International Journal of Cardiology 186 (2015) 144–145

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International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard

Letter to the Editor

Acute myocardial infarction in a young woman with rheumatoid arthritis Yong Zhang, Lijing Zhang ⁎, Xian Wang, Liang Zheng, Jie Lv, Wei Zhang, Huaibing Zhao Dongzhimen Hospital, The First Affiliated Hospital of Beijing University of Chinese Medicine, Beijing 100700, China

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Article history: Received 28 January 2015 Accepted 7 March 2015 Available online 20 March 2015 Keywords: Acute myocardial infarction Rheumatoid arthritis Young woman

A 27-year-old Chinese woman was admitted for an episode of prolonged chest pain, accompanied by sweating and nausea for 5 h. Her blood pressure was 110/70 mm Hg symmetrical over both arms and her pulse was 70 beats/min. Her physical examination was normal. The electrocardiogram showed sinus rhythm with ST-segment elevation in leads V1–V5. The laboratory data revealed a cardiac troponin I of 0.9 ng/ml (relative index b 0.02 ng/ml), a creatine kinase MB of 146.0 ng/ml (relative index b 7.0 ng/ml), and a myoglobin of 682.0 ng/ml (relative index b 112.0 ng/ml). Acute myocardial infarction (AMI) was strongly suspected and coronary angiography was performed. The result revealed smooth angiographic appearance except for a total occlusion in the proximal segment of the left anterior descending artery and TIMI grade 0 flow (see Fig. 1). A 3.5 × 30 mm resolute RX drug-eluting stent was implanted and subsequently postdilated with an excellent final angiographic result (see Fig. 2). The percutaneous coronary intervention was successfully performed without any complications. The patient was afterward transferred into the coronary care unit and was treated accordingly before she was discharged 10 days later. The patient had been diagnosed of rheumatoid arthritis (RA) and treated with hydroxychloroquine sulfate (200 mg once a day) and prednisone (5 mg once every other day) for more than 10 years. She had regular menstruation period and was not pregnant. She had no history of smoking, drinking, or family history of coronary artery disease. Her temperature, heart rate, blood pressure and body mass index were normal. The chest X-ray and CT, abdominal and gynecological ultrasound examinations were also normal. Carotid and limbs' arteriovenous ⁎ Corresponding author at: Coronary Care Unit, Dongzhimen Hospital, Beijing 100700, China. E-mail address: [email protected] (L. Zhang).

http://dx.doi.org/10.1016/j.ijcard.2015.03.291 0167-5273/© 2015 Elsevier Ireland Ltd. All rights reserved.

ultrasound examinations revealed smooth appearance. Her echocardiographic examination revealed segmental wall motion abnormalities and an estimated left ventricular ejection fraction of 50%. Other laboratory data including blood and urine routines, blood lipid and glucose, renal and liver function tests, coagulation factors, and electrolytes were within normal range. Further tests revealed nothing special in erythrocyte sedimentation rate, female hormones, thyroid function, and tumor markers. Studies for immunoglobulin (IgM, IgA, IgE, and IgG), antiphospholipid antibodies, vasculitis antibodies, complement (C3 and C4), antistreptolysin O, and circulating lupus anticoagulant. The only positive results were an increased rheumatoid factor (RF) of 110.0 IU/ml (relative index b 15 IU/ml), an increased C-reactive protein (CRP) of 51.4 mg/l (relative index b 10 mg/l), and a positive titer of the antinuclear antibodies (ANA) were also negative. What made this case unique was that the patient was a young woman and revealed no conventional risk factors of AMI. Previous studies demonstrated that the main risk factors for young adults with AMI included smoking, hyperlipidemia, family history of coronary artery disease, hypertension, diabetes mellitus, and obesity [1,2]. But all of these risk factors were excluded in our patient. Consistent with her history of RA and treatment with hydroxychloroquine sulfate and prednisone, we found positive results in RF, ANA and CRP in the search of possible causes for the occurrence of her AMI. Thus, we believe that RA and its medication may potentially play a role in the development of AMI in this young woman. A recent retrospective cohort study indicated that the incidence of AMI in patients with RA was increased by 38% compared to the general population [3]. This increased incidence is predominantly due to endothelial dysfunctions, atherosclerosis, cardiomyopathies, pericarditis, valvular diseases, arrhythmias, and other complications. It is believed that RA confers a prothrombotic state featured by abnormalities in coagulation and fibrinolytic systems, together with an altered state of platelet reactivity. Furthermore, chronic inflammation induced by RA can promote endothelial cell activation and vascular dysfunction which may explain the reason of the occurrence of AMI in RA patients. However, in the present case, various laboratory tests were done to detect a possible prothrombotic risk factor but without any significant results and there were not any findings to support a hypercoagulable state. In addition, the remainder of the coronary artery system was smooth and without any signs of atherosclerosis. Given that she had a medical history of RA for more than 10 years, we speculated that the reason could be explained that she was not in the active period of RA. As for RA clinical manifestations, the young woman revealed only slight tumidness in the interphalangeal joint of her right middle finger and a 10 angle limitation of dorsiflexion in her right wrist. She scored only

