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com
Original article
1
Royal Brompton and Harefield
Hospitals NHS Trust, London,
UK
2
CRY Centre for Cardiac
Pathology, NHLI Imperial College
London, UK
Correspondence to
Dr Mary N Sheppard,
Department of Pathology, Royal
Brompton Hospital, Sydney
Street, London SW 3 6NP, UK;
m.sheppard@rbht.nhs.uk
Received 30 November 2011
Accepted 2 February 2012
Published Online First
29 February 2012
512
Myocardial infarction with normal coronaries:
an autopsy perspective
Anna Silvanto,1 Sofia Victoria de Noronha,2 Mary N Sheppard1,2
ABSTRACT
Aim To analyse postmortem cases of myocardial
infarction (MI) with normal coronary arteries in terms of
patient characteristics, features of the MI and risk
factors.
Methods This retrospective non-case controlled study
was carried out at a specialist cardiac pathology
department at a tertiary cardiac referral centre. Cases of
histologically confirmed MI and normal coronary arteries
during the period 1996e2010 were identified and
analysed for the presence of risk factors.
Results Nineteen cases of histologically confirmed
MI and normal coronary arteries were identified with
a similar gender ratio 1:1.1 (male:female) and mean age
of 33612 years (range 14e58). All patients died
suddenly. The location of the infarct was variable, with
left anterior descending artery territory being the single
most prevalent (47%). Risk factors were identified in the
majority of cases (n¼14), with some cases experiencing
more than one association, including alcohol and/or
predominately class A drug use (n¼7), including
cocaine, inflammation (n¼2), hypercoagulable state
(n¼3) and exertion (n¼2).
Conclusions Current data regarding prognosis in MI
with normal coronary arteries suggests a favourable
outcome in the context of major cardiovascular events.
No large series of fatal cases have been reported. This
study highlights that this entity can be fatal and its
prognosis may be less favourable than currently
considered. This autopsy series also demonstrates that
the causation of MI with normal coronary arteries is
complex and multifactorial, including a history of alcohol
and/or drug use. It also highlights the importance of
accurate epidemiological data from referring
pathologists.
While the leading cause of myocardial infarction
(MI) in patients with coronary heart disease is
plaque rupture, MI with normal coronary arteries
has been recognised for many years. Its prevalence
ranges from 1% to 12% according to the angio-
graphic definition of normal or near-normal used.
Some studies define ‘normal’ as coronary arteries
with smooth contours and no focal luminal
reduction.1 Others view a less than 30% stenosis as
insignificant,2 while many more studies have
considered only greater than 50% stenoses as
significant in causing acute coronary syndrome.3e5
Patients with MI and normal coronary arteries tend
to be younger,6 and have a lower prevalence of
cardiovascular risk factors compared with patients
with obstructive coronary artery disease.7e9
A number of mechanisms have been postulated to
account for this phenomenon, including coronary
artery vasospasm, concealed atherosclerosis, throm-
bosis and hypercoagulability, embolisation and
inflammation.1 10 Furthermore, coronary artery
spasm can be induced by catecholamine excess,
alcohol and cocaine abuse, cigarette smoking, with-
drawal of calcium antagonists, minimal but diffuse
coronary atherosclerosis and endothelial dysfunction.
Thrombosis secondary to hypercoagulability can be
inherited, such as factor V Leiden mutation, or
acquired, for example, oestrogen therapy, pregnancy
or postoperative state. Embolisation is thought to
account for a very small percentage of cases, and
may be caused by the presence of native or pros-
thetic valve disease, endocarditis or left atrial
