World Journal of Cardiovascular Diseases, 2013, 3, 483-486 WJCD Published Online November 2013 (
Acute myocardial infarction with normal coronary artery
(MINCA) in a patient with multiple sclerosis
Murat Celik1*, Mehmet Ata Akil2, Mustafa Tuncer2
1Department of Cardiology, School of Medicine, Gulhane Military Medical Academy, Ankara, Turkey
2Department of Cardiology, Van Medicalpark Hospital, Van, Turkey
Email: *
Received 24 August 2013; revised 25 September 2013; accepted 9 October 2013
Copyright © 2013 Murat Celik et al. This is an open access article distributed under the Creative Commons Attribution License,
which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Interestingly, some patients with ST elevation myo-
cardial infarction have normal coronary artery ana-
tomy at cooronary angiography. This situation is call-
ed as MINCA (acute myocardial infarction with nor-
mal coronary artery). The incidence of MINCA va-
ries between 1.0% and 8.5%. Although some reasons
have been propounded, the exact underlying mecha-
nism remains unclear. Nevertheless, thoracic myelitis
can be as a possible cause of myocardial infarction.
Herein, we report a case of acute myocardial infarc-
tion with normal coronary artery in a patient with
multiple sclerosis.
Keywords: Acute Myocardial İnfarction; Normal
Coronary Artery; Multiple Sclerosis
Although it is known that rupture of atherosclerotic
plaque and subsequent intra-luminal thrombus formation
is the main cause of acute myocardial infarction, some
patients have normal coronary arteries at coronary an-
giography in the setting of acute myocardial infarction.
The existence of acute myocardial infarction despite an-
giographically normal coronary arteries (MINCA) was
recognized for more than 30 years and its incidence varied
between 1.0% and 8.5% [1-5]. The aetiology and patho-
genesis of the condition are still a source of debate. Some
reasons such as cocaine ingestion, coronary vasospasm,
endothelial dysfunction, thrombosis, embolization and
inflammation, coagulopathies (inherited or acquired),
perimyocarditis and stress cardiomyopathy (Takotsubo
syndrome) may explain some of these occurrences [3].
Additionally, myocardial infarctions may have been
caused by vasospastic reactions secondary to spinal cord
pathology such as thoracic myelitis.
Abnormal cardiac function has been described after
upper-spinal-cord lesions due to acute autonomic imbal-
ance by the disruption of sympathetic pathways [6].
Nevertheless, coronary vasospastic reactions secondary
to spinal cord pathology may lead to myocardial infarc-
tion [7-9]. However, the number of case report de-
scriging the relationship between myocardial ischemia
and multiple sclerosis (MS) is limited and pathogenesis
of this condition is still being debated. We hereby wanted
to draw attention to this rare togetherness by reporting a
case of MINCA in a patient with MS and tried to explain
the relationship between MINCA and MS.
A 40-year-old woman without a history of any cardio-
vascular disease was admitted to our hospital because of
typical chest pain for 1 hour. She had a history of MS for
5 years. An admission 12-lead electrocardiogram (ECG)
showed ST elevation in leads II, III, aVF and reciprocal
changes in leads V1,V2, suggesting an acute inferior
myocardial infarction (Figure 1). Vital parameters and
standart biochemical tests at admission were with in nor-
mal ranges. Coronary angiography (CAG) was per-
formed. Interestingly, CAG did not reveal any stenosis,
luminal irregularities, thrombus or coronary spasm in
any of 3 coronary arteries (Figures 2(a) and (b)). Addi-
tionally, we performed aortography for the suspicion of
occlusion of any anomalous coronary artery, but there
was not a coronary artery anomaly. The patient took in
coronary intensive care unit and treated with infusion of
unfractioned heparin and glyceryl trinitrate at recom-
mended dose for the possibility of coronary vasopasm
and/or spontenous resolution of thrombus and emboliza-
tion into the microvascular integrity. Cardiac enzymes
were elevated 2.5 hours later: peak creatine kinase 3045
IU/L; peak creatine kinase MB 405 IU/L; and troponin,
*Corresponding author.
