Complications of Myocardial Infarction (MI)

Complications of AcuteComplications of Acute
Myocardial InfarctionMyocardial Infarction

OverviewOverview
 Recurrent Ischemia/InfarctionRecurrent Ischemia/Infarction
 Congestive Heart Failure/LV FailureCongestive Heart Failure/LV Failure
 Cardiogenic ShockCardiogenic Shock
 Interventricular Septal RuptureInterventricular Septal Rupture
 Free Wall RuptureFree Wall Rupture
 Acute Mitral RegurgitationAcute Mitral Regurgitation
 Right Ventricular InfarctionRight Ventricular Infarction
 ArrhythmiasArrhythmias
 Pericardial Effusion and PericarditisPericardial Effusion and Pericarditis

Recurrent Ischemia andRecurrent Ischemia and
InfarctionInfarction
 Incidence of postinfarction angina withoutIncidence of postinfarction angina without
reinfarction is 20-30%reinfarction is 20-30%
 Reduced incidence with primary PTCAReduced incidence with primary PTCA
 May be due to occlusion of an initiallyMay be due to occlusion of an initially
patent vessel, reocclusion of an initiallypatent vessel, reocclusion of an initially
recanalized vessel, or coronary spasm.recanalized vessel, or coronary spasm.

Ischemic complications
These can include infarct extension, recurrent infarction, and recurrent
angina.
Prevalence
Infarct extension is a progressive increase in the amount of
myocardial necrosis within the infarct zone of the original
MI. This may manifest as an infarction that extends and
involves the adjacent myocardium or as a subendocardial
infarction that becomes transmural.
Reocclusion of an infarct-related artery (IRA) occurs in
5% to 30% of patients following fibrinolytic therapy.
These patients also tend to have a poorer outcome.1
Reinfarction is more common in patients with diabetes
mellitus or prior MI.

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Infarction in a separate territory (recurrent infarction) may
be difficult to diagnose within the first 24 to 48 hours after
the initial event. Multivessel coronary artery disease is
common in patients with acute myocardial infarction. 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, which occurs from a few hours to 30 days after
acute MI, is defined as postinfarction angina. The
incidence of postinfarction angina is highest in patients
with non–ST-elevation MI (approximately 25%) and
those treated with fibrinolytics compared with mechanical
revascularization (percutaneous coronary intervention
[PCI]).

Pathophysiology
Reinfarction occurs more frequently 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 fibrinolytic
therapy, reocclusion is found on angiograms of 5% to 30%
of patients and is associated with a worse outcome.
The pathophysiologic mechanism of postinfarction angina
is similar to that of unstable angina and 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.

Signs and Symptoms
Patients with infarct extension or
postinfarction angina usually have continuous
or recurrent chest pain, with protracted
elevation in the creatine kinase (CK) level
and, occasionally, new electrocardiographic
changes.

Diagnostic Testing
The diagnosis of infarct expansion, reinfarction, or
postinfarction ischemia can be made with
echocardiography or nuclear imaging.
A new wall motion abnormality, 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, nitrates, and beta
blockers is indicated in patients who have had a myocardial
infarction and have ongoing ischemic symptoms. An intra-
aortic balloon pump (IABP) should be inserted promptly in
patients with hemodynamic instability or severe LV systolic
dysfunction. Coronary angiography should be performed in
patients who are stabilized with medical therapy, but
emergency angiography may be undertaken in unstable
patients. Revascularization, percutaneous or surgical, is
associated with improved prognosis.

Left Ventricular FailureLeft Ventricular Failure
 THE single most important predictor of mortalityTHE single most important predictor of mortality
after AMIafter AMI
 Characterized by either systolic dysfunction aloneCharacterized by either systolic dysfunction alone
or both systolic and diastolic dysfunctionor both systolic and diastolic dysfunction
 Increased clinical manifestations as the extent ofIncreased clinical manifestations as the extent of
the injury to the LV increasesthe injury to the LV increases
 Other predictors of development of symptomaticOther predictors of development of symptomatic
LV dysfunction include advanced age and diabetesLV dysfunction include advanced age and diabetes
 Mortality increases with the severity of theMortality increases with the severity of the
hemodynamic deficithemodynamic deficit

 LV failure – Congestive Heart FailureLV failure – Congestive Heart Failure
 Characteristically develop hypoxemia dueCharacteristically develop hypoxemia due
to pulmonary vascular engorgementto pulmonary vascular engorgement
 Managed most effectively first by reductionManaged most effectively first by reduction
of ventricular preload and then, if possible,of ventricular preload and then, if possible,
by lowering afterloadby lowering afterload

 Treatment:Treatment:
– DiureticsDiuretics
– NitroglycerinNitroglycerin
– VasodilatorsVasodilators
– DigitalisDigitalis
– Beta-adrenoceptor agonistsBeta-adrenoceptor agonists
– Other positive inotropic agentsOther positive inotropic agents

