Successful coronary intervention for spontaneous coronary dissection in a patient with fibromuscular dysplasia

Successful coronary intervention for spontaneous coronary dissection in a patient with fibromuscular dysplasia

Journal of Cardiology Cases 8 (2013) 158–160 Contents lists available at www.sciencedirect.com Journal of Cardiology Cases journal homepage: www.els...

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Journal of Cardiology Cases 8 (2013) 158–160

Contents lists available at www.sciencedirect.com

Journal of Cardiology Cases journal homepage: www.elsevier.com/locate/jccase

Case Report

Successful coronary intervention for spontaneous coronary dissection in a patient with fibromuscular dysplasia Atsuko Uema (MD), Masaru Araki (MD) ∗ , Shinjo Sonoda (MD, FJCC), Akiyoshi Shimizu (MD), Kuninobu Kashiyama (MD), Yoshitaka Muraoka (MD), Yoshiyuki Suzuki (MD), Fumihiko Kamezaki (MD), Yuki Tsuda (MD), Masaaki Takeuchi (MD, FJCC), Masahiro Okazaki (MD, FJCC), Yutaka Otsuji (MD, FJCC) Department of Cardiology and Renal Medicine, University of Occupational and Environmental Health, 1-1 Iseigaoka, Yahatanishi-ku, Kitakyushu 807-8556, Japan

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Article history: Received 4 May 2013 Received in revised form 3 July 2013 Accepted 25 July 2013 Keywords: Spontaneous coronary artery dissection Fibromuscular dysplasia Myocardial infarction Intravascular ultrasound

a b s t r a c t Spontaneous coronary artery dissection (SCAD) is a reported rare cause of acute coronary syndrome (ACS) and sudden death among middle-aged women. Some institutes have recently reported fibromuscular dysplasia (FMD) concomitant with SCAD. Therefore, a survey of the presence of comorbid FMD in SCAD patients is important to obtain a definitive diagnosis and for the prediction of possible SCAD recurrence. The optimal treatment of ACS due to SCAD remains undetermined, and technical failures are frequently encountered in primary percutaneous coronary intervention (PCI) owing to the unusual nonatherosclerotic cause of the disease. We report a case of SCAD successfully treated with cutting balloon PCI under intravascular ultrasound guidance without stent implantation, in which FMD was detected in the right external iliac artery through screening by noncoronary angiography, not duplex ultrasound. © 2013 Japanese College of Cardiology. Published by Elsevier Ltd. All rights reserved.

Introduction Spontaneous coronary artery dissection (SCAD) is a reported rare cause of acute coronary syndrome (ACS). Although >400 cases and reviews on SCAD have been published on Medline, the existing information on the clinical future, prognosis, and optimal treatment of SCAD is insufficient to provide a better understanding of the disease [1,2]. In addition to the current investigations on the predilection of SCAD for young women without atherosclerosis, recent reports have focused on fibromuscular dysplasia (FMD) concomitant with SCAD [1,3]. These reports indicated that >50% of SCAD patients have FMD formation at the carotid, renal, and iliac arteries, as determined by angiography, suggesting that SCAD is associated with a predisposition of patients to coronary artery FMD, besides vasculitides, coronary spasm, and intense exercise, as reported in previous studies [4–6]. Therefore, a survey of the presence of noncoronary FMD as a causative factor of ACS concomitant with SCAD is important because of the associated high recurrence

∗ Corresponding author. Tel.: +81 93 603 1611; fax: +81 93 691 6913. E-mail address: [email protected] (M. Araki).

of coronary dissection among patients [3]. The optimal treatment of ACS due to SCAD remains undetermined, and technical failures are frequently encountered during primary percutaneous coronary intervention (PCI), even in an institution performing refined PCI [3]. We report a case of SCAD in a patient treated with PCI under intravascular ultrasound (IVUS) guidance, in whom FMD was detected at the right external iliac artery through screening angiography. Case report A 42-year-old woman with a history of hyperlipidemia presented at the emergency department of our hospital with severe chest pain. Before arriving at the hospital, the symptoms had improved. At presentation, no abnormality was observed on an electrocardiogram and blood test results were negative. After 4 days, she returned to our hospital with continuing severe chest pain, this time with ST-segment elevation in the precordial leads of the electrocardiogram. Coronary angiography revealed an occluded mid-left anterior descending coronary artery (LAD) (Fig. 1A). We performed IVUS to distinguish between plaque rupture and SCAD as a cause of acute myocardial infarction. IVUS analysis revealed

