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Post Myocardial Infarction Left Ventricular
Dysfunction And Failure
Introduction
In the post-myocardial infarction (MI) patient with coronary
artery disease (CAD) and left ventricular dysfunction (LVD),
ischemia and adverse remodeling hinder myocardial performance
and increase electrical instability. Collectively, the coronary
arteries, myocardium, and conduction system represent the
principal pathophysiologic targets in MI complicated by LVD and
subsequent failure. Patients with reduced left ventricular ejection
fractions (LVEFs) and previous myocardial infarction (MI) or heart
failure are at increased mortality risk. Clinical, angiographic, and
electrocardiographic characteristics at the time of STEMI must be
evaluated to predict LVEF at ≥90 days. Consequently, an accurate
assessment of disease severity in these targets is essential for the
design of an effective therapeutic program.This review describes
the current modalities for assessing the key pathophysiologic
targets in post-MI patients with LVD and the effects of systemic
factors on cardiac disease severity.
Coronary atherosclerosis is the principal cause of ischemic heart
disease. Plaques can evolve into stenotic lesions with a hard
fibrous composition leading to stable angina. Plaques can also be
vulnerable to rupture without being necessarily obstructive and
can lead to thrombus formation and the development of acute
ischemic syndromes, including unstable angina and MI.1
Assessing Coronary Artery Disease
Coronary angiography remains the “gold standard” technique
for assessing the presence, extent, and severity of CAD and for
determining appropriate therapy. Current American College of
Cardiology/American Heart Association (ACC/AHA) guidelines
strongly recommend (class 1) that coronary angiography be
performed in patients with suspected CAD, including post-MI
patients who are candidates for primary or rescue percutaneous
coronary intervention.2 Likewise, early angiography with the goal
of revascularization is also strongly recommended (class 1) in
patients with unstable angina/non-ST-segment elevation MI (nonSTEMI) and any high-risk features, including elevated cardiac
biomarkers, ST-segment depression, a reduced left ventricular
ejection fraction (LVEF), or signs of heart failure (HF).3Angiography
can also identify candidates for revascularization among patients
with post-MI Left ventricular dysfunction (LVD) who present late
Amal Kumar Banerjee,
Dipankar Ghosh Dastidar, Kolkata
or have had clinically “silent” MI.The technique is especially useful
in patients with ongoing angina, ischemia, or HF. Angiography may
also be necessary to identify obvious bypass surgery candidates,
such as those with LVD and significant left main CAD.
Multislice spiral computed tomographic angiography is a promising
noninvasive imaging modality for the assessment of CAD.Although
it is not as accurate as angiography for characterizing CAD, partly
because of the rapid motion of the beating heart and the small
dimensions of the coronary arteries, it could prove to be a useful
method for ruling out coronary stenoses in low-risk patients
reporting possible symptoms of ischemia.4
Assessing Left Ventricular Dysfunction
Left ventricular function has long been recognized as a major
predictor of both short- and long-term survival after MI.Although
a higher LVEF is associated with increased survival, SCD risk
does not correlate well with LVEF. This was demonstrated in
the Oregon Sudden Unexpected Death Study, where an LVEF
of ≤0.35 was observed in only 30% of cases of sudden cardiac
death (SCD) in which left ventricular function had been assessed
within the preceding 2 years.5 This seeming discrepancy might
exist because although LVEF is primarily a measure of chronic risk
associated with the burden of myocardial scar, there are a number
of transient functional disturbances and electrophysiologic events
that can precipitate a fatal arrhythmia without a lowered LVEF.
Conditions such as transient ischemia and reperfusion, electrolyte
disturbances, and autonomic fluctuations would not be detected
by an LVEF assessment, but they could precede a fatal arrhythmia.6
Many recent trials have addressed the issue of assessing the
prognostic power of different indices of left ventricular function
by studying post-MI patients who have undergone reperfusion.