Incidence of Heart Failure in
Acute Myocardial Infarction
Killip Class Characteristics
I No evidence of congestive heart failure
II Rales, ↑ jugular venous distention, or S3
III
Pulmonary edema
IV Cardiogenic shock

Class of CHF - KillipClass of CHF - Killip
 Derived retrospectively in the 60’s, post-MI ptsDerived retrospectively in the 60’s, post-MI pts
I - No CHF - 5% mortalityI - No CHF - 5% mortality
II - Mild CHF (bibasilar rales and S3) - 15-25%II - Mild CHF (bibasilar rales and S3) - 15-25%
mortalitymortality
III - Frank pulmonary edema - 40% mortalityIII - Frank pulmonary edema - 40% mortality
IV - Cardiogenic shock - 80% mortalityIV - Cardiogenic shock - 80% mortality
Killip T 3rd, Kimball JT. Treatment of myocardial infarction in a coronary care unit. A twoKillip T 3rd, Kimball JT. Treatment of myocardial infarction in a coronary care unit. A two
year experience with 250 patients. Am J Cardiol. 1967 Oct;20(4):457-64.year experience with 250 patients. Am J Cardiol. 1967 Oct;20(4):457-64.

NYHA ClassificationNYHA Classification
 Class IClass I: No limitation of physical activity: No limitation of physical activity
 Class IIClass II: Slight limitation of activity. Dyspnea: Slight limitation of activity. Dyspnea
and fatigue with moderate activity (>2flights ofand fatigue with moderate activity (>2flights of
stairs)stairs)
 Class IIIClass III: Marked limitation of activity. Dyspnea: Marked limitation of activity. Dyspnea
and fatigue with minimal activity (i.e. < 2 flightsand fatigue with minimal activity (i.e. < 2 flights
of stairsof stairs
 Class IVClass IV: Severe limitation of activity. Sx are: Severe limitation of activity. Sx are
present at restpresent at rest

Cardiogenic ShockCardiogenic Shock
 Most severe clinical expression of leftMost severe clinical expression of left
ventricular failureventricular failure
 Occurs in up to 7% of patients with AMIOccurs in up to 7% of patients with AMI
 Low output state characterized by elevatedLow output state characterized by elevated
ventricular filling pressures, low cardiacventricular filling pressures, low cardiac
output, systemic hypotension, and evidenceoutput, systemic hypotension, and evidence
of vital organ hypoperfusionof vital organ hypoperfusion

 At autopsy, more than 2/3 of patients withAt autopsy, more than 2/3 of patients with
cardiogenic shock demonstrate stenosis ofcardiogenic shock demonstrate stenosis of
75 percent or more of the luminal diameter75 percent or more of the luminal diameter
of all 3 major coronary vessels and loss ofof all 3 major coronary vessels and loss of
about 40 percent of LV massabout 40 percent of LV mass

 Medical ManagementMedical Management
– Same as tx for LV failureSame as tx for LV failure
– Intraaortic balloon counterpulsationIntraaortic balloon counterpulsation
– RevascularizationRevascularization

Mechanical complications
Mechanical complications of acute MI include
ventricular septal rupture, papillary muscle
rupture or dysfunction, cardiac free wall
rupture, ventricular aneurysm, LV failure with
cardiogenic shock, dynamic left ventricular
outflow tract obstruction, and right ventricular
failure.

Ventricular Septal Rupture
Independent predictors of ventricular septal rupture
(VSR) are shown in
Older age
Female gender
Nonsmoker
Anterior infarct
Worse Killip class on admission
Increasing heart rate on admission

Prevalence
VSR formerly occurred in 1% to
2% of patients after acute MI in the
prethrombolytic era . The incidence
has dramatically decreased with
reperfusion therapy.2
The GUSTO-
I trial has demonstrated an
incidence of VSR of approximately
0.2%.3,4
VSR may develop as early as 24
hours after MI but was commonly
seen 3 to 7 days after MI in the
prefibrinolytic era and 2 to 5 days
currently. Fibrinolytic therapy is
not associated with an increased
risk of VSR.2,5

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. VSR almost
always occurs in the setting of a transmural MI
and is more frequently seen in anterolateral MIs.
The defect may not always be a single large
defect; it can be a meshwork of serpiginous
channels that can be identified in 30% to 40% of
patients.

Signs and Symptoms
Early in the disease process, patients with
VSR may appear relatively comfortable, with
no clinically significant cardiopulmonary
symptoms. Rapid recurrence of angina,
hypotension, shock, or pulmonary edema may
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
profile and biventricular failure. Therefore, it is
important that all patients with MI have a well-
documented cardiac examination at presentation and
daily thereafter daily thereafter.

An electrocardiogram (ECG) may show atrioventricular (AV)
nodal or infranodal conduction delay abnormalities in
approximately 40% of patients. Echocardiography with color flow
imaging is the best method for diagnosing VSR.
There are two types of VSR, which can best be visualized in
different echocardiographic planes.
A basal VSR is best visualized in the parasternal long axis with
medial angulation, apical long axis, and subcostal long axis. An
apical VSR is best visualized in the apical four-chamber view.
Echocardiography can define LV and right ventricular (RV)
function—important determinants of mortality—as well as the size
of defect and degree of left-to-right shunt by assessing flow
through the pulmonary and aortic valves. In some cases, it may be
necessary to use transesophageal echocardiography to assess the
ventricular septal defect.

