Acute Complications of Myocardial Infarction in the Current Era

Abstract

Coronary heart disease is a major cause of mortality and morbidity worldwide. The incidence of mechanical complications of acute myocardial infarction (AMI) has gone down to less than 1% since the advent of percutaneous coronary intervention, but although mortality resulting from AMI has gone down in recent years, the burden remains high. Mechanical complications of AMI include cardiogenic shock, free wall rupture, ventricular septal rupture, acute mitral regurgitation, and right ventricular infarction. Detailed knowledge of the complications and their risk factors can help clinicians in making an early diagnosis. Prompt diagnosis with appropriate medical therapy and timely surgical intervention are necessary for favorable outcomes.

Full text

Acute Complications of Myocardial Infarction in
the Current Era: Diagnosis and Management
Anurag Bajaj, MD, FACP,* Ankur Sethi, MD, FACP,†Parul Rat ho r, MB B S , ‡
Nissi Suppogu, MD,* and Arjinder Sethi, MD, FACP§
Abstract: Coronary heart disease is a major cause of mortality and mor-
bidity worldwide. The incidence of mechanical complications of acute
myocardial infarction (AMI) has gone down to less than 1% since the
advent of percutaneous coronary intervention, but although mortality
resulting from AMI has gone down in recent years, the burden remains
high. Mechanical complications of AMI include cardiogenic shock, free
wall rupture, ventricular septal rupture, acute mitral regurgitation, and right
ventricular infarction. Detailed knowledge of the complications and their
risk factors can help clinicians in making an early diagnosis. Prompt diag-
nosis with appropriate medical therapy and timely surgical intervention are
necessary for favorable outcomes.
Key Words: myocardial infarction, percutaneous coronary intervention,
thrombolytic
(JInvestigMed2015;63: 844–855)
Cardiovascular disease is a leading cause of death in people
older than 65 years in the United States.
1
According to
2015 American Heart Association's (AHA) heart disease and
stroke statistics, approximately 635,000 new cases and 300,000
recurrent attacks of acute myocardial infarction (MI, AMI) occur
each year. Coronary heart disease causes 1 of every 7 deaths in
the United States and there were 375,295 deaths in 2011.
1
There
has been a significant drop in the incidence of mechanical compli-
cations with the advent of percutaneous coronary intervention
(PCI), as shown in Figure 1. The incidence of mechanical compli-
cations after acute ST elevation MI (STEMI) where primary PCI
was the reperfusion strategy was 0.9% in the Assessment of
Pexelizumab in Acute Myocardial Infarction (APEX-MI) trial.
2
Another trend that was observed in the PCI era was the timing
of onset of mechanical complications; it is occurring earlier in
the course of AMI than in the preperfusion era. The mean time
of onset of complications is 23.5 hours in the APEX-AMI trial.
Although the incidence has decreased in recent years, mortality
in patients with complications of AMI still remains very high, as
shown in Figure 2.
In a national registry of AMI of US hospitals, overall mortal-
ity decreased from 10.45% in 1994 to 6.3% in 2006, and a similar
drop in mortality was observed in other countries, as shown in
Figure 3.
4–6
Complications of AMI can be broadly divided into
the following 5 categories (Table 1): mechanical, electrical, in-
flammatory (ie, pericarditis), ischemic, and embolic complications.
However, this article will focus only on mechanical compli-
cations and right ventricular infarction (RVI). Detailed know-
ledge of the complications and their risk factors can help
clinicians make an early diagnosis and offer timely treatment. For
the purpose of this review, we searched PubMed for the latest stud-
ies on mechanical complications of AMI restricted to humans pub-
lished in English and reviewed reference lists of identified articles.
The most current recommendations of professional societies are
provided when available.
CARDIOGENIC SHOCK
Cardiogenic shock is the most common mechanical compli-
cation and cause of death after AMI.
7
The most common etiology
of cardiogenic shock is left ventricle dysfunction secondary to ex-
tensive infarct; isolated right ventricle dysfunction only contrib-
utes to 5% of all cases of cardiogenic shock.
8
Other causes
include ventricular septal rupture (VSR), papillary muscle rupture
(PMR), and free wall rupture (FWR), and they contribute to 12%
of all cases.
8
Various registries reported conflicting temporal
trends in the incidence of cardiogenic shock. In 1 registry that
collected data from 2003 to 2010, the incidence of cardiogenic
shock in STEMI surprisingly went up from 6.5% to 10.1%.
9
Other
registries such as the National Hospital Discharge Survey in
the United States, the population-based study of residents in
the Worcester, MA, metropolitan area, and the AMIS (AMI in
Switzerland) Plus Registry in Switzerland showed decreasing
rates of cardiogenic shock in patients with AMI (non-STEMI
[NSTEMI] and STEMI) from 1979 to 2004, 1975 to 2005, and
1997 to 2006, respectively.
10–12
Cardiogenic shockoccurred more
commonly in STEMI, and it contributes to 6.9% to 7.2% of cases
in STEMI and 2.5% to 3.4% in NSTEMI.
13
Cardiogenic shock is a state of inadequate tissue perfusion
because of low cardiac output. It is defined as persistent hypoten-
sion (systolic blood pressure < 80 or 90 mm Hg or mean arterial
pressure < 30 mm Hg below the baseline) with severe reduction
in cardiac index less than 1.8 L/min per m
2
without support or less
than 2.2 L/min per m
2
with support and adequate or elevated fill-
ing pressure, for example, left ventricular end diastolic pressure
(LVEDP) greater than 18 or right ventricular end diastolic pres-
sure (RVEDP) greater than 10 to 15 mm Hg.