myxoma. Patients with MI and normal coronary
arteries have also been shown to have significantly
more frequent upper respiratory tract infections
within 2 weeks before MI. However, the mechanism
linking this type of inflammation to MI is
unknown.10 MI with near normal coronary arteries
following strenuous exercise has also been reported.11
Begieneman et al12 reported basement membrane
thickening in intramyocardial arteries in acute
MI, identified electron microscopically, indicating
a further contributing mechanism.
Prognosis in patients with MI and normal coro-
nary arteries is often viewed as favourable. A recent
paper by Ong et al5 found that during a 3-year
follow-up there was no cardiac death or non-fatal
MI in a group of 76 patients without a culprit
lesion, defined as a greater than 50% stenosis. Other
groups have also demonstrated an excellent prog-
nosis with no major cardiac events at follow-up.2 9
Other studies disagree; major cardiac events
including death, heart failure, stroke or re-infarction
occurred in 25% of a cohort of 91 patients during
a 3-year follow-up.1 Also, Raymond et al8 found
that nine of 74 (12%) patients with MI and normal
coronary arteries died of a cardiovascular cause,
with six dying suddenly.
To date no large autopsy series has been
published on this entity. We report all cases of
sudden cardiac death (SCD) with MI and in whom
the coronary arteries were entirely normal on
detailed examination referred to our tertiary cardiac
pathology centre.
METHODS
Criteria for case selection
Our database includes 1980 cases of non-athero-
matous SCD referred to a specialist tertiary cardiac
pathology centre, part of the National Heart and
Lung Institute and the Royal Brompton Hospital.
From this database we retrieved cases of MI with
normal coronary arteries.
Pathological analysis of all cardiac tissue
including the histology was performed by MNS
J Clin Pathol 2012;65:512e516. doi:10.1136/jclinpath-2011-200597
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with the consent of the coroner and the family of the deceased.
Heart tissue was examined thoroughly and MI was confirmed
using histological criteria for acute and chronic ischaemic
damage.13 Major epicardial coronary arteries, including left main
stem, left anterior descending, left circumflex and right coronary
arteries (RCA) were cross-sectioned at 3e5-mm intervals and
verified to be entirely normal macroscopically and histologically,
with no atherosclerotic plaques. The presence of other pathol-
ogies, including myocarditis, inflammatory cell infiltration of
the endothelial layer of the coronary arteries or abnormalities in
the intramyocardial vessels, was excluded by light microscopic
examination of H&E stained slides.
This study was approved by the ethics committee of the
Royal Brompton Hospital, reference number 07/Q0404/9 and
10/H0724/38 and complies with the requirements of the Human
Tissue Act, 2004.
Patient demographics and detection of risk factors
Data on age, sex, circumstances of death, antecedent cardiac
symptoms, past medical history and toxicology were obtained
for each patient from the referring pathologist or coroner when
available.
Characteristics of MI
The location of each infarct in the ventricular myocardium was
determined. The age of each infarct was estimated on well-
established histological criteria that can be observed during the
evolution of an MI. In the first 17e24 h MI is impossible to
recognise both macroscopically and microscopically. Features of
an acute MI in the first 24e48 h include contraction band
necrosis, myocyte swelling, loss of myocyte nuclear detail and
a neutrophilic infiltrate. Days 3e7 are characterised by an infil-
trate of lymphocytes and macrophages around necrotic
myocytes. Granulation tissue with myocyte loss, pigmented