The Global Utilization of Streptokinase and Tissue Plasminogen
Activator for Occluded CoronaryArteries (GUSTO) angiographic
investigators assessed left ventricular function 90 minutes after
thrombolysis in patients with acute MI. They found that multiple
markers of left ventricular function, including LVEF, ESV, and
Medicine Update 2010  Vol. 20
Fig. 1 : Indices of left ventricular function 90 minutes after
thrombolysis in patients who survived 30 days after an acute
myocardial infarction (MI) and in patients who died before 30
days after an acute MI (p = 0.001). ESVI = end-systolic volume
index; LVEF = left ventricular ejection fraction.7
Fig. 3 Annual mortality rates for patients with coronary artery
disease and left ventricular dysfunction stratified by coronary
revascularization (revasc.) medical treatment and myocardial
viability.11
target. Recently, it was demonstrated that post-MI patients
with silent ischemia randomized to balloon-only percutaneous
coronary intervention had markedly reduced cardiac events
and a higher average LVEF through 10 years of follow-up versus
medical management alone.9 In post-MI patients without ongoing
ischemia, myocardial viability may be an important therapeutic
target. Because left ventricular function can improve significantly in
patients with a dysfunctional but viable myocardium who undergo
coronary revascularization, viability testing offers a means for
predicting the reversibility of LVD. Viable but dysfunctional
myocardium may either be “hibernating” or “stunned,” with the
former representing myocardium that has adapted to a chronic
state of underperfusion and the latter an adequately perfused
myocardium that is dysfunctional because of active ischemia.10
In a meta-analysis of 24 published studies, Allman et al11 assessed
late survival after revascularization or medical therapy in patients
with CAD and LVD who underwent myocardial viability testing. In
patients with myocardial viability, annual mortality was significantly
lower in patients treated with revascularization than it was in
the group receiving medical treatment alone. In contrast, among
patients without myocardial viability, there were no significant
differences in mortality rates between those undergoing
revascularization and those receiving medical therapy alone
(Figure 3).11
Fig. 2 : Kaplan-Meier survival curves for cardiac death in patients with and without left ventricular remodeling at 6 months
after primary percutaneous coronary intervention for acute
myocardial infarction (p = 0.005).8
regional wall motion, were predictive of 30-day post-MI survival
(Figure 1).7 Meanwhile, Bolognese and colleagues8 reported that
remodeling assessed by left ventricular dilation (≥20% increase
in EDV) was a good predictor of 5-year cardiac mortality in
patients with MI who were treated with primary percutaneous
transluminal coronary angioplasty (Figure 2).
A recent retrospective observational study examined
approximately 4,000 patients with HF and CAD, most of whom
(78.2%) had LVD. Patients who underwent revascularization
had substantially reduced mortality at 1 year (11.8% vs 21.6%;
hazard ratio, 0.52; 95% confidence interval, 0.47–0.58), which was
Assessing Ongoing Ischemia And
Myocardial Viability
Ongoing ischemia after MI can be an important therapeutic
252
Post Myocardial Infarction Left Ventricular Dysfunction and Failure
before revascularization. Among dysfunctional myocardial
segments, the likelihood of improvement in regional contractility
after revascularization was significantly and inversely related to
the transmural extent of hyperenhancement. In addition, the
percentage of the left ventricle that was dysfunctional but viable
before revascularization was strongly correlated with the degree
of improvement in the global wall motion score and LVEF after
revascularization.14 In a subsequent study, the same group found
a strong correlation between infarct transmurality at baseline,
as measured by CMR, and improvement in contractile function
at 8–12 weeks in post-MI patients who underwent successful
revascularization. Patients with transmural scarring do not
respond to β-blockers as effectively as patients with more viable
myocardium.15
Fig. 4 : Predictive value of myocardial viability assessment
tools for improvement in regional left ventricular (LV) function after coronary revascularization. CABG = coronary
artery bypass graft surgery; Echo = echocardiography; FDG =
18
F-fluorodeoxyglucose; MBF = myocardial blood flow; PET =
positron emission tomography; PTCA = percutaneous transluminal coronary angioplasty; SPECT = single-photon emission
computed tomography.10
Assessing Microvascular Obstruction
maintained through 7 years of follow-up.12
A number of noninvasive imaging methods are used to identify viable
myocardium in patients with LVD. Positron emission tomography
imaging uses enhanced 18F-fluorodeoxyglucose uptake relative
to myocardial blood flow as a marker for myocardial viability.
Thallium-201 single-photon emission computed tomography
imaging assesses membrane integrity and myocardial perfusion by
measuring uptake several hours after radioisotope administration.