13
Reduced cardiac
output due to left ventricle dysfunction or other mechanical com-
plication leads to inadequate tissue perfusion. Hypoperfusion
leads to catecholamine's release, which may improve mean arterial
pressure by peripheral vasoconstriction and/or increasing cardiac
contractility but at an expense of increased myocardial demand
and risk of arrhythmia. Reduction in arterial pressure decreases
coronary perfusion and, therefore, lowers cardiac output, which
in turn causes further tissue hypoperfusion. The management of
cardiogenic shock revolves around breaking this vicious cycle.
Release of inflammatory mediators further complicates the situation
in AMI. According to Kohsaka et al.,
14
AMI is an inflammatory
state and may cause systemic inflammatory response syndrome via
From the *Department of Medicine, The Wright Center for Graduate Medical
Education, Scranton, PA; †Department of Cardiology, Rosalind Franklin Uni-
versity of Medicine and Science, Chicago, IL; ‡Department of Medicine,
Zhengzhou University, Henan, China; and §Department of cardiology, Medical
Associates of Monroe County, Stroudsburg, PA.
Received March 12, 2015, and in revised form April 17, 2015.
Accepted for publication July 17, 2015.
Reprints: Anurag Bajaj, MD, FACP, Department of Medicine, The Wright
Center for Graduate Medical Education, 707 Tall Trees Dr, Scranton, PA.
E-mail: dr.anuragbajaj@ gmail.co m.
The study was performed at The Wright Center for Graduate Medical
Education, 501 Madison Ave, Scranton, PA 18505.
Conflict of interest: No conflict of interest.
Copyright © 2015 by The American Federation for Medical Research
ISSN: 1081-5589
DOI: 10.1097/JIM.0000000000000232
REVIEW ARTICLE
844 Journal of Investigative Medicine •Volume 63, Number 7, October 2015
Copyright © 2015 American Federation for Medical Research. Unauthorized reproduction of this article is prohibited.

release of inflammatory mediators such as interleukins and nitric ox-
ide. Release of inflammatory mediators may cause vasodilatation,
negating the effect of reflex vasoconstriction and further compli-
cating the situation. Systemic vascular resistance varied widely
in cardiogenic shock, and in fact, there is relatively more vasodi-
latation than vasoconstriction in these patients.
13
It is interesting
to note that many patients with very low ejection fraction do not
have shock and many patients with shock do not have very low
ejection fraction; thus, there is no correlation between severity
of cardiogenic shock and ejection fraction.
15
However, left ventri-
cle ejection fraction and left ventricle motion abnormality are im-
portant determinants of prognosis.
16
At the age older than 65 years, left ventricle ejection fraction
less than 35%, large infarct with creatine kinase greater than
160 U/L, anterior wall MI, history of diabetes mellitus, previous
MI, left bundle branch block, multivessel disease, and STEMI
are independent predictors of cardiogenic shock.
17
Recognizing
these factors early and using urgent revascularization strategies
may decrease mortality of cardiogenic shock. Clinically, these pa-
tients present with pulmonary edema, hypotension, and signs of
hypoperfusion—altered mental status, decreased urine output,
and cool and clammy skin. They may have resting tachycardia.
Up to 5.2% of the patients may present with a low cardiac output
state in the absence of hypotension, and almost 20% may manifest
no signs of pulmonary congestion, the so-called silent lung syn-
drome.
18
Most patients with STEMI developed cardiogenic shock
early on (ie, within the first 24 hours) and only approximately
26% presented with shock late (ie, >24 hours).
19
In a SHOCK
trial, median time from symptom onset to cardiogenic shock
was 5.5 hours. Late onset of shock after symptom onset is
associated with higher mortality.
19
The onset of shock is delayed
in NSTEMI elevation MI rather than STEMI.
19,20
The main goals of management include prevention of tissue
hypoperfusion and hypoxia by improving cardiac output and re-
ducing filling pressure without undue increase in myocardial oxy-
gen demand and wall stress. Immediate resuscitative measures are
taken as soon as cardiogenic shock is diagnosed. It is imperative to
consider emergent revascularization if not already performed. In a
SHOCK trial, medical management was compared with PCI and
coronary artery bypass graft (CABG), and mortality reduction
did not reach statistical significance at 30 days, but at 6 months
and 1 year, the mortality was significantly reduced.
21
Antiplatelet
agents, including aspirin, P2Y inhibitors, glycoprotein IIb/IIIA in-
hibitors, and anticoagulants, should be used to maintain patency of
the culpritvessel. The AHA guidelines give a level 1A recommen-
dation for emergency revascularization with either PCI or CABG
in suitable patients with cardiogenic shock due to pump failure
after STEMI, irrespective of the time delay from MI onset.
22
In the absence of contraindications, fibrinolytic therapy
should be administered to patients with STEMI and cardiogenic
shock who are unsuitable candidates for either PCI or CABG.
22
Most patients will require invasive monitoring with pulmonary
artery catheterization (PAC) to guide management. Different
studies reported conflicting results on the use of the PAC in car-
diogenic shock.
23–25
Pulmonary artery catheterization use has
declined in the last few years because of unclear benefit. In 1 study,
PAC was associated with increased mortality in acute coronary
syndrome except among patients with cardiogenic shock.
23
Sup-
plemental oxygen, noninvasive mechanical ventilation, and inva-
sive mechanical ventilation should be used on the basis of the
patient's respiratory status and mentation. If mechanical ventilation
is required, the use of the lowest tidal volume and end expiratory
pressure to maintain oxygen saturation greater than 92% is sug-
gested.
26
Negative inotropes including β-blockers or calcium
FIGURE 1. Graph comparing incidence of complications of AMI in
preperfusion and PCI era.