macrophages and myofibroblasts are seen on days 7e42. The
presence of fibrosis indicates an infarct more than 6 weeks
before death.13
RESULTS
Case selection
Histology confirmed the presence of acute MI in 16 patients, and
an old fibrosed MI in three patients. The coronary arteries in all
19 cases were entirely normal with smooth contours, no luminal
irregularities and no atheroma. The intramyocardial arteries
were normal.
Patient characteristics
Gender was similarly distributed (men n¼10; women n¼9) and
the mean age was 33.8612.2 years (range 14e58). There was no
significant difference in the age distribution between male and
female patients. The distribution of age at death is shown
in figure 1.
Circumstances of death
All 19 patients died suddenly. Twelve (63%) patients were found
dead at home, mostly dying at rest (n¼7). Two patients (cases 3
and 11) died within 12 h of strenuous exertion in sport. Images
of the infarct post-exertion for case 11 are shown in figure 2;
a macroscopic cross-section of the left ventricle (A) and
a microscopic image of haemorrhagic reperfusion of the
same infarct (B). The remaining cases died in the community
(n¼3), following hip replacement (n¼1) or died in unknown
circumstances (n¼3) (table 1).
J Clin Pathol 2012;65:512e516. doi:10.1136/jclinpath-2011-200597
Original article
Figure 1 Age and gender distribution of patients who died suddenly
with a myocardial infarction and normal coronaries.
Antecedent symptoms, medical history and risk factors
Of the 19 cases, just over a quarter (n¼5) had experienced one or
more antecedent cardiac symptoms, including chest pain (n¼4),
shortness of breath (n¼1) or palpitations (n¼1). Risk factors
were identified in the majority of cases (n¼14, 68%) with some
experiencing more than one risk factor (table 1). The most
common association was alcohol consumption (n¼5, chronic
alcoholism n¼2), of whom three patients also had a history of
drug use (cocaine n¼1, heroin n¼1, cannabis n¼1). Three
patients had positive toxicology results (alcohol n¼1, 80 mg/dl,
morphine n¼1, 0.012 mg/dl, cocaine n¼1, positive for cocaine
metabolites, quantity not specified). Both patients with
a history of heroin use were hepatitis C positive. Other associ-
ated factors included exertion (n¼2), epilepsy (n¼2), oral
contraceptive pill use (n¼2), pregnancy (n¼1), bronchitis (n¼1)
and phaeochromocytoma (n¼1) (table 1).
Infarct characteristics
Location of infarct
The majority of the cases (n¼9, 47%) had transmural infarcts
located in the anterolateral region of the left ventricle supplied
by the left anterior descending artery. Four infarcts (21%) were
located in the posterobasal region of RCA territory. Two infarcts
(11%) were transmural in both the RCA and left coronary artery
territories, and four infarcts were subendocardial (21%).
Age of infarct
Eleven of 19 infarcts were estimated to be 24e48 h old, two
infarcts were 3e7 days old (example in figure 2C) and three
infarcts were 7e42 days old (example in figure 2D), while three
cases had established regional fibrosis transmurally with no
evidence of acute changes (cases 5, 13, 16). Five cases of acute
infarction had evidence of established regional fibrosis within
the myocardium in the same territory, indicating reinfarction
(cases 3, 10, 11, 14, 17).
DISCUSSION
Our study is to our knowledge the first large autopsy series on
MI with completely normal coronary arteries. A previous study
of ours examining non-atherosclerotic causes of SCD found six
cases of infarction with normal coronary arteries.14 Our current
study demonstrates that MI with normal coronary arteries is
rare but is associated with a definite risk of mortality, presenting
a contrast to reports suggesting a favourable prognosis. Our
513
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Original article

