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Intravascular imaging as a tool for definite diagnosis of acute coronary syndrome caused by spontaneous coronary artery dissection
International Journal of Cardiology 214 (2016) 43–45
Contents lists available at ScienceDirect
International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard
Correspondence
Intravascular imaging as a tool for definite diagnosis of acute coronary syndrome caused by spontaneous coronary artery dissection Dario Buccheri a,b, Davide Piraino a,b, Bernardo Cortese a,⁎ a b
Interventional cardiology, A.O. Fatebenefratelli, Milano, Italy Interventional cardiology, A.O.U.P. Paolo Giaccone, Palermo, Italy
a r t i c l e
i n f o
Article history: Received 12 February 2016 Accepted 19 March 2016 Available online 26 March 2016
A number of patients presenting with acute coronary syndrome (ACS)/myocardial infarction (MI) show angiographic non-obstructive coronary artery disease (NOCAD) [1]. Among the causes of this event, spontaneous coronary artery dissection (SCAD) is a rare and often misdiagnosed phenomenon that represents 0.1%–4% of all ACSs [2,3] and 3% of all NOCADs [1]. A 70-year-old male with arterial hypertension, type II diabetes and a history of myocardial infarction (2008) due to left circumflex coronary artery spasm treated with calcium-channel blockers was admitted at our department for an ACS with dynamic shift of the ST segment in the inferior leads at the ECG. Coronary angiography showed a moderate stenosis of the distal segment of the right coronary artery. Instant wavefree ratio™ (iFR®) for assessment of coronary artery stenosis severity was 1.00, confirming that the lesion was not hemodynamically significant (Fig. 1A), thus medical treatment was prescribed. The following day the patient experienced a sudden chest pain with transient STsegment elevation in the inferior leads. Urgent coronary angiography confirmed previous findings; optical coherence tomography analysis (OCT) was thus performed, and showed clear signs of right coronary artery spontaneous dissection with an intimal tear at the entry point (Fig. 1B) and a clear image of intimal flap and false lumen downstream (Fig. 1C). Notably, the atherosclerotic burden was low in that segment. We thus treated the lesion with a 3.00/18 mm Absorb bioresorbable vascular scaffold (BVS, Abbott Vascular, Santa Clara, US) implantation obtaining good angiographic result confirmed by the OCT (Fig. 1D–E). At 12 month follow-up, the patient was in good clinical condition and the coronarography confirmed good angiographic result without signs of dissection (Fig. 2A–B).
⁎ Corresponding author at: Interventional Cardiology, A.O. Fatebenefratelli Milano, Bastioni di Porta Nuova 21, 20100 Milano, Italy. E-mail address: [email protected] (B. Cortese).
http://dx.doi.org/10.1016/j.ijcard.2016.03.114 0167-5273/© 2016 Elsevier Ireland Ltd. All rights reserved.
Here we present a case of SCAD causing an ACS in a senior man in which coronary angiography was not useful for the diagnosis (or even suspicion) of dissection, with normal iFR®. Only the OCT analysis, performed during the second urgent coronarography, allowed us to diagnose the SCAD. SCAD etiopathogenesis often remains unclear but some evidences correlate it with connective/collagen tissue alterations, arteritis with or without an intimal damage caused by higher vessel wall shear stress finally determining the separation of tunica intima and media or media and adventitia, due to an intramural hematoma that determines the creation of a false lumen, sometimes with impairment of the anterograde coronary blood flow and subsequent myocardial ischemia/infarction [2]. Renown risk factors for this entity are: 1) female gender, especially b50 years; 2) peripartum period or with multiple prior pregnancies; 3) coronary artery tortuosity and extracoronary vascular abnormalities, especially fibromuscular dysplasia; 4) a common angiographic presentation with diffuse, typically smooth arterial narrowing rather than pathognomonic contrast staining in the arterial wall; and 5) frequent recurrences [2,4]. Its clinical presentation may consist in angina pectoris, any type of ACS, cardiogenic shock or even sudden cardiac death [3], and a number of patients show mild lumen obstruction (often b50%) at coronary angiography without the pathognomonic appearance of multiple radiolucent lumen [5,6]. