Complications of Acute Myocardial Infarction

8/6/2016
Complications of Acute Myocardial Infarction
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Complicationsof
AcuteMyocardialInfarction
AdamW.Grasso
SorinJ.Brener
Published:July2014
Contents
Complications of acute myocardial infarction (MI) include ischemic, mechanical, arrhythmic, embolic, and
inammatory disturbances (Table 1). Nevertheless, circulatory failure from severe left ventricular (LV)
dysfunction or one of the mechanical complications of MI account for most fatalities.
Table1:ComplicationsofAcuteMyocardialInfarction
Complication
Type
Manifestations
Ischemic
Angina, reinfarction, infarct extension
Mechanical
Heart failure, cardiogenic shock, mitral valve dysfunction, aneurysms, cardiac

rupture
Arrhythmic
Atrial or ventricular arrhythmias, sinus or atrioventricular node dysfunction
Embolic
Central nervous system or peripheral embolization
Inammatory
Pericarditis
Ischemic complications
Ischemic complications can include infarct extension, recurrent infarction, and postinfarction angina.
Prevalence
Infarct extension is a progressive increase in the amount of myocardial necrosis within the infarct zone of the
original MI. This can manifest as an infarction that extends and involves the adjacent myocardium, or as a
subendocardial infarction that becomes transmural.
Following brinolytic therapy, reocclusion of the infarct-related artery (IRA) occurs in approximately 5% to
10% of patients by the time of discharge, and in 25% to 30% of patients at 1 year.1 These patients also tend to
have a poorer outcome.2,3 Reinfarction is more common in patients with diabetes mellitus or prior MI. With
the advent of primary percutaneous coronary intervention (PCI) and stent placement, risk of reinfarction has
dropped substantially, to approximately 3% during the rst 90 days after MI.4
Recurrent infarction in a separate territory may be difcult to diagnose within the rst 24 to 48 hours after the
initial event. Multivessel coronary artery disease is common in patients with acute MI. In fact, angiographic
evidence of complex or ulcerated plaques in noninfarct-related arteries is present in up to 40% of patients
with acute MI.
Angina that occurs from a few hours to 30 days after acute MI is dened as postinfarction angina. The
incidence of postinfarction angina is highest in patients with nonST-elevation MI (approximately 25%), and
in those treated with brinolytics rather than with PCI.
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Pathophysiology
Reinfarction occurs more often when the IRA reoccludes than when it remains patent; however, reocclusion
of the IRA does not always cause reinfarction because of abundant collateral circulation. After brinolytic
therapy, reocclusion is found on angiograms of 5% to 10% of patients and is associated with a worse
outcome. When primary PCI is used for reperfusion, the incidence of IRA reocclusion is much lower. Of
particular concern is the development of acute stent thrombosis, usually within the rst few hours after
primary PCI in ~1% of patients.5
The pathophysiologic mechanism of postinfarction angina is similar to that of unstable anginaplaque
ruptureand should be managed in a similar manner. Patients with postinfarction angina have a worse
prognosis with regard to sudden death, reinfarction, and acute cardiac events, compared with those without
such symptoms.
SignsandSymptoms
Patients with infarct extension or postinfarction angina usually have continuous or intermittent chest pain,
with protracted elevation in the creatine kinase (CK) level and occasionally, new electrocardiographic
changes.
DiagnosticTesting
The diagnosis of infarct expansion, reinfarction, or postinfarction ischemia can be made with
echocardiography or nuclear imaging. New wall motion abnormalities, larger infarct size, new area of
infarction, or persistent reversible ischemic changes help substantiate the diagnosis. CK-MB is a more useful
marker for tracking ongoing infarction than troponin, given its shorter half-life. Re-elevation and subsequent
decline in CK-MB levels suggest infarct expansion or recurrent infarction. Elevations in the CK-MB level of
more than 50% over a previous nadir are diagnostic for reinfarction.
Treatment
Medical therapy with aspirin, heparin, nitroglycerin, beta blocker, and statin is indicated in patients who have
had a MI and are experiencing ongoing ischemic symptoms.6 Depending upon the clinical situation,
additional anti-platelet therapy (clopidogrel, prasugrel, ticagrelor) and a glycoprotein IIb/IIIa inhibitor
(eptibatide) may also be given. An intra-aortic balloon pump (IABP) should be inserted promptly in patients
with hemodynamic instability or severe LV systolic dysfunction. However, it must be borne in mind that
severe peripheral vascular disease of the aortoiliac and femoral arteries is a contraindication to IABP
placement, due to increased risk of lower extremity ischemia. IABP use is also contraindicated in patients
with severe aortic valve insufciency (AI), because their AI will be worsened by the balloon pump. Coronary
angiography should be performed in patients who are stabilized with medical therapy, but emergency
angiography also may be undertaken in unstable patients, since restoration of coronary arterial blood ow,
either by percutaneous or surgical means, is associated with an improved prognosis.
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Mechanical Complications
Mechanical complications of acute MI include ventricular septal defect (VSD), papillary muscle rupture or
dysfunction, cardiac free wall rupture (FWR), ventricular aneurysm, LV failure with cardiogenic shock,
dynamic LV outow tract (LVOT) obstruction, and right ventricular (RV) failure.
VentricularSeptalDefect
Independent predictors of VSD are shown in Box 1.
Box 1: Independent Predictors of Ventricular Septal Defect
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Older age
Female gender
Nonsmoking status
Anterior infarct
Worse Killip class on admission
Increased heart rate on admission
Prevalence
VSD formerly occurred in 1% to 2% of patients after acute MI in

the prethrombolytic era (Figures 1 and 2). The incidence has
decreased dramatically with reperfusion therapy. For example, the GUSTO-I (Global Utilization of
Streptokinase and Tissue plasminogen activator for Occluded coronary arteries) trial demonstrated an
incidence of VSD of approximately 0.2%.7 Similar rates of VSD occurrence post-MI have been obtained
from studies utilizing primary PCI.8 VSD was commonly seen 3 to 7 days after MI in the prebrinolytic era,
but now is generally diagnosed within the rst 24 hours after MI.7,8
Pathophysiology
The defect usually occurs at the junction of preserved and infarcted myocardium in the apical septum with
anterior MI, and in the basal posterior septum with inferior MI. VSD almost always occurs in the setting of a
transmural MI and is more often seen in anterolateral MIs. The defect might not always be a single large
defect; in 30% to 40% of patients, a meshwork of serpiginous channels can be identied.
SignsandSymptoms
Early in the disease process, patients with VSD may appear relatively comfortable, with no clinically
signicant cardiopulmonary symptoms. Rapid recurrence of angina, together with hypotension, pulmonary
edema, and frank cardiogenic shock can develop later in the course.
Diagnosis
Rupture of the ventricular septum is often accompanied by a new harsh holosystolic murmur best heard at the
left lower sternal border. The murmur is accompanied by a thrill in 50% of cases. This sign is generally
accompanied by a worsening hemodynamic prole and biventricular failure. Therefore, it is important that all
patients with MI undergo a careful, well-documented cardiac examination at presentation and daily thereafter.
An electrocardiogram (ECG) may show atrioventricular (AV) nodal or infranodal conduction delay
abnormalities in approximately 40% of patients. Echocardiography with color ow Doppler imaging is the
best method for diagnosing VSD. There are two types of VSD, which can be visualized best in different
echocardiographic planes. A posterobasal VSD is best visualized in the parasternal long axis with medial
angulation, apical long axis, and subcostal long axis. An apical-septal VSD is best visualized in the apical
four-chamber view. Echocardiography can dene LV and RV dysfunctionimportant determinants of
mortalityas well as the size of the defect and degree of left-to-right shunt by assessing ow through the
pulmonary and aortic valves. In some cases, it may be necessary to use transesophageal echocardiography to
assess the VSD.
VSD can also be diagnosed by demonstrating an increase or "step-up" in oxygen saturation in the right
ventricle and pulmonary artery (PA) on right-heart catheterization. The location of the step-up is signicant,
because there have been case reports of increased peripheral PA oxygen saturation due to acute mitral
regurgitation (MR). Diagnosis involves uoroscopically-guided measurement of oxygen saturation in the
superior and inferior vena cava, right atrium, right ventricle, and PA. With a left-to-right shunt across the
ventricular septum, one will generally detect an increase in oxygen saturation of more than 8% when going
from the right atrium to the right ventricle and PA. A shunt fraction can be calculated as follows:
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where
is the pulmonary ow,
is the systemic ow, SaO2 is the arterial oxygen saturation, MvO2 is the
mixed venous oxygen saturation, PvO2 is the pulmonary venous oxygen saturation, and PaO2 is the
pulmonary arterial oxygen saturation. A calculated
be well-tolerated by the patient.
>2 suggests a large shunt, which is not likely to
Treatment
Early surgical closure is the treatment of choice, even if the patient's condition is stable. Initial reports
suggested that delaying surgery could reduce surgical mortality.9 However, these perceived benets were
probably the result of selection bias,10 because the mortality rate in patients with VSD treated medically is
24% at 72 hours and 75% at 3 weeks. Therefore, in order to reduce mortality, patients with postinfarction
VSD should be strongly considered for early urgent surgical repair.
Cardiogenic shock and multisystem failure are associated with a high surgical mortality. This further supports
earlier operative management before complications develop.11 Mortality is highest in patients with basal
septal rupture associated with inferior MI (70%, compared with 30% in patients with rupture due to anterior
infarction). The mortality rate with basal septal rupture is higher because of increased technical difculty and
the frequent need for mitral valve repair or replacement in the patients with MR.12 Regardless of the VSD
location and the patient's hemodynamic condition, surgery should always be considered, because it is
associated with a lower mortality rate than conservative management.6
Intensive medical management should be started to support the patient before surgery. Unless there is
signicant aortic regurgitation, an IABP should be inserted urgently as a bridge to a surgical procedure. The
IABP will decrease the systemic vascular resistance (SVR) and shunt fraction while increasing coronary
perfusion and maintaining blood pressure. After the IABP is inserted, vasodilators can be used, with close
hemodynamic monitoring. Vasodilators can also reduce left-to-right shunting and increase systemic ow by
reducing SVR. Caution should be exercised to avoid a greater decrease in pulmonary vascular resistance than
in SVR and a consequent increase in shunting. The vasodilator of choice is intravenous sodium nitroprusside
(SNP), which is started at 0.5 to 1.0 g/kg/min and titrated to a mean arterial pressure (MAP) of 60 to 75 mm
Hg.
MitralRegurgitation
Prevalence
MR after acute MI portends a poor prognosis, as demonstrated in multiple trials.1316 MR of mild-tomoderate severity is found in 13% to 45% of patients following acute MI. Whereas most MR is transient in
duration and asymptomatic, MR caused by papillary muscle rupture (Figure 3) is a life-threatening
complication of acute MI. Fibrinolytic agents decrease the incidence of rupture; however, when present,
rupture can occur earlier in the post-MI period than in the absence of reperfusion. Although papillary muscle
rupture was reported to occur between days 2 and 7 in the prebrinolytic era, the SHOCK (SHould we
emergently revascularize Occluded Coronaries in cardiogenic shocK?) Trial Registry demonstrated a median
time to papillary muscle rupture of 13 hours.17 Papillary muscle rupture is found in 7% of patients in
cardiogenic shock and contributes 5% of the mortality after acute MI.18,19
Pathophysiology
MR can occur as a result of a number of mechanisms, including mitral valve annular dilatation secondary to
LV dilatation, papillary muscle dysfunction with associated ischemic regional wall motion abnormality in
close proximity to the insertion of the posterior papillary muscle, and partial or complete rupture of the
chordae tendineae or papillary muscle.18
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Papillary muscle rupture is most common with an inferior MI. The posteromedial papillary muscle is most
often involved because of its single blood supply through the posterior descending coronary artery.20 The
anterolateral papillary muscle has a dual blood supply, being perfused by the left anterior descending (LAD)
and left circumex coronary arteries. In 50% of patients with papillary muscle rupture, the infarct is
relatively small.
SignsandSymptoms
Complete transection of both papillary muscles is rare and usually results in immediate pulmonary edema,
cardiogenic shock, and death. Physical examination of the patient with anterolateral papillary muscle rupture
usually demonstrates a new pansystolic murmur, which is audible at the cardiac apex and radiates to the
axilla or the base of the heart. If there is a posteromedial papillary muscle rupture, the murmur radiates to the
left sternal border and may be confused with the murmur of VSD or aortic stenosis (intensity of the murmur
does not always predict the severity of MR). It is important to remember that in patients with severe heart
failure, poor cardiac output, or elevated left atrial pressures, the murmur of severe MR may be soft or absent.
DiagnosticTesting
The ECG usually shows evidence of a recent inferior or posterior MI. The chest radiograph generally shows
pulmonary edema. Focal pulmonary edema can occur in the right upper lobe when ow is directed at the
right pulmonary veins.
The diagnostic test of choice is two-dimensional echocardiography with color ow Doppler imaging. In
severe MR, the mitral valve leaet is usually ail. Color ow imaging can be useful in distinguishing
papillary muscle rupture with severe MR from VSD. Transthoracic echocardiography may not fully reveal
the amount of MR in some patients with posteriorly-directed jets. In these individuals, transesophageal
echocardiography can be particularly useful.
Hemodynamic monitoring with a PA catheter can reveal large (>50 mm Hg), early v waves in the pulmonary
capillary wedge pressure (PCWP). Patients with VSD can also have large v waves as a result of augmented
pulmonary venous return in a left atrium of normal size and decreased compliance, but they appear later in
the cardiac cycle. Further complicating the diagnostic picture, patients with severe MR and reected v waves
in the PA tracing may have an increase in oxygen saturation in the PA.21 With Swan-Ganz catheterization,
MR can be distinguished from VSD by two characteristics: First, prominent v waves in the PCWP tracing
preceding the incisura on the PA tracing are almost always secondary to severe MR. Second, in order to
identify a signicant increase in oxygen content associated with VSD, blood for oximetry should be obtained
with uoroscopic control from the central PA rather than from its more distal branches.
Treatment
Patients with papillary muscle rupture should be rapidly identied and receive aggressive medical treatment
while being considered for surgery. Medical therapy includes vasodilator therapy. SNP is useful in the
treatment of patients with acute MR. SNP directly decreases SVR, thereby reducing the regurgitant fraction
and increasing the forward stroke volume and cardiac output. SNP can be started at 0.5 to 1.0 g/kg/min and
titrated to a MAP of 60 to 75 mm Hg. An IABP should be inserted to decrease LV afterload, improve
coronary perfusion, and increase forward cardiac output. Patients with hypotension may tolerate vasodilators
after an IABP is inserted, but certainly not before.
Patients with papillary muscle rupture should be considered for emergency surgery, because the prognosis is
dismal in medically treated patients. Coronary angiography should be performed before surgical repair, since
revascularization during mitral valve repair or replacement is associated with improved short-term and longterm mortality.19,22 Additional surgical candidates include patients with moderate MR who do not clinically
improve with afterload reduction.
LeftVentricularFreeWallRupture
Prevalence
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While LV FWR was more common before the era of reperfusion, it now affects only 0.5% of MI patients.
However, FWR carries with it a substantial mortality rate of 20%.8,23 The timing of cardiac rupture is within
5 days of infarction in 50% of patients and within 2 weeks in 90% of patients. FWR occurs only among
patients with transmural MI (Figure 4). Risk factors include advanced age, female gender, hypertension, rst
MI, and poor coronary collateralization.
Pathophysiology
Compared with individuals who did not receive brinolytic agents, MI patients administered such drugs were
found to experience FWR earlier in their clinical course. However, their overall risk of FWR was not
increased.2325 Although any wall can be involved, cardiac rupture most commonly occurs at the lateral wall.
FWR occurs at three distinct intervals, with three distinct pathologic subsets. Type I increases with the use of
brinolytics, occurs early (within the rst 24 hours) and is a full-thickness rupture. Type II rupture occurs 1 to
3 days after MI and is a result of erosion of the myocardium at the site of infarction. Type III rupture occurs
late and is located at the border zone between infarcted and normal myocardium.
The reduction in Type III ruptures as a result of the advent of brinolytics has resulted in no change in the
overall FWR rate. It has been postulated that Type III ruptures may occur as a result of dynamic LVOT
obstruction and the resultant increased wall stress.26
SignsandSymptoms
Sudden onset of chest pain with straining or coughing can suggest the onset of myocardial rupture. Acutely
ruptured patients often have pulseless electrical activity (electromechanical dissociation) and sudden cardiac
death. Other patients may have a more subacute course as a result of a contained rupture, or pseudoaneurysm.
They may complain of nausea, pain suggestive of pericarditis, and are usually hypotensive. In an older study
evaluating 1,457 patients with acute MI, 6.2% had FWR. Approximately one third of these patients presented
with a subacute course.27
Jugular venous distention, pulsus paradoxus, diminished heart sounds, and a pericardial rub suggest subacute
rupture. New to-and-fro murmurs may be heard in patients with subacute rupture or pseudoaneurysm. A
junctional or idioventricular rhythm, low-voltage complexes, and tall precordial T waves may be evident on
the ECG. Additionally, a large number of patients have transient bradycardia just before rupture, as well as
other signs or symptoms of increased vagal tone.
DiagnosticTesting
Although there is generally insufcient time for thorough diagnostic testing in the management of patients
with acute rupture, transthoracic echocardiography is the emergent test of choice. Echocardiography typically
demonstrates a pericardial effusion with ndings of cardiac tamponade. These ndings include right atrial
(RA) and RV diastolic collapse, dilated inferior vena cava, and marked respiratory variations in mitral and
tricuspid inow. Additionally, a Swan-Ganz PA catheter may reveal hemodynamic signs of tamponade, with
equalization of the RA, RV diastolic, and PCWPs.
Treatment
The goal of therapy is to diagnose the problem early, and perform emergency open heart surgery to correct
the rupture. Emergency pericardiocentesis may be performed immediately on patients with tamponade and
severe hemodynamic compromise while arrangements are being made for transport to the operating room.
The procedure carries with it considerable risk because as the intrapericardial pressure is relieved,
communication is re-established between the intra- and extraventricular spaces, often leading to further
bleeding into the pericardium. Medical management has no role in the treatment of these patients, except for
the use of vasopressors to maintain blood pressure temporarily as the patient is rushed to the operating room.
Pseudoaneurysm
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Pathophysiology
Pseudoaneurysm is caused by contained rupture of the LV free wall. The aneurysm may remain small or
undergo progressive enlargement. The outer wall is formed by the pericardium and mural thrombus. The
pseudoaneurysm communicates with the body of the left ventricle through a narrow neck whose diameter is
by denition less than 50% of the diameter of the fundus.
SignsandSymptoms
Some pseudoaneurysms remain clinically silent and are discovered during routine investigations. However,
some patients have recurrent tachyarrhythmia, systemic embolization, and heart failure. Some patients have
systolic, diastolic, or to-and-fro murmurs related to the ow of blood across the neck of the pseudoaneurysm
during LV systole and diastole. A chest radiograph may show cardiomegaly, with an abnormal bulge on the
cardiac border. There may by persistent ST-segment elevation on the ECG. The diagnosis may be conrmed
by echocardiography, magnetic resonance imaging, or computed tomography.
Treatment
Spontaneous rupture occurs without warning in approximately one third of patients with a pseudoaneurysm.
Therefore, surgical intervention is recommended for all patients, regardless of symptoms or the size of the
aneurysm, to prevent sudden death.
LeftVentricularFailureandCardiogenicShock
Prevalence
LV dysfunction is to be expected after an acute MI. The degree of dysfunction correlates with the extent and
location of myocardial injury. Non-infarcted myocardium can also become temporarily hypokinetic or
akinetic due to ischemic "stunning." Patients with small, more distal infarctions may have discrete regional
wall motion abnormalities with preserved overall LV function because of compensatory hyperkinesis of the
unaffected segments.28 Prior MI, older age, female gender, diabetes, and anterior infarction are risk factors
for development of cardiogenic shock.29,30
In the late 1960's, Killip and Kimball31 developed a classication scheme to categorize patients' prognosis
based on their physical exam ndings (Table 2). Individuals were classied into four subsets, from "no
evidence of congestive heart failure" (Class I) to "cardiogenic shock" (Class IV). The authors reported a 67%
mortality rate for Class IV patients.
Table2:IncidenceofHeartFailureinAcuteMyocardialInfarction
Killip Class
Characteristics
Patients (%)
30-Day Mortality (%)
No evidence of congestive heart failure
32
II
Rales, jugular venous distention, or S3
38
17
III
Pulmonary edema
10
38
IV
Cardiogenic shock
19
67
Forrester and colleagues32,33 classied patients by their hemodynamic prole using a PA catheter to dene
PCWP and cardiac index. They reported a 50% mortality rate in the most compromised subset (PCWP >18
mm Hg; cardiac index <2.2 L/min/m2). Results of the GUSTO-I trial have indicated that 7% to 8% of acute
MI patients develop cardiogenic shock. Fibrinolysis did not materially affect mortality, which remained high
at 58%.34,35 In contrast, in the SHould we emergently revascularize Occluded Coronaries for cardiogenic
shocK (SHOCK) trial, urgent percutaneous or surgical revascularization markedly reduced early and late
mortality, when compared with continued medical therapy, including IABP.36 Finally, when the study
population of GUSTO-I was restricted to those with non-ST-elevation MI, the 30-day risk of mortality for
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pooled Killip Class III and IV patients was considerably lower, at 14%.37
Pathophysiology
Patients can develop cardiogenic shock in association with an acute MI due to multiple causes, including
large LV infarction, severe RV infarction, VSD, FWR, acute MR, or pharmacologic depression of LV
function (beta blockers in MI from a proximal LAD lesion). Patients who have cardiogenic shock as a result
of acute MI typically have severe multivessel disease, with signicant involvement of the LAD.38,39
Generally, at least 40% of the LV mass is affected in patients who present in cardiogenic shock as a result of a
rst MI.40,41 In patients with prior MI and baseline depressed LV function, a smaller acute insult can result in
cardiogenic shock (Figure 5).
SignsandSymptoms
Patients who present in Killip Class III often have respiratory distress, diaphoresis, and cool, clammy
extremities in addition to the typical signs and symptoms of acute MI. Patients in Killip Class IV
(cardiogenic shock) can have severe orthopnea, dyspnea, and oliguria and may have altered mental status, as
well as multisystem organ failure from hypoperfusion. It may be possible to palpate an area of dyskinesia on
the precordium. An S3 gallop, pulmonary rales, and elevated jugular venous pressure are common ndings on
physical examination.
