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Very late multiple recurrent spontaneous coronary artery dissection in a young woman with recidivating acute myocardial infarction
International Journal of Cardiology 223 (2016) 168–170
Contents lists available at ScienceDirect
International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard
Correspondence
Very late multiple recurrent spontaneous coronary artery dissection in a young woman with recidivating acute myocardial infarction Sophie Degrauwe a, Andrea Zuffi a, Olivier Muller a, François Schiele b, Eric Eeckhout a, Juan F. Iglesias a,⁎ a b
Department of Cardiology, Lausanne University Hospital, Switzerland Department of Cardiology, Besançon University Hospital, France
a r t i c l e
i n f o
Article history: Received 8 July 2016 Accepted 5 August 2016 Available online 07 August 2016 Keywords: Spontaneous coronary artery dissection Acute myocardial infarction Women
Spontaneous coronary artery dissection (SCAD) is an uncommon and potentially underdiagnosed cause of acute coronary syndrome (ACS) with a prevalence ranging from 0.1 to 1.1% among patients undergoing coronary angiography (CA). Accordingly, limited information is currently available related to the optimal management strategy and long-term clinical outcome of patients with SCAD. Large contemporary retrospective series report an excellent long-term prognosis with low rates of SCAD or ACS recurrences [1,3], as well as major adverse clinical events (MACE) [2,3] up to 3 years after the initial event. Longterm recurrence of SCAD is an extremely rare clinical condition [2,4], but current evidence remains limited to retrospective series reporting small total number of patients with mainly a single recurrent SCAD event and a relatively short-term follow-up period. Herein, we report on a 52-year-old Caucasian female, active smoker with history of non-ST elevation-ACS (NSTE-ACS) caused by a SCAD of the mid- to distal left anterior descending (LAD) artery nine years earlier, who underwent percutaneous coronary intervention (PCI) with two paclitaxel-eluting stents due to persistent chest pain on medical treatment (Fig. 1, Panels A-D, Movie clip 1). Three years later, the patient was admitted with recurrent NSTE-ACS. The CA showed patent stents on the LAD but revealed a recurrent SCAD of the distal posterior descending artery, which was managed conservatively (Fig. 1, Panels E-F, Movie clip 2). The patient has been thereafter free from cardiovascular symptoms over an eight-year period. On current admission, the patient presented to the emergency department with typical exertional chest pain and shortness of breath. The 12-lead ECG ⁎ Corresponding author: Department of Cardiology, Lausanne University Hospital (CHUV), Rue du Bugnon 46, 1011 Lausanne, Switzerland. E-mail address: [email protected] (J.F. Iglesias).
http://dx.doi.org/10.1016/j.ijcard.2016.08.124 0167-5273/© 2016 Elsevier Ireland Ltd. All rights reserved.
showed no acute ischemic changes, but cardiac biomarkers were elevated. The urgent CA showed patent stents on the LAD and no left circumflex artery disease (Fig. 2, Panels A–B, Movie clip 3), but a SCAD involving the proximal to mid right coronary artery (RCA) with Thrombolysis in Myocardial Infarction 2 anterograde flow (Fig. 2, Panel C, Movie clip 4). PCI to the proximal to distal RCA was performed with three drug-eluting stents (DES). The final CA demonstrated restored TIMI 3 anterograde flow from the proximal to the distal RCA despite small residual distal coronary dissection, which was left untreated in the absence of significant residual stenosis or abnormal coronary blood flow (Fig. 2, Panel D, Movie clip 5). On coronary care unit admission, the patient developed acute chest pain, inferior STsegment elevation and ventricular fibrillation (VF) arrest requiring immediate cardio-pulmonary resuscitation (CPR). Return of spontaneous circulation (ROSC) was obtained after delivery of one defibrillation shock and the patient was transferred for urgent CA. On catheterization laboratory