1878-5409/$ – see front matter © 2013 Japanese College of Cardiology. Published by Elsevier Ltd. All rights reserved. http://dx.doi.org/10.1016/j.jccase.2013.07.011

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Fig. 1. Coronary angiography revealed a total occlusion of the mid left anterior descending artery (LAD) (+) (A). Initial intravascular ultrasound (IVUS) image of the normal proximal LAD (*corresponding to A) (B). IVUS image showing intramural hematoma in the distal LAD (+ corresponding to A) (C).

a diffuse intramural hematoma ranging from the middle to the distal part of the LAD and an unremarkable atherosclerotic formation (Fig. 1B and C), indicating coronary artery dissection as a pathogenesis of the hematoma. Intracoronary isosorbide dinitrate injection could not improve the LAD obstruction, persistent chest pain, and ST-segment elevation. We performed PCI using a 3.0mm-diameter cutting balloon (Flextome Cutting Balloon; Boston Scientific, Natick, MA, USA) for re-entry to avoid implantation of long and small-diameter stents. After cutting balloon angioplasty,

thrombolysis in myocardial infarction (TIMI) grade 3 flow was detected in the LAD. Oral administration of aspirin, statin, angiotensin receptor antagonist, and beta-blocker was started along with cardiac rehabilitation. Plasma sex hormone levels were within the normal limits, and serum antinuclear antibody titer was low. A computed tomographic angiogram revealed no evidence of carotid artery dissection or FMD. Although noncoronary FMD was not detected by duplex ultrasound, follow-up angiography (day 13) revealed TIMI grade 3 flow in the LAD (Fig. 2A), and FMD formation

Fig. 2. Follow up coronary angiography (day 13) revealed thrombolysis in myocardial infarction grade 3 flow in the left anterior descending artery with dissection (arrow) (A). Aortography showed no fibromuscular dysplasia (FMD) at bilateral renal arteries. No FMD could be identified even in the selective angiography of each renal artery (B). Iliac angiography showed diffuse mild FMD in the right external iliac artery (arrow) (C).

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– mild scalloping of the lumen edge – in the right external iliac artery without involvement of the left external iliac and bilateral renal arteries (Fig. 2B and C). The patient was discharged 14 days after the initial procedure, free from symptoms. Discussion SCAD is a rare but well-known cause of ACS and sudden cardiac death. Although a substantial proportion of SCAD cases have undetermined causes, some underlying conditions have been proposed, such as peripartum state among women, connective tissue disorders, coronary spasm, vasculitides, and intense exercise [2,4–8]. Two institutes have recently reported a possible association between FMD and SCAD. Tweet et al. [3] reported an analysis of 87 SCAD cases, in which they incidentally found FMD of the iliac artery in 8 of 16 femoral angiograms obtained before closure device placement and in the carotid arteries of 2 others with carotid dissection. The incidence of FMD concomitant with SCAD was not so high because of incomplete FMD screening at noncoronary territories. Saw et al. [1] reported FMDs in noncoronary territories (cerebral, renal, and iliac arteries) in 43 of 50 SCAD patients. According to the high comorbidity, they suspected that the SCAD patients had an underlying coronary FMD, which was too subtle to detect by standard angiography or IVUS. Thus, examination for noncoronary FMD is important for the clinical diagnosis and identification of a possible comorbidity such as carotid dissection; otherwise, the pathological mechanism of SCAD should be considered. The present case was of a relatively young woman with no atherosclerotic LAD on IVUS. Although she was young with a major coronary risk factor (high low-density lipoprotein cholesterol level) for developing ACS with atherosclerosis, the presence of FMD in the right external iliac artery detected by screening of the noncoronary territory validated SCAD diagnosis. In this case, duplex ultrasound was unable to detect the FMD, which was evident on angiography, because the FMD formation was subtle and did not display the typical features of medial fibroplasia, such as a “string of beads” appearance or intimal fibroplasia. Although non-invasive screening such as duplex ultrasound is preferable to invasive angiography, catheter-based angiography has been considered the criterion standard for the diagnosis of FMD because ultrasound has disadvantages in terms of evaluating whole arterial structure, such as turbulence, tortuosity, and velocity shift of the distal portion [9]. Therapeutic strategies for ACS caused by SCAD have not been established. The treatment of choice – medication, PCI, or bypass surgery – depends on the extent of coronary artery dissection and the severity of clinical conditions. Tweet et al. [3] reported a high rate (15 of 43 patients) of complications by technical failures in PCI, which may be attributed to the unusual mechanism of ACS. Atherosclerotic etiology and male sex have comparatively better prognosis in this condition [10]. In fact, our case also had the atypical clinical features of ACS patients, such as young female, and few coronary risk factors, which led to a misdiagnosis. In addition,