M. Celik et al. / World Journal of Cardiovascular Diseases 3 (2013) 483-486
Figure 1. 12-lead electrocardiogram (ECG) at admission shows ST elevation in leads DII, DIII and aVF.
(a) (b)
Figure 2. Left (a) and right (b) coronary angiograms show normal coronary artery.
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M. Celik et al. / World Journal of Cardiovascular Diseases 3 (2013) 483-486 485
7.22 ng/mL. The erythrocyte sedimentation rate was 16
mm/h, total leukocyte count was 9600 cells/μL, C-reac-
tive protein level was 0.3 mg/dl. Echocardiogram show-
ed inferior hypokinesis without any finding of pericardi-
tis. Her chest pain recurred and same ECG finding sug-
gesting an acute inferior myocardial infarction were
found at the 2nd day of hospitalization. CAG repeated
and revealed normal coronary arteries once more. At that
time, she also complained of dizziness, nausea and vom-
iting. Magnetic resonance imaging (MRI) was performed
and revealed multiple foci of increased T2 signal inten-
sity, but there was not any finding of new foci suggesting
MS exacerbation. The patient was treated with infusion
of methylprednisolone at recommended dose for five
days. Her all complaints including chest pain did not
occurred again during hospitalization. On the 4th day of
hospitalization, creatine kinase was 164 IU/L; creatine
kinase MB was 32 IU/L; and troponin was 2.63 ng/mL.
Then, the patient was discharged in a very good condi-
tion on the 7th day of hospitalization.
We presumed that the patient had an acute myocardial
infarction. We thought about the possibility of coronary
vasospasm or intra-luminal thrombosis resolved sponta-
neously. However, either clear atherosclerosis or throm-
bus formation was not present at CAG. Thus, we could
not point out the underlying mechanism exactly.
MINCA is a rare but fair clinical entity. Patients with
MINCA are younger and less likely to have traditional
risk factors for atherosclerosis than those of identifiable
CAD [3]. The incidence and the underlying etiology of
MINCA remain unclear. A number of possible mecha-
nisms have been suggested. The most known are coro-
nary vasospasm and thromboembolic disease. Changes in
autonomic neural control, changes in contractile function,
locally released vasoactive mediators in contact with
dysfunctional endothelium, history of smoking, mental
stress and oral contraceptive use may be responsible for
coronary artery vasospasm [7]. In their study, Bulkley et
al. [10] described the autopsy findings of nine patients
with progressive systemic sclerosis and evidence of
ischemic heart disease but morphologically normal coro-
nary arteries. They observed contraction band necrosis,
as a form of reperfusion lesion, in seven of nine patients,
and suggested that intermittent vascular spasm at some
level of the microcirculation would account for the con-
traction band type of necrosis and cause myocardial in-
farction with morphologically normal coronary arteries
in patients with progressive systemic sclerosis. Larsen et
al. [3] showed a trend toward a higher prevalence of ma
lignancy in patients with MINCA, and suggested that
malignancy—induced hypercoagulability or inflammation
—might be the underlying mechanism of MINCA. Also,
myocarditis is one of the possible causes of MINCA, es-
pecially in patients below the age of 35 years [11]. Other
potential mechanisms are cocaine ingestion, coagulo-
pathies (inherited or acquired), stress cardiomyopathy or
Takotsubo syndrome, myocardial bridging and sponta-
neous coronary artery dissection [1,12,13].
Sympathetic innervation of the heart originates from
the cervical and the upper four or five thoracic segments
of the spinal cord and has an important role in regulat-
ing cardiac function and myocardial blood flow [14].