admission, the patient developed refractory VF arrest requiring prolonged CPR with ROSC after 20 min. The urgent CA showed patent stents on the RCA, but revealed anterograde progression of the SCAD to the distal RCA (Fig. 2, panel E, Movie clip 6). The patient underwent PCI to the distal RCA with an additional DES guided by intravascular ultrasound imaging to ensure the correct intraluminal position of the coronary guidewire (Fig. 2, Panel F, Movie clip 7). The transthoracic echocardiogram at discharge showed only mild left ventricular systolic dysfunction (ejection fraction 53%), with basal inferior akinesia, mid-inferior and inferolateral hypokinesia. Invasive angiography and Doppler ultrasonography excluded fibromuscular dysplasia of the iliac and renal arteries. In-hospital course was uneventful and the patient was discharged at day 8. At 2 years follow-up, the patient remained free from recurrent SCAD or ACS, up to eleven years after the initial SCAD event. SCAD is considered a rare but increasingly recognized cause of ACS, accounting for 0.1% to 4% of all patients and up to 25% of women younger than 50 years [1,3]. SCAD corresponds to a non-traumatic and non-iatrogenic separation of coronary arterial walls between either the intima and media, or the media and adventitia by an intramural hematoma creating a false lumen, with or without associated intimal tear [1,3]. SCAD affects predominantly young women without conventional cardiac risk factors and is commonly associated with underlying predisposing arteriopathy (fibromuscular dysplasia in up to 50–72% of patients), multiple pregnancy or peripartum, systemic inflammation (systemic lupus erythematosus, Crohn's disease, polyarteritis nodosa,
S. Degrauwe et al. / International Journal of Cardiology 223 (2016) 168–170
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Fig. 1. Coronary angiogram (CA) performed nine years prior to current admission demonstrating a spontaneous coronary artery dissection (SCAD) involving the mid- to distal left anterior descending artery (LAD) (Panels A and B, white arrows). Due to persistent ischemic symptoms on medical therapy, the patient underwent percutaneous coronary intervention (PCI) with two drug-eluting stents (DES) achieving a good final angiographic result (Panels C and D, white arrows). Coronary angiogram performed three years after initial SCAD event showing recurrent SCAD of the distal posterior descending artery (Panels E and F, white arrows), which was managed conservatively in the absence of persisting ischemic symptoms.
sarcoidosis), connective tissue disease (Marfan's syndrome, EhlersDanlos syndrome, cystic medial necrosis), (hormonal therapy, or coronary artery spasm) and a precipitating stress factor (intense exercise or emotional stress, labor, delivery, intense Valsalva-like activities, or
sympathomimetic drugs) [3]. The optimal management and longterm therapy after SCAD remains controversial [1,3], but large contemporary prospective series report favorable clinical outcomes, with in-hospital mortality rates ranging from 0 to 4% [3] and 2-year
Fig. 2. Urgent CA performed during current admission demonstrating favorable long-term result of DES on mid- to distal LAD nine years earlier (Panels A and B, white arrows) and recurrent SCAD of the proximal to mid-right coronary artery (RCA) (Panel C, white arrow). The patient underwent PCI to proximal to distal RCA with three DES (Panel D, white arrow) with a good final angiographic result, despite residual distal coronary artery dissection (Panel D, black arrow), which was initially managed conservatively. Urgent CA after ventricular fibrillation cardiac arrest showing patent stents on proximal to distal RCA (Panel E, white arrow) and anterograde progression of the initial SCAD to the distal RCA (Panel E, black arrow). The patient underwent PCI to distal RCA with a DES (Panel F, white arrow) allowing restoration of normal distal anterograde flow, despite a small persistent coronary artery dissection (Panel F, black arrow), which was left untreated.
