Complications of myocardial infarction

Susan Wilansky, MD, FACC, FRCPC; Carlos A. Moreno, BS; Steven J. Lester, MD, FACC, FRCPC

Echocardiography is a most useful bedside tool to help in the
diagnosis and management of critically ill patients after acute
myocardial infarction. In most instances, the mechanism of un-
explained shock will be elucidated. Transesophageal echocardi-
ography can further delineate the mechanical complications of
myocardial infarction when the transthoracic echocardiogram
may not be adequate. This article will focus on the mechanical
complications of myocardial infarction in patients who most often
present with cardiogenic shock or acute pulmonary edema. Each
clinical entity is discussed, and illustrative echocardiograms are
provided. (Crit Care Med 2007; 35[Suppl.]:S348–S354)
KEY WORDS: myocardial infarction; mitral regurgitation; contin-
uous-wave Doppler echocardiography; color flow imaging; ven-
tricular rupture

E
chocardiography is the ideal
imaging technique for diag-
nosing all complications of
myocardial infarction (MI). In
fact, in the 2003 American College of
Cardiology/American Heart Association/
American Society of Echocardiography
guideline update for the clinical applica-
tions of echocardiography (1), the use of
echocardiography in the assessment of
mechanical complications of MI is a class
1 indication.
Complications of MI include the devel-
opment of congestive heart failure (sys-
tolic and diastolic), pericardial effusion,
left ventricular (LV) thrombus, right ven-
tricular (RV) infarction, LV aneurysm, LV
pseudoaneurysm, free wall rupture, ven-
tricular septal rupture, mitral regurgita-
tion, and dynamic LV outflow tract ob-
struction causing hemodynamic collapse.
This article will focus primarily on the
acute mechanical complications, or those
causing cardiogenic shock, commonly
encountered in the intensive care setting.
Left Ventricular Free Wall
Rupture
Acute free wall rupture in the pre-
interventional era occurred in approxi-
mately 6% of patients with acute MI (2),
From the Division of Cardiovascular Diseases,
Mayo Clinic Arizona, Scottsdale, AZ.
Dr. Wilansky has not disclosed any potential con-
flict of interest.
For information regarding this article, E-mail:
Wilansky.Susan@mayo.edu
Copyright © 2007 by the Society of Critical Care
Medicine and Lippincott Williams & Wilkins
DOI: 10.1097/01.CCM.0000270244.90395.67
with a marked reduction in the angio-
plasty era of ⬍1% (3). About half the
ruptures occur as out-of-hospital sudden
cardiac death (4). Ruptures account for
8 –17% of the mortality after MI (3, 5).
After MI, 40% of ruptures occur within the
first 24 hrs and 85% within the first week.
Rupture does not usually occur after 10
days, when healing has taken place (5, 6).
Risk factors for free wall rupture in-
clude (1, 5–7):
1. Age (⬎65)
2. Gender (women more often than
men)
3. First MI
4. Single-vessel disease (often total
occlusion)
5. Absence of LV hypertrophy
6. Acute transmural MI (ⱖ20% of
the wall)
7. Anterior location (more frequent
in for early rupture)
Clinical Presentation. Complete rup-
ture can cause sudden hemopericardium,
with electromechanical dissociation and
death (2, 7). The symptoms of those who
survive to the hospital include persistent
or recurrent chest pain, syncope, agita-
tion, nausea, and vomiting (2, 7). Up to
one fifth of patients may have a paradoxic
bradycardia (8). Table 1 shows the most
common clinical predictors of rupture.
Signs include cardiogenic shock, elevated
neck veins, arrhythmia, and transient
electromechanical dissociation (7, 9). Ap-
proximately one third of patients have a
more subacute presentation, with persis-
tent chest pain and disproportionate
right-sided heart failure, followed by he-
modynamic deterioration (5, 9).
Electrocardiography. Hallmarks of
end-stage rupture are bradycardia and
electromechanical dissociation (7, 9). The
electrocardiographic signs are otherwise
nonspecific and not sensitive (Table 2).
Echocardiography. Echocardiography
is the most reliable diagnostic modality
to diagnose LV free wall rupture. The
most common finding is pericardial effu-
sion. It should be noted, however, that up
to 25% of patients with MI may have
pericardial effusion. Echodense masses,
representing pericardial thrombus, noted
in the pericardial space adjacent to a wall
motion abnormality increase the sensitiv-
ity and specificity (7). Color flow Doppler
may localize the rupture site. Injection of
contrast agents may demonstrate extrav-
asation of contrast into the pericardial
space, and this would be diagnostic of
rupture (10). Figures 1 and 2 demon-
strate an echocardiogram of a patient
with a rupture that occurred 4 days after
an acute MI.
Management. Once the echocardio-
gram suggests the diagnosis of rupture,
and there remains uncertainty, urgent
diagnostic pericardiocentesis should be
performed. If bloody, the patient should
undergo urgent operation and be medi-
cally stabilized with fluids, pressors, and
if needed, an intraaortic balloon pump.
The condition is uniformly fatal without
intervention.
Ventricular Septal Rupture
Ventricular septal rupture (VSR) is a
less frequent complication of MI, occur-
ring in approximately 0.2% of patients in
the reperfusion era (11). The tear usually
occurs within the thin, akinetic segment