Abnormalities of cardiac function have been described
after acute injuries to the cervical spinal cord and/or spi-
nal cord pathologies such as thoracic myelitis. Lehmann
et al. [6] evaluated cardiac functions after acute injury to
the spinal cord in 71 consecutive patients and they found
that acute severe injury to the cervical spinal cord is
regularly accompanied by arrhythmias (persistent bra-
dycardia, marked sinus slowing, supraventricular ar-
rhythmias) and hemodynamic abnormalities (hypoten-
sion) resolved spontaneously within 2 to 6 weeks. They
suggested the primary mechanism underlying these ob-
servations appears to involve the acute autonomic im-
balance created by the disruption of sympathetic path-
ways located in the cervical cord [6].
Multiple sclerosis (MS), also known as disseminated
sclerosis or encephalomyelitis disseminate, is an inflam-
matory autoimmune disorder in which the body’s own
immune system destroys the fatty myelin sheath protects
and insulates the neurons of the brain and the spinal cord.
MS is typically a relapsing-remitting neurologic disorder
and usually occurs in young adults, and it is more
common in women [15]. Nevertheless, patients with MS
have been shown to be at risk for various forms of car-
diovascular dysfunction related to involvement of reflex
pathways in the brainstem and parasympathetic dysfunc-
tion [16]. Additionally, coronary vasospasm and/or
myocardial ischemia can be seen in patients with MS and
normal coronary arteries. A search of the literature re-
veals only 3 case reports of indicating the relationship
between myocardial infarction and spinal cord pathology.
Lalouschek et al. [8] reported a 53-year-old woman with
normal coronary arteries who had angina at rest, which
was associated with myelitis of the thoracic spinal cord.
Joing et al. [7] reported a case of 38-year-old woman
who experienced Prinzmetal variant angina during a
multiple sclerosis relapse. Lappegard et al. [9] reported
myocardial infarction in a 45-year-old male with acute
and documented inflammatory changes in the spinal cord.
In all of the 3 case reports, the thoracic spinal cord lesion
led to coronary vasoconstriction due to the fact that in-
tense activation of cardiac sympathetic nerves had been
suggested as the most plausible explanation by authors. In
our patients, the coronary arteries were angiographically
completely normal indicating the fact that patients’
Copyright © 2013 SciRes. OPEN ACCESS
M. Celik et al. / World Journal of Cardiovascular Diseases 3 (2013) 483-486
symptoms might be due to vasospastic coronary occlu-
sion and no obvious cause could be found except MS.
We did not observe any significant neurological finding
related to patient’s lower or upper extremities. So, we did
not perform MRI of spinal cord. Although we did not
perform a MRI of spinal cord, a lesion in the stated seg-
ments of the spinal cord might be the cause of the find-
ings of myocardial ischemia in our patient.
Patients with MINCA have a significantly better
prognosis than those of angiographically documented
coronary artery disease (CAD) [3]. Long-term outcomes
appear favourable in the majority of patients [1]. It was
reported that there was no recurrence of anginal symp-
toms in any of the MINCA patients and no patient un-
derwent a revascularization procedure within 1 year [1,
3]. However, patients’ chest patin was repeated 2 days
later in our case indicating acute myocardial infarctions
in the same coronary territories. The optimal treatment of
MINCA is currently controversial. There is no consensus
about the use of heparin, aspirin, antiplatelet drugs and
statins, even after the angiographic finding of normal
coronary arteries. It is reasonable to make a cause-spesi-
fic treatment. It was shown that no further episodes of
angina pectoris were observed after administration of high
dose methylprednisolone treatment in patient with MS [8].
In conclusion, MINCA is a rare entity, but its inci-
dence seems to be more increased than expected by the
frequent use of CAG. The prognosis of this condition is
much better than myocardial infarction with coronary
artery disease, and prognosis is likely variable according
to the underlying mechanism. Cardiologist should be
aware of the possible underlying mechanism in the sett-
ing of the MINCA, because treatment is likely variable
according to the underlying mechanism. Multiple sclero-
sis may be one of these possible explanations.
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