A third method, low-dose dobutamine echocardiography, detects
viability by measuring myocardial contractile reserve during
inotropic stimulation.10
The techniques used to assess myocardial viability can differ in
their accuracy for predicting improvement after revascularization
(Figure 4). Although the combined results of 34 studies involving
926 patients showed that positron emission tomography and
dobutamine echocardiography displayed similar accuracy for
predicting improvement in regional left ventricular function after
revascularization, thallium single-photon emission computed
tomography imaging showed a lower positive predictive value
than the other 2 methods. It did, however, demonstrate a better
negative predictive value.10
A newer method of identifying regions of viable myocardium
after MI involves the use of contrast-enhanced cardiac magnetic
resonance imaging (CMR). In animal studies, hyperenhancement
on CMR was found to coincide with both the extent of myocyte
necrosis developing days after injury and with the extent of scar
tissue measured weeks later. In human studies, the signal intensity
of hyperenhanced regions, which correspond to infarcted areas,
was much higher than it was for normal myocardium, indicating
that CMR can accurately differentiate between normal and injured
regions of myocardium.13
Kim et al14 used CMR to identify reversible myocardial dysfunction
253
Another predictor of outcome is the degree of microvascular
obstruction after MI. Obstruction of the microcirculation has
been associated with both poor recovery of global and regional
left ventricular function soon after successful reperfusion and with
a higher risk for developing HF16.Wu et al 17 used CMR to visualize
regions of significant microvascular obstruction at the infarct core
in patients after MI. After an average follow-up of 16 months, the
presence of microvascular obstruction was found to be predictive
of serious cardiovascular complications. Even with the infarct size
controlled, the presence of microvascular obstruction remained
a prognostic indicator of post-MI complications.17
Assessing Electrical Markers Of
Arrhythmic Risk
Post-MI patients with LVD are at an increased risk of SCD, usually
from ventricular tachyarrhythmias. Because electrical instability is
a precursor to fatal arrhythmia, identifying indices of myocardial
electrical activity might help to predict SCD risk.
A number of measures have been theorized to have prognostic
value for identifying patients at high risk for SCD, especially in
the first year after MI.Among such measures is the occurrence of
ambient arrhythmias, such as frequent premature depolarizations
and nonsustained ventricular tachycardia.18 Although early studies
suggested an association with SCD, a survival benefit has not been
demonstrated for suppression of such arrhythmias.19 In contrast,
spontaneous nonsustained ventricular tachycardia and a low LVEF
have been shown to be important predictors of improved survival
in post-MI patients with LVD who have received an implantable
cardioverter defibrillator (ICD).
Standard electrocardiographic measures, such as the length of
the QRS and QT intervals, have also been proposed as markers
of arrhythmic risk in post-MI patients. A longer QRS interval
duration on initial electrocardiography before reperfusion therapy
was associated with an increase in 30-day mortality in patients
with MI who were treated with thrombolysis.20 Similarly, a longer
QRS duration observed on discharge electrocardiography was
Medicine Update 2010  Vol. 20
make suppression of its activity an important component of postMI treatment.Angiotensin II is a potent peripheral vasoconstrictor
that can induce ventricular hypertrophy. Angiotensin II also
stimulates secretion of aldosterone, which causes sodium
retention, further contributing to the development of ventricular
hypertrophy
STEMI
Primary Invasive Strategy
Fibrinolytic Therapy
Cath
Performed
No Cath
Performed
EF>0.40
No High-Risk
Features
Revascularization
as Indicated
No Reperfusion Therapy
EF>0.40
EF<0.40
EF<0.40
Catheterization and
Revascularization as
Indicated
High-Risk
Features
High-Risk
Features
No High-Risk
Features
Among comorbid conditions, type 2 diabetes mellitus causes
significant metabolic, hemodynamic, and neurohormonal
changes, which collectively increase cardiovascular risk in the
post-MI patient. Insulin resistance plays a central role through
its impact on multiple regulatory pathways. The compensatory
hyperinsulinemia associated with insulin resistance raises blood
pressure by increasing SNS activity. It also activates RAAS, causing
an increase in angiotensin levels. Increased level of circulating free
fatty acids causes arrhythmias.The use of a glucose-insulin infusion
followed by an extended course of subcutaneous insulin has been
shown to improve long-term survival in patients with diabetes
presenting with an acute MI.27
Functional
Evaluation
ECG Interpretable
ECG Uninterpretable
Unable to Exercise
Able to Exercise
Able to Exercise
Pharmacologic Stress
Submaximal
Exercise Test
Before Discharge
Catheterization and
Revascularization as
Indicated
Symptom-Limited
Exercise Test
Before or After Discharge
Adenosine
or Dipyridamole
Nuclear Scan
Clinically Significant
Ishchemia†
Dobutamine
Echo
No Clinically Significant
Ishchemia†
Exercise
Echo
Exercise
Nuclear
Medical Therapy
Fig. 5 : Algorithm for assessing patients with ST-segment elevation myocardial infarction (STEMI). Cath = catheterization;
ECG = electrocardiography; Echo = echocardiography; EF = left
ventricular ejection fraction.