DiagnosticTesting
Patients with cardiogenic shock caused by acute MI generally have extensive electrocardiographic changes
demonstrating a large infarct, diffuse ischemia, or prior infarcts. If these changes are absent, another cause of
shock such as sepsis should be considered. Chest radiography usually reveals pulmonary edema. Laboratory
tests may demonstrate lactic acidemia, renal failure, and arterial hypoxemia.
The patient in cardiogenic shock should be monitored with a PA catheter and an arterial line. These can help
distinguish between primary LV failure and other mechanical causes of cardiogenic shock, as discussed
above.
Transthoracic echocardiography helps determine the extent of dysfunctional myocardium. It also helps
identify other mechanical complications of MI that may be contributing to cardiogenic shock, such as
papillary muscle rupture.
Treatment
A patient in cardiogenic shock should have a LV assist device (IABP, Impella, TandemHeart) placed
urgently to reduce afterload, improve cardiac output, and enhance coronary perfusion. Medical therapy with
vasodilators (e.g., nitroglycerin and SNP), angiotensin-converting enzyme (ACE) inhibitors and loop
diuretics should be used as tolerated. Intravenous nitroglycerin is the rst-line drug of choice among
vasodilators because it is less likely to produce coronary steal than SNP and helps protect against ischemia.
The starting dose is 10 to 20 g/min and it may be increased by 10 g/min every 2 to 3 minutes to a goal
MAP of 70 mm Hg. Intravenous SNP can be added if further reduction in afterload is necessary. SNP is
started at 0.5 to 1.0 g/kg/min and is also titrated to a MAP of approximately 70 mm Hg. Patients who are
hypotensive on presentation (MAP <70 mm Hg) may not tolerate vasodilators or other blood pressurelowering agents prior to placement of an assist device.
ACE inhibitors improve LV performance and decrease myocardial oxygen consumption by reducing the
cardiac afterload of patients with heart failure and acute MI. ACE inhibitors can reduce infarct expansion if
started in the rst 12 hours of an MI if the patient is not already in cardiogenic shock. It is recommended that
captopril be started early, at 3.125 to 6.25 mg every 8 hours, with each dose subsequently doubled as
tolerated to a maximum dose of 50 mg every 8 hours. Patients with mild pulmonary edema can be treated
with diuretics such as intravenous (IV) furosemide, adjusted for serum creatinine and history of diuretic use.
Beta-adrenergic agonists such as dobutamine or dopamine may be needed for patients with severe heart
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failure and cardiogenic shock. This therapy should generally be reserved for those who have failed
mechanical LV support and maximal vasodilator therapy, or for those with a RV infarct. Phosphodiesterase
inhibitors such as milrinone may be benecial for some patients, but can increase ventricular ectopy. The
bolus may be omitted in patients with marginal blood pressures. Some patients may need norepinephrine to
maintain arterial pressure. Norepinephrine is started at 2 g/min and titrated to maintain the MAP at
approximately 70 mm Hg.
PCI and emergency coronary bypass surgery have been associated with improved prognosis for patients in
cardiogenic shock, reducing the mortality rate from 80% to 50%. Emergency PCI or surgical
revascularization is indicated for patients with severe multivessel disease.6 Substantial left main coronary
artery stenosis is also an indication for coronary bypass, as ongoing studies evaluate the efcacy of left main
stenting in this situation. Other surgical modalities that may be considered include implantation of LV or
biventricular assist devices or extracorporeal membrane oxygenation as a bridge to heart transplantation.
Some patients may be gradually weaned from ventricular assist devices after the stunned portion of
myocardium recovers, without the need for cardiac transplantation.
RightVentricularFailure
Prevalence
Mild RV dysfunction is common after MI of the inferior or inferoposterior wall, with an incidence of
approximately 40%. Hemodynamically signicant RV impairment occurs in only 10% of patients with these
types of MI, however (Figure 6).
Pathophysiology
The degree of RV dysfunction depends on the location of the right coronary artery occlusion. Only proximal
occlusions of the right coronary artery (proximal to the acute marginal branch) result in marked
dysfunction.42 The degree of RV involvement also depends on the amount of collateral ow from the LAD
and the degree of blood ow through the thebesian veins. Because the right ventricle is thin-walled and has
lower oxygen demand, there is coronary perfusion during the entire cardiac cycle; therefore, widespread
irreversible infarction is rare.
SignsandSymptoms
The triad of hypotension, jugular venous distention with clear lungs, and absence of dyspnea has high
specicity but low sensitivity for RV infarction.43 Severe RV failure can manifest with signs and symptoms
of a low cardiac output state, including diaphoresis, cool clammy extremities, and altered mental status.
Patients often have oliguria and hypotension. Other causes of severe hypotension in the setting of an inferior
MI include bradyarrhythmia, acute severe MR, and VSD.
Patients with isolated RV failure have elevated jugular venous pressure and right-ventricular S3 heart sound
in the setting of a normal lung examination. The presence of jugular venous pressure greater than 8 cm H2O
and Kussmaul's sign is highly sensitive and specic for severe RV failure. A rare but clinically important
complication of RV infarction is right-to-left shunting secondary to increased pressures in the RA and RV and
opening of the foramen ovale. This should be considered in patients with RV infarction and persistent
hypoxemia.
Electrocardiographically, patients present with inferior ST elevation in conjunction with ST elevation in the
V4R lead. These ndings have a positive predictive value of 80% for RV infarction.44 The chest radiograph
usually does not show pulmonary venous hypertension.
DiagnosticTesting
Echocardiography is the diagnostic study of choice for RV infarction. It will demonstrate RV dilation and
dysfunction and usually LV inferior wall dysfunction as well. It is also helpful in excluding cardiac
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tamponade, which can mimic RV infarction hemodynamically. The hemodynamic prole of acute RV
infarction can also be due to an acute pulmonary embolism in the absence of a cardiac ischemic event.
