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MINI-SYMPOSIUM
The pathology of myocardial infarction in the pre-
and post-interventional era
M Pasotti, F Prati, E Arbustini
...............................................................................................................................
Heart 2006;92:1552–1556. doi: 10.1136/hrt.2005.086934
T
he clinical diagnosis of myocardial infarction (MI) relies
on symptoms, electrocardiographic findings, and bio-
chemical markers (troponin, serum creatine kinase,
creatine kinase-MB).
12
Acute ischaemic syndromes are now
classified as unstable angina/non-ST-elevation MI (UA/
NSTEMI) and acute ischaemic syndromes with ST-elevation
MI (STEMI).
12
The new diagnostic criteria and markers are
leading to increased proportions
3
of acute ischaemic syn-
dromes being recognised as acute MI. Obviously, elevated
troponin concentrations are not, by themselves, synonymous
with acute MI and can occur in a variety of cardiac and non-
cardiac disorders (for example, sepsis or septic shock,
pulmonary embolism, acute exacerbation of chronic obstruc-
tive pulmonary disease).
4
Therefore, the diagnosis of acute
MI relies on the combination of all clinical and biochemical
tools, each providing its own diagnostic contribution.
The pathological hallmark of acute MI is coagulative
necrosis of the myocardium. All recent advances in the
definition, diagnostic work-up and treatment of MI are
essential to perform an informative pathological investiga-
tion. In fatal MI, the pathological study must be performed at
the appropriate technical and interpretative level to confirm,
extend and improve information useful for the clinical
understanding of the event (why one infarction proves fatal
while other clinically similar MIs are not) and, eventually,
contribute towards improving knowledge that may help
future research in the MI setting.
PATHOLOGY
The pathological diagnosis of MI relies on the identification
of coagulative necrosis in the myocardium, or of repairing
features according to the ‘‘age’’ of the MI,
5
or, if death
occurred before the time necessary for coagulative necrosis to
become visible at routine histopathology, on the detection of
occlusive coronary thrombosis of an epicardial coronary
artery (International classification of diseases, 9th revision (ICD-
9) classification 410, 411). When coronary thrombosis is not
detected at autopsy in individuals with MI who did not
receive reperfusion, plaque complications such as rupture and
haemorrhage can be considered the potential substrate of an
acute thrombotic event that spontaneously thrombolysed. In
less than 5% of cases, MI is reported as not being associated
with coronary atherosclerotic plaques. Coronary spasm
(toxic,
6
drug-induced (Kounis syndrome)
7
or associated with
systemic disease
8
), coronary emboli, and myocardial bridges
9
have been considered as exceptional causes of MI; for these
coronary substrates, the pathologic identification of the
culprit lesion may be difficult. Cases with clinically diagnosed
MI in which neither coagulative necrosis nor acute events in
the culprit plaque are found at autopsy are exceptional.
Most patients with acute MI who are admitted to coronary
care units (CCUs) and coronary interventional labs shortly
after the onset of the ischaemia have a favourable prog-
nosis.
10
In the modern cardiology setting, fatal MIs are
usually those occurring out of the hospital, or are seen in
patients who came late to the CCU, did not receive
appropriate treatments, or died suddenly from life-threaten-
ing arrhythmias.
10
With respect to transmural versus subendocardial MI, the
recent identification of small intramural foci of coagulative
necrosis, clinically recognised with the additional informa-
tion derived from troponin measurements (fig 1),
1
indicates
the need for modified investigation protocols at autopsy with
extensive search for microfoci of necrosis in multiple
myocardial samples. These MIs are unlikely to be fatal unless
the acute ischaemia triggers life-threatening arrhythmias
and, in any case, the corresponding clinical phenotype should
be UA/NSTEMI.
PRE-INTERVENTIONAL AND PRE-THROMBOLYTIC
ERA
Myocardium
Non-reperfused MI shows typical ischaemic coagulative
necrosis.
5
During the first 30–40 minutes of ischaemia, the
changes are visible only at electron microscopy and are
reversible. The macroscopic appearance depends on the
interval of time between the onset of MI and death. A
macroscopic early diagnosis (few hours from onset) relies on
the immersion of the infarcted myocardium in a solution of
triphenyltetrazolium chloride. This histochemical stain
imparts a brick-red stain to the non-infarcted area preserving
the dehydrogenase enzymes. From 12–24 hours the myocar-
dium appears as dark mottling; from days 1–3, the mottling is
centred by a yellow-tan core; from days 3–7 the central
yellow-tan softening area is surrounded by hyperaemic
borders; from days 7–10, the infarction area is yellow-tan
and soft, and the margins are red-tan and depressed; from
10–14 days, the borders assume a red-grey colour; from 2–
8 weeks the scar starts to develop from the periphery to the
centre; after the second month, the scarring process should
be completed.
