Coronary artery stenting in acute coronary syndrome associated with giant cell arteritis

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JCCASE-854; No. of Pages 5 Journal of Cardiology Cases xxx (2017) xxx–xxx

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Case Report

Coronary artery stenting in acute coronary syndrome associated with giant cell arteritis Lillian Armellin (MD)a,*, Anthony Michael Sammel (MBBS)b, Ben Ng (BSc, MBBS, FRACP)a, Kiran Sarathy (MBBS)b, John Lambros (MBBS, FRACP, DDU, FCSANZ)b, Taraneh Amir-Nezami (MD)b, Shannon Dean Thomas (MBBS, FRACS)b, John Highton (MD, FRACP)c, Arvin Damodaran (BSc, MBBS, MMedEd, FRACP)a a

Prince of Wales Clinical School, University of New South Wales, Sydney, Australia Prince of Wales Hospital, University of New South Wales, Sydney, Australia c University of Otago, Dunedin, New Zealand b

A R T I C L E I N F O

A B S T R A C T

Article history: Received 7 February 2017 Received in revised form 15 May 2017 Accepted 22 May 2017

Coronary vasculitis is a rare but devastating complication of giant cell arteritis, otherwise known as temporal arteritis. Originally named for its propensity to attack the superficial temporal arteries, it is now recognized that it commonly involves a number of medium and large arteries throughout the body. Here we describe two cases of giant cell arteritis affecting the coronary arteries, one discovered at postmortem and one which was successfully treated with immunosuppressive therapy and drug-eluting coronary stents. © 2017 Japanese College of Cardiology. Published by Elsevier Ltd. All rights reserved.

Keywords: Giant cell arteritis Coronary artery disease Coronary stenting

Introduction Giant cell arteritis (GCA), also known as temporal arteritis, is a medium to large vessel vasculitis affecting people over the age of 50 years. While it classically has a predilection for the temporal arteries, computed tomographic (CT) angiography has demonstrated involvement of other large arteries (particularly aorta, brachiocephalic trunk, carotid arteries, subclavian arteries, and femoral arteries) in up to two thirds of patients [1]. Coronary arteritis has classically been associated with medium and small vessel vasculitis such as Kawasaki disease and is a potential and known complication of Takayasu arteritis. However, there are a few reports of coronary arteritis caused by GCA, most of which were in the context of fatal myocardial infarctions, with autopsy evidence of coronary GCA [2]. GCA involving the coronary arteries has been treated with bare metal stents [3]. Stenting has

also been used successfully in GCA affecting the subclavian, axillary, brachial, renal [4], and vertebral arteries [5]. Here we describe two cases of critical coronary artery stenosis in acute GCA, one which was only discovered at post-mortem, and one which is the first case reported to have been effectively revascularized with drug-eluting stents. Case A An elderly woman had a sudden death in the community which was referred to the coroner. Upon post-mortem, the aorta had ruptured, resulting in hemopericardium and cardiac tamponade. The aorta, coronary arteries, and pulmonary arteries demonstrated granulomatous inflammatory skip lesions and giant cells, consistent with GCA (Fig. 1a). Case B

* Corresponding author at: Prince of Wales Hospital, Barker St., Randwick, NSW 2031, Australia. Fax: +61 2 9382 4748. E-mail address: [email protected] (L. Armellin).

A 76-year-old woman presented to her ophthalmologist in November 2015 with a 3-week history of transient left-sided vision loss associated with headache, jaw claudication, weight loss, and

http://dx.doi.org/10.1016/j.jccase.2017.05.008 1878-5409/© 2017 Japanese College of Cardiology. Published by Elsevier Ltd. All rights reserved.

Please cite this article in press as: Armellin L, et al. Coronary artery stenting in acute coronary syndrome associated with giant cell arteritis. J Cardiol Cases (2017), http://dx.doi.org/10.1016/j.jccase.2017.05.008

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Fig. 1.

Pathology of Patient A’s coronary artery (a) and Patient B’s temporal artery (b). (1) Partial lumen occlusion. (2) Intimal fibroplasia. (3) Disrupted internal elastic lamina. (4) Histocytes and lymphocytes.