2,33,43–45,47,49
FIGURE 2. Graph comparing survival after acute mechanical
complication of MI.
3
FIGURE 3. Graph showing mortality trend in AMI in
different countries.
4–6
TABLE 1. Types of Complications After AMI
Complications Types
Mechanical complications Cardiogenic shock, FWR, VSR, acute
MR, and true ventricular aneurysm
Electrical complications Bradyarrhythmias, tachyarrhythmia,
bundle branch blocks and
fascicular blocks
Inflammatory complications Peri-infraction pericarditis and
Dressler syndrome
Ischemic complications Postinfarction angina (infarct extension
and reinfarction)
Embolic complications Mural thrombus and systemicembolism
Journal of Investigative Medicine •Volume 63, Number 7, October 2015 Complications of Myocardial Infarction
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channel blockers are best avoided in the early post-MI period until
hemodynamic status is stabilized. The best evidence comes from
the Clopidogrel and Metoprolol in Myocardial Infarction Trial/
Second Chinese Cardiac Study 2 trial, which reported a 29% in-
crease risk of death related to cardiogenic shock with the use of
metoprolol in AMI, a particularly accentuated effect in high-risk
patients.
27
Inotropes and vasopressors should be used to maintain
mean arterial pressure to prevent end organ damage. Dobutamine
and milrinone are the inotropes, and norepinephrine and dopamine
are the vasopressors commonly used in clinical practice. Dopamine
is an alpha and beta agonist with rapid escalation of alpha effect at
high doses, whereas norepinephrine is a predominantly alpha-
adrenergic agent. In a subgroup analysis of a randomized trial, do-
pamine was associated with increased risk of mortality at 30 days
compared with norepinephrine in cardiogenic shock.
28
These pharmacological agents increase cardiac contractility
and blood pressure,but at the expense of increased myocardial ox-
ygen requirements. Still, their use is always required to maintain
perfusion of end organs. Dobutamine is recommended in predom-
inant left heart failure but its use best avoided in profound hypo-
tension because of its vasodilatingproperties.The2004American
College of Cardiology (ACC)/AHA guidelines for management
of hypotension complicating AMI suggest the use of dobutamine
as a first-line agent if systolic blood pressure ranges between 70
and 100 mm Hg in the absence of signs and symptoms of shock.
29
When response to dobutamine is inadequate or the patient's present-
ing systolic blood pressure is less than 70 mm Hg, the use of vaso-
pressors, preferably norepinephrine, is suggested on the basis of
the recent data.
28
Cardiogenic shock carries significant mortality
with 30-day mortality of approximately 40% and 1 year mortality
of 51.5%.
30,31
The overall in-hospital mortality has gone down
from 62.8% to 47.7% with the use of timely reperfusion
therapy, as shown in Figure 4.
11
Many patients with profound cardiogenic shock do not re-
spond adequately to the previous measures and require mechani-
cal support to restore perfusion to vital organs and unload the
ventricle. An intra-aortic balloon pump (IABP) is one of the oldest
percutaneous mechanical support devices used in clinical practice.
Previous studies, mostlyobservational, have shown improved out-
comes with IABP use.
32,33
However, 2 recent randomized trials—
Counterpulsation Reduces Infarct Size Pre-PCI-Acute Myocar-
dial Infarction and IABP shock—have cast doubt on the efficacy
of IABP.
30,31,34
Some authors have critiqued IABP shock, the
largest randomized trial till date, for low power because of lower
than expected mortality, high crossover to IABP, and insertion of
IABP after the PCI. However, on the basis of these trials, the
ACC/AHA recently downgraded the recommendation to use
IABP to IIA.
35
Recent meta-analysis of 12 studies on the use of
IABP in AMI did not show any mortality benefit.
36
One potential
reason for no benefit of IABP may be inadequate hemodynamic
support. Newer percutaneously inserted devices such as
Impella 2.5 (Abiomed) may provide superior hemodynamic
support compared with IABP.
37
However so far, there is no strong
evidence to support their efficacy over IABP in AMI complicated
by shock.
38
As per recent AHA/ACC STEMI update, their use
may be considered in patients with refractory shock.
35
FREE WALL RUPTURE
The incidence of FWR was 2% to 6.2%
39–43
in the pre-
perfusion era and it accounted for 15% of mortality after
AMI
41,42,44
; however, the incidence has declined significantly in
the perfusion era. In a multinational Global Registry of Acute Cor-
onary Events registry, one of the largest, the incidence of FWR
was 0.2% with in-hospital mortality of 80%.
3
Inastudyby
Moreno et al.,
45
PCI independently reduces the risk of FWR in
comparison with thrombolytic. The short-term mortality remains
very high even with rapid diagnosis and timely surgery. Most of
the ruptures occurred within the first 3 to 5 days but may happen
up to 2 weeks.
46
Some factors associated with FWR include the
following: age older than 55 years, female sex, no history of
previous MI, totally occluded left anterior descending (LAD),
transmural MI, hypertension, Killip class greater than 2, persistent
ST elevation, and use of corticosteroids and nonsteroidal inflam-
matory drugs (Table 2).
3,39,47,48
Recognizing these factors early
and carefully observing at-risk patients for early signs of cardiac
rupture may help decrease the mortality. The relationship between
the use of thrombolytics and the risk of rupture has been contro-
versial.
49,50
Many observational studies have reported an in-
creased risk of rupture with the use of thrombolytics.
44,51
The
Valsartan in Acute Myocardial Infarction trial reported an in-
creased use of thrombolytics in patients who died of FWR than
other causes; however, it reduces the incidence of adverse out-
comes.