S348 Crit Care Med 2007 Vol. 35, No. 8 (Suppl.)

Table 1. Common clinical predictors of
rupture (9)

Pericarditis
Repeated emesis
Agitation
Persistent or recurrent ST-segment elevation
Lack of typical T-wave evolutionary changes of
myocardial infarction

Table 2. Electrocardiographic findings of free

wall rupture (8, 10)

Sinus tachycardia
Non-specific ST-T-wave changes
New conduction delay
Persistent or recurrent ST-segment elevation
Pseudonormalization of T waves
ST-segment elevation in AVL (anteroseptal
myocardial infarction)
New Q waves in at least two leads

of myocardium and may be simple or

complex. The complex tear may form a
dissection plane in a serpiginous fashion
connecting the ventricles at different lev-
els (12). VSR occurs more commonly in
single-vessel disease, and the left anterior Figure 1. Apical four-chamber view demonstrating moderate–large apical pericardial effusion. PE,
descending artery is more frequently the pericardial effusion; LV, left ventricle; RV, right ventricle. Image courtesy of Dr. R. Click.
culprit (12–14). Clinical risk factors for
developing VSR can be seen in Table 3
(11).
In ⬎70% of patients (13), the clinical
presentation is that of hemodynamic col-
lapse and a new systolic murmur (often
with a thrill) at the left sternal border. A
smaller subset may not present with car-
diovascular collapse or a murmur.
Risk factors for mortality include
complex tears, RV infarction (12), older
age, and inferior location (11).
Echocardiography. Echocardiography
with color flow imaging is a highly sen-
sitive tool for diagnosing and character-
izing VSR (12–14). Off-axis views may be
very useful to localize the defect. Contin-
uous-wave Doppler through the color
flow defect (in the most parallel to flow
angle) can be used to estimate the RV
systolic pressure. Using the modified Ber-
noulli equation (4V2), where V is the peak
velocity of the ventricular septal defect
(VSD) jet, one obtains the pressure differ-
ence between the left and right ventri-
cles. Subtracting this from the systolic
blood pressure yields the RV systolic pres-
sure. Using the inferior vena cava dynam-
ics to estimate the right atrial pressure,
one can add this estimate to the RV sys-
tolic pressure to obtain the pulmonary Figure 2. Magnification of pericardial effusion demonstrating echodense mass confirmed to be
artery pressure. thrombus at surgery. PE, pericardial effusion. Image courtesy of Dr. R. Click.