Treatment
Early surgical closure is the treatment of choice, even if the patient's
condition is stable. Initial reports have suggested that delaying surgery is
likely to result in improved surgical mortality.6
These benefits were
probably the result of selection bias,7
because the mortality rate in
patients with VSD treated medically is 24% at 72 hours and 75% at 3
weeks. Therefore, patients should be considered for urgent surgical
repair.
There is a high surgical mortality associated with cardiogenic shock and
multisystem failure. This further supports earlier operation before
complications develop.8
Mortality is highest in patients with basal septal
rupture associated with inferior MI (70%, compared with 30% in patients
with anterior infarcts). The mortality rate is higher because of increased
technical difficulty and the frequent need for mitral valve repair or
replacement in the patients with mitral regurgutation.9
Regardless of the
location and hemodynamic condition of the patient, surgery should
always be considered, because it is associated with a lower mortality rate
than conservative management.10

Intensive medical management should be started to support the
patient before surgery. Unless there is significant 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 insertion of the IABP, vasodilators
can be used, with close hemodynamic monitoring. Vasodilators can
also reduce left-to-right shunting and increase systemic flow by
reducing SVR. Nevertheless, 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 (IV) nitroprusside, which is started at 0.5 to 1.0
μg/kg/min and titrated to a mean arterial pressure (MAP) of 60 to 75
mm Hg.

Interventricular Septal RuptureInterventricular Septal Rupture
 Occurs in 0.2 percent of patients with AMIOccurs in 0.2 percent of patients with AMI
 Clinical features associated with increased risk ofClinical features associated with increased risk of
rupture:rupture:
– Lack of development of collateral networkLack of development of collateral network
– Advanced ageAdvanced age
– HypertensionHypertension
– Anterior location of infarctionAnterior location of infarction
– thombolysisthombolysis
 Higher 30-day mortality (74%) compared to thoseHigher 30-day mortality (74%) compared to those
patients who do not develop this complicationpatients who do not develop this complication
(7%)(7%)

 The size of the defect determines:The size of the defect determines:
– The magnitude of the left-to-right shuntThe magnitude of the left-to-right shunt
– Extent of hemodynamic deteriorationExtent of hemodynamic deterioration
– Likelihood of survivalLikelihood of survival
 Associated with complete heart block, rightAssociated with complete heart block, right
bundle branch block, and atrial fibrillationbundle branch block, and atrial fibrillation
in 20-30 percent of casesin 20-30 percent of cases

 Characterized by the appearance of a newCharacterized by the appearance of a new
harsh, loud holosystolic murmurharsh, loud holosystolic murmur
 Best heard at the lower left sternal borderBest heard at the lower left sternal border
 Usually accompanied by a thrillUsually accompanied by a thrill
 Can be recognized by 2-DCan be recognized by 2-D
echocardiographyechocardiography
 Catheter placement of an umbrella-shapedCatheter placement of an umbrella-shaped
device within the ruptured septumdevice within the ruptured septum

Free Wall Rupture
Prevalence
Free wall rupture occurs in 3% of MI patients and accounts
for approximately 10% of mortality after MI . The timing
of cardiac rupture is within 5 days in 50% of patients and
within 2 weeks of MI in 90% of patients. Free wall rupture
occurs only among patients with transmural MI. Risk
factors include advanced age, female gender, hypertension,
first MI, and poor coronary collateral vessels.

Pathophysiology
Free wall rupture accounts for part of the early hazard in patients
treated with fibrinolytic agents. Nevertheless, the overall incidence
of free wall rupture is not higher in patients treated with
fibrinolytics.21–23
Although any wall can be involved, cardiac rupture
most commonly occurs at the lateral wall.
Free wall rupture occurs at three distinct intervals, with three distinct
pathologic subsets. Type I increases with the use of fibrinolytics. It
occurs early (within the first 24 hours) and is a full-thickness
rupture. Type II rupture occurs 1 to 3 days post-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 of the infarction and
normal myocardium. The reduction in type III ruptures as a result of
the advent of fibrinolytics has resulted in no change in the overall
free wall rupture rate. It has been postulated that type III ruptures
can occur as a result of dynamic left ventricular outflow tract
obstruction and the resultant increased wall stress.24

Signs and Symptoms
Sudden onset of chest pain with straining or coughing may suggest
the onset of myocardial rupture. Acute rupture patients often have
electromechanical dissociation and sudden death. Other patients may
have a more subacute course as a result of a contained rupture. They
might complain of pain consistent with pericarditis, nausea, and
hypotension. In a study evaluating 1457 patients with acute MI, 6.2%
of patients had free wall rupture. Approximately one third of these
patients presented with a subacute course.22
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 manifestations of increased vagal
tone.