52
It was demonstrated by Honan et al.
53
in a meta-
analysis that timely thrombolytics reduces the risk of rupture
and mortality, but the risk of rupture increases if thrombolytics
were administered beyond 14 hours of symptom onset. The
mean time of FWR has decreased from 3 to 5 days in the
prethrombolytic era to 12 to 24 hours in the thrombolytic era.
54
Overall, it decreases mortality but mortality increases in the first
24 to 48 hours.
54,55
On the contrary, PCI reduces the incidence
of FWR and improves mortality and morbidity because of AMI.
56
There are 3 different types of cardiac rupture as follows:
acute, subacute, and chronic.
46
Among patients, 70% have acute
FWR and they presented with sudden cardiac death and electro-
mechanical dissociation. In a few cases, the bleeding is stopped
because of fibrin clot formation or pericardial adhere to the myo-
cardium resulting in formation of pseudoaneurysm or chronic
FWR. Patients with chronic rupture either remain hemodynami-
cally stable or they can present with worsening shortness of breath
and arrhythmias. Sometimes, patient may have slow bleeding be-
cause of incomplete tear. The latter type of rupture is called sub-
acute rupture and emergent intervention can be lifesaving.
Clinical manifestation depends on rapidity of bleeding. Patients
may present with sudden cardiac death if bleeding is massive or
hypotension with cardiogenic shock if there is a slow progressive
bleeding.
57,58
Patients may or may not have premonitory symp-
toms, but if present, they are persistent chest pain, agitation, and
recurrent emesis. Patients with subacute rupture almost always
present with hypotension. Sudden onset hypotension with brady-
cardia in a patient with AMI is highly suspicious for cardiac rup-
ture and should never be ignored. A patient may have persistent
ST elevation or positive T-wave deflection that persists beyond
72 hours but is neither sensitive nor specific for subacute rupture.
FIGURE 4. Graph showing mortality in cardiogenic shock versus
PCI trend.
11
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846 © 2015 The American Federation for Medical Research
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The accurate diagnosis of subacute FWR requires the presence
of high degree of suspicion.
40
Echocardiogram typically shows
pericardial effusion, which can be present in up to 28% of patients
in a post-MI period in absence of cardiac rupture.
59
The presence
of echogenic masses increases both sensitivity (97%) and speci-
ficity (93%).
59
According to Lopez-Sendon et al.,
40
false positives
are very low if pericardial effusion is greater than 5 mm and
pericardiocentesis should be performed before taking the patient
for surgery; clear pericardial fluid essentially rules out cardiac
rupture. In a patient with hypotension, an echocardiogram sugges-
tive of pericardial effusion greater than 5 mm with intrapericardial
echoes carries a sensitivity of 90.9% for cardiac rupture.
40
The
presence of moderate to severe pericardial effusion (>10 mm) in
patient with STEMI is associated with 43% of 30-day mortality;
therefore, the presence of moderate pericardial effusion in patients
with recent MI should be considered secondary to FWR unless
proven otherwise.
60
The treatment of subacute cardiac rupture is surgery. Medical
treatment aimed at stabilizing the patient acts as bridge to surgery
and it includes intravenous fluids, inotropes, and small-volume
pericardiocentesis as guided by clinical status. The 30-day sur-
vival is approximately 37%, according to the APEX-AMI trial.
2
Hence, subacute cardiac rupture is a potentially treatable condition
with good long-term survival if recognized early and surgery is
performed in a timely manner.
VENTRICULAR SEPTAL RUPTURE
The incidence of VSR in AMI was approximately 1% to 3%
before the reperfusion era
61–64
; however, with the advent of reper-
fusion therapy, the incidence has decreased to 0.26%.
3,61–64
Ac-
cording to the APEX-AMI trial, its incidence is 0.17% in the
PCI era.
2
It accounts for 5% of all deaths in AMI.
3
It carries a sig-
nificant mortality rate: approximately 46% of the patients die
within the first week and 62% to 82% within 2 months without
surgical treatment.
65,66
Even after surgery, there is 40% mortality.
2
It typically occurs 3 to 5 days after AMI and rarely after 2 weeks,
but there are case reports of VSR even after 30 days.
63,67
With the
advent of thrombolytic and PCI, VSRs occur earlier in patients
with thrombolytic and PCI, and the mean time of onset of VSR
has been reduced to 24 hours, probably because of intramyo-
cardial hemorrhage.
18,67
The risk factors of VSR include hyper-
tension, old age, female, absence of angina, previous MI and
extensive MI, and single vessel disease.
18,63
More extensive in-
farct leads to greater expansion and cavitary dilatation. Complete
occlusion of an infarct-related artery also has been identified as a
risk factor.
18,63
Septal rupture has been categorized morphologi-
cally as simple—a through-and-through defect at the same level
and usually located anteriorly—or complex—serpiginous dissec-
tion tract remote from the primary septal defect and usually lo-
cated inferiorly. The ventricle septum is supplied by LAD in the
upper two thirds and by the right coronary artery (RCA) in the
lower one third in many cases when RCA is dominant and left cir-
cumflex when RCA is nondominant. In some cases, however, the
LAD extends beyond the left ventricular apex, wrapping around to
supply the distal inferior wall and inferior septum.
Patients with AMI due to occlusion of a “wraparound”LAD
artery seem to have an elevated risk of septal rupture.
68
Studies re-
ported increased incidence of VSR with anterior-apical wall MI,
and LAD almost always is the culprit artery.
18,63
However, when
it is associated with inferior wall MI, it is more complex and more
likely to have associated posterobasal aneurysm and right ventri-
cle infarct and carries poor prognosis.
65
More than 50% of patients with VSR present with cardio-
genic shock.