Although the microscopic appearance before 12 hours is
poorly informative, hypereosinophilic changes of the myocyte
sarcoplasms are present before neutrophilic infiltrates
(fig 1A,B). The so-called ‘‘waviness’’ may be seen at the
border of the ischaemic MI. Isolated myocyte waviness
(without other findings such as hypereosinophilia of the
sarcoplasms or contraction bands and coagulative necrosis)
do not have diagnostic value. Focal waviness of single
myocytes or groups of these cells can be seen in hearts of
patients who died from proven non-cardiac causes; they
constitute the morphologic expression of terminal changes in
pre-agonic and agonic phases. The lack of significance of
Abbreviations: CCU, coronary care unit; MI, myocardial infarction;
MR, mitral regurgitation; PCI, percutaneous coronary intervention;
PTCA, percutaneous transluminal coronary angioplasty; STEMI, ST-
elevation myocardial infarction, UA/NSTEMI, unstable angina/non-ST-
elevation myocardial infarction
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isolated myocyte waviness has been experimentally demon-
strated.
11
After 12 hours, coagulative necrosis starts and progresses
with loss of the nuclei (days 1–3), neutrophilic infiltration
(early days 1–3) (fig 1C,D, fig 2A,B), myocyte fragmentation
(days 3–7) and early phagocytosis at the border of the MI
(days 3–7) after the first week; the granulation tissue
progresses and evolves through loose (week 2) and progres-
sively dense collagen deposition (from 3–8 weeks) and scar
that is completed by the second month. After that date, the
scar becomes acellular and collagen appears dense and
compact.
5
The above time intervals indicate the onset and
peaks of the features but do not reflect the ending. In large
transmural MI, layers of necrotic myocytes can be observed
after intervals longer than two months.
Coronary arteries
A culprit plaque with acute thrombosis is found at autopsy in
more than 90%
12
of patients who have died from MI and were
not treated with either thrombolysis or percutaneous translum-
inal coronary angioplasty (PTCA). The plaque substrate for
thrombosis is rupture in about 75% of the cases and erosion in a
minority of cases,
12
mostly women and smokers.
13
The typical
culprit lesion is a large atherosclerotic plaque with cap
ulceration and superimposed acute thrombosis. The acute
thrombus is red, with a small platelet-rich small head, a fibrin-
and red cell-rich body, and a red cell-rich tail.
14
POST-THROMBOLYTIC AND POST-PTCA ERA
Reperfusion in MI restores the coronary flow interrupted by
the acute coronary event. It can be obtained using thrombo-
lysis or mechanical interventions such as PTCA with or
without stenting. The greatest effectiveness is obtained with
PTCA which dramatically modifies the natural history of MI
and is now available in nearly all tertiary cardiologic centres
in Europe.
2
Thrombolysis and percutaneous coronary interventions
(PCI) with or without stenting is usually performed when
the interval between the onset of symptoms and opening of
the culprit coronary artery is less than 12 hours (the gold
standard is six hours, while the benefit derived from
reperfusion between 12–24 hours is debatable). Guidelines
for STEMI indicate 12 hours after onset of symptoms, and
then distinguish the indications on the basis of the presence
or absence of a PCI centre in the hospital. In hospitals where
a PCI centre is active, all patients with STEMI should
undergo primary PCI. If the interval between onset of
symptoms and arrival at a hospital without a PCI centre is
between 3–12 hours, the patient should be immediately
transferred to a hospital with an active PCI centre. If the
interval is , 3 hours, then thrombolysis can be performed.
12
Myocardium
Reperfusion strategies are introduced in the cardiopathological
setting for the so-called reperfusion-associated pathologies,
Figure 1 Small foci of coagulative necrosis can be recognised on haematoxylin and eosin (H&E) stained sections: ischaemic myocytes typically show
the hypereosinophilia that characterises early phases of coagulative necrosis. (A) The ischaemic myocytes are located in the left side of the panel; (B) the
ischaemic myocytes are positioned bottom left; (C) low magnification view showing a small area of acute myocardial infarction in which granulocyte
infiltration is clearly visible among the myocytes showing coagulative necrosis (squared area and (D), inset at higher magnification). The front of the
myocardial ischaemia is in the top half of the figure.
