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 Table of Contents  
CASE REPORT
Year : 2018  |  Volume : 2  |  Issue : 2  |  Page : 57-59

Cardiogenic shock from acute myocardial infarction induced by large-vessel Arteritis


1 Shenzhen Research Institute of Shandong University, Shenzhen, Guangdong; Department of Radiology, Shandong University Qilu Hospital, Jinan, Shandong, China
2 Shenzhen Research Institute of Shandong University, Shenzhen, Guangdong; Department of Cardiology, Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese National Health Commission and Chinese Academy of Medical Sciences, Shandong University Qilu Hospital, Jinan, Shandong, China

Date of Web Publication22-Aug-2019

Correspondence Address:
Panpan Hao
Department of Cardiology, Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese National Health Commission and Chinese Academy of Medical Sciences, Shandong University Qilu Hospital, Jinan 250012, Shandong
China
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/hm.hm_15_18

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  Abstract 

Coronary artery involvement in large-vessel arteritis is not uncommon, but rarely fatal. Here, we present a case of a young female with arteritis who was admitted to our hospital with acute myocardial infarction-induced cardiogenic shock. Imaging and laboratory results demonstrate that anticardiolipin antibody-related large-vessel arteritis is a possible cause of coronary ostial stenosis in patients with no other risk factors.

Keywords: Anticardiolipin antibody, arteritis, large vessel, myocardial infarction, ostial stenosis


How to cite this article:
Liu Y, Hao P. Cardiogenic shock from acute myocardial infarction induced by large-vessel Arteritis. Heart Mind 2018;2:57-9

How to cite this URL:
Liu Y, Hao P. Cardiogenic shock from acute myocardial infarction induced by large-vessel Arteritis. Heart Mind [serial online] 2018 [cited 2019 Oct 17];2:57-9. Available from: http://www.heartmindjournal.org/text.asp?2018/2/2/57/265158


  Introduction Top


Large-vessel arteritis is characterized by inflammation due to invasion of the arterial wall by leukocytes.[1] Coronary artery involvement in this disease is not uncommon, but rarely fatal. Herein, we present a case of a young female with large-vessel arteritis who was admitted to our hospital with acute myocardial infarction (AMI)-induced cardiogenic shock.


  Case Report Top


A 23-year-old Chinese woman without medical history was brought to the emergency room after acute chest pain and palpitation developed at rest. Her systolic blood pressure on hospital admission was 69 mmHg. Cardiothoracic examination revealed bilateral fine rales. A 12-lead electrocardiogram showed sinus tachycardia, ST-segment elevation in lead aVR, and ST-segment depression in leads I, II, III, aVF, and V2 through V6 [Figure 1]a. Serum concentration of cardiac troponin I was 0.98 ng/mL. Initial assessment of the patient suggested the possibility of cardiogenic shock from AMI. Because of the profound hemodynamic instability, she was immediately transferred for cardiac catheterization. Urgent coronary angiography revealed isolated bilateral coronary ostial stenoses without thrombus [Figure 1]b and [Figure 1]c. An intra-aortic balloon pump was used to provide hemodynamic support, and then, a stent was deployed at the ostium of the left main coronary artery [Figure 1]d and the right coronary artery [Figure 1]e, respectively.
Figure 1: (a) Urgent 12-lead electrocardiogram. (b) Urgent angiography for the left main coronary, the left anterior descending artery, and the left circumflex artery. (c) Urgent angiography for the right coronary artery. (d) Angiography for the left main coronary, the left anterior descending artery, and the left circumflex artery after stenting. (e) Angiography for the right coronary artery after stenting

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Computed tomography (CT) arteriography revealed no obvious abnormalities of the main arteries of the thorax and abdomen [Video 1]. Serum anticardiolipin immunoglobulin G (IgG) and IgM antibodies were moderately elevated. Anticardiolipin IgG was at a concentration of 31 IgG phospholipid units (<14 is considered negative), and IgM was at a concentration of 36 IgM phospholipid units (<12 is considered negative). However, levels of other autoimmune biomarkers were within normal ranges, including high-sensitivity C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), antineutrophil cytoplasmic antibodies, antinuclear antibodies, anti-double-stranded DNA, lupus anticoagulants, and anti-beta 2 glycoprotein 1 antibodies. She was discharged home on a regimen of aspirin, clopidogrel, and prednisone. During a 3-year follow-up, no other autoimmune diseases or complications of antiphospholipid antibodies occurred in this patient.