18,68
Ventricular septal ruptures with inferior wall
MI are more likely to present with shock.
68
Patients may present
with recurrent chest pain because of new onset of recurrent myo-
cardial necrosis, shortness of breath, decreased urine output, and
TABLE 2. Characteristics of FWR, VSR, and PMR
Characteristics FWR VSR PMR
Incidence 2%–6.2% before thrombolytic era
and 0.2% in PCI era
1%–3% before thrombolytic era
and 0.3% in PCI era
1%–3% before thrombolytic era and
0.26% in PCI era
Effect of
thrombolytics
Does not reduce risk, increase
risk in high-risk patients.
Decrease risk
Effect of PCI Decreases risk Decreases risk
Mortality 15% of all MI death 5% of all MI death 5% of all MI death
Timing 1–14 days, peak time 3–5days.
12–24 hours in thrombolytic era
3–14 days, peak time 3–7days.
24 hours in thrombolytic era.
1–14 days. Peak time 2–7days
Risk factors Elderly, age older than 55 years, women,
first MI, totally occluded LAD, low GFR,
Q-wave MI, hypertension, Killip class > 2,
and persistent ST elevation
Hypertension, old age, female,
absence of smoking, absence of
angina, previous MI, extensive MI,
and single vessel disease
First MI, single vessel disease
Clinical
symptoms
Sudden death, recurrent chest pain,
hypotension, recurrent emesis, agitation
Recurrent chest pain, shortness
of breath, hypotension
Shortness of breath, pulmonary
edema, and hypotension
Physical
examinations
Electromechanical dissociation, hypotension,
JVD, pulsus paradoxus, bradycardia
Hypotension, loud harsh,
holosytolic murmur with a thrill
Hypotension, soft holosystolic
murmur without a thrill,
pulmonary edema
Diagnostic
imaging
Transthoracic echocardiogram showing
pericardial effusion > 5 mm with
intrapericardial echoes. Pericardiocentesis
may be needed sometimes.
Transthoracic echocardiogram with
Doppler imaging highly sensitive
but may need right heart
catheterization in some cases,
which shows step up in O
2
saturation > 10% from right atria
to right ventricle.
Transthoracic echocardiogram
has a sensitivity of 65%–85%.
Transesophageal echo has a
sensitivity of 100%.
GFR indicates glomerular filtration rate; JVD, jugular venous distension; MI, myocardial infarction.
Journal of Investigative Medicine •Volume 63, Number 7, October 2015 Complications of Myocardial Infarction
© 2015 The American Federation for Medical Research 847
Copyright © 2015 American Federation for Medical Research. Unauthorized reproduction of this article is prohibited.

altered mentation secondary to decreased cardiac output. Typically,
a new loud, harsh holosystolic murmur radiating to the axilla
and apex is heard but associated with a thrill; murmur and thrill
are less pronounced if the patient is in cardiogenic shock. In com-
parison to VSR, acute mitral regurgitation (MR) has a soft holo-
systolic murmur without a thrill. The patient may have bundle
branch block because of disruption of conduction system pathway.
Approximately 20% of patients who died of VSR also had associ-
ated FWR and PMR
30
; 10% to 20% of cases have coexistent se-
vere MR.
64
Patients may have a big “a”and “v”wave because
of increase RVEDP and increase pulmonary blood flow. Echocar-
diogram with Doppler imaging is a highly sensitive and specific
technique and diagnostic in almost all cases. It also helps identify
other structural abnormalities that may be contributing to a decline
in the patient's condition. Because of widespread availability of
echocardiograms, PAC is rarely used. A high pulmonary artery
saturation (>80%) is suggestive of left to right shunt, and step
up of oxygen saturation in right ventricle rather than pulmonary
artery differentiates it from severe MR. Left ventriculography
also may be used although it is rarely required to make a diagnosis
of VSR.
Medical therapy should be aimed at stabilizing the hemody-
namics and acts as a bridge to surgery. It consists of respiratory
support, mechanical support with the use of IABP, and afterload
reduction with the help of vasodilators. Inotropic support often
is needed in hypotensive patients. Surgery is almost always re-
quired in VSR. A recently published review of the Society of Tho-
racic Surgeons National Database (STS Database) identified 2876
individuals aged 18 years or older who underwent post-MI VSR
repair between 1999 and 2010.
69
The overall operative mortality
was 42.9%. Operative mortality was much lower for procedures
considered elective (13.2% mortality) versus emergent (56.0%
mortality) versus salvage (80.5% mortality).
69
In the Global Utili-
zation of Streptokinase and Tissue Plasminogen Activator for
Occluded Coronary Arteries-1 trial, there was 94% mortality at
30 days without surgery, suggesting that conservative manage-
ment is associated with very high mortality.
63
There has been
considerable debate in the past on the timing of surgery. Late sur-
gery after 6 weeks was preferred more than early surgery, and
studies reported longer survival.
70–72
Patients who underwent sur-
gery within 7 days of presentation had a 54.1% mortality com-
pared with 18.4% mortality if repair was delayed until after
7days.
69
In a systematic review on postinfarction VSR done by
Papalexopoulou et al.,
73
early surgery was recommended if VSR
was greater than 15 mm with a significant shunt causing hemody-
namic compromise; otherwise, surgery can be delayed up to 3 to
4 weeks in case of hemodynamically stable patient. Emergent sur-
gery should be performed if there is clinical deterioration.
73
Mor-
tality is highest in patients with basal septal rupture associated
with inferior wall 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 MR.
18
Data about concomitant
revascularization along with septal repair are rather controversial;
however, revascularization reduces the ischemic burden, increases
the collateral blood flow, and should be performed whenever i n-
dicated.