Figure 2 Acute myocardial infarction

in a 17-year-old man after exertion. (A)
Macroscopic mid-ventricular short-axis
view of circumferential subendocardial
infarction. (B) Haemorrhage reperfusion
of an acute myocardial infarction (H&E,
magnification 1003). (C) Infiltrate of
neutrophils around necrotic myocytes in
an infarct on days 3e7 (H&E,
magnification 2003). (D) Granulation
tissue with myocyte loss, pigmented
macrophages and myofibroblasts are
seen on days 7e42 (H&E, magnification
4003). This figure is produced in colour
in the online journaldplease visit the
website to view the colour figure.

series suggest that MI with normal coronary arteries can occur
in the territories of any single or multiple coronary arteries,
similar to previous studies,15 16 with an effect on a predomi-
nantly younger population. While vasospasm cannot be
confirmed as the underlying mechanism of infarction in
postmortem hearts, several of the associated factors are linked
to vasospasm, as is described below. Our cases illustrate
several possible associations and multifactorial mechanisms,17
and a single aetiology does not appear to exist for this
condition.

Table 1 Patient demographics, circumstances of SCD, relevant medical history, location and timing of infarction
Circumstances Location of acute
Case Sex Age (years) of SCD Medical history LVHz infarct LV wall* Timing of infarct
1 M 44 Sitting/home Heroin use, alcoholism and hepatitis C positive 0 Anterior, lateral, posterior 1e6 weeks
2 F 16 Home Pregnancy, family history of HHT 0 Anterior, lateral, septal 24e48 h
3 F 42 Post-exertion On contraceptive pill. BMI 23.5 0 Antero and posteroseptal 1e6 weeks +
(community) lateroseptal fibrosis
4 M 58 N/A Asthma and emphysema 1 (septal) Anterolateral 24e48 h
5 M 32 Bed/home Chest pain. BMI 27.0 1 (septal) Anteroseptal Fibrosis
6 M 37 N/A Heroin use, on detoxification and 0 Anteroseptal 24e48 h
chlorpromazine. Hepatitis C+. BMI 20.2.
Toxicology positive for morphine.
7 M 45 Home Alcohol and cannabis use, chest pain 1 Anteroseptal 1e6 weeks
8 F 35 Home Alcoholism, ischaemic ECG and chest pain, 0 Anteroseptal 24e48 h
toxicology positive for cocaine, BMI 20.7
9 F 39 N/A N/A 0 Anteroseptal 24e48 h
10 F 49 Hospital Hypertension, asthma, phaeochromocytomay 0 Anteroseptal 24-48 h + LV fibrosis
11 M 17 Post-exertion Dyspnoea and chest pain 1 Circumferential 24e48 h +
(bed/home) posterior LV fibrosis
12 F 16 Bed/home Consumption of alcohol before death 0 Lateral 24e48 h
13 M 38 Sitting/home Gout. BMI 23.0 0 Posterior Fibrosis
14 F 26 Bed/home On contraceptive pill 0 Posterobasal 24e48 h +
posterior LV fibrosis
15 M 14 Community Epilepsy, consumption of cannabis before 0 Posterolateral 24e48 h
death, BMI 20.0
16 M 32 Bed/home Epilepsy, BMI 21.5 0 Posteroseptal fibrosis
17 F 25 Bed/home Palpitations, consumption of alcohol before 0 Subendocardial, inc. 1e6 weeks +
death. Toxicology positive for alcohol papillary muscle papillary muscle fibrosis
18 F 36 Home Bronchitis, chest pain 0 Subendocardial RV (and LV) 24e48 h
19 M 41 Community Smoker 1 Subendocardial 1e6 weeks
*Unless otherwise specified.
yDiagnosed at autopsy.
zLeft ventricular hypertrophy was mild (16-18 mm).
BMI, body mass index; HHT, hereditary haemorrhagic telangiectasia; HTN, hypertension; LV, left ventricle(ular); N/A, not available; RV, right ventricle; SCD, sudden cardiac death.