Diagnostic Testing
Although often there is not enough time for diagnostic testing in the
management of patients with acute rupture, echocardiography is the
test of choice. Echocardiography will demonstrate a pericar-dial
effusion with findings of cardiac tamponade. These findings include
right atrium and RV diastolic collapse, dilated inferior vena cava,
and marked respiratory variations in mitral and tricuspid inflow.
Additionally, a Swan-Ganz pulmonary catheter may reveal
hemodynamic signs of tamponade, with equalization of the right
atrium, RV diastolic, and pulmonary capillary wedge pressures.

Treatment
The goal of therapy is to diagnose the problem and perform early
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 hospital. The procedure may be
dangerous because of reopening of communication with the
pericardium as the intrapericardial pressure is relieved. 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.

Free Wall RuptureFree Wall Rupture
 Usually leads to hemopericardium andUsually leads to hemopericardium and
death from cardiac tamponadedeath from cardiac tamponade
 Occasionally, rupture of the free wall of theOccasionally, rupture of the free wall of the
ventricle occurs as the first clinicalventricle occurs as the first clinical
manifestation in patients with undetected ormanifestation in patients with undetected or
silent MI, and then it may be considered asilent MI, and then it may be considered a
form of “sudden cardiac death”form of “sudden cardiac death”

Free Wall RuptureFree Wall Rupture
 The coarse of rupture can vary fromThe coarse of rupture can vary from
catastrophic, with an acute tear leading tocatastrophic, with an acute tear leading to
immediate death, to subacute, with nausea,immediate death, to subacute, with nausea,
hypotension, and pericardial type ofhypotension, and pericardial type of
discomfortdiscomfort
 Survival depends on the recognition of thisSurvival depends on the recognition of this
complication, on hemodynamic stabilizationcomplication, on hemodynamic stabilization
of the patient, and most importantly, onof the patient, and most importantly, on
prompt surgical repairprompt surgical repair

PseudoaneurysmPseudoaneurysm
 Incomplete rupture of the heart, withIncomplete rupture of the heart, with
organizing thrombus and hematoma,organizing thrombus and hematoma,
together with pericardium, seal a rupture oftogether with pericardium, seal a rupture of
the left ventriclethe left ventricle
 With time this area of organized thrombusWith time this area of organized thrombus
and pericardium can become aand pericardium can become a
pseudoaneurysm that maintainspseudoaneurysm that maintains
communication with the cavity of the leftcommunication with the cavity of the left
ventricle.ventricle.

PseudoaneurysmPseudoaneurysm
 Can become quite large, even equaling theCan become quite large, even equaling the
true ventricular cavity in size, and theytrue ventricular cavity in size, and they
communicate with the LV cavity through acommunicate with the LV cavity through a
narrow necknarrow neck
 Diagnosis: 2-D echocardiography andDiagnosis: 2-D echocardiography and
contrast angiographycontrast angiography

Mitral Regurgitation
Prevalence
Mitral regurgitation (MR) after acute MI predicts poor prognosis, as
demonstrated in the Global Utilization of Streptokinase and Tissue
Plasminogen Activator for Occluded Coronary Arteries (GUSTO-I)
trial. Nevertheless, MR of mild to moderate severity is found in 13%
to 45% patients following acute MI.11–14
Whereas most MR is transient
in duration and asymptomatic, MR caused by papillary muscle rupture
(Fig. 3) is a life-threatening complication of acute MI. Fibrinolytic
agents decrease the incidence of rupture; however, when present,
rupture may 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 prefibrinolytic era, the SHOCK Trial
Registry demonstrated a median time to papillary muscle rupture of 13
hours.15
Papillary muscle rupture is found in 7% of patients in
cardiogenic shock and contributes to 5% of the mortality after acute
MI.16,17

Pathophysiology
Mitral regurgitation can occur as a result of a number of mechanisms,
including the following: (1) mitral valve annular dilation secondary to
LV dilation; (2) papillary muscle dysfunction with associated
ischemic regional wall motion abnormality in close proximity to the
insertion of the posterior papillary muscle; and (3) partial or complete
rupture of the chordae or papillary muscle.16
Papillary muscle rupture is most common with an inferior MI. The
posteromedial papillary muscle is most frequently involved because of
its single blood supply through the posterior descending coronary
artery.18
The anterolateral papillary muscle has dual blood supply,
being perfused by the left anterior descending (LAD) and left
circumflex coronary arteries. In 50% of patients with papillary muscle
rupture, the infarct is relatively small

Signs and Symptoms
Complete transection of the papillary muscles is rare and usually
results in immediate pulmonary edema, cardiogenic shock, and
death. Physical examination 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 posterior 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). In patients with severe heart failure, poor cardiac output or
with elevated left atrial pressures, the murmur may be soft or
absent.