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S. Degrauwe et al. / International Journal of Cardiology 223 (2016) 168–170
MACE rates of 10–17% [2,3]. Recurrent SCAD occurs in 13–17% of patients according to large modern series with a median follow-up period ranging from 3.9 to 6.9 years [2,4]. Nevertheless, little information is available on the longer-term risk of SCAD recurrence, which may be particularly important, especially for women who experience a first SCAD event before age 50 years. Current evidence on the very longterm risk of SCAD recurrence remains limited to retrospective series reporting small total number of patients and relatively short-term clinical follow-up periods, precluding therefore any definite conclusion about the true prevalence and very long-term prognosis of SCAD patients and leading to a potential underestimation of very late recurrent SCAD rates. Multiple very late recurrences of SCAD in a patient with underlying FMD have been previously reported [5]. Here, we describe for the first time to our knowledge a unique case of multiple and multivessel very late recurrent SCAD in a young woman not affected by FMD resulting in recurrent ACS presentations. Our case underscores the paramount importance of close very long-term follow-up of patients, particularly young women, with SCAD by cardiovascular specialists owing to the unpredictable very long-term risk of multiple recurrent SCAD that may result in potentially fatal MACE and recurrent ACS.
Supplementary data to this article can be found online at http://dx. doi.org/10.1016/j.ijcard.2016.08.124. Conflict of interest No conflict of interest to disclose. References [1] J. Saw, Spontaneous coronary artery dissection, Can. J. Cardiol. 29 (9) (2013) 1027–1033. [2] J. Saw, E. Aymong, T. Sedlak, C.E. Buller, A. Starovoytov, D. Ricci, S. Robinson, T. Vuurmans, M. Gao, K. Humphries, G.B. Mancini, Spontaneous coronary artery dissection: association with predisposing arteriopathies and precipitating stressors and cardiovascular outcomes, Circ. Cardiovasc. Interv. 7 (5) (2014) 645–655. [3] A. Yip, J. Saw, Spontaneous coronary artery dissection—a review, Cardiovasc. Diagn. Ther. 5 (1) (2015) 37–48. [4] M.S. Tweet, S.N. Hayes, S.R. Pitta, R.D. Simari, A. Lerman, R.J. Lennon, B.J. Gersh, S. Khambatta, P.J. Best, C.S. Rihal, R. Gulati, Clinical features, management, and prognosis of spontaneous coronary artery dissection, Circulation 126 (5) (2012) 579–588. [5] A. Khosla, J. Saw, Recurrent spontaneous coronary artery dissection in a woman with fibromuscular dysplasia, J. Invasive Cardiol. 27 (6) (2015 Jun.) E110–E112.
Contents lists available at ScienceDirect
International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard
Correspondence
Very late multiple recurrent spontaneous coronary artery dissection in a young woman with recidivating acute myocardial infarction Sophie Degrauwe a, Andrea Zuffi a, Olivier Muller a, François Schiele b, Eric Eeckhout a, Juan F. Iglesias a,⁎ a b
Department of Cardiology, Lausanne University Hospital, Switzerland Department of Cardiology, Besançon University Hospital, France
a r t i c l e
i n f o
Article history: Received 8 July 2016 Accepted 5 August 2016 Available online 07 August 2016 Keywords: Spontaneous coronary artery dissection Acute myocardial infarction Women
Spontaneous coronary artery dissection (SCAD) is an uncommon and potentially underdiagnosed cause of acute coronary syndrome (ACS) with a prevalence ranging from 0.1 to 1.1% among patients undergoing coronary angiography (CA). Accordingly, limited information is currently available related to the optimal management strategy and long-term clinical outcome of patients with SCAD. Large contemporary retrospective series report an excellent long-term prognosis with low rates of SCAD or ACS recurrences [1,3], as well as major adverse clinical events (MACE) [2,3] up to 3 years after the initial event. Longterm recurrence of SCAD is an extremely rare clinical condition [2,4], but current evidence remains limited to retrospective series reporting small total number of patients with mainly a single recurrent SCAD event and a relatively short-term follow-up period. Herein, we report on a 52-year-old Caucasian female, active smoker with history of non-ST elevation-ACS (NSTE-ACS) caused by a SCAD of the mid- to distal left anterior descending (LAD) artery nine years earlier, who underwent percutaneous coronary intervention (PCI) with two paclitaxel-eluting stents due to persistent chest pain on medical treatment (Fig. 1, Panels A-D, Movie clip 1). Three years later, the patient was admitted with recurrent NSTE-ACS. The CA showed patent stents on the LAD but revealed a recurrent SCAD of the distal posterior descending artery, which was managed conservatively (Fig. 1, Panels E-F, Movie clip 2). The patient has been thereafter free from cardiovascular symptoms over an eight-year period. On current admission, the patient presented to the emergency department with typical exertional chest pain and shortness of breath. The 12-lead ECG ⁎ Corresponding author: Department of Cardiology, Lausanne University Hospital (CHUV), Rue du Bugnon 46, 1011 Lausanne, Switzerland. E-mail address: [email protected] (J.F. Iglesias).