Y. Zhang et al. / International Journal of Cardiology 186 (2015) 144–145

Fig. 1. Coronary angiography showing a total occlusion in the proximal segment of the left anterior descending artery.

2.56 according to the disease activity scores in 28 joints (DAS28) which indicated the level of clinical remission of her RA activity. A recent case report described a premenopausal woman with RA who was diagnosed as having large right and left ventricular thrombus and myocardial infarction. She also revealed no prothrombotic risk factors and no findings were found to explain her hypercoagulable state [4]. The authors proposed that RA itself was responsible for the cardiovascular event. RA medication may also be responsible for the occurrence of AMI in this case. Our patient had been taking hydroxychloroquine sulfate and prednisone for more than 10 years. It has been reported that hydroxychloroquine could decrease cardiovascular risk by lowering total cholesterol levels. However, a previous study demonstrated that, regardless of RA clinical manifestations, glucocorticoid exposure was associated with carotid plaque and atherosclerosis which may lead to cardiovascular diseases in RA patients [5]. Another recent study also confirmed that immediate and past cumulative effects of glucocorticoids were associated with an increased risk of myocardial infarction in RA patients [6]. In conclusion, we report a rare case of an AMI solely associated with RA and its medications. Our case suggests that, for young patients whose AMI cannot be explained with the conventional risk factors, RA and its medications may serve as possible risk factors of AMI related to non-atherosclerotic processes. However, information in this regard

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Fig. 2. Final angiographic result after percutaneous coronary intervention.

is scarce and further studies are still in need to unravel the underlying pathophysiology. Conflict of interest All authors cared for the patient and written consent to publish was obtained from the patient. The authors report no relationships that could be construed as a conflict of interest. References [1] J. Huang, H.Y. Qian, Z.Z. Li, J.M. Zhang, Comparison of clinical features and outcomes of patients with acute myocardial infarction younger than 35 years with those older than 65 years, Am. J. Med. Sci. 346 (1) (2013) 52–55. [2] C.P. Wong, S.Y. Loh, K.K. Loh, P.J. Ong, D. Foo, H.H. Ho, Acute myocardial infarction: clinical features and outcomes in young adults in Singapore, World J. Cardiol. 4 (6) (2006) 206–210. [3] W.S. Chung, C.L. Lin, C.L. Peng, Y.F. Chen, C.C. Lu, F.C. Sung, C.H. Kao, Rheumatoid arthritis and risk of acute myocardial infarction — a nationwide retrospective cohort study, Int. J. Cardiol. 168 (5) (2013) 4750–4754. [4] E. Acikgoz, C. Yayla, S.K. Acikgoz, A. Sahinarslan, Biventricular thrombus and associated myocardial infarction in a rheumatoid arthritis patient: a case report and literature review, Clin. Rheumatol. 32 (6) (2013) 909–912. [5] I. del Rincon, D.H. O'Leary, R.W. Haas, A. Escalante, Effect of glucocorticoids on the arteries in rheumatoid arthritis, Arthritis Rheum. 50 (12) (2004) 3813–3822. [6] J.A. Avina-Zubieta, M. Abrahamowicz, M.A. De Vera, H.K. Choi, E.C. Sayre, M.M. Rahman, M.P. Sylvestre, W. Wynant, J.M. Esdaile, D. Lacaille, Immediate and past cumulative effects of oral glucocorticoids on the risk of acute myocardial infarction in rheumatoid arthritis: a population-based study, Rheumatology (Oxford) 52 (1) (2013) 68–75.

Acute myocardial infarction in a young woman with rheumatoid arthritis.

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