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Most infarcts in our study were acute. However, our study
also suggests that a proportion of patients have recurrent MI
with normal coronary arteries.
Associated factors
Alcohol and drug use
Alcohol misuse is widespread in the UK.18 Epidemiological
studies show higher rates of alcohol abuse in men younger than
40 years, with a first MI and higher rates of sudden death in
heavy alcohol consumers.19 Ethanol generally induces vasodila-
tion but can produce concentration-dependent coronary vaso-
spasm in animal studies,20 subsequently confirmed in humans.21
With the increasing trend towards binge drinking this entity
may become more prevalent. The role of cocaine in causing
cardiovascular complications, including myocardial ischaemia
and infarction, is well documented.22 Aslibekyan et al23 showed
that 18e45 year olds had a significantly elevated prevalence of
MI in association with cocaine use. Alcohol and cocaine can
have synergistic or additive adverse effects on coronary artery
blood flow.24 Marijuana is a rare trigger of acute MI, ventricular
tachycardia and fibrillation by the induction of coronary artery
spasm being reported in the background of other associations
such as cigarette smoking, obesity and coronary artery disease.25
Two cases consumed alcohol and one case consumed cannabis
within 12 h of death. As these infarcts were greater than 24 h in
duration, this may indicate that a fatal arrhythmia may have
been triggered by these substances in a heart already infarcting.
A case report by Yu et al26 described MI after heroin injection
with a normal coronary angiogram. It is possible that morphine
usage in a detoxification programme in one further patient may
have caused cardiac ischaemia by the same mechanism as heroin.
However, this patient was also on an antipsychotic medication
known to induce coronary vasospasm. In a cohort of schizo-
phrenia, users of typical antipsychotic agents had a fivefold risk
of MI compared with control subjects.27
Hypercoagulable state
Acute MI during pregnancy and puerperium is well documented,
with the highest incidence occurring in the third trimester, as in
case 2. Normal coronary arteries have been reported in 29% of
cases.28 Coronary artery spasm associated with a probable hyper-
coagulable state is the most likely mechanism. Our patient also
had a family history of hereditary haemorrhagic telangiectasia.
Acute MI with normal coronary arteries in this disorder has been
reported.29 It is well established that contraceptive medications
thath include oestrogen increase the risk of vascular thrombosis.
Exertion
MI following strenuous exercise also featured in this study. Post-
exercise ST elevation MI has been described.11 Physical exertion
may precipitate epicardial coronary spasm related to an
increased catecholamine output leading to arterial vasocon-
striction and platelet aggregation.30 31
Adrenal tumours
Phaeochromocytoma identified in one patient in our series is
a rare neuroendocrine tumour that can secrete high levels of
catecholamines and has been linked to apical ballooning (or
takotsubo syndrome) and may cause coronary vasospasm with
infarction.32
Epilepsy
In a recent study, patients with epilepsy were at an increased
risk of an acute MI, which may explain the sudden death of our
J Clin Pathol 2012;65:512e516. doi:10.1136/jclinpath-2011-200597
Original article
Take-home messages
< MI with normal coronary arteries is associated with a definite
risk of mortality.
< This study highlights its risk factors, particularly alcohol and/
or drug use. With both being on the increase, this entity may
be encountered more frequently in the future.
Interactive multiple choice questions
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patients with this condition. Epileptic seizures may induce
cardiac ischaemia and increase the risk of subsequent acute MI
in the absence of structural disease.33
Inflammation
Inflammation has been implicated in the pathogenesis of MI. C-
reactive protein, an acute phase protein has been shown to be an
independent predictor of future coronary events in apparently
healthy individuals.34 Acute myocarditis and an inflammatory
response to specific infectious agents, such as EpsteineBarr virus
and Chlamydia pneumoniae have been proposed as a mechanism
for acute coronary syndrome.35 36
Study limitations
Our autopsy series is a retrospective study and subject to the
limitations of such studies, including reliance on information
obtained from the referring pathologist and the coroner
regarding epidemiological data and past medical history. A
definite causative link between the risk factors and MI cannot be
demonstrated and the presence of vasospasm can only be
assumed in this study. It must also be stated that infarction as
a result of spasm occurring within 24 h of the spasm may not be
detected at autopsy.
CONCLUSION
Our autopsy series demonstrates a small but definite risk of
mortality associated with MI and normal coronary arteries. Our
study highlights that this entity can be fatal and its prognosis
may be less favourable than currently considered. This autopsy
series also demonstrates that the causation of MI with normal
coronary arteries is complex and multifactorial. It suggests an
association of this entity with a history of alcohol and/or drug
use. However, studies such as ours rely on clinical information
provided by referring pathologists. Only with complete clinical
histories and investigations, including toxicology results, can we
obtain better epidemiological data and identify the multifacto-
rial causes more accurately.
515
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Original article

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516 J Clin Pathol 2012;65:512e516. doi:10.1136/jclinpath-2011-200597

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Myocardial infarction with normal

coronaries: an autopsy perspective
Anna Silvanto, Sofia Victoria de Noronha and Mary N Sheppard

J Clin Pathol 2012 65: 512-516 originally published online February 29,
2012
doi: 10.1136/jclinpath-2011-200597

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