neck stiffness. She had a past medical history of hyperlipidemia, multinodular goiter, vitiligo, intermittent supraventricular tachycardia, and minor non-obstructive coronary artery disease, which had been diagnosed on an angiogram in 2013 when she had presented with atypical chest pain. She denied a history of stroke, hypertension, diabetes, or smoking but reported limited mobility due to bilateral lower limb claudication type pain which she had been experiencing for the past few months at a distance of 200 m. Medications prior to presentation were aspirin 100 mg daily, sotalol 40 mg twice daily, and rosuvastatin 5 mg daily. Examination that day was suspicious for left retinal artery embolus and she was referred for urgent cardiology review for suspected atrial fibrillation. At this stage, electrocardiogram (ECG) showed normal sinus rhythm with no evidence of ischemia or previous infarction and transthoracic echocardiogram (TTE) was normal. Erythrocyte sedimentation rate and C-reactive protein were elevated to 59 mm/h (normal range 1–35 mm/h) and 58.9 mg/L (normal range 0.0–5.0 mg/L), respectively and she was commenced on oral prednisone 50 mg daily for possible GCA. Over the subsequent two days, she experienced intermittent chest and neck pain which was attributed to gastro-oesophageal reflux in the context of prednisone use. She was admitted to hospital two days after initial cardiology review for a transesophageal echocardiogram looking for an intracardiac source of embolus. Unexpectedly, this showed marked anterior left ventricular wall hypokinesis, consistent with recent ischemia. There were corresponding new deep anterior Q waves on ECG (Fig. 2a). Urgent coronary angiography showed 90% stenoses of the proximal left anterior descending (LAD) and large caliber intermediate arteries, 70% stenosis of the mid right coronary artery, and 30% stenosis of the left main artery. The appearances were suggestive of widespread vasospasm but were unresponsive to intra-arterial glyceryl trinitrate. This was in stark comparison to an angiogram performed 2 years previously, where she had only

30% stenosis of the mid-LAD and mild irregularity of the remaining vessels. Troponin T was elevated at 353 ng/L (normal range <14 ng/ L). Given the rapid progression of disease in the absence of other risk factors for cardiovascular disease, the possibility of superimposed coronary vasculitis was raised. Due to the complexity of the coronary anatomy, initial resolution of symptoms on medical therapy, confounding comorbidities and potential for requiring surgical intervention, the decision was made to defer an attempt for percutaneous revascularization, pending further discussion. She was commenced on medical therapy for presumed missed ST-elevation myocardial infarction (STEMI) with aspirin, clopidogrel, and a heparin infusion and pulsed with intravenous methylprednisolone 1 g daily for 3 days. Further examination revealed palpable strong femoral pulses with absent popliteal and pedal pulses on both lower limbs, a left axillary bruit, a blood pressure gradient of 14 mmHg between arms, delayed radial pulse on the left, and bilateral tender temporal arteries. The following evening, she developed acute chest discomfort and ECG showed ST elevation in the anterior leads (Fig. 2b). She underwent primary percutaneous coronary intervention (PCI) with drug-eluting stents to the ostial LAD (3.0  20 mm Synergy, Boston Scientific, Marlborough, MA, USA), the proximal intermediate (2.75  8 mm Xience Xpedition, Abbott Vascular, Santa Clara, CA, USA), and the ostial circumflex (3.25  8 mm Xience Xpedition) (Fig. 3) arteries. A tirofiban infusion was commenced and an intra-aortic balloon pump inserted for peri-procedural hemodynamic support. Post-procedural TTE 4 days later showed complete normalization of left ventricular function. She was transitioned to 60 mg daily of oral prednisone and 10 mg weekly of oral methotrexate. Inflammatory markers normalized, ECG changes resolved (Fig. 2c) she had no further chest pain, and subsequent ophthalmology examination was normal.

Please cite this article in press as: Armellin L, et al. Coronary artery stenting in acute coronary syndrome associated with giant cell arteritis. J Cardiol Cases (2017), http://dx.doi.org/10.1016/j.jccase.2017.05.008

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Fig. 2.

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Patient B’s electrocardiograms from hospital admission. (a) Upon presentation to hospital. (b) During ST-elevation myocardial infarction. (c) Shortly before discharge from hospital.

A temporal artery biopsy performed 13 days after initial presentation was consistent with GCA with histopathological features of partial lumen occlusion, intimal fibroplasia, disrupted internal elastic lamina, multinucleated giant cells, and a cellular infiltrate consisting of histocytes and lymphocytes (Fig. 1b). Subsequent CT angiography revealed typical vasculitic changes

of beading and multifocal stenotic lesions involving the left subclavian, right vertebral, bilateral superficial femoral, and popliteal arteries (more severe on the right side) with mild disease at the origin of profunda femoris. At 12-month follow up she remained on methotrexate 20 mg weekly, prednisone 5 mg daily, folic acid 10 mg weekly, aspirin/

Please cite this article in press as: Armellin L, et al. Coronary artery stenting in acute coronary syndrome associated with giant cell arteritis. J Cardiol Cases (2017), http://dx.doi.org/10.1016/j.jccase.2017.05.008

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Fig. 3.