  Discussion Top


Imaging and laboratory results demonstrate that anticardiolipin antibody-related large-vessel arteritis is a possible cause of coronary ostial stenosis in patients with no other risk factors. Large-vessel arteritis is frequent in younger females and is characterized by infiltration of the arterial wall by mononuclear cells and/or multinucleated giant cells, leading to concentric medial hyperplasia, fibrosis, stenosis, and/or even occlusion.[1] Takayasu arteritis (TA), one chronic vessel inflammation predominantly involving the aorta and its main branches, is mostly seen in females in the second or third decade of life, whereas giant cell arteritis (GCA), which has a predilection for cranial vessels, almost exclusively strikes people over age 50 years.[2]

In our present case, this female fell into cardiogenic shock and was rescued by the combination of intra-aortic balloon pump counterpulsation with reperfusion therapy. We ruled out other causes of the shock other than AMI at the trunk lesion. The early detection and diagnosis of large-vessel arteritis before progression to such a severe condition are important. Large-vessel arteritis is diagnosed according to clinical presentation, imaging, laboratory values, and arterial biopsy. Patients usually present with focal symptoms induced by end-organ ischemia related to the vessels affected by stenotic or occlusive lesions, as well as constitutional complaints, including fever, malaise, and anorexia.[3] Both TA and GCA have been reported to involve the coronary arteries and aggravate atherosclerosis, and these patients tend to present with symptomatic myocardial ischemia.[4]

Early diagnosis of large-vessel arteritis is difficult since it is a rare disease and is accompanied by various nonspecific clinical symptoms. However, recent advances in noninvasive imaging modalities, including magnetic resonance angiography, CT angiography, sonography, and fluorodeoxyglucose positron emission tomography (FDG-PET)/CT, have facilitated earlier and more accurate diagnoses of this condition.[5] Arterial wall thickening with crescents and indistinct vascular borders are almost exclusively displayed in CT and magnetic resonance angiography.[6] Coronary artery involvement is not uncommon and most frequently includes the ostia and proximal segment,[7] as in our case. Sonography and FDG-PET/CT are useful in evaluating active inflammation in the arteries involved.[8],[9] As conventional invasive angiography has limited ability to detect arterial wall inflammation and remodeling, intracoronary imaging with intravascular ultrasound or optical coherence tomography might be required.[6] ESR and CRP levels should be used for initial testing, with a sensitivity of 99% when taken in combination.[10] Other autoimmune biomarkers may be nonspecific elevated as well. In line with our patient, ESR and CRP were normal in some case reports of arteritis patients; thus, treatment should not be withheld when a patient is under high clinical suspicion of this disease.

Given the high mortality rate associated with severe stenosis and occlusion, revascularization is recommended, but the procedure modality has a great impact on the prognosis. Surgical bypasses exhibit better outcomes than percutaneous interventions, which are frequently burdened with postoperative complications, including restenosis, stent detachment, new arterial lesions, and so on.[11] Therefore, it is crucial that disease activity is controlled with adequate immunosuppressive treatments, regardless of revascularization or not.[12] Finally, a long-term follow-up is mandatory for all these young patients.

Predicting outcome of patients with this disease is challenging due to the large variation in the course. The presence of a major complication and/or a progressive course might be indicators of poor prognosis.[13] Recently, type V angiographic classification was identified as an independent predictive factor for disease activity.[14] Nevertheless, data regarding long-term prognosis are lacking.