Dyslipidemia also contributes to CAD progression and increases
the risk of future coronary events. For example, in men with
cardiovascular disease and high total cholesterol, the risk of death
from cardiovascular disease is much higher than for similarly
affected men with normal serum cholesterol levels. A study of
middle-aged men,which was a follow-up to the Primary Prevention
Study in Göteborg, Sweden, found that 76% of healthy men with
low cholesterol and 65% of healthy men with high cholesterol
were still alive 16 years after enrollment. By contrast, among men
with prior MI, 50% of those with low cholesterol were still alive
compared with only 21% of those with high cholesterol.28
reported to be predictive of worse 4-year survival after a first
MI.21 For post-MI patients who go on to develop symptomatic
HF, a prolonged QRS duration is an indicator of ventricular
dyssynchrony, which is predictive of a therapeutic response to
cardiac resynchronization therapy.22
Other markers of electrical instability predict fatal arrhythmias with
varying degrees of success.These include QT dispersion,23 microvolt
T-wave alternans,24 and signal-averaged electrocardiography for
detecting microvolt level signals in the terminal QRS complex.25
Systemic Factors Affecting
Pathophysiologic Targets
Although the structural and proarrhythmic consequences of
ischemia are most important in determining the prognosis in
post-MI patients, systemic factors play a significant role, as well.
Among these is the neurohormonal activation that occurs in
patients with LVD after MI and several comorbid conditions.
Neurohormonal Activation
A complex set of maladaptive neurohormonal changes occurs
in the post-MI patient with LVD. These include activation of the
sympathetic nervous system (SNS) and the renin-angiotensinaldosterone system (RAAS). Neurohormonal activation can cause
electrical instability, increasing the risk of ventricular arrhythmia,
and it can induce ventricular remodeling, leading to a worsening
of LVD and the development of HF.
In LVD, a baroreceptor-mediated increase in SNS activity has
a number of consequences, including tachycardia, arterial
vasoconstriction, and venoconstriction.26 The increased regional
and circulating concentrations of norepinephrine that accompany
SNS activation can be toxic to cardiac myocytes, an effect that can
be reversed by β-blockade.Another important effect of increased
SNS activity is RAAS activation.26The adverse effects of angiotensin
Preexisting hypertension in patients with MI is another comorbid
condition that can negatively affect patient prognoses. Richards et
al 29 compared patients with MI who had antecedent hypertension
with those who did not. Plasma neurohormones, which
included norepinephrine and the cardiac natriuretic peptides,
were significantly higher in the hypertensive group than in the
normotensive group days after MI, and these increases were still
apparent several months later. Patients with hypertension had
larger left ventricular systolic and diastolic volumes and a lower
average LVEF compared with patients who were normotensive.
Workup and Management Goals in the
Post-MI Patient
An algorithm for appropriate workup of the patient with STEMI is
presented in Figure 5. A similar scheme can be used for a patient
with non-STEMI, although there may not be the same urgency to
achieve immediate reperfusion. Determining the LVEF is crucial
to the early assignment of risk, but information beyond LVEF is
also essential for further elaborating mortality risk and deciding
on a therapeutic strategy. Angiography, electrocardiography,
echocardiography, exercise testing, and viability imaging all may
play a role in a comprehensive assessment.
There are 4 principal goals for management of the post-MI patient
254
Post Myocardial Infarction Left Ventricular Dysfunction and Failure
Table 1 : Goals in the management of post-myocardial
infarction with left ventricular dysfunction and recommended therapies
Table 2 : American College of Cardiology/American
Heart Association/European Society of Cardiology
guidelines for implantable cardioverter defibrillator
(ICD)
Goal
Improve symptoms
Therapy
Therapies aimed at ischemia and/or
congestion
Prevent future coronary events
Statins
(CAD progression)
Antiplatelet agents
ACEIs/ARBs
Coronary revascularization (PCI or
CABG)
Attenuate progressive pathologic LV ACEIs/ARBs
remodeling
β-blockers
Aldosterone antagonists
CRT
Prolong survival by preventing SCD β-blockers
or progression of HF
ICD
CRT
LVAD
Class
Class I
with LVD, each associated with ≥1 therapeutic options (Table
1). The particular treatment prescribed for an individual patient
should be guided by an assessment of the key pathophysiologic
targets:the coronary arteries,the myocardium,and the conduction
system.
Device Therapies
Current device therapies used in patients with LVD include CRT
with biventricular pacing,ICDs,and rate-responsive atrioventricular
sequential (dual-chamber) pacemakers in patients with disease- or
drug-mediated chronotropic incompetence (or ventriculoatrial
conduction with ventricular pacing).
The American College of Cardiology, American Heart
Association, and European Society of Cardiology (ACC/AHA/
ESC) 2006 guidelines for management of patients with ventricular
arrhythmias and the prevention of sudden cardiac death provide
recommendations for the use of ICDs (Table 2).31 In addition,
both ICDs and CRT received class I recommendations for use
in patients without contraindications in recent guidelines for the
management of ST-segment elevation MI and chronic HF.
