A Case of Cardiac Arrest due to Multivessel, Diffuse Coronary Spasm in Moyamoya Disease

Young Min Choi; Jung Woo Choi; Dong Ho Kang; Choong Hwan Kwak; Jin Yong Hwang; Jin Sin Koh

doi:10.7180/kmj.2017.32.1.111

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Choi, Choi, Kang, Kwak, Hwang, and Koh: A Case of Cardiac Arrest due to Multivessel, Diffuse Coronary Spasm in Moyamoya Disease

Case Report

Kosin Medical Journal 2017;32(1):111-117.

Published online: 19 January 2017

DOI: https://doi.org/10.7180/kmj.2017.32.1.111

A Case of Cardiac Arrest due to Multivessel, Diffuse Coronary Spasm in Moyamoya Disease

Young Min Choi¹, Jung Woo Choi¹, Dong Ho Kang², Choong Hwan Kwak¹, Jin Yong Hwang¹, Jin Sin Koh¹

¹Division of Cardiology, Department of Internal Medicine, Gyeongsang National University Hospital, Korea

²Department of Neurosurgery, Gyeongsang National University, School of Medicine, Korea

Corresponding Author: Jin Sin Koh, Division of Cardiology, Department of Internal Medicine, Gyeongsang National University Hospital, 79, Gangnam-ro, Jinju-si, Gyeongsangnam-do, 52727, Korea Tel: +82-55-750-8873, Fax: +82-55-758-9122, E-mail address: kjs0175@gmail.com

Received 20 August 201530 September 2015 Accepted 26 October 2015

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Moyamoya disease is characterized by progressive stenosis of the distal portion of the internal carotid arteries and fragile collateral vessels in the brain. The precise pathogenesis is still not known. Although extracranial vessel involvement is very rare, coronary arterial involvement has recently been reported. Here, we report a case of diffuse, multivessel coronary spasm leading to cardiac arrest and myocardial infarction in a 47-year-old man with moyamoya disease with no underlying emotional or physical stress.

Keywords: Moyamoya disease, Stress-induced cardiomyopathy, Sudden cardiac death

REFERENCES

1.Scott RM., Smith ER. Moyamoya disease and moya-moya syndrome. N Engl J Med. 2009. 360:1226–37.

2.Ikezaki K., Kono S., Fukui M. Etiology of moya-moya disease. Pathology, pathophysiology, and genetics in moyamoya disease. Ikezaki K, Loftus CM, editors. editors.Moyamoya disease. New York: Rolling Meadows;2001. p. 55–64.

3.Lee JH., Youn TJ., Yoon YE., Park JJ., Hong SJ., Chun EJ, et al. Coronary artery stenosis in Moyamoya disease: tissue characterization by 256-slice multi-detector CT and virtual histology. Circulation. 2013. 127:2063–5.

4.Choi W., Kim YN., Kim KH. Variant angina in moyamoya disease--a correlative etiology and different presentation: a case report. J Med Case Rep. 2015. 9:86.

5.Prasad A., Lerman A., Rihal CS. Apical ballooning syndrome (Tako-Tsubo or stress cardiomyopathy): a mimic of acute myocardial infarction. Am Heart J. 2008. 155:408–17.

6.Akashi YJ., Nef HM., Lyon AR. Epidemiology and pathophysiology of Takotsubo syndrome. Nat Rev Cardiol. 2015. 12:387–97.

7.Deepika A., Reddy M., Shukla D. Paroxysmal sympathetic hyperactivity in a child with moyamoya disease. J Neurosurg Anesthesiol. 2014. 26:87–8.

Fig. 1

Cerebral angiogram after injection of contrast demonstrates stenosis in both internal carotid arteries, with net-like collaterals (black arrow) typical for moyamoya disease.

Fig. 2

Local hospital ECG 3 years ago for acute chest pain showed ST elevation in leads Ⅱ, Ⅲ, aVF, and V2-V6 (A). ECG after electro-cardioversion: the irregular rhythm converted to sinus rhythm with ST elevation in Ⅰ, Ⅱ, Ⅲ, and V2-6, with frequent ventricular premature complexes (B). Follow-up ECG 5 days later showed ST resolution in Ⅰ, Ⅱ, Ⅲ, and V2-6, and Q waves in V1-5 (C).

Fig. 3

Echocardiography demonstrated akinesis in the entire mid- to apical segments of the left ventricular (LV) wall, with severe LV dysfunction (LV ejection fraction 25%) and mild apical dilatation (white arrow), which suggest stress induced cardiomyopathy (A: systolic phase, B: diastolic phase). Follow up echocardiography demonstrated true apical akinesis, and hypokinesis of the apical anterior septum and anterior LV wall, with improved LV function; LV ejection fraction 45% (C: systolic phase, D: diastolic phase).

Fig. 4

Angiography reveals diffuse spasm of the right (A) and left (B) coronary arteries (black arrow). After intracoronary nitroglycerin injection, spasm was relieved in both coronary arteries (C, D).

Fig. 5

Cardiac magnetic resonance imaging showed subendocardial perfusion defects in the septum, anterior wall, apex, and inferior and lateral walls (A,B), and late enhancement in the same territories (C,D).

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