Hemodynamic monitoring with a PA catheter typically reveals high RA pressures with a low PCWP, because
RV failure results in underlling of the left ventricle and a low cardiac output. A RA pressure of higher than
10 mm Hg and a RA pressure-to-PCWP ratio of 0.8 or greater strongly suggest RV infarction.45 If severe LV
dysfunction is also present, the PCWP can be higher. In some patients, RV dilatation can impair LV
performance by attening or bowing of the septum into the left ventricle. This can restrict ventricular lling
and elevate the PCWP.
Treatment
Volume loading to increase LV preload and cardiac output is key to the management of RV infarction. Some
patients require several liters in 1 hour to reach a target central venous pressure of 15 mm Hg and a target
PCWP of 15 mm Hg. It is important to have hemodynamic monitoring with a PA catheter in these patients,
because overzealous uid administration can further decrease LV output. This occurs as a result of septal shift
toward the left ventricle and an intrapericardial pressure shift. When volume loading is insufcient to
improve cardiac output, inotropes are indicated. Administration of dobutamine can increase cardiac index and
improve RV ejection fraction. Vasodilators such as nitroglycerin and SNP, while effective for afterload
reduction in acute LV infarction, will almost universally cause hypotension and hemodynamic
decompensation in acute RV infarction.43
Patients may benet from reperfusion therapy, because those who undergo successful reperfusion of RV
branches have enhanced RV function and a lower 30-day mortality rate.46,47 Patients with RV infarction and
bradyarrhythmias or loss of sinus rhythm may have signicant improvement with AV sequential pacing.
Optimal pacer settings tend to utilize longer AV delays (approximately 200 msec) and a heart rate of 80 to 90
beats per minute.
Although an IABP acts primarily on the LV, there have been case reports of IABP improving the cardiac
index when used in combination with dobutamine for acute RV infarction. Pericardiectomy may be
considered for patients with refractory shock because it reverses the septal impingement on LV lling. Most
patients with RV infarction improve after 48 to 72 hours. An RV assist device is indicated for patients who
remain in cardiogenic shock in spite of these measures.
VentricularAneurysm
Prevalence
Patients who do not receive reperfusion therapy are at greatest risk for developing this complication (in
10%-30%). Among the various infarct locations, patients with apical transmural MIs are at the highest risk
for aneurysm formation, followed by those with posterior-basal infarcts.
Pathophysiology
The early open artery hypothesis states that early reperfusion should result in improved myocardial salvage
and prevention of infarct expansion. Even late reperfusion limits infarct expansion through a number of
mechanisms, including immediate change in infarction characteristics, preservation of small amounts of
residual myobrils and interstitial collagen, accelerated healing, the scaffold effect of a blood-lled
vasculature, and elimination of ischemia in viable but dysfunctional myocardium. Persistent occlusion of the
IRA, on the other hand, can lead to infarct expansion and progressive LV dilation. The aneurysm consists of a
stretched portion of the myocardium which contains all three tissue layers and is connected to the ventricle by
a wide neck (greater than half the diameter of the fundus). The differences between a pseudoaneurysm (false
aneurysm) and true aneurysm are highlighted in Table 3.
Table3:DifferencesBetweenTrueAneurysmsandPseudoaneurysms
Parameter
True Aneurysm
Pseudoaneurysm
Cause
Infarction
Contained rupture
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Cause
Infarction
Contained rupture
Incidence
1%-5%
Rare
Neck
Wide
Narrow
Wall
All three layersscar
Pericardium and thrombus
Rupture
Very rare
Common
SignsandSymptoms
Acute decompensated heart failure and even cardiogenic shock can develop as a result of a large LV
aneurysm. Because acute aneurysms expand during systole, contractile energy generated by a normal
myocardium is wasted and puts the entire ventricle at a mechanical disadvantage. Chronic aneurysms persist
for more than 6 weeks after the acute event, are less compliant than acute aneurysms, and are less likely to
expand during systole. Patients with chronic aneurysms may have heart failure, ventricular arrhythmias, and
systemic embolization, or they may be asymptomatic. Palpation of the precordium can reveal a dyskinetic
segment of the ventricle. An S3 gallop may be heard in patients with poor ventricular function.
DiagnosticTesting
Typical electrocardiographic ndings include Q waves and ST elevation, which can persist despite
application of reperfusion therapy. When electrocardiographic changes (ST elevation) persist for more than 6
weeks, patients may have a chronic ventricular aneurysm. A chest radiograph may reveal a localized bulge in
the cardiac silhouette. Echocardiography is the gold standard for accurate identication of the aneurysmal
segment. It may also demonstrate the presence of a mural thrombus. Additionally, echocardiography is useful
in differentiating true aneurysms from pseudoaneurysms. Magnetic resonance imaging may also be useful
and diagnostic for delineating the aneurysmal section.
Treatment
Acute decompensated heart failure with acute aneurysms is managed with IV vasodilators. ACE inhibitors
have been shown to reduce infarct expansion and unfavorable LV remodeling. As tolerated by blood pressure,
ACE inhibitors are best started within the rst 12 to 24 hours of onset of acute MI because infarct expansion
starts early. Corticosteroids and nonsteroidal anti-inammatory drugs (NSAIDs) should be avoided in the
acute setting because they have been shown to promote infarct expansion and aneurysm formation in
experimental models. Chronic heart failure with chronic aneurysms can be managed with ACE inhibitors,
beta-blockers, and diuretics.
Anticoagulation with warfarin is indicated for patients with a mural thrombus. Patients should be treated
initially with IV heparin, with a target partial thromboplastin time of 50 to 70 seconds. Warfarin is started
simultaneously. Patients should be treated with warfarin at a target international normalized ratio (INR) of 2
to 3 for a period of 3 to 6 months. It is controversial whether patients who have large aneurysms without
thrombus should receive anticoagulants. Many clinicians prescribe anticoagulants for 6 to 12 weeks after the
acute phase. Patients with LV aneurysms and a low global ejection fraction (<40%) have a higher stroke rate
and should take anticoagulants for at least 3 months after the acute event. Subsequently, they will undergo
regular surveillance with echocardiography (usually every year). Anticoagulation should be reinitiated if a
new thrombus develops.
