by nonarrhythmic events;
therefore, the use of an ICD before
40 days after myocardial infarction
is not currently recommended.59
Both studies included a sizable proportion of patients with asymptomatic LVSD, thus current ACC/AHA
guidelines for patients who have had
comes.71 In the Duke Heart Failure
Program, clinicians used significantly more β-blocker therapy after
pathway implementation, more
patients reached target β-blocker
doses, and cost of care decreased
throughout the hospital system.72
Management pathways for myocardial infarction can serve as the
framework for developing and instituting optimal in-hospital management of patients after myocardial
infarction by reminding caregivers
to assess for LVSD and noting recommended treatments. Education of
patients, assessment of social support and depression, discharge planning, follow-up, and outpatient
monitoring can also be improved
through critical pathways that pro-
administration in appropriate
patients. The results of an observational analysis of hospital care in
64 775 patients with acute coronary
syndrome who were enrolled in the
CRUSADE National Quality
Improvement Initiative were
assessed to evaluate use of the
ACC/AHA guideline recommendations.75 In 74% of cases, care decisions were consistent with the
ACC/AHA guidelines. The overall
rate for adherence to guidelines was
significantly associated with inhospital mortality: mortality rates
decreased from 6.31% for the lowest
adherence quartile to 4.15% for the
highest adherence quartile (P < .001).
Every 10% (risk-adjusted) increase in
composite adherence in a hospital
was associated with a 10% decrease
in its patients’ likelihood of inhospital mortality (P < .001).75 The
significant association between care
process and outcomes supports the
use of broad, guideline-based performance metrics as a means of
assessing and helping improve hospital quality.
The ACC/AHA guidelines recommend that critical pathways, protocols, and other quality
improvement tools be used by caregivers and institutions to improve
the application of evidence-based
treatments for patients with STsegment elevation myocardial infarction.40 In the AHA Get With the
Guidelines program, many tools can
be used to improve care. For example, an online patient management
tool provides source documentation
of performance measures and also is
the source of patient education
materials and treatment plan summaries used to educate or facilitate
communication among health care
providers.76 Analyses of data from
the patient management tool can be
used to identify factors related to
patients and hospital systems that
can be altered to improve patients’
outcomes or delivery of cardiovascular care.
third of patients have LVSD after
myocardial infarction, and about
one-half of patients with LVSD are
asymptomatic. The risk of death or
heart failure depends on the extent
of injury of the left ventricle. Mortality in asymptomatic LVSD can be
from progressive heart failure, recurrent myocardial infarction, or lethal
arrhythmias. The lack of signs or
symptoms of heart failure after
myocardial infarction may create a
false sense of health and deprive
patients of proven lifesaving therapies. Timely diagnosis of asymptomatic LVSD by echocardiography,
ventriculography, or radionuclide
imaging is crucial.
Evidence-based management of
asymptomatic LVSD in patients who
have had a myocardial infarction
centers on early and continued neurohormonal antagonism of the
renin-angiotensin-aldosterone and
sympathetic nervous systems with
an ACE inhibitor or angiotensinreceptor blocker and β-blocker therapy because these agents reduce risk
of mortality and the likelihood of
heart failure developing. Although
recent clinical guidelines do not
specifically recommend any particular
agent, captopril, enalapril, and
carvedilol have the most evidence of
effectiveness in patients with asympConclusions
tomatic LVSD after myocardial
Nurse clinicians play a critical
infarction. Of major importance is
role in caring for patients after
treatment of risk factors for progresmyocardial infarction. About onesion of heart failure and coronary
artery disease, including hypertension, diabetes, and dyslipidemia, and
placement of an ICD as indicated for
primary or secondary prevention of
To learn more about heart failure, read
sudden cardiac arrest. Hospital nurse
“Evidence-Based Practice for Acute Decompensated Heart Failure” by Nancy M. Albert, clinicians, advanced practice nurses,
Cathy A. Eastwood, and Michelle L. Edwards
and nurse educators should develop
in Critical Care Nurse 2004:24:14-29. Aavailable online at ccn.aacnjournals.org.
and use critical pathways to improve
•
d t
recognition and treatment of LVSD
after myocardial infarction and to
educate patients. The prevention of
disease progression in patients with
asymptomatic LVSD after myocardial infarction is based on early
intervention and education. CCN
Financial Disclosures
Nancy Albert is on the speaker’s bureau and is a consultant for GlaxoSmithKline and is a consultant for
Medtronic Inc.