Diagnostic Testing
The ECG usually shows evidence of a recent inferior or posterior
MI. The chest radiograph shows evidence of pulmonary edema.
Focal pulmonary edema can occur in the right upper lobe when
flow is directed at the right pulmonary veins.
The diagnostic test of choice is two-dimensional echocardiography
with Doppler and color flow imaging. In severe MR, the mitral
valve leaflet is usually flail. Color flow imaging can be useful in
distinguishing papillary muscle rupture with severe MR from
VSR. Transthoracic echocardiography may not fully appreciate the
amount of MR in some patients with posteriorly directed jets. In
these patients, transesophageal echocardiography (TEE) may be
particularly useful.
Hemodynamic monitoring with a PA catheter may reveal large V
(more than 50 mm Hg) waves in the pulmonary capillary wedge
pressure (PCWP). Nevertheless, patients with VSR can also have

Treatment
Patients with papillary muscle rupture should be rapidly
identified and receive aggressive medical treatment while
being considered for surgery. Medical therapy includes
vasodilator therapy. Nitroprusside is useful in the treatment of
patients with acute MR. Nitroprusside directly decreases SVR,
thereby reducing the regurgitant fraction and increasing the
forward stroke volume and cardiac output. Nitroprusside can
be started at 0.5 to 1.0 μ/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 the insertion of an IABP.

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, because revascularization
during MVR is associated with improved short-term and
long-term mortality.17,20
Additional surgical candidates
include patients with moderate MR who do not improve
with afterload reduction
Treatment

Right Ventricular InfarctionRight Ventricular Infarction
 Frequently accompanies inferior LVFrequently accompanies inferior LV
infarction or rarely occurs in isolated forminfarction or rarely occurs in isolated form
 Right-sided filling pressures are elevated,Right-sided filling pressures are elevated,
whereas left ventricular filling pressure iswhereas left ventricular filling pressure is
normal or only slighty raisednormal or only slighty raised
 Cardiac output is often markedly depressedCardiac output is often markedly depressed

 Common among patients with inferior LVCommon among patients with inferior LV
infarctioninfarction
 Unexplained systemic arterial hypotensionUnexplained systemic arterial hypotension
or diminished cardiac output or markedor diminished cardiac output or marked
hypotension in response to small doses ofhypotension in response to small doses of
nitroglycerine in patients with inferiornitroglycerine in patients with inferior
infarction should lead to the promptinfarction should lead to the prompt
consideration of this diagnosisconsideration of this diagnosis

 Most patients with RV infarction have STMost patients with RV infarction have ST
segment elevation in lead V4R (rightsegment elevation in lead V4R (right
precordial lead in V4 position)precordial lead in V4 position)
 2-D echocardiography : abnormal wall2-D echocardiography : abnormal wall
motion of the right ventricle as well as rightmotion of the right ventricle as well as right
ventricular dilitation and depressed RVventricular dilitation and depressed RV
ejection fractionejection fraction

 Medications routinely prescribed for LVMedications routinely prescribed for LV
infarction may produce profoundinfarction may produce profound
hypotension in patients with RV infarctionhypotension in patients with RV infarction
(especially nitroglycerine)(especially nitroglycerine)
 Initial treatment of hypotension in patientsInitial treatment of hypotension in patients
with RV infarction include volumewith RV infarction include volume
expansionexpansion

Embolic Complications
Prevalence
The incidence of clinically evident systemic embolism after MI is
lower 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.47,48
Pathophysiology
Most emboli arise from the left ventricle as a result of wall motion
abnormalities or aneurysms. Atrial fibrillation in the setting of is-
chemia may also contribute to systemic embolization.

Signs and Symptoms
The most common clinical manifestation of embolic
complications is stroke, although patients may have limb
ischemia, renal infarction, or intestinal ischemia. Most
episodes of systemic emboli occur in the first 10 days after
acute MI. Physical findings vary with the site of the
embolism. Focal neurologic deficits occur in patients with
central nervous system emboli. Limb ischemia manifests
with limb pain in a cold pulseless extremity. Renal
infarction manifests with flank pain and hematuria.
Mesenteric ischemia manifests with abdominal pain out of
proportion to physical findings and bloody diarrhea.

Treatment
IV heparin should be started immediately with a
target PTT of 50 to 70 seconds and continued
until the INR is in therapeutic range. Warfarin
sodium therapy should also 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.

Post Cardiac Injury Syndrome
(Dressler’s Syndrome)
Definition: Dressler’s Syndrome occurs in 5%-6% of
patients with acute myocardial infarction4. It
characteristically presents with fever, malaise and
pleuropericardial chest pain, the onset of whichnis 2-3
weeks after the acute event7. About 28% develop pleural
or pericardial effusion2,6. The acute event can also be
anything causing inflammation or penetration of the
pericardium, cardiac operation, a stab wound, a non-
penetrating blow to the chest, or perforation of the heart
with a heart catheter, or post-operative cytomegalovirus
(CMV) infection. In these cases it is called post-
pericardotomy5 or post cardiac injury syndrome1.