In 2005, on the basis of large-scale clinical trials, the ACC and the
AHA issued an update to their 2001 joint HF treatment guidelines,
assigning a class I indication (level of evidence, A) to CRT (with
or without defibrillation) in patients who meet the following
criteria: (1) ischemic or nonischemic dilated cardiomyopathy; (2)
an LVEF ≤0.35; (3) sinus rhythm; (4) NYHA functional class III or
ambulatory class IV; (5) cardiac dyssynchrony, defined as a QRS
duration ≥120 msec; and (6) optimal pharmacologic therapy for
HF.
Emerging Pharmacotherapies
Some experimental agents are being developed for post-MI patients
with LVD in an effort to improve outcomes (Table 3).The following
is a description of a few investigational pharmacotherapies.
255
Recommendations
If coronary revascularization cannot be carried out and
evidence of prior MI and significant LVD exists, ICD should
be primary therapy for patients resuscitated from VF who are
receiving chronic OMT and for those who have reasonable
expectation of survival with good functional status for >1 year.
ICD therapy is recommended for primary prevention to reduce
total mortality by reducing SCD in patients with LVD due to
prior MI who are ≥40 days post MI, have LVEF ≤0.30–0.40, are
NYHA functional class II or III, are receiving chronic OMT, and
who have reasonable expectation of survival with good functional status for >1 year.
ICD is effective in reducing mortality by reducing SCD in
patients with LVD due to prior MI who present with hemodynamically unstable sustained VT, are receiving chronic OMT,
and who have reasonable expectation of survival with good
functional status for >1 year.
Class IIa ICD implantation is reasonable in patients with LVD due to
prior MI who are ≥40 days post MI, have LVEF ≤0.30–0.35,
are NYHA functional class I on chronic OMT, and who have
reasonable expectation of survival with good functional status
for >1 year.
Adjunctive therapies to the ICD, including catheter ablation or
surgical resection, and pharmacologic therapy with agents such
as amiodarone or sotalol are reasonable to improve symptoms
due to frequent episodes of sustained VT or VF in patients with
LVD due to prior MI.
Amiodarone is reasonable therapy to reduce symptoms due to
recurrent hemodynamically stable VT in patients with LVD due
to prior MI in whom an ICD is contraindicated.
ICD implantation is reasonable for treatment of recurrent
sustained VT in post-MI patients with normal or near normal
LV function who are receiving chronic OMT, and who have
reasonable expectation of survival with good functional status
for >1 year.
Class IIb Curative catheter ablation or amiodarone may be considered as
an alternative to ICD therapy to improve symptoms in patients
with LVD due to prior MI and recurrent hemodynamically
stable VT whose LVEF is >0.40.
Amiodarone may be reasonable therapy for patients with LVD
due to prior MI in whom an ICD is contraindicated
Conclusion
Collectively, the coronary arteries, myocardium and conduction
system represent the principal pathophysiological targets in MI
complicated by LVD. Systemic factors, such as neurohormonal
activation and comorbid conditions, also impact prognosis and
therapies. An accurate assessment of disease severity in these
targets is essential for the design of a therapeutic program.The post
myocardial infarction (MI) patient with left ventricular dysfunction
(LVD) is at risk for ventricular arrhythmias resulting in sudden
cardiac death. In high-risk post-MI patients with a depressed left
Medicine Update 2010  Vol. 20
Table 3 : Promising therapies for post–myocardial infarction left ventricular dysfunction
Therapy
Aliskiren
6. Myerburg R.J., Kessler K.M., Castellanos A.: Sudden cardiac death:
structure, function, and time-dependence of risk. Circulation 1992;
85 (suppl): S2-S10
Mechanism
Direct renin inhibitor
Target
More thorough RAAS
blockade via sustained
reduction in PRA
BAY 58-2667
Selective guanylate cyclase Reduced peripheral vascuactivator
lar resistance and increased
cardiac output
CK-1827452
Selective myosin activator Enhanced myocardial
contractility
Clenbuterol
Reverse remodeling and
β2 receptor agonist that
enhances IGF-1 expression LV recovery when used
in conjunction with LVAD
implantation
Ivabradine
Sinoatrial node blocker
Reduced myocardial work
Stem cell therapy Myocardial regeneration
Preservation and recovery
of myocardial contractility
Angiogenesis
Preservation and recovery
Thymosin β4
of myocardial contractility
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patients with ST-elevation myocardial infarction—executive summary:
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