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Now that you’ve read the article, create or contribute to an online discussion about this topic
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397-402.
43. Bolognese L, Neskovic AN, Parodi G, et al.
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coronary angioplasty: patterns of left ventricular dilation and long-term prognostic
implications. Circulation. 2002;106(18):
2351-2357.
44. Savoye C, Equine O, Tricot O, et al. Left ventricular remodeling after anterior wall acute
myocardial infarction in modern clinical
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45. Amin A. Improving the management of
patients after myocardial infarction, from
admission to discharge. Clin Ther.
2006;28(10):1509-1539.
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mortality and the development of heart failure in asymptomatic patients with reduced
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SOLVD Investigators. N Engl J Med. 1992;
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47. Kober L, Torp-Pedersen C. Clinical characteristics and mortality of patients screened
for entry into the Trandolapril Cardiac Evaluation (TRACE) study. Am J Cardiol. 1995;
76(1):1-5.
48. Exner DV, Dries DL, Waclawiw MA, Shelton B, Domanski MJ. Beta-adrenergic blocking agent use and mortality in patients with
asymptomatic and symptomatic left ventricular systolic dysfunction: a post hoc
analysis of the Studies of Left Ventricular
Dysfunction. J Am Coll Cardiol. 1999;33(4):
916-923.
49. Vantrimpont P, Rouleau JL, Wun CC, et al.
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to angiotensin-converting enzyme
inhibitors in the Survival and Ventricular
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al. Valsartan, captopril, or both in myocardial infarction complicated by heart failure,
left ventricular dysfunction, or both. N Engl
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Dickstein K, Kjekshus J. Effects of losartan
and captopril on mortality and morbidity in
high-risk patients after acute myocardial
infarction: the OPTIMAAL randomised
trial. Optimal Trial in Myocardial Infarction
with Angiotensin II Antagonist Losartan.
Lancet. 2002;360(9335):752-760.
Moss AJ, Zareba W, Hall WJ, et al. Prophylactic implantation of a defibrillator in
patients with myocardial infarction and
reduced ejection fraction. N Engl J Med.
2002;346(12):877-883.
Kadish A, Dyer A, Daubert JP, et al. Prophylactic defibrillator implantation in patients
with nonischemic dilated cardiomyopathy.
N Engl J Med. 2004;350(21):2151-2158.
Goldberg LR, Jessup M. Stage B heart failure: management of asymptomatic left ventricular systolic dysfunction. Circulation.
2006;113(24):2851-2860.
St John Sutton M, Pfeffer MA, Plappert T, et
al. Quantitative two-dimensional echocardiographic measurements are major predictors of adverse cardiovascular events after
acute myocardial infarction: the protective
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Doughty RN, Whalley GA, Walsh HA,
Gamble GD, Lopez-Sendon J, Sharpe N.
Effects of carvedilol on left ventricular
remodeling after acute myocardial infarction: the CAPRICORN Echo Substudy.
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reduces mortality 30 days after randomization following acute myocardial infarction
in patients with left ventricular systolic dysfunction and heart failure. J Am Coll Cardiol.
2005;46(3):425-431.
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Faergeman O, Pyorala K. The effects of simvastatin on the incidence of heart failure in
patients with coronary heart disease. J Card
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effect of pravastatin on coronary events
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average cholesterol levels. Cholesterol and
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Amiodarone Trial Investigators. Lancet.
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ME, Prystowsky EN, Hafley G. A randomized study of the prevention of sudden
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Get with the guidelines. American Heart
Association Web site. http://www
.americanheart.org/presenter.jhtml?identifier
=1165. Accessed January 8, 2008.