Patient B’s coronary angiography with radiographic projections labelled. (a) Coronary angiogram prior to GCA. (b) Upon presentation to hospital, 3 weeks after onset of typical GCA symptoms. (c) During STEMI pre-PCI. (d) Post PCI. GCA, giant cell arteritis; LAD, left anterior descending artery; LAO, left anterior oblique; PCI, percutaneous coronary intervention.

clopidogrel 100/75 mg daily, bisoprolol 5 mg daily, and ezetimibe/ atorvastatin 10/40 mg daily. She has had no further coronary events. CT coronary angiography (CTCA) in April 2016 showed patent stents (Fig. 4). In the absence of ischemic rest pain or tissue loss, her lower limb claudication symptoms have been managed conservatively, and have continued to improve. Discussion Coronary GCA is a rare but potentially lethal condition. In an older patient with acute cardiovascular disease in conjunction with raised inflammatory markers or clinical features of GCA, coronary arteritis should be considered. Conversely, in a patient with known GCA, clinicians need to consider coronary vasculitis in the differential diagnosis for new-onset cardiac symptoms. While Case A unequivocally demonstrates that GCA can involve the coronary arteries, to date, the literature is inconclusive on any population-wide association between GCA and cardiovascular disease. Being a rare condition, it is difficult to adequately power prospective studies for cardiovascular endpoints. Studies by Ray et al. and Tomasson et al. have suggested an increased risk in GCA of myocardial infarction (MI), stroke, aortic dissection/aneurysm, and peripheral vascular disease, possibly either due to the vasculitis directly attacking the coronary, cerebral or peripheral circulation, or a generalized inflammatory state accelerating the underlying atherosclerosis [6,7]. However, a systematic review of 6 studies by Ungprasert et al. in 2015 was unable to demonstrate any statistically increased risk of coronary artery disease with GCA, but the analysis had high statistical heterogeneity (I2 = 97%),

mostly due to differences in the definition of coronary artery disease [8]. Patients with GCA are also an older population with a higher baseline risk of coronary atherosclerosis. Furthermore, corticosteroid treatment may play an independent role in increasing cardiovascular risk via inducing hyperlipidemia, hypertension, and hyperglycemia, or could theoretically also lower the risk due to anti-inflammatory effects [8]. Case B is the first case to demonstrate that primary PCI with drug-eluting stents can be used to successfully revascularize coronary vessels in acute GCA even in the context of complex anatomy. The normalization of left ventricular wall motion post intervention, which successfully reperfused the LAD and circumflex territories, is also consistent with a component of myocardial stunning rather than widespread infarction. We believe the patient’s coronary lesions likely represent longstanding atherosclerotic plaque with superimposed vasculitic inflammation, similar to a case published in 2007 of an 83-yearold woman who unexpectedly died during corticosteroid treatment for GCA and was discovered on autopsy to have coexisting atherosclerosis and GCA of the coronary arteries [9]. While impossible to prove without autopsy, the rapid progression of lesions in two years since previous coronary angiogram, histopathological evidence of active arteritis on temporal artery biopsy and characteristic vasculitic angiographic changes in subclavian, vertebral, and femoral arteries, as well as the patient’s relative paucity of cardiovascular risk factors, argues against this being a purely atherosclerotic process. Furthermore, although coronary atherosclerosis is common in the elderly, Case B’s CTCA after nearly 6 months demonstrated not only stent patency, but a calcium score

Please cite this article in press as: Armellin L, et al. Coronary artery stenting in acute coronary syndrome associated with giant cell arteritis. J Cardiol Cases (2017), http://dx.doi.org/10.1016/j.jccase.2017.05.008

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for bypass procedures. These high rates possibly argue for a trial of medical therapy and early institution of immunosuppression in the absence of acute end-organ ischemia. Our experience with Case B with the absence of coronary events out to 12 months post revascularization suggest that drug-eluting stents may be effective in both the short and longer-term treatment of unstable acute coronary GCA in conjunction with immunosuppression. Conflict of interest None. Acknowledgment We would like to acknowledge Professor Han-Seung Yoon, Professor of Medicine (Pathology), Nagoya Medical Centre, Department of Pathology, Japan, who kindly provided the pathology slides for Patient A. References

Fig. 4.

Images from computed tomography coronary angiogram April 2016 showing patency of stents. (a) Left anterior descending (LAD) and intermediate stents. (b) LAD and circumflex (Cx) stents.

of only 21 Agatston units. According to the Multi-Ethnic Study of Atherosclerosis coronary artery calcium score reference values, this places her in the lower 34th percentile for her age and sex [10]. There are limited data to predict in-stent thrombosis and restenosis rates for GCA, however studies of vascular interventions in Takayasu arteritis [11] point to rates of long-term restenosis or occlusion as high as 78% for angioplasty including stents and 36%

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Please cite this article in press as: Armellin L, et al. Coronary artery stenting in acute coronary syndrome associated with giant cell arteritis. J Cardiol Cases (2017), http://dx.doi.org/10.1016/j.jccase.2017.05.008