Acute myocardial infarction with normal coronary artery (MINCA) in a patient with multiple sclerosis

doi:10.4236/wjcd.2013.38076

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World Journal of Cardiovascular Diseases, 2013, 3, 483-486 WJCD

http://dx.doi.org/10.4236/wjcd.2013.38076 Published Online November 2013 (http://www.scirp.org/journal/wjcd/)

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: *[email protected]

Received 24 August 2013; revised 25 September 2013; accepted 9 October 2013

which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

ABSTRACT

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

1. INTRODUCTION

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.

2. CASE REPORT

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.

OPEN ACCESS

M. Celik et al. / World Journal of Cardiovascular Diseases 3 (2013) 483-486

484

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.

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.

3. DISCUSSION

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’

M. Celik et al. / World Journal of Cardiovascular Diseases 3 (2013) 483-486

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.

REFERENCES

[1] Ahmar, W. and Lefkovits, J. (2008) Acute ST elevation

myocardial infarction with angiographically normal cor-

onary arteries: Causes and outcomes. International Jour-

nal of Cardiology, 128, 131-133.

http://dx.doi.org/10.1016/j.ijcard.2007.05.053

[2] Ammann, P., Marschall, S., Kraus, M., et al. (2000) Cha-

racteristics and prognosis of myocardial infarction in

patients with normal coronary arteries. Chest, 117, 333-

338. http://dx.doi.org/10.1378/chest.117.2.333

[3] Larsen, A.I., Galbraith, P.D., Ghali, W.A., et al. (2005)

Characteristics and outcomes of patients with acute my-

ocardial infarction and angiographically normal coronary

arteries. American Journal of Cardiology, 95, 261-263.

http://dx.doi.org/10.1016/j.amjcard.2004.09.014

[4] Sharifi, M., Frohlich, T.G. and Silverman, I.M. (1995)

Myocardial infarction with angiographically normal cor-

onary arteries. Chest, 107, 36-40.

http://dx.doi.org/10.1378/chest.107.1.36

[5] Gehani, A.A., Al-Mulla, A.W., Chaikhouni, A., et al.

(2001) Myocardial infarction with normal coronary an-

giography compared with severe coronary artery disease

without myocardial infarction: The crucial role of

smoking. Journal of Cardiovascular Risk, 8, 1-8.

http://dx.doi.org/10.1097/00043798-200102000-00001

[6] Lehmann, K.G., Lane, J.G., Piepmeier, J.M., et al. (1987)

Cardiovascular abnormalities accompanying acute spinal

cord injury in humans: Incidence, time course and

severity. Journal of the American College of Cardiology,

10, 46-52.

http://dx.doi.org/10.1016/S0735-1097(87)80158-4

[7] Joing, S., Casey, R. and Forgosh, L. (2004) Prinzmetal

variant angina associated with multiple sclerosis. Journal

of the American Board of Family Medicine, 17, 71-73.

http://dx.doi.org/10.3122/jabfm.17.1.71

[8] Lalouschek, W., Muller, C., Gamper, G., et al. (1997)

Myocardial ischemia with normal coronary arteries as-

sociated with thoracic myelitis. The New England Jour-

nal of Medicine, 337, 1920.

http://dx.doi.org/10.1056/NEJM199712253372612

[9] Lappegard, K.T., Justad, G., Prytz, J.F., et al. (2005)

Thoracic myelitis as a possible cause of myocardial

infarction. Journal of Internal Medicine, 257, 558-560.

http://dx.doi.org/10.1111/j.1365-2796.2005.01487.x

[10] Bulkley, B.H., Klacsmann, P.G. and Hutchins, G.M.

(1978) Angina pectoris, myocardial infarction and sudden

cardiac death with normal coronary arteries: A clinico-

pathologic study of 9 patients with progressive systemic

sclerosis. American Heart Journal, 95, 563-569.

http://dx.doi.org/10.1016/0002-8703(78)90297-1

[11] Agewall, S., Eurenius, L., Hofman-Bang, C., et al. My-

ocardial infarction with angiographically normal coronary

arteries. Atherosclerosis, 95, 398-400.

[12] Kardasz, I. and De Caterina, R. (2007) Myocardial in-

farction with normal coronary arteries: A conundrum

with multiple aetiologies and variable prognosis: An

update. Journal of Internal Medicine, 261, 330-348.

http://dx.doi.org/10.1111/j.1365-2796.2007.01788.x

[13] Wittstein, I.S., Thiemann, D.R., Lima, J.A., et al. (2005)

Neurohumoral features of myocardial stunning due to

sudden emotional stress. The New England Journal of

Medicine, 352, 539-548.

http://dx.doi.org/10.1056/NEJMoa043046

[14] Di Carli, M.F., Tobes, M.C., Mangner, T., et al. (1997)

Effects of cardiac sympathetic innervation on coronary

blood flow. The New England Journal of Medicine, 336,

1208-1215.

http://dx.doi.org/10.1056/NEJM199704243361703

[15] Noseworthy, J.H., Lucchinetti, C., Rodriguez, M., et al.

(2000) Multiple sclerosis. The New England Journal of

Medicine, 343, 938-952.

http://dx.doi.org/10.1056/NEJM200009283431307

[16] Acevedo, A.R., Nava, C., Arriada, N., et al. (2000) Car-

diovascular dysfunction in multiple sclerosis. Acta Neu-

rologica Scandinavica, 101, 85-88.

http://dx.doi.org/10.1034/j.1600-0404.2000.101002085.x