occluded coronary artery is rather difficult to clearly distinguish from atherosclerotic plaque rupture merely by angiography. Many reports recommend using imaging devices such as IVUS or optical coherence tomography for optimal diagnosis and PCI [11–13]. We obtained a good reperfusion of the dissected LAD, which is an axial extension of intramural hematoma, using IVUS imaging and cutting balloon and unusual long stenting for the treatment of hematoma, without complications. However, drug therapy and prognosis remain controversial. Although we chose to administer statin because of the patient’s history of high low-density lipoprotein cholesterol level and aspirin for antiplatelet action, no consensus exists among clinical trials as to their efficacy. The longterm recurrence rates of SCAD and major adverse cardiac events have been reported to be 30–50% [3,13]; hence, close follow-up is also needed in such cases. In conclusion, we report a case of SCAD successfully treated with cutting balloon angioplasty under IVUS guidance, in which FMD was detected in the right external iliac artery through screening by noncoronary angiography. References [1] Saw J, Ricci D, Starovoytov A, Fox R, Buller CE. Spontaneous coronary artery dissection: prevalence of predisposing conditions including fibromuscular dysplasia in a tertiary center cohort. JACC Cardiovasc Interv 2013;6:44–52. [2] Adlam D, Cuculi F, Lim C, Banning A. Management of spontaneous coronary artery dissection in the primary percutaneous coronary intervention era. J Invasive Cardiol 2010;22:549–53. [3] Tweet MS, Hayes SN, Pitta SR, Simari RD, Lerman A, Lennon RJ, Gersh BJ, Khambatta S, Best PJ, Rihal CS, Gulati R. Clinical features, management, and prognosis of spontaneous coronary artery dissection. Circulation 2012;126:579–88. [4] Stoukas V, Dragovic LJ. Sudden deaths from eosinophilic coronary monoarteritis: a subset of spontaneous coronary artery dissection. Am J Forensic Med Pathol 2009;30:268–9. [5] Tsujita K, Miyazaki T, Kaikita K, Chitose T, Takaoka N, Soejima H, Tayama S, Hokimoto S, Sugiyama S, Ogawa H. Premenopausal woman with acute myocardial infarction caused by spontaneous coronary artery dissection and potential association with coronary vasospasm. Cardiovasc Interv Ther 2012;27:121–6. [6] Tehrani S, Khawaja MZ, Redwood S. Successful treatment of a late presentation exercise-induced spontaneous left anterior descending artery dissection. J Invasive Cardiol 2011;23:E260–2. [7] Hampole CV, Philip F, Shafii A, Pettersson G, Anesi GL, Patel JB, Menon V. Spontaneous coronary artery dissection in Ehlers-Danlos syndrome. Ann Thorac Surg 2011;92:1883–4. [8] Koul AK, Hollander G, Moskovits N, Frankel R, Herrera L, Shani J. Coronary artery dissection during pregnancy and the postpartum period: two case reports and review of literature. Catheter Cardiovasc Interv 2001;52:88–94. [9] Olin JW, Sealove BA. Diagnosis, management, and future developments of fibromuscular dysplasia. J Vasc Surg 2011;53:826–36.e1. [10] Celik SK, Sagcan A, Altintig A, Yuksel M, Akin M, Kultursay H. Primary spontaneous coronary artery dissections in atherosclerotic patients. Report of nine cases with review of the pertinent literature. Eur J Cardiothorac Surg 2001;20:573–6. [11] Miki K, Fujii K, Nakata T, Shibuya M, Fukunaga M, Kawai K, Kawasaki D, Masutani M, Ohyanagi M, Masuyama T. The utility of intravascular ultrasound for the diagnosis and management of spontaneous coronary artery dissection in a middle-aged woman with acute inferior myocardial infarction. J Cardiol Cases 2012;6:e78–80. [12] Saw J, Poulter R, Fung A. Intracoronary imaging of coronary fibromuscular dysplasia with OCT and IVUS. Catheter Cardiovasc Interv 2012, August, http://dx.doi.org/10.1002/ccd.24640 [Epub ahead of print]. [13] Kansara P, Graham S. Spontaneous coronary artery dissection: case series with extended follow up. J Invasive Cardiol 2011;23:76–80.