Case Report

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American Journal of Emergency Medicine

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American Journal of Emergency Medicine 31 (2013) 1721.e1-1721.e2

Acute myocardial infarction with Normal coronary arteries associated with subclinical Graves disease?

Abstract

Myocardial infarction occurring with angiographically normal coro- nary arteries is rare and often described in Young people. This report describes a case of myocardial infarction with normal coronary arteries in a young female patient related to Coronary thrombosis complicated by left ventricular apical thrombus in the setting of an unknown and subclinical Graves disease.

A 23-year-old overweight female patient without history of alcohol, tobacco, recreational drug abuse or inherited Cardiovascular risk factors presented with chest pain. On presentation, heart rate was 78 beats per minute and blood pressure 130/65 mm Hg. Diffuse ST segment elevation was found on electrocardiogram (Fig. A). Echocar- diography showed apical akinesia filled with thrombus despite normal ejection fraction (video 1). Coronary angiography revealed a distal left anterior descending artery thrombosis with no sign of coronary dissection or atherosclerosis (Fig. B, videos 2, 3). Throm- boaspiration was not the chosen option with a TIMI III flow artery and a distal thrombosis. Medical treatment was then decided. Troponin I levels rose to 16.35 ng/mL (normal b 0.05 ng/mL) and C-reactive protein to 7 mg/L. Lipid profile was normal. cardiac magnetic resonance imaging showed transmural apical late enhance- ment related to myocardial infarction (Fig. C) and apical thrombus. There were no clinical or biological signs suggestive of myocarditis, Behcet’s disease, lupus erythematosus, Antiphospholipid syndrome, Takayasu disease, nor Kawasaki disease. Graves disease was diag- nosed on laboratory findings without any clinical sign of hyperthy- roidism (thyroid stimulating hormone b 0.005 uUI/mL, presence of specific auto-antibodies: anti-thyroid peroxidase, anti-thyroglobulin and anti-thyrotropin binding-inhibitory immunoglobulin). Follow- up was uneventful while the patient received antiplatelet, warfarin, angiotensin-converting enzyme inhibition and beta blockade ther- apy in addition to carbimazole. Thrombus disappearance was confirmed on 3-month cardiac MRI (Fig. D). The patient is doing well at 3-year follow-up.

Myocardial infarction occurring with angiographically normal

coronary arteries is rare and often described in young people [1]. Smoking, cocaine and alcohol abuse have been shown to trigger Coronary vasospasm in normal coronary arteries [2]. Prolonged coronary vasospasm itself may in turn induce endothelial damage and platelet aggregation resulting in local thrombosis [3]. Oral

? Conflict of interest: none.

contraceptives and inherited thrombophilia are also factors that may promote coronary thrombosis [4]. Hyperthyroidism results in a physiologic state that resembles activation of the sympathetic nervous system. Rare observations have reported an association between hyperthyroidism and myocardial infarction with normal coronary arteries [5]. The complex pathogenesis of coronary thrombosis in patients with hyperthyroidism associates coronary vasospam and Hypercoagulable state [6]. Hyperthyroidism was found to be associated with increased plasma factor X activity, increase in plasma concentrations Factor VIII, von Willebrand antigen and activity, and decreased tissue plasminogen activator inhibitor-1 activity [7]. Abnormal endothelial NO release and exaggerated vasoconstrictive response have also been demonstrat- ed in the setting of hyperthyroidism [7]. Return to a euthyroid state may result in complete resolution of Vascular abnormalities [7]. Lastly, local stasis due to a dysfunctional infarcted myocar- dium along with endocardial inflammation favors local thrombosis in our patient.

In conclusion subclinical hyperthyroidism may be an under recognized etiology of acute myocardial infarction with normal coronary arteries.

Supplementary data to this article can be found online at http://dx. doi.org/10.1016/j.ajem.2013.07.023.

Nadia Bouabdallaoui MD Department of Cardiology, Georges Pompidou European Hospital Assistance Publique des Hopitaux de Paris (AP-HP)

Paris, France

Frederic Mouquet MD, PhD

Polyclinique du Bois

Lille, France

Pierre Vladimir Ennezat MD, PhD

Centre Hospitalier Regional et Universitaire de Lille

Lille, France E-mail address: [email protected]

http://dx.doi.org/10.1016/j.ajem.2013.07.023

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   0735-6757/$ - see front matter (C) 2013

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   Fig. A, 12-lead electrocardiogram showing an extensive ST elevation (arrow). B, videos 2, 3: Coronary angiography, zoom view showing a distal left anterior descending Artery thrombosis (arrow). C, Image from cardiac MRI at admission, long axis view, late enhancement sequences showing apical transmural late enhancement suggestive of left ventricular apical myocardial infarction associated with apical thrombosis (arrow). D, Image from 3-month cardiac MRI, long axis view, late enhancement sequences showing the persistence of an apical transmural late enhancement as a scar of myocardial infarction. The left ventricular thrombus is no longer present.

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