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whose clinical manifestations include arrhythmias and pro-
longed ischaemic dysfunction, the pathological evidence for
which includes myocardial haemorrhage with contraction
bands, myocyte reperfusion injury distinct from, and additional
to, coagulative necrosis, and small vessel damage. Contraction
bands are seen in irreversibly injured myocytes: their morphol-
ogy is characterised by intensely eosinophilic transverse bands
comprising closely packed hypercontracted sarcomeres. The
macroscopic appearance of reperfused MI is typically haemor-
rhagic. Microscopic examination of reperfused infarction areas
shows myocytes with coagulative necrosis surrounded by red
cell infiltration (fig 2C,D), contraction band necrosis and small
vessels which are either damaged or showing small thrombo- or
athero-emboli. Small vessel damage may further worsen the
haemorrhagic invasion of the myocardium and leads to
endothelial cell swelling which is potentially occlusive (espe-
cially at the capillary level), thus preventing local reperfusion of
ischaemic myocardium. This phenomenon is known as no-
reflow.
15 16
If reperfusion is done before irreversible necrosis, the
blood flow restoration of the area at risk may rescue the entire
ischaemic myocardium. Alternatively, the rescued area is
proportional to the interval elapsed between onset of ischaemia
and blood flow restoration. Scars of reperfused MI show more
angiogenesis processes than non-reperfused MI. In the majority
of cases, the result of reperfusion is a limitation of the infarct
area and size, with improvement of short and long term
function and prolonged survival.
2
Coronary arteries
In reperfused MI the culprit lesion is expected to be patent: it
may show ulceration with haemorrhagic invasion of the core
or mural thrombus layered over the plaque ulceration.
Pultaceous material and thrombotic fragments may reach
the small vessels of the area around the culprit vessel.
17
This
deleterious consequence of infarct-related artery reperfusion
can be addressed by the upstream use of glycoprotein IIb/IIIa
inhibitors, which were found to improve microcirculatory
function and clinical outcome.
18
Alternatively, new filters or
aspirating devices are being used in clinical practice to collect
or suck up both plaque and thrombus derived fragments in
order to limit small vessel impairment. However, these
devices were not found to sufficiently antagonise the no-
reflow phenomenon and improve clinical results.
19
MYOCARDIAL INFARCTION COMPLICATIONS
Acute pulmonary oedema
Pulmonary oedema is associated with a 20–40% 30-day
mortality rate, even in the fibrinolytic era.
20
Pulmonary
oedema may occur as an acute event with the onset of STEMI
Figure 2 (A and B) Typical, non-reperfused myocardial infarction: the basophilic areas indicate the front of granulocyte infiltration. In non-reperfused
MI the repair starts at the borders of the MI and the front progresses from the periphery to the centre. (C and D) Typical reperfusion pattern of a
consolidated myocardial infarction: note the extensive haemorrhagic invasion of the myocardium with coagulative necrosis and the absence of
haemorrhage in subendocardial layers with morphologically ‘‘viable’’ myocytes.
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or reinfarction, or as the culmination of slowly progressive
congestive heart failure during the first days after MI.
Heart rupture
The main risk factors for heart rupture include longstanding
hypertension, female sex, advanced age, and no history of
prior infarction.
21 22
N
Left ventricular free-wall rupture—Cardiac rupture occurs in
1–6% of all patients admitted with STEMI. The frequency
of cardiac rupture shows two peaks: one early within
24 hours, and one late from 3–5 days after STEMI. Risk
factors for cardiac rupture include: first MI, anterior
infarction, old age, female sex, hypertension during the
acute phase of STEMI, lack of prior angina and MI, lack of
collaterals, Q waves on the ECG, symptoms of pericarditis,
peak MB creatine kinase . 150 IU/l, intake of corticoster-
oids or non-steroidal anti-inflammatory drugs, and
fibrinolytic therapy more than 14 hours after onset of
symptoms.
21 22
The most important determinants in pre-
venting rupture are successful early reperfusion and the
presence of collateral circulation.
21 22
N
Ventricular septal rupture—During the reperfusion era the
frequency of acute rupture of the interventricular septum
has declined. It occurs in less than 1% of patients with
STEMI.
23
In patients treated with fibrinolytic therapy, the
highest risk is within the first 24 hours after MI. The
rupturesitecanrapidlyexpandandcausesudden
haemodynamic collapse, even in patients who appear to
be clinically stable with normal left ventricular function.
N
Papillary muscle rupture—Papillary muscle rupture occurs in
less than 1% of cases. The diagnosis is made on the basis of
clinical and imaging findings.
Left ventricular aneurysm
Aneurysm after STEMI usually occurs in the left anterior
wall, in association with left anterior descending occlusion
and a wide infarcted area. Patients with STEMI treated with
fibrinolytic therapy and a patent infarct-related artery have a
significantly reduced incidence of left ventricular aneurysm
compared with those who do not (7.2% v 18.8%).
24
Ventricular pseudoaneurysm
Ventricular pseudoaneurysm is a rare complication. It occurs
as a consequence of rupture of the ventricular free wall and is
contained by overlying, adherent pericardium, producing
what has been termed a ‘‘false aneurysm or pseudoaneur-
ysm’’ of the left ventricle. The pathologic features depend on
the interval of time elapsed from onset of MI and death and
from the extent of haemorrhage between the pericardium
and the myocardial wall. The myocardial wall shows
interruption or fissuring. The myocardial changes include
coagulative necrosis with or without reperfusion pattern,
according to the administered treatments.