70
Barker et al.
74
reported t hat incomplete myocardial
revascularization is a significant predictor of late mortality after
surgical repair of postinfarction VSR. In view of this, concomitant
CABG to all stenotic coronary arteries, including those supplying
the noninfarcted area, is recommended for patients undergoing
surgical repair of VSR.
75
A postoperative course is really crucial
in these patients for survival. Those who survive the initial event
and operation tend to have favorable 5- and 10-year outcomes.
Studies reported that incidenceof recurrent shunt is approximately
25% and it could be due to missed defect or dehiscence of a patch
or extension of defect.
76
Most of the shunts are well tolerated;
however, repeat surgery is performed in cases with severe ventric-
ular failure and it carries a mortality of 60%.
77
Transcatheter clo-
sure of VSR is an alternative to surgery in an anatomically suitable
rupture and has shown promising results with both good short-
term and long-term outcomes.
78
ACUTE MITRAL REGURGITATION
There are 2 main mechanisms of development of MR in AMI;
one is sudden rupture of the PMR and the second is ischemia-
related papillary muscle wall dysfunction. Ischemic MR is much
more common than PMR. Prevalence of PMR after AMI is
0.26% in the PCI era.
2
The prevalence of ischemic MR varies
from 8% to 74%
79–84
if determined by Doppler echocardiogram
and 1.6% to 9%
85–90
if determined by angiography. Such a wide
range is because of variability in studies that estimated the preva-
lence of acute MR. The studies differ in terms of design, timing of
imaging, severityof MR, and techniques used. Posteromedial rup-
ture is more common than anterolateral rupture because of a dual
blood supply of the anterolateral muscle from LAD and left cir-
cumflex and posteromedial muscle supplied only by posterior de-
scending artery. Autopsy studies conducted on 22 patients with
PMR after AMI showed that 82% occurred in the first MI and
50% had single vessel disease.
91
It usually occurs 2 to 7 days after
AMI and symptoms typically range from acute decompensated
heart failure to cardiogenic shock, leading to hypotension and
acute respiratory failure due to pulmonary edema. Varying de-
grees of systolic murmur can be heard, ranging from severe to
no murmur. The systolic murmur can be holosystolic, mid or late.
Murmur is not always heard because of concomitant left ventricu-
lar dysfunction leading to decrease in regurgitation jet volume and
rapid equalization of pressure in the ventricle and atria. Transtho-
racic echocardiogram is the initial imaging modality of choice
with a sensitivity of 65% to 85%; however, transesophageal echo-
cardiogram may be required because of its higher diagnostic accu-
racy of 95% to 100%.
92,93
Emergent or urgent surgery in the form
of mitral valve repair or replacement is warranted; otherwise, 90%
of the patients die within the first week.
94
There are no random-
ized studies that compare repair and replacement or different re-
pair techniques for MR due to post-MI PMR.
95
When PMR is
complete, repair is not feasible because the tissue is very friable.
A segmental prolapse secondary to a partial PMR with limited
adjacent tissue damage is often amenable to a reliable repair.
96,97
In terms of medical management, patients should be stabilized
with oxygen, vasodilators, IABP, and inotropic support until sur-
gery is arranged. Mitral valve surgery for PMR carries a very high
operative mortality; however, it has decreased in recent years
because of advances in surgical techniques and concomitant re-
vascularization surgery. Long-term outcome of patients after sur-
gery is really good, with a 5-year survival rate of 60% to
70%.
98,99
In a study by Russo et al.,
99
long-term outcomes of pa-
tients with PMR who survived PMR surgery have been similar to
patients without PMR. Concomitant coronary revascularization
should be performed because it is shown to improve short-term
and long-term survival in these patients.
96,99
Ischemic MR is far more common than PMR and has short-
term and long-term prognostic significance. Patients with MR
after AMI carry poor prognosis as compared with patients without
MR. In an analysis from the Controlled Abciximab and Device In-
vestigation to Lower Late Angioplasty Complications trial of
1976 patients with STEMI, 10% had mild MR and 3% had mod-
erate to severe MR. Patients with worse MR had significantly
higher mortality rates at 30 days and at 1 year.
90
The etiology of
Bajaj et al Journal of Investigative Medicine •Volume 63, Number 7, October 2015
848 © 2015 The American Federation for Medical Research
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TABLE 3. American Heart Association Guidelines on Management of Mechanical Complications After AMI
22,29,106
Cardiogenic shock
Class I
1. Emergency revascularization with either PCI or CABG is recommended in suitable patients with cardiogenic shock due to pump
failure after STEMI irrespective of the time delay from MI onset (level of evidence: B).
2. In the absence of contraindications, fibrinolytic therapy should be administered to patients with STEMI and cardiogenic shock
who are unsuitable candidates for either PCI or CABG (level of evidence: B).
3. Inotropic support (level of evidence: B).
4. Surgical correction of mechanical complications (level of evidence: B).
Class IIa
1. The use of IABP counterpulsation can be useful for patients with cardiogenic shock after STEMI who do not quickly
stabilize with pharmacological therapy (level of evidence: B).
Class IIb
1. Alternative LVassist devices for circulatory support may be considered in patients with refractory cardiogenic shock (level of evidence: C).
PMR
Class I
1. Patients with acute PMR should be considered for urgent cardiac surgical repair unless further support is considered futile because
of the patient's wishes or contraindications/unsuitability for further invasive care (level of evidence: B). Mitral valve replacement is
required in these patients.
2. Coronary artery bypass graft surgery should be undertaken at the same time as mitral valve surgery (level of evidence: B).