Dressler’s syndrome: In Dressler’s syndrome,
the pericarditis develops after a myocardial
infarction. The theory is that the infarction can
cause a pericardial injury that in turn causes a
pericardial effusion. This is sometimes a sub-
clinical effusion. This is supported by the fact
that serial ECHO’s done on post-MI patients
show pericardial effusions in 28% of patients
which sometimes go undetected7.

Clinical Features: Fever with pericarditis, pleuritis, and/or pneumonitis are the main
features of PCIS. The illness usually lasts for one to two weeks. The pericarditis can
be fibrinous or
serosanguineous, rarely causes tamponade, and can be associated with arthralgias.
Some clinical features to look for are:
• Prior injury of the pericardium, myocardium, or both.
• Latent period between the injury and the development of pericarditis or pericardial
effusion.
• Tendency for recurrence.
• Stabbing chest pain pleuritic in nature
• Responsiveness to nonsteroidal antiinflammatory drugs and corticosteroids.
• Fever (as high as 104 degrees), leukocytosis, and elevated erythrocyte
sedimentation rate. C-reactive protein and other markers of inflammation.
• Pericardial and sometimes pleural effusion, with or without a pulmonary infiltrate
• Pericardial friction rub.
• Alteration in the populations of lymphocytes in peripheral blood.

Treatment: Most cases of PCIS can be
adequately treated with non-steroidal anti-
inflammatory drugs. For refractory cases,
corticosteroids can be used, but they can slow
the healing of the already injured myocardium
so they should be avoided if possible. Lastly, in
patients with frequent recurrences, colchicine
has been shown to be effective in some case
studies (3).

Early Pericarditis:
• Epidemiology: occurs in 10% of patients with acute MI.
• Risk factors: transmural MI.
• Timing: usually occurs 1-4 days after MI.
• Symptoms: worse pain while supine, radiation of pain to the
trapezius ridge.
• Physical exam: pericardial friction rub.
• Diagnosis: ECG may show evidence of pericarditis; echo may show
pericardial effusion.
• Treatment: aspirin. Avoid NSAIDs and corticosteroids (may
interfere with healing of infarcted
myocardium)

Prevalence
The incidence of early pericarditis after acute MI is
approximately 10%. The inflammation usually develops
between 24 and 96 hours after MI.49,50
Dressler's syndrome,
or late pericarditis, occurs with an incidence between 1%
and 3%, 1 to 8 weeks after MI.
Pathophysiology
The pathogenesis of acute pericarditis is an inflammatory
reaction in response to necrotic tissue. As such, acute
pericarditis develops more often in patients with transmural
MI. The pathogenesis of Dressler's syndrome is unknown,
but an autoimmune mechanism has been suggested.

Signs and Symptoms
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 postural—worse in the supine position—and are
alleviated by sitting up and leaning forward. The pain tends to
be pleuritic in nature and is therefore exacerbated with deep
inspiration, coughing, and swallowing. Radiation of pain to the
trapezius ridge is almost pathognomonic for acute pericarditis.
The pain also may radiate to the neck and, less frequently, to the
arm or back. A pericardial friction rub on examination is
pathognomonic for acute pericarditis; however, it can be
ephemeral. The rub is best heard at the left lower sternal edge
with the diaphragm of the stethoscope.

Signs and Symptoms
The rub has three components—atrial systole, ventricular systole, and
ventricular diastole. In about 30% of patients, the rub is biphasic and
in 10%, it is uniphasic. A pericardial effusion may cause fluctuation
in the intensity of the rub.
Evolving MI changes may mask the diagnosis of pericarditis.
Pericarditis produces generalized ST-segment elevation, which is
concave or saddle-shaped. As pericarditis evolves, T waves become
inverted after the ST segment becomes isoelectric. Conversely, in
acute MI, T waves may become inverted when the ST segment is still
elevated. Four phases of electrocardiographic abnormalities have
been described in association with pericarditis.

Electrocardiographic Changes of
Pericarditis
Stage Electrocardiographic Change
I ST elevation, upright T waves
II ST elevation resolves, upright to flat T
waves
III ST isoelectric, inverted T waves
IV ST isoelectric, upright T waves
A pericardial effusion on echocardiography is strongly
suggestive of pericarditis. Nevertheless, the lack of an
effusion does not rule out pericarditis.

Treatment
Aspirin is the therapy of choice for post-MI
pericarditis, 650 mg every 4 to 6 hours. NSAIDs and
corticosteroids should be avoided less than 4 weeks
after the acute event. These agents may interfere with
myocardial healing and contribute to infarct
expansion. In late pericarditis, NSAIDs and even
corticosteroids may be indicated if severe symptoms
persist beyond 4 weeks after MI. Colchicine may be
beneficial for patients with recurrent pericarditis.