25
Most pseudo-
aneurysms are formed within seven days after an AMI, only
exceptionally forming later.
Arrhythmias
Cardiac arrhythmias are common in patients with STEMI
and occur most frequently early after the development of
symptoms. The mechanisms for ventricular tachyarrhythmia
include loss of transmembrane resting potential, re-entrant
mechanisms due to dispersion of refractoriness in the border
zones between infracted and non-ischaemic tissues, and the
development of foci of enhanced automaticity.
26
Reperfusion
arrhythmias likely involve washout of toxic metabolites and
various ions such as lactate and potassium.
26
Lethal arrhythmias/sudden death
Ventricular arrhythmias are one of the most frequent causes
of death in non-hospitalised patients with acute MI.
27
They
are the most common form of sudden ischaemic death.
Cardiogenic shock
Cardiogenic shock in patients with STEMI is commonly
(75%) caused by extensive left ventricular dysfunction.
28
Other relevant causes include mechanical complications
(acute severe mitral regurgitation, ventricular septal rupture,
and subacute free-wall rupture with tamponade).
Cardiogenic shock may be mimicked by aortic dissection
and haemorrhagic shock.
Mitral regurgitation
After STEMI, mitral regurgitation (MR) may occur as a result
of infarction of the papillary muscle, infarction involving the
lateral wall, large infarction with left ventricular dilation, and
displacement/dysalignment of the papillary muscle. Severe
MR with cardiogenic shock has a poor prognosis. In the
SHOCK trial registry, approximately 10% of patients with
shock presented with severe MR (overall hospital mortality
55%).
28
When severe MR is caused by infarction of the
papillary muscle and wall, the area of infarction tends to be
less extensive than in patients in whom the MR is caused by
papillary displacement/dysalignment and severe left ventri-
cular dysfunction. The presence of acute pulmonary oedema
or cardiogenic shock in posterior/posterolateral STEMI
should point to the possibility of acute MR caused by
papillary muscle rupture.
Figure 3 Light micrographs showing (A) typical pulmonary oedema
(H&E stain) versus (B) pulmonary haemorrhage in a patient who died of
acute adult-type respiratory distress related to abciximab (peroxidase-
antiperoxidase; anti-glycoforin A immunostain).
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Pericarditis
Pericarditis occurs in transmural STEMI involving the full
thickness of the myocardial wall to the epicardium. Patients
with pericarditis have larger infarcts, lower ejection fraction
and higher incidence of congestive heart failure. Pericarditis
may appear up to several weeks after STEMI. The Dressler
syndrome (post-MI syndrome) has essentially disappeared in
the reperfusion era.
29
Acute pulmonary haemorrhage
This is a rare complication that may occur in patients who
undergo primary PTCA and are treated with glycoprotein IIb/
IIIa inhibitors.
30 31
When it occurs, it is difficult and costly to
treat and may result in death. The pathologic diagnosis is
essential to confirm the alveolar invasion by red blood cells
(fig 3A,B). Bleeding complications are higher in women than
in men. In pooled analysis of the results from EPIC, EPILOG
and EPISTENT, major bleeding rates were 3% and 1.3%
(p = 0.004) and minor bleeding rates were 6.7% and 2.2%
(p , 0.001) in women and men, respectively. Rare intracra-
nial and gastrointestinal haemorrhages have also been
reported.
32
CONCLUSIONS
The pathology of MI in the post-interventional era includes
specific features mostly resulting from the reperfusion of
necrotic myocardium. The contribution of the pathologic
study should add information to the clinical data and should
match new sensitive diagnostic markers. The complication
scenario is also modified: prevalence and evolution are
significantly different in non-reperfused and reperfused MI.
Authors’ affiliations
.....................
M Pasotti, Center for Inherited Cardiomyopathies, IRCCS Policlinico San
Matteo, Pavia, Italy
F Prati, Interventional Cardiology, S. Giovanni Hospital, Roma, Italy
E Arbustini, Molecular Genetics, Cardiovascular and Transplant
Pathology, IRCCS Policlinico San Matteo, Pavia, Italy
Supported by grants: Ricerche Finalizzate granted by the Ministry of
Health to the IRCCS Policlinico San Matteo, Pavia, Italy
Correspondence to: Dr Eloisa Arbustini, Centre for Inherited
Cardiovascular Diseases, Cardiovascular Pathology, Area
Trapiantologica, Piazzale Golgi 2, 27100 Pavia, Italy; e.arbustini@
smatteo.pv.it
Published Online First 18 April 2006
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