Ischemic MR
Class IIa
1. Mitral valve surgery is reasonable for patients with chronic severe secondary MR (stages C and D) who are undergoing
CABG or AVR (level of evidence: C).
Class IIb
1. Mitral valve repair or replacement may be considered for severely symptomatic patients (New York Heart Association class III-IV)
with chronic severe secondary MR (stage D) who have persistent symptoms despite optimal Guideline Determined Medical Therapy
for heart failure (level of evidence: B).
2. Mitral valve repair may be considered for patients with chronic moderate secondary MR (stage B) who are undergoing other cardiac
surgery (level of evidence: C).
VSR
Class I
1. Patients with acute VSR should be considered for urgent cardiac surgical repair unless further support is considered futile because
of the patient's wishes or contraindications/unsuitability for further invasive care (level of evidence: B).
2. Coronary artery bypass graft surgery should be undertaken at the same time as mitral valve surgery (level of evidence: B).
FWR
Class I
1. Patients with FWR should be considered for urgent cardiac surgical repair unless further support is considered futile because of the
patient's wishes or contraindications/unsuitability for further invasive care (level of evidence: B).
2. Coronary artery bypass graft surgery should be undertaken at the same time as mitral valve surgery (level of evidence: C).
RVI
Class I
1. Patients with inferior STMI and hemodynamic compromise should be assessed with right-sided V4 lead to detect for ST elevation
and echocardiogram to screen for RVI (level of evidence: B).
2. The following principles apply to therapy with STEMI and RVI:
a. Early reperfusion should be achieved (level of evidence: C).
b. Atrioventricular synchrony should be achieved and bradycardia should be corrected (level of evidence: C).
c. Right ventricular preload should be optimized, which usually requires initial volume challenge in patients with hemodynamic
instability provided the jugular venous pressure is normal or low (level of evidence: C).
d. Right ventricular afterload should be optimized, which usually requires therapy for concomitant LV dysfunction (level of evidence: C).
e. Inotropic support should be used for hemodynamic instability not responding to volume challenge (level of evidence: C).
Class IIa
1. After infarction that leads to clinically significant right ventricular dysfunction, it is reasonable to delay CABG for 4 weeks to allow
time for recovery of contractile performance (level of evidence: C).
Corticosteroids and NSAID's use
Class III
1. Glucocorticoids and nonsteroidal anti-inflammatory drugs are potentially harmful for treatment of pericarditis after
STEMI (level of evidence: B).
Journal of Investigative Medicine •Volume 63, Number 7, October 2015 Complications of Myocardial Infarction
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ischemic MR had been long known because of papillary muscle
dysfunction until Kaul et al.,
100
Yiu et a l.,
101
and Levine et al.
102
demonstrated the pathophysiology of ischemic MR.
100–102
Ische-
mia causes displacement of apical and posterior papillary muscle
and wall motion abnormalities. This induces mitral valve tethering
and causes systolic tenting of mitral valve leaflet away from the
annulus with incomplete closure of the valve. It is this alteration
in the geometric relationship between ventricle and valve appara-
tus that causes MR. It is more common in women, elderly, mul-
tivessel disease, and previous MI.
79,85,86
Medical management
plays a major role in treatment of ischemic MR, unlike PMR,
where surgery is required. Prompt revascularization should be
done if not already performed. Early revascularization has shown
to be effective in reducing MR and increases survival.
103–105
Angiotensin-converting enzyme inhibitors and β-blockers prevent
remodeling of LVand, hence, decrease ischemic MR. Aldosterone
antagonist should be used in addition to the previous therapy, if in
heart failure and there are no contraindications. Diuretics often are
needed for volume overload. The role of mitral valve surgery is
unclear in ischemic MR because of the absence of randomized
control trials, but surgery in ischemic MR carries high mortality
in comparison with surgery for structural MR. The AHA and
the European Society of Cardiology recommendations for mitral
valve surgery in ischemic MR are mentioned in Tables 3 and
4.
106,107
The recurrencerate for MR is very high in these cases be-
cause of continuous left ventricular remodeling.
108
The data
about type of surgery and repair versus replacement remain un-
clear. Previous studies and AHA guidelines favor repair more than
replacement; however, recent RCT in which repair was compared
with chordal sparing replacement showed no difference in out-
comesat30daysand1year.
109
The percutaneous mitral clip pro-
cedure may be considered in patients with symptomatic severe
secondary MRdespite optimal medical therapy (including cardiac
resynchronization therapy if indicated) if they fulfill the echo
criteria of eligibility, are considered high risk, and have a life ex-
pectancy greater than 1 year (recommendation class IIb, level of
evidence: C ).
107
RIGHT VENTRICLE INFARCTION
Right ventricle infarction is associated with approximately
50% of all cases of inferior wall MI.
110,111
There is a variability
in reported incidence among the studies because of different diag-
nostic methodologies used. The right ventricle has a complex
shape and its evaluation can sometimes be challenging with
2-dimensional echocardiography. According to late-enhancement
cardiac magnetic resonance studies, the incidence of RVI is ap-
proximately 45% to 57% in inferior wall MI and 11% to 65% in
anterior wall MI.
109,112,11 3
Rarely, RVI presents as isolated MI
without inferior or anterior wall involvement, and it accounts for
3% of cases of STEMI.
114
It usually occurs as a complication of
PCI of RCA; however, cases have been reported of isolated
RVI with occlusion of right ventricular branch of RCA without
PCI.
108,115,11 6
Occlusion of RCA proximal to origin of right
ventricular branch most commonly leads to right ventricular is-
chemia, but many cases donot progressto infarction. The possible
explanations for this observation include the following: (1) thin
right ventricle muscle mass has less oxygen requirement and bi-
phasic blood supply during both systole and diastole as compared
with LV; (2) diffusion of blood to the right ventricle through the
right ventricle cavity; and (3) extensive collateral circulation from
left coronary system.