CE Test Test ID C082: Recognizing and Managing Asymptomatic Left Ventricular Dysfunction After Myocardial Infarction
Learning objectives: 1. Identify the definitive measurement for the diagnosis of asymptomatic left ventricular systolic dysfunction (LVSD) after
myocardial infarction 2. Describe the pathophysiology of asymptomatic LVSD after myocardial infarction 3. Discuss the pharmacologic management of
asymptomatic LVSD after myocardial infarction
1. Which percentage of myocardial infarctions is accompanied by left ventricular
systolic dysfunction (LVSD)?
a. 20%
b. 40%
c. 60%
d. 80%
7. Which of the following medication classes decreased progression from asymptomatic LVSD to clinical heart failure by 37% in the SAVE trial?
a. Calcium-channel blocker
b. Antiplatelet
c. β-Blocker
d. ACE inhibitor
2. Which of the following left ventricular end-diastolic pressures were associated
with higher rates of death or severe heart failure in the SAVE trial?
a. 15 mm Hg
b. 20 mm Hg
c. 25 mm Hg
d. 30 mm Hg
8. Which of the following medication classes was just as effective as an ACE
inhibitor in patients with asymptomatic LVSD in the VALIANT trial?
a. Aldosterone receptor antagonist
b. Angiotensin receptor blocker
c. Adrenergic agonist
d. Antiplatelet
3. Which of the following was most apparent among patients with low ejection
fractions in the VALIANT trial?
a. Cardiac rupture
b. Recurrent myocardial infarction
c. Sudden cardiac death
d. Cardioembolic stroke
9. Which of the following medication classes increased left ventricular ejection
fraction by 5% after 6 months of treatment in the CAPRICORN trial?
a. Statin
b. Aldosterone receptor antagonist
c. β-Blocker
d. ACE inhibitor
4. In asymptomatic LVSD after myocardial infarction, which of the following
leads to loss of cardiomyocytes, left ventricular remodeling, and functional
deterioration?
a. Neurohormonal activation
b. Normalized end-systolic wall stress
c. Endogenous vasodilation
d. Increased cardiac output
10. Which of the following medication classes added to an ACE inhibitor and
beta-blocker reduced the risk of mortality in patients with LVSD in the EPHESUS
trial?
a. Statin
b. Aldosterone receptor antagonist
c. Loop diuretic
d. Calcium-channel blocker
5. Which of the following measurements is a definitive diagnostic cue of
asymptomatic LVSD after myocardial infarction?
a. Creatine phosphokinase
b. Brain natriuretic peptide
c. Ejection fraction
d. Left ventricular end-diastolic pressure
11. Which of the following medication classes reduced the risk of new nonfatal
myocardial infarction and heart failure in asymptomatic LVSD after myocardial
infarction in the Scandinavian Survival Study?
a. ACE inhibitor
b. Heparin
c. Antiplatelet
d. Statin
6. Which of the following pharmacologic regimens should be considered for
patients with asymptomatic LVSD after myocardial infarction?
a. Angiotensin-converting enzyme (ACE) inhibitor, β-blocker, aldosterone receptor
antagonist, statin
b. β-Blocker, statin, ACE inhibitor, loop diuretic
c. Aldosterone receptor antagonist, calcium-channel blocker, β-blocker, ACE
inhibitor
d. Calcium-channel blocker, ACE inhibitor, statin, β-blocker
12. Which of the following ejection fractions was a criterion for an implantable
cardioverter defibrillator in the MADIT II trial?
a. 30%
b. 35%
c. 40%
d. 45%
Test answers: Mark only one box for your answer to each question. You may photocopy this form.
1. K a
Kb
Kc
Kd
2. K a
Kb
Kc
Kd
3. K a
Kb
Kc
Kd
4. K a
Kb
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Kd
5. K a
Kb
Kc
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6. K a
Kb
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7. K a
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8. K a
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9. K a
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11. K a
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10. K a
Kb
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12. K a
Kb
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Test ID: C082 Form expires: April 1, 2010 Contact hours: 1.5 Fee: AACN members, $0; nonmembers, $11 Passing score: 9 correct (75%) Category: A, Synergy CERP B
Test writer: John P. Harper, RN-BC, MSN
Program evaluation
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Recognizing and Managing Asymptomatic Left Ventricular Dysfunction: After Myocardial Infarction

Transcription

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