Crit Care Med 2007 Vol. 35, No. 8 (Suppl.) S349

 Agitated saline may be used to identify a
defect that may have been missed by color
Doppler. Ten milliliters of agitated saline
(agitated in three-way stopcock) with 0.5–
1.0 mL of air is injected into a peripheral
vein. A positive contrast study is defined by
the presence of contrast within the LV
within three cardiac cycles. Because LV
pressure is much higher than RV pressure,
the presence of a VSD is often characterized
by a “negative” contrast effect, which ap-
pears as nonuniform opacification of the
RV at the site of the defect. In those patients
with technically challenging transthoracic
echocardiograms, transesophageal echo-
Table 3. Clinical risk factors for ventricular
septal rupture
Older age
Female gender
Hypertension
Absence of smoking history
Anterior myocardial infarction location
Tachycardia
Killip class 3–4
Figure 3. Apical four-chamber view demonstrating the color flow jet of the ventricular septal defect
(VSD) at the distal septum. LV, left ventricle; RV, right ventricle; LA, left atrium; RA, right atrium.
Image courtesy of Dr. F. Mookadam.
S350
cardiography may be useful for localizing
the defect. Multiplane imaging may allow
for better tomographic assessment of the
right ventricle.
Management. Unless there are contra-
indications, urgent surgery with aorto-
coronary bypass is a class 1 indication for
VSR (15, 16). Patients should be stabi-
lized with an intraaortic balloon pump,
pressors, and vasodilators, as needed, be-
fore cardiac catheterization and surgery
(16, 17). Surgical mortality is high with
cardiogenic shock (87% in the SHOCK
[SHould we emergently revascularize Oc-
cluded Coronaries in cardiogenic shocK?]
registry (17)), with 1 of 24 patients sur-
viving with medical management. In the
GUSTO (Global Utilization of Streptoki-
nase and TPA for Occluded Coronary Ar-
teries) trial (11), mortality for medical vs.
surgical management was 94% and 47%.
Percutaneous closure of VSR has been
reported in a small number of patients
(18) and may become a viable option for
inoperable patients or for those who de-
cline surgery.
Figures 3 and 4 are illustrative exam-
ples of a simple VSR, and Figures 5 and 6
are examples of a complex VSR.
Left Ventricular Outflow Tract
Obstruction and Acute
Myocardial Infarction
Several small case series describe this
unusual entity of LV outflow tract (LVOT)
obstruction secondary to the develop-
ment of severe systolic anterior motion of
the mitral valve in the setting of acute
coronary syndromes (19 –22). The basis
for this hemodynamic derangement is
not entirely understood but is often
found in the setting of apical MI with
hyperdynamic basal septal contraction,
with resultant systolic anterior motion of
the mitral valve and LVOT obstruction.
The clinical scenario often entails a new
systolic murmur and hypotension refrac-
tory to usual management (i.e., inotropes
or intraaortic balloon pump). In one of
the series (20), apical wall motion abnor-
malities were found in the presence of
normal coronary angiography, suggest-
ing the diagnosis of what is currently
known as Takostubo cardiomyopathy.
Echocardiography. Echocardiography
is a class 1 indication in all patients with
a new murmur or cardiogenic shock in
the setting of acute MI (1). Systolic ante-
rior motion is best visualized on M-mode
of the mitral valve on the parasternal
long-axis view (Fig. 7B) or two-dimen-
sional imaging on the parasternal long-
axis (Fig. 7A) or apical long axis views.
Color flow Doppler reveals turbulence in
the LVOT (at the level of systolic anterior
motion–septal contact) (Fig. 7C), and
continuous-wave Doppler through the
LVOT will quantitate the magnitude of
the LVOT obstruction (Fig. 7D). The
spectral display is dagger shaped, as is
seen in obstructive hypertrophic cardio-
myopathy. Using the modified Bernoulli
equation (4V2) of the peak velocity ob-
tained in the LVOT, the pressure gradient
is thereby obtained.
Management. Therapy is directed at
reversing the LVOT obstruction (Fig. 8).
First-line therapy is volume expansion.
The reminder of management is, at first
glance, counterintuitive. Beta-blockers
are the drug of choice to reduce obstruc-
tion, by reducing the hyperdynamic con-
traction of the base of the heart (19, 20).
Alpha agonists, pure vasoconstrictors,
may be used to improve the blood pres-
sure (19, 20).
Crit Care Med 2007 Vol. 35, No. 8 (Suppl.)
 Right Ventricular Infarction

RV infarction is associated with infe-

rior wall MI and is noted pathologically in
approximately 35% of inferior MIs (23),
but it is clinically evident in far fewer.
Significant RV dysfunction should be sus-
pected clinically with the triad of hypo-
tension, clear lungs, and elevated neck
veins. An inspiratory rise in the “a” wave
is sensitive and specific bedside finding
(23). Other findings include RV S3, tri-
cuspid regurgitation, and atrioventricu-
lar block (23).
The diagnosis is also confirmed by the
use of a right-sided electrocardiogram, in
which ST elevation in right chest lead
V4R (and also V5R and V6R) is often seen
(16, 24).
Echocardiography. Although imaging
of the right ventricle is sometimes diffi-
cult, the subcostal view is often most
useful. The most common echocardio-
graphic findings are (Fig. 9) (23, 25):
1. Dilated right ventricle with re-
gional wall motion abnormalities
or global dysfunction.
Figure 4. Continuous-wave Doppler through the ventricular septal defect jet. Peak velocity of 4 m/sec. 2. Reduced descent of the base of the
Using the modified Bernoulli equation (4V2, where V is the peak velocity of the ventricular septal defect jet), RV free wall (apical four-chamber
the right ventricle/left ventricle pressure difference is 64 mm Hg. The patient’s systolic blood pressure was view).
100 mm Hg; therefore, the right ventricle systolic pressure was 36 mm Hg. Image courtesy of Dr. F. 3. Inferior vena cava plethora.
Mookadam.
Normal inferior vena cava diameter is
⬍2.5 cm. Normal dynamics of the infe-
rior vena cava reveal an inspiratory col-
lapse of ⱖ50%. Dilated inferior vena cava
with lack of respiratory variability is
highly sensitive and specific for elevated
right atrial pressure (26).
Other echocardiographic findings in-
clude flattening of the interventricular sep-
tum on the short-axis view in diastole (23),
indicative of elevated RV diastolic pressure.
Other signs of right atrial hypertension,
Figure 5. Gastric view on transesophageal echocardiography of a patient with complex ventricular such as the bowing of the interatrial sep-
septal rupture (VSR). A, rupture site at the level of the inferior septum; B, color flow shunting from tum toward the left atrium, may be present.
the left ventricle (LV) to right ventricle (RV). Images courtesy of Dr. R. Click. Depending on the extent of the RV
dilation, tricuspid regurgitation may be
present in varying degrees. The pulmo-
nary artery pressure may be obtained us-
ing the modified Bernoulli equation of
the peak tricuspid regurgitant jet plus the
estimate of the right atrial pressure using
the inferior vena cava dynamics.
It is important to remember that if a
patient with RV MI presents with unex-
plained hypoxemia, a patent foramen
ovale with right-to-left shunting should
be considered (27). This occurs when
Figure 6. A, gastric view, at slightly more caudal level, in the same patient with complex ventricular right atrial pressure exceeds that of the
septal rupture (VSR) as in Figure 5, showing a serpiginous dissection plane through the ventricular left atrium and may open the foramen
septum. B, color flow left-to-right shunting. LV, left ventricle; RV, right ventricle. ovale. The diagnosis is confirmed by the