http://dx.doi.org/10.1016/j.ijcard.2016.08.124 0167-5273/© 2016 Elsevier Ireland Ltd. All rights reserved.
showed no acute ischemic changes, but cardiac biomarkers were elevated. The urgent CA showed patent stents on the LAD and no left circumflex artery disease (Fig. 2, Panels A–B, Movie clip 3), but a SCAD involving the proximal to mid right coronary artery (RCA) with Thrombolysis in Myocardial Infarction 2 anterograde flow (Fig. 2, Panel C, Movie clip 4). PCI to the proximal to distal RCA was performed with three drug-eluting stents (DES). The final CA demonstrated restored TIMI 3 anterograde flow from the proximal to the distal RCA despite small residual distal coronary dissection, which was left untreated in the absence of significant residual stenosis or abnormal coronary blood flow (Fig. 2, Panel D, Movie clip 5). On coronary care unit admission, the patient developed acute chest pain, inferior STsegment elevation and ventricular fibrillation (VF) arrest requiring immediate cardio-pulmonary resuscitation (CPR). Return of spontaneous circulation (ROSC) was obtained after delivery of one defibrillation shock and the patient was transferred for urgent CA. On catheterization laboratory admission, the patient developed refractory VF arrest requiring prolonged CPR with ROSC after 20 min. The urgent CA showed patent stents on the RCA, but revealed anterograde progression of the SCAD to the distal RCA (Fig. 2, panel E, Movie clip 6). The patient underwent PCI to the distal RCA with an additional DES guided by intravascular ultrasound imaging to ensure the correct intraluminal position of the coronary guidewire (Fig. 2, Panel F, Movie clip 7). The transthoracic echocardiogram at discharge showed only mild left ventricular systolic dysfunction (ejection fraction 53%), with basal inferior akinesia, mid-inferior and inferolateral hypokinesia. Invasive angiography and Doppler ultrasonography excluded fibromuscular dysplasia of the iliac and renal arteries. In-hospital course was uneventful and the patient was discharged at day 8. At 2 years follow-up, the patient remained free from recurrent SCAD or ACS, up to eleven years after the initial SCAD event. SCAD is considered a rare but increasingly recognized cause of ACS, accounting for 0.1% to 4% of all patients and up to 25% of women younger than 50 years [1,3]. SCAD corresponds to a non-traumatic and non-iatrogenic separation of coronary arterial walls between either the intima and media, or the media and adventitia by an intramural hematoma creating a false lumen, with or without associated intimal tear [1,3]. SCAD affects predominantly young women without conventional cardiac risk factors and is commonly associated with underlying predisposing arteriopathy (fibromuscular dysplasia in up to 50–72% of patients), multiple pregnancy or peripartum, systemic inflammation (systemic lupus erythematosus, Crohn's disease, polyarteritis nodosa,
S. Degrauwe et al. / International Journal of Cardiology 223 (2016) 168–170
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Fig. 1. Coronary angiogram (CA) performed nine years prior to current admission demonstrating a spontaneous coronary artery dissection (SCAD) involving the mid- to distal left anterior descending artery (LAD) (Panels A and B, white arrows). Due to persistent ischemic symptoms on medical therapy, the patient underwent percutaneous coronary intervention (PCI) with two drug-eluting stents (DES) achieving a good final angiographic result (Panels C and D, white arrows). Coronary angiogram performed three years after initial SCAD event showing recurrent SCAD of the distal posterior descending artery (Panels E and F, white arrows), which was managed conservatively in the absence of persisting ischemic symptoms.