Refractory heart failure or ventricular arrhythmias in patients with aneurysms are indications for surgical
resection, also referred to as LV reconstructive surgery. Resection of the aneurysm may be followed by
conventional closure or newer techniques to maintain LV geometry. Revascularization is benecial for
patients with a large amount of viable myocardium around the aneurysmal segment.
DynamicLeftVentricularOutflowTractObstruction
Prevalence
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Dynamic LVOT obstruction is an uncommon complication of acute anterior MI and was rst described in a
case report by Bartunek and associates.48
Pathophysiology
This event is dependent on compensatory hyperkinesis of the basal and midsegments of the left ventricle in
patients with distal LAD infarcts. Predictors of enhanced regional wall motion in noninfarct zones are the
absence of multivessel disease, female gender, and higher ow in the infarct-related vessel. The increased
contractile force of these regions decreases the cross-sectional area of the LVOT during systole. The resulting
increased velocity of blood through the outow tract can produce decreased pressure below the mitral valve
and cause the leaet to be displaced anteriorly toward the septum (Venturi effect). This results in further
LVOT obstruction resulting from systolic anterior motion (SAM) of the anterior mitral valve leaet, and in
posteriorly-directed MR.
It has been postulated that dynamic LVOT obstruction can play a role in causing FWR. LVOT obstruction
leads to increased end-systolic intraventricular pressure, which induces increased wall stress of the weakened,
necrotic infarct zone. This frequently fatal complication occurs most often in women, in older patients (older
than 70 years), and in those without prior MI.
SignsandSymptoms
Patients may have respiratory distress, diaphoresis, and cool, clammy extremities in addition to the typical
signs and symptoms of acute MI. Patients with severe LVOT obstruction may appear to be in cardiogenic
shock with severe orthopnea, dyspnea, and oliguria, and may have altered mental status from cerebral
hypoperfusion. Patients may present with a new systolic ejection murmur heard best at the left upper sternal
border, with radiation to the neck. Additionally, a new holosystolic murmur can be heard at the apex, with
radiation to the axilla as a result of SAM of the mitral leaet. An S3 gallop, pulmonary rales, hypotension,
and tachycardia can also be present.
DiagnosticTesting
Echocardiography is the diagnostic test of choice and can accurately characterize the hyperkinetic segment,
LVOT obstruction, and mitral leaet SAM.
Treatment
Treatment centers on decreasing myocardial contractility and heart rate while expanding intravascular
volume and increasing afterload (modestly). Beta blockers should be added slowly and with careful
monitoring of heart rate, blood pressure, and SvO2. Patients can receive gentle IV hydration with several
small (250 mL) boluses of saline to increase preload and decrease LVOT obstruction and SAM. The patient's
hemodynamic and respiratory status should be monitored closely during this therapeutic intervention with a
PA catheter. Vasodilators, inotropes, and balloon pumps should be avoided because they can increase LVOT
obstruction. In contrast, the pure peripheral vasoconstrictor phenylephrine can be useful, since it will increase
afterload and diminish the LVOT gradient.
ArrhythmicComplications
Ventricular arrhythmia is a common complication of acute MI, occurring in almost all patients, even before
monitoring is possible. It is related to the formation of re-entry circuits at the conuence of the necrotic and
viable myocardium, as well as to irritable ischemic myocardium.
Premature ventricular contractions occur in approximately 90% of patients with acute MI. At the other end of
the spectrum, the incidence of ventricular brillation (VF) is approximately 2% to 4%. Although lidocaine
has been demonstrated to reduce somewhat the rate of primary VF in patients with MI, there is no survival
benet and there may be excess mortality. Therefore, it is not recommended that patients receive prophylactic
lidocaine therapy.49 Amiodarone may be used in patients with MI with nonsustained ventricular tachycardia
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(VT), or after debrillation for VF. The recommended dosing is a bolus of 150 mg and then administration of
1 mg/min for 6 hours, followed by 0.5 mg/min. When starting this medication for VF or pulseless VT, the
bolus should be increased to 300 mg (the 150 mg bolus can be repeated in 10 minutes). Ventricular
arrhythmias not responding to amiodarone may be treated with lidocaine (1 mg/kg bolus to a maximum of
100 mg, followed by a 1-4 mg/min drip),50 or with procainamide. Polymorphic VT is a rare complication of
acute MI, usually associated with recurrent ischemia. It can be treated with amiodarone, lidocaine,
procainamide, or a combination of drugs, as described for the more commonly-observed monomorphic VT.
Accelerated idioventricular rhythm, sometimes referred to as "slow VT," often occurs during the reperfusion
phase of PCI, is self-limited, and usually does not require treatment.
The importance of VF in the setting of MI has been re-evaluated in the context of the interaction between
severe systolic dysfunction and the potential for sudden cardiac death. Implantable cardioverter-debrillators
have been shown to reduce mortality in post-MI patients with an ejection fraction less than or equal to 30%,
regardless of whether or not ventricular dysrhythmia has been observed.51
Supraventricular arrhythmias occur in less than 10% of patients with acute MI, and are not directly ischemic
in origin. Because patients who develop these arrhythmias tend to have more severe ventricular dysfunction
than those who do not, they will generally experience a worse outcome. Although isolated RA infarction or
small inferior infarcts leading to atrial arrhythmias are not associated with higher mortality rates, the
appearance of atrial arrhythmias usually heralds the onset of heart failure in the setting of acute anterior MI.