ArrhythmiasArrhythmias
 Ventricular arrhythmiasVentricular arrhythmias
– Ventricular Premature BeatsVentricular Premature Beats
– Accelerated Idioventricular RhythmAccelerated Idioventricular Rhythm
– Ventricular TachycardiaVentricular Tachycardia
– Ventricular FibrillationVentricular Fibrillation
 BradyarrhythmiasBradyarrhythmias
– Sinus BradycardiaSinus Bradycardia

ArrhythmiasArrhythmias
 Atrioventricular and Intraventricular BlockAtrioventricular and Intraventricular Block
– First-Degree AV blockFirst-Degree AV block
– Second-Degree AV Block (Mobitz I / II)Second-Degree AV Block (Mobitz I / II)
– Third degree (Complete) AV blockThird degree (Complete) AV block
– Intraventricular BlockIntraventricular Block
– AsystoleAsystole
 Supraventricular TachyarrhythmiasSupraventricular Tachyarrhythmias
– Sinus TachycardiaSinus Tachycardia
– Atrial Premature ContractionsAtrial Premature Contractions
– Atrial FlutterAtrial Flutter
– Atrial FibrillationAtrial Fibrillation
– Paroxysmal Supraventricular TachycardiaParoxysmal Supraventricular Tachycardia

Ventricular ArrhythmiasVentricular Arrhythmias
 Ventricular Premature Beats (PVCs)Ventricular Premature Beats (PVCs)
 Commonly seen in patients with acute MICommonly seen in patients with acute MI
 Usually pursue a conservative approach andUsually pursue a conservative approach and
do not routinely prescribe antiarrhythmicdo not routinely prescribe antiarrhythmic
drugs but instead determine whetherdrugs but instead determine whether
recurrent ischemia or electrolyte/metabolicrecurrent ischemia or electrolyte/metabolic
disturbances are presentdisturbances are present

 Accelerated Idioventricular RhythmAccelerated Idioventricular Rhythm
 Defined as a ventricular rhythm with a rate of 60-Defined as a ventricular rhythm with a rate of 60-
125 beats/min125 beats/min
 Frequently called “slow v. tach”Frequently called “slow v. tach”
 Seen in up to 20% of patients with AMISeen in up to 20% of patients with AMI
 Occurs frequently during the first 2 daysOccurs frequently during the first 2 days
 Probably results from enhanced automaticity ofProbably results from enhanced automaticity of
the Purkinje fibersthe Purkinje fibers
 Often observed shortly after successfulOften observed shortly after successful
reperfusionreperfusion

 Ventricular TachycardiaVentricular Tachycardia
 When continuous ECG recordings duringWhen continuous ECG recordings during
the first 12 hours of AMI are analyzed,the first 12 hours of AMI are analyzed,
nonsustained paroxysms of VT may be seennonsustained paroxysms of VT may be seen
in up to 67% of patientsin up to 67% of patients
 Hypokalemia and hypomagnesemia mayHypokalemia and hypomagnesemia may
increase the risk of developing VTincrease the risk of developing VT
 Treatment may include: lidocaine,Treatment may include: lidocaine,
procainamide, amiodaroneprocainamide, amiodarone

 Ventricular FibrillationVentricular Fibrillation
 Ventricular fibrillation occuring inVentricular fibrillation occuring in
association with marked LV failure orassociation with marked LV failure or
cardiogenic shock entails a poor prognosis,cardiogenic shock entails a poor prognosis,
with an in-hospital mortality rate of 40-60%with an in-hospital mortality rate of 40-60%
 Tx : defibrillatorTx : defibrillator
 Management : lidocaine, amiodarone,Management : lidocaine, amiodarone,
bretyliumbretylium

BradyarrhythmiasBradyarrhythmias
 Sinus BradycardiaSinus Bradycardia
 Common arrhythmia occuring during the earlyCommon arrhythmia occuring during the early
phases of AMIphases of AMI
 Particularly frequent in patients with inferior andParticularly frequent in patients with inferior and
posterior infarctionposterior infarction
 Isolated sinus bradycardia, unaccompanied byIsolated sinus bradycardia, unaccompanied by
hypotension or ventricular ectopy, should behypotension or ventricular ectopy, should be
observed rather than treated initiallyobserved rather than treated initially
 Atropine should be utilized if hypotensionAtropine should be utilized if hypotension
accompanies any degree of sinus bradycardiaaccompanies any degree of sinus bradycardia

Atrioventricular andAtrioventricular and
Intraventricular BlockIntraventricular Block
 First Degree AV BlockFirst Degree AV Block
 Occurs in less than 15% of patients withOccurs in less than 15% of patients with
AMI admitted to CCUsAMI admitted to CCUs
 Generally does not require specificGenerally does not require specific
treatmenttreatment
 (Digitalis, B-blockers, Calcium antagonists)(Digitalis, B-blockers, Calcium antagonists)

 Second-Degree AV blockSecond-Degree AV block
– Mobitz Type I or WenckebachMobitz Type I or Wenckebach
 Usually transient and does not persist moreUsually transient and does not persist more
than 72 hours after infarctionthan 72 hours after infarction
 Rarely progresses to complete AV blockRarely progresses to complete AV block
 Do not appear to affect survivalDo not appear to affect survival
 Caused by ischemia of the AV nodeCaused by ischemia of the AV node
 Specific therapy not requiredSpecific therapy not required