Crit Care Med 2007 Vol. 35, No. 8 (Suppl.) S351

 use of an agitated saline injection into a
vein of the right arm, with immediate
opacification of contrast from the right
atrium to the left atrium.
Management of Hemodynamically
Compromising Right Ventricular Myo-
cardial Infarction. Although mortality
and morbidity is higher in patients with
RV MI (24), significant improvement in
RV function is the norm at 3 months (23,
28). The principles of management of RV
MI (16) and hypotension include avoid-
ance of agents that reduce preload (i.e.,
nitrates and diuretics) and increasing
preload with normal saline loading. Of-
ten, this will ameliorate the hypotension.
If no response occurs after 1 L of saline,
dobutamine should be administered for
inotropic support of the RV. Consider-
ation of Swan-Ganz catheterization may
be warranted to best manage volume and
inotropic support. Temporary pacing may
be of benefit in situations of high-degree
atrioventricular block (16).

Figure 7. Series of images in a patient who presented with increased troponins, anterior wall motion Mitral Regurgitation
abnormality, and shock not responsive to inotropic agents. A, parasternal long-axis view, demonstrat-
ing severe systolic anterior motion of the mitral valve (arrow). B, M-mode through the mitral valve, Mitral regurgitation (MR) after MI con-
illustrates severe systolic anterior motion of the mitral valve; note the early onset and prolonged fers a worse prognosis in terms of cardio-
contact with the septum, suggesting a high-pressure gradient. C, parasternal long axis view, showing vascular morbidity and mortality than in
turbulent flow in the left ventricular outflow tract with concomitant posteriorly directed mitral those without MR. The mechanisms of MR
regurgitation (MR). D, continuous-wave Doppler through the left ventricular outflow tract. Peak are shown in Table 4 (29 –33).
velocity of 6 m/sec. Using the modified Bernoulli equation, the calculated left ventricular outflow tract
Ruptured papillary muscle will be dis-
gradient was 144 mm Hg. LV, left ventricle; Ao, aorta; LA, left atrium; s, systole; MV, mitral valve; d,
cussed separately in a later section. Clinical
diastole; IVS, interventricular septum.
risk factors associated with the development
of MR can be seen in Table 5 (29, 30, 33).
Ischemic MR may be clinically silent.
The audibility of the murmur is a func-
tion of the regurgitant orifice, LV func-
tion, and left atrial compliance (29, 33).
Echocardiography. Echocardiography
will elucidate the mechanism of the MR,
with transesophageal echocardiography
being most useful in this regard. Further-
more, the transthoracic echocardiogram
can reliably estimate the degree of MR.
Quantification utilizing the continuity
equation (34 –37) provides the regurgi-
tant volume and effective regurgitant or-
ifice. Norms for severity of ischemic MR
are lower than for nonischemic MR (38).
Other Doppler indicators of severe MR
include a vena contracta of ⬎7 mm, peak
mitral E velocity of ⬎1.2 m/sec, dense
continuous-wave Doppler signal, systolic
flow reversal in the pulmonary veins, and
Figure 8. M-mode through the mitral valve before (PRE) and after (POST) medical intervention. PRE,
severe systolic anterior motion of the mitral valve while patient was in shock and receiving dobut-
significant pulmonary hypertension (37).
amine. POST, abolition of systolic anterior motion of the mitral valve (and hence the gradient and Other important information such as LV
mitral regurgitation) after discontinuing the dobutamine and giving high-dose beta-blockers and size, function, and wall motion abnor-
alpha-agonists. Blood pressure and heart rate normalized with these maneuvers. IVS, interventricular malities, left atrial volume, and right
septum. atrial pressure can readily be obtained.