Bradyarrhythmias, including AV block and sinus bradycardia, occur most commonly with inferior MI.
Complete AV block occurs in approximately 20% of patients with acute RV infarction. Infranodal conduction
disturbances with wide complex ventricular escape rhythms occur most often in large anterior infarctions and
portend a very poor prognosis.
Temporary transvenous pacing is indicated for patients who present with Mobitz type 2 second-degree AV
block, complete AV block, or asystole. Consideration for transvenous pacing should be given to patients with
bifascicular block or "trifascicular block" (bifascicular block with concurrent rst-degree AV block) in the
setting of acute MI.52 Pacing is not indicated for the patient in sinus bradycardia or AV dissociation with a
slow sinus rate and a more rapid ventricular escape rhythm as long as the patient is maintaining adequate
hemodynamics. If mild symptoms exist, the initial treatment for these rhythm disturbances is IV atropine, 0.5
to 1.0 mg. This may be repeated every 5 minutes, to a maximum dose of 2 mg.
EmbolicComplications
Prevalence
The incidence of clinically evident systemic embolism after MI is less than 2%. The incidence increases in
patients with anterior wall MI. The overall incidence of mural thrombus after MI is approximately 20%.
Large anterior MI may be associated with mural thrombus in as many as 60% of patients.53,54
Pathophysiology
Most emboli arise from the left ventricle as a result of wall motion abnormalities or aneurysms. Atrial
brillation in the setting of ischemia can also contribute to systemic embolization.
SignsandSymptoms
The most common clinical manifestation of embolic complications is stroke, although patients may have limb
ischemia, renal infarction, or mesenteric ischemia. Most episodes of systemic emboli occur within the rst 10
days after acute MI. Physical ndings vary with the site of the embolism. Focal neurologic decits occur in
patients with central nervous system emboli. Limb ischemia manifests with limb pain in a cold, pulseless
extremity. Renal infarction manifests with ank pain, hematuria, and acute renal insufciency. Mesenteric
ischemia manifests with abdominal pain out of proportion to physical ndings, anorexia and bloody diarrhea.
Treatment
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In the absence of active bleeding, IV heparin should be started immediately with a target partial
thromboplastin time of 50 to 70 seconds and continued until warfarin treatment has brought the INR into the
therapeutic range. Warfarin therapy should be started immediately, with a goal INR of 2 to 3, and continued
for at least 3 to 6 months for patients with mural thrombi and for those with large akinetic areas detected by
echocardiography.
Pericarditis
Prevalence
The incidence of early pericarditis after acute MI is approximately 10%. This inammatory condition usually
develops between 24 and 96 hours after MI.55,56 Dressler's syndrome, or late pericarditis, occurs with an
incidence between 1% and 3%, typically 2 to 8 weeks after MI.
Pathophysiology
The pathogenesis of acute post-MI pericarditis is an inammatory reaction in response to necrotic tissue.
Acute pericarditis thus develops more often in patients with transmural MI. The pathogenesis of Dressler's
syndrome is unknown, but an autoimmune mechanism involving circulating myocardial antigens has been
suggested.
SignsandSymptoms
Most patients with early pericarditis report no symptoms. Patients with symptoms from early or late
pericarditis describe progressive, severe chest pain that lasts for hours. The symptoms are posturalworse in
the supine positionand are alleviated by sitting up and leaning forward. The pain is pleuritic in nature and
therefore tends to be exacerbated by deep inspiration, coughing, and swallowing. Radiation of pain to the
trapezius ridge is almost pathognomonic for acute pericarditis. The pain also can radiate to the neck and, less
commonly, to the arm or back.
A pericardial friction rub on examination is a very specic nding to support acute pericarditis; however, it
can be ephemeral, and is not found in all patients with pericarditis (low sensitivity). Frequent cardiac physical
examinations will increase the chance of hearing the rub. It is best heard at the left lower sternal edge with
the diaphragm of the stethoscope. The rub has three components: atrial systole, ventricular systole, and
ventricular diastole. In about 30% of patients with rubs it is biphasic, and in 10% it is uniphasic. A pericardial
effusion can cause uctuation in the intensity of the rub.
Evolving MI changes can mask the diagnosis of pericarditis. Pericarditis produces generalized ST-segment
elevation, which is concave-upwards or saddle-shaped. As pericarditis evolves, T waves become inverted
after the ST segment becomes isoelectric. Conversely, in acute MI, T waves can become inverted when the
ST segment is still elevated. Four sequential phases of electrocardiographic abnormalities have been
described in association with pericarditis (Table 4).57
Table4:ElectrocardiographicChangesofPericarditis
Stage
Electrocardiographic Change
ST elevation, upright T waves
II
ST elevation resolves, upright to at T waves
III
ST isoelectric, inverted T waves
IV
ST isoelectric, upright T waves
A pericardial effusion on echocardiography strongly suggests pericarditis, but the lack of an effusion does not
rule it out.
Treatment
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Aspirin is the therapy of choice for post-MI pericarditis, 650 mg every 4 to 6 hours, for at least 4 weeks.
During this time, a proton-pump inhibitor or other anti-secretagogue should be co-administered for gastric
protection. NSAIDs and corticosteroids should be avoided, as they can interfere with myocardial healing and
contribute to expansion of the infarct. NSAIDs should also be avoided in patients with coronary artery
disease, due to the increased risk of further cardiac events on such drugs. The anti-inammatory agent
colchicine can be used as initial therapy, and is also the preferred add-on drug in the treatment of chronic or
recurrent post-MI pericarditis if aspirin monotherapy is ineffective.
Back to Top
Suggested Reading
Kutty RS, Jones N, Moorjani N. Mechanical complications of acute myocardial infarction [published
online ahead of print August 13, 2013]. Cardiol Clin 2013; 31:519531. doi:10.1016/j.ccl.2013.07.004.
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