 Second Degree AV blockSecond Degree AV block
– Mobitz Type IIMobitz Type II
 Rare conduction defect after AMIRare conduction defect after AMI
 Often progresses suddenly to complete AVOften progresses suddenly to complete AV
blockblock
 Treated with a temporary external orTreated with a temporary external or
transvenous demand pacemakertransvenous demand pacemaker

 Complete (Third Degree) AV blockComplete (Third Degree) AV block
 Often develops gradually, progressing fromOften develops gradually, progressing from
first-degree or type II second-degree blockfirst-degree or type II second-degree block
 Treat with temporary external orTreat with temporary external or
transvenous demand pacemakertransvenous demand pacemaker

 Intraventricular BlockIntraventricular Block
– Isolated fasicular blocksIsolated fasicular blocks
» LAFBLAFB
» LPFBLPFB
– Right bundle branch blockRight bundle branch block
– Bifasicular blockBifasicular block

SupraventricularSupraventricular
TachyarrhythmiasTachyarrhythmias
 Sinus TachycardiaSinus Tachycardia
 Typically associated with augmentedTypically associated with augmented
sympathetic activity (anxiety, persistentsympathetic activity (anxiety, persistent
pain, LV failure, hypovolemia, epinephrine,pain, LV failure, hypovolemia, epinephrine,
atropine, etc.)atropine, etc.)
 Beta-adrenoceptor blocking agentsBeta-adrenoceptor blocking agents
frequently utilizedfrequently utilized

 Paroxysmal Supraventricular TachycardiaParoxysmal Supraventricular Tachycardia
 Requires aggressive management becauseRequires aggressive management because
of the rapid ventricular rateof the rapid ventricular rate
 Augmentation of vagal tone – manualAugmentation of vagal tone – manual
carotid massagecarotid massage
 Drug of choice – adenosine (in non-AMIDrug of choice – adenosine (in non-AMI
patients)patients)
 Alternatives: IV verapamil, diltiazem,Alternatives: IV verapamil, diltiazem,
metoprololmetoprolol

 Atrial Flutter and FibrillationAtrial Flutter and Fibrillation
 Atrial flutter – usually transientAtrial flutter – usually transient
 Atrial Fibrillation occurs in 10-20% ofAtrial Fibrillation occurs in 10-20% of
patients with AMIpatients with AMI
 The increased ventricular rate and the lossThe increased ventricular rate and the loss
of atrial contribution to LV filling result in aof atrial contribution to LV filling result in a
significant reduction in cardiac outputsignificant reduction in cardiac output
 Atrial fibrillation in AMI is associated withAtrial fibrillation in AMI is associated with
increased mortality and strokeincreased mortality and stroke

Pericardial EffusionPericardial Effusion
 Generally detected by 2-DGenerally detected by 2-D
echocardiographyechocardiography
 More common in patients with anterior MIMore common in patients with anterior MI
and with larger infarcts and whenand with larger infarcts and when
congestive heart failure is presentcongestive heart failure is present
 Majority do not cause hemodynamicMajority do not cause hemodynamic
compromise; when tamponade occurs, it iscompromise; when tamponade occurs, it is
usually due to ventricular rupture orusually due to ventricular rupture or
hemorrhagic pericarditishemorrhagic pericarditis

PericarditisPericarditis
 When secondary to transmural MI,When secondary to transmural MI,
pericarditis may produce pain as early aspericarditis may produce pain as early as
the first day and as late as 6 weeks after MIthe first day and as late as 6 weeks after MI
 Treatment of pericardial discomfort consistsTreatment of pericardial discomfort consists
of aspirin at does as high as 650mg every 4-of aspirin at does as high as 650mg every 4-
6 hours. (corticosteroids should be avoided6 hours. (corticosteroids should be avoided
because they may interfere with myocardialbecause they may interfere with myocardial
scar formation)scar formation)
 Dressler SyndromeDressler Syndrome

Dressler SyndromeDressler Syndrome
 Post-myocardial infarction syndromePost-myocardial infarction syndrome
 Usually occurs 1 to 8 weeks after infarctionUsually occurs 1 to 8 weeks after infarction
 Patients present with malaise, fever,Patients present with malaise, fever,
pericardial discomfort, leukocytosis,pericardial discomfort, leukocytosis,
elevated ESR,and a pericardial effusionelevated ESR,and a pericardial effusion
 Cause of this syndrome not clearlyCause of this syndrome not clearly
established (? Immunopathological process)established (? Immunopathological process)
 Treatment : ASA 650mg Q4hrsTreatment : ASA 650mg Q4hrs

SummarySummary
 Be aware of all the potential complicationsBe aware of all the potential complications
that can arise from myocardial infarction,that can arise from myocardial infarction,
diagnose these complications when theydiagnose these complications when they
occur, and treat the patient appropriately inoccur, and treat the patient appropriately in
a timely manner to reduce morbidity anda timely manner to reduce morbidity and
mortality.mortality.

Complications of Myocardial Infarction (MI)

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