117
Symptoms and signs of RVI are variable
and range from asymptomatic patients to cardiogenic shock. The
classical clinical triad of hypotension, distended neck veins, and
clear lung field in a setting of inferior wall MI has a very low
sensitivity for RVI, approximately 25%.
118
An elevated jugular
venous pressure and Kussmaul sign in the setting of inferior
wall MI carries very high sensitivity of 88% and specificity of
100%.
118
Electrocardiogram plays a very important role in mak-
ing diagnosis of RVI. In the setting of inferior wall MI, right-
sided leads should always be taken and ST elevation in V1 to
V6R confirms the diagnosis. Isolated ST elevation of 1 mm or
more in V4R is enough to diagnose RVI.
119,120
According to
Robalino et al.,
120
isolated ST elevation of 1 mm or more in
V4R has sensitivity of 100% and specificity of 88% in diagnosing
RVI. Higher ST elevation in V4R as compared with other leads
carries a bad prognosis with higher complications and in-hospital
mortality.
121
Two-dimensional echocardiogram is a noninvasive
and inexpensive imaging modality to assess the function of the
right ventricle; however, its close proximity to the sternum some-
times makes it difficult to fully assess the walls and function of
the right ventricle. Cardiovascular magnetic resonance imaging
using late gadolinium enhancement imaging enables the accurate
characterization of ischemic myocardial injury. Studies have shown
that contrast-enhanced CMR is more sensitive for the detection of
right ventricular involvement than physical examination, electrocar-
diography, and echocardiography in patients with an inferior MI.
However, at the present time, we do not recommend its use,
because it has not been shown to improve patient care in this set-
ting.
109
Hemodynamic monitoring rarely is needed to make a di-
agnosis when echocardiogram is nondiagnostic. Disproportionate
elevation of right-sided pressure as compared with left-sided pres-
sure is the hallmark of RVI. Elevated right atrial pressure (RAP)
greater than 10 mm Hg and ratio of RAP/pulmonary artery pres-
sure greater than 0.8 suggest hemodynamically significant RVI.
122
Therapy for patients with RVI is the same as for any other MI:
dual antiplatelet therapy, statin, anticoagulants, and early reperfu-
sion therapy. Early revascularization improves right ventricular
function and decreases mortality and morbidity in RVI.
123,124
In
a study by Assali et al.,
125
complete revascularization of the right
ventricular branch of RCA decreased 30-day mortality and signif-
icantly improved right ventricular function.
125
Right ventricular
infarction is an independent predictor of mortality after inferior
wall MI and increases both hospital and 30-day mortality (shown
in Fig. 5); however, long-term outcomes of these patients are
good.
125,126
Early recognition of RVI is important to decrease
TABLE 4. European Society of Cardiology Guidelines for Mitral Valve Surgery in Chronic Ischemic Mitral Regurgitation
107
Class I
1. Surgery is indicated in patients with severe MR undergoing CABG and LVEF > 30% (level of evidence: C).
Class IIa
1. Surgery should be considered in patients with moderate MR undergoing CABG (level of evidence: C).
2. Surgery should be considered in symptomatic patients with severe MR, LVEF < 30%, option for revascularization, and evidence of viability
(level of evidence: C).
Bajaj et al Journal of Investigative Medicine •Volume 63, Number 7, October 2015
850 © 2015 The American Federation for Medical Research
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mortality. Opiods, nitrates, and β-blockers should be avoided. The
initial management of RVI may include intravenous fluids to opti-
mize the preload; however, giving too many fluids to the patients
can be detrimental because it further increases RVEDP, pushes the
septum toward the left, increases LVEDP, and further decreases
cardiac output of the left ventricle. According to Berisha et al.,
127
a maximum right ventricle stroke work index is achieved when
RAP is 10 to 14 mm Hg and RAP greater than 14 is associated
with reduced stroke work index. Invasive hemodynamic monitor-
ing can be very helpful in these circumstances to measure right-
sided pressures accurately and guide fluid therapy. When blood
pressure does not improve even after achieving RVEDP of
15 mm Hg with fluids, an inotropic agent is needed to increase
cardiac output. Patients with right ventricular infarct have fixed
stroke volume, and adequate heart rate is important to maintain
sufficient cardiac output. Therefore, maintenance of adequate
heart, atrial ventricular synchrony, and prevention of tachyar-
rhythmia is of paramount importance. Some patients may require
temporary ventricular and atrioventricular sequential pacing to
improve shock. Unfortunately, transvenous pacing of the right
ventricle may be difficult because of sensing failure and right-
sided chamber enlargement.
In a patient with refractory cardiogenic shock, the use of
IABP can be useful; it improves perfusion of coronary arteries
and improves right ventricle function. Percutaneous left ventricle
assist device such as Tandem-heart (Cardiac Assist, Pittsburgh,
PA) may be employed in extreme cases to support RV function.
Percutaneous ventricular assist devices (VADs) are expected to
allow time for the recovery of RV function in acute conditions
or to serve as a bridge to other interventions, such as surgical
VAD implantation.
CONCLUSIONS
The purpose of this review article is to emphasize the high
mortality and morbidity associated with complications of AMI.
Even with advances in management of AMI such as reperfusion
therapies and coronary care unit, complication rates are still high.
A high index of clinical suspicion and rapid imaging such as echo-
cardiogram is needed for early recognition of these complications.
Early recognition of these complications is very important because
appropriate intervention in a timely manner can be lifesaving.
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