sarcoidosis), connective tissue disease (Marfan's syndrome, EhlersDanlos syndrome, cystic medial necrosis), (hormonal therapy, or coronary artery spasm) and a precipitating stress factor (intense exercise or emotional stress, labor, delivery, intense Valsalva-like activities, or
sympathomimetic drugs) [3]. The optimal management and longterm therapy after SCAD remains controversial [1,3], but large contemporary prospective series report favorable clinical outcomes, with in-hospital mortality rates ranging from 0 to 4% [3] and 2-year
Fig. 2. Urgent CA performed during current admission demonstrating favorable long-term result of DES on mid- to distal LAD nine years earlier (Panels A and B, white arrows) and recurrent SCAD of the proximal to mid-right coronary artery (RCA) (Panel C, white arrow). The patient underwent PCI to proximal to distal RCA with three DES (Panel D, white arrow) with a good final angiographic result, despite residual distal coronary artery dissection (Panel D, black arrow), which was initially managed conservatively. Urgent CA after ventricular fibrillation cardiac arrest showing patent stents on proximal to distal RCA (Panel E, white arrow) and anterograde progression of the initial SCAD to the distal RCA (Panel E, black arrow). The patient underwent PCI to distal RCA with a DES (Panel F, white arrow) allowing restoration of normal distal anterograde flow, despite a small persistent coronary artery dissection (Panel F, black arrow), which was left untreated.
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MACE rates of 10–17% [2,3]. Recurrent SCAD occurs in 13–17% of patients according to large modern series with a median follow-up period ranging from 3.9 to 6.9 years [2,4]. Nevertheless, little information is available on the longer-term risk of SCAD recurrence, which may be particularly important, especially for women who experience a first SCAD event before age 50 years. Current evidence on the very longterm risk of SCAD recurrence remains limited to retrospective series reporting small total number of patients and relatively short-term clinical follow-up periods, precluding therefore any definite conclusion about the true prevalence and very long-term prognosis of SCAD patients and leading to a potential underestimation of very late recurrent SCAD rates. Multiple very late recurrences of SCAD in a patient with underlying FMD have been previously reported [5]. Here, we describe for the first time to our knowledge a unique case of multiple and multivessel very late recurrent SCAD in a young woman not affected by FMD resulting in recurrent ACS presentations. Our case underscores the paramount importance of close very long-term follow-up of patients, particularly young women, with SCAD by cardiovascular specialists owing to the unpredictable very long-term risk of multiple recurrent SCAD that may result in potentially fatal MACE and recurrent ACS.
Supplementary data to this article can be found online at http://dx. doi.org/10.1016/j.ijcard.2016.08.124. Conflict of interest No conflict of interest to disclose. References [1] J. Saw, Spontaneous coronary artery dissection, Can. J. Cardiol. 29 (9) (2013) 1027–1033. [2] J. Saw, E. Aymong, T. Sedlak, C.E. Buller, A. Starovoytov, D. Ricci, S. Robinson, T. Vuurmans, M. Gao, K. Humphries, G.B. Mancini, Spontaneous coronary artery dissection: association with predisposing arteriopathies and precipitating stressors and cardiovascular outcomes, Circ. Cardiovasc. Interv. 7 (5) (2014) 645–655. [3] A. Yip, J. Saw, Spontaneous coronary artery dissection—a review, Cardiovasc. Diagn. Ther. 5 (1) (2015) 37–48. [4] M.S. Tweet, S.N. Hayes, S.R. Pitta, R.D. Simari, A. Lerman, R.J. Lennon, B.J. Gersh, S. Khambatta, P.J. Best, C.S. Rihal, R. Gulati, Clinical features, management, and prognosis of spontaneous coronary artery dissection, Circulation 126 (5) (2012) 579–588. [5] A. Khosla, J. Saw, Recurrent spontaneous coronary artery dissection in a woman with fibromuscular dysplasia, J. Invasive Cardiol. 27 (6) (2015 Jun.) E110–E112.