S352 Crit Care Med 2007 Vol. 35, No. 8 (Suppl.)


Figure 9. Transesophageal echocardiography of RV myocardial infarction and patent foramen ovale. A,
severely dilated right ventricle (RV). On real-time imaging, the RV was severely hypokinetic. Note the
dilated right atrium (RA) and the bowing of the interatrial septum toward the left, suggestive of high RA
pressure. B, positive contrast study. Agitated saline injected into the right forearm immediately crossed over
from the RA to the left atrium (LA), indicating the presence of a patent foramen ovale, which was the
explanation for the patient’s hypoxemia. LV, left ventricle. Images courtesy of Dr. R. Click.
Table 4. Mechanisms of mitral regurgitation
after myocardial infarction
Incomplete closure because of systolic tenting
of the valve
Dilated annulus with severe left ventricular
dysfunction
Ruptured (partial or complete) papillary muscle
Ruptured chordae tendineae
Worsening of pre-existing mitral regurgitation
Table 5. Clinical risk factors for mitral
regurgitation
Older age
Female sex
Previous myocardial infarction
Multivessel coronary artery disease
Recurrent ischemia
Hypertension
Extensive myocardial infarction
Congestive heart failure
Table 6. Clinical risk factors for ruptured
papillary muscle
Older age
Female sex
Inferoposterior myocardial infarction
Single-vessel disease
No diabetes
Management of MR depends on the
severity of MR, LV function, and the ex-
tent of coronary artery disease and is be-
yond the scope of this discussion.
Crit Care Med 2007 Vol. 35, No. 8 (Suppl.)
Figure 10. Transesophageal echocardiography of
a ruptured papillary muscle. LA, left atrium; PM,
ruptured head of papillary muscle; LV, left ven-
tricle; RV, right ventricle. Image courtesy of Dr.
R. Click.
Papillary Muscle Rupture
Ruptured papillary muscle is a surgical
emergency, with a mortality rate of 50%
within the first 24 hrs in those who do not
undergo operative intervention (39). It typ-
ically occurs a few days after MI. The pos-
teromedial papillary muscle is 6 –12 times
more likely to rupture than the anterolat-
eral papillary muscle, which has a dual
blood supply (6, 39). The anterolateral
muscle is fed by the left anterior descend-
ing and circumflex coronary arteries. The
posteromedial receives its blood supply
from the posterior descending branch of
the right coronary artery (6).
The clinical presentation of papillary
muscle rupture is that of acute pulmo-
nary edema, a loud systolic murmur
(50%) with no thrill, and ensuing cardio-
genic shock, most typically in inferior
wall MI. Clinical risk factors for develop-
ing papillary muscle rupture can be seen
in Table 6 (29).
Echocardiography. Transthoracic echo-
cardiography will demonstrate severe MR
(Fig. 10). Often, the flail papillary muscle
will be seen to prolapse into the left
atrium. Partial rupture has been de-
scribed (40) and is seen as a mobile mass
within the LV cavity in the region where
the papillary muscle should be. Trans-
esophageal echocardiography is the best
modality to confirm the diagnosis. In
65% of the patients described by Moursi
et al. (41), direct visualization of the pap-
illary muscle head was seen in the left
atrium. In ⬎90% in this series of surgi-
cally proven rupture, what was described
as a “large amplitude erratic motion” in
the body of the left ventricle was observed
(41). In the absence of obvious prolapse
into the left atrium with severe MR, thor-
ough scanning of the body of the left
ventricle should be performed.
Management. Prompt diagnosis can
be made by transthoracic echocardiogra-
phy and transesophageal echocardiogra-
phy. Immediate stabilization of the pa-
tient includes afterload reduction with
nitroprusside and an intra-aortic balloon
pump (16) and diuretics for congestion, if
needed. Prompt catheterization of the left
side of the heart will define coronary
anatomy, followed by urgent surgery. Al-
though operative mortality is high (25–
40%) (16, 42), survival thereafter is good
(43). Concomitant coronary revascular-
ization improves long-term survival (43),
as do attempts to repair rather than re-
place the valve.
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