Concluding remarks

Coronary artery involvement in arteritis is not uncommon, but rarely fatal. Anticardiolipin antibody-related large-vessel arteritis is a possible cause of coronary ostial stenosis in patients with no other risk factors.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

This work was supported by the Shenzhen Science and Technology Research and Development Fund (No. JCYJ20160331183804137) and the Planned Science and Technology Project of Guangdong Province (No. 2017A020215005).

Conflicts of interest

There are no conflicts of interest.

 
  References Top

1.
Ozen S, Batu ED. Vasculitis pathogenesis: Can we talk about precision medicine? Front Immunol 2018;9:1892.  Back to cited text no. 1
    
2.
Espígol-Frigolé G, Planas-Rigol E, Lozano E, Corbera-Bellalta M, Terrades-García N, Prieto-González S, et al. Expression and function of IL12/23 related cytokine subunits (p35, p40, and p19) in giant-cell arteritis lesions: Contribution of p40 to Th1-and Th17-mediated inflammatory pathways. Front Immunol 2018;9:809.  Back to cited text no. 2
    
3.
Humayun MA, Masood A, Waseem T, Ahmad F, Raza T. An unusual cause of stroke in a young female. Am J Emerg Med 2014;32:685.e3-5.  Back to cited text no. 3
    
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Rav-Acha M, Plot L, Peled N, Amital H. Coronary involvement in Takayasu's arteritis. Autoimmun Rev 2007;6:566-71.  Back to cited text no. 4
    
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Misra DP, Naidu GS, Agarwal V, Sharma A. Vasculitis research: Current trends and future perspectives. Int J Rheum Dis 2019;22 Suppl 1:10-20.  Back to cited text no. 5
    
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Keser G, Aksu K. Diagnosis and differential diagnosis of large-vessel vasculitides. Rheumatol Int 2019;39:169-85.  Back to cited text no. 6
    
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Cavalli G, Tomelleri A, Di Napoli D, Baldissera E, Dagna L. Prevalence of Takayasu arteritis in young women with acute ischemic heart disease. Int J Cardiol 2018;252:21-3.  Back to cited text no. 7
    
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Versari A, Pipitone N, Casali M, Jamar F, Pazzola G. Use of imaging techniques in large vessel vasculitis and related conditions. Q J Nucl Med Mol Imaging 2018;62:34-9.  Back to cited text no. 8
    
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Braun J, Baraliakos X, Fruth M. The role of 18F-FDG positron emission tomography for the diagnosis of vasculitides. Clin Exp Rheumatol 2018;36 Suppl 114:108-14.  Back to cited text no. 9
    
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Parikh M, Miller NR, Lee AG, Savino PJ, Vacarezza MN, Cornblath W, et al. Prevalence of a normal C-reactive protein with an elevated erythrocyte sedimentation rate in biopsy-proven giant cell arteritis. Ophthalmology 2006;113:1842-5.  Back to cited text no. 10
    
11.
Saadoun D, Lambert M, Mirault T, Resche-Rigon M, Koskas F, Cluzel P, et al. Retrospective analysis of surgery versus endovascular intervention in Takayasu arteritis: A multicenter experience. Circulation 2012;125:813-9.  Back to cited text no. 11
    
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Luqmani RA. State of the art in the treatment of systemic vasculitides. Front Immunol 2014;5:471.  Back to cited text no. 12
    
13.
Ishikawa K, Maetani S. Long-term outcome for 120 Japanese patients with Takayasu's disease. Clinical and statistical analyses of related prognostic factors. Circulation 1994;90:1855-60.  Back to cited text no. 13
    
14.
Hong S, Bae SH, Ahn SM, Lim DH, Kim YG, Lee CK, et al. Outcome of Takayasu arteritis with inactive disease at diagnosis: The extent of vascular involvement as a predictor of activation. J Rheumatol 2015;42:489-94.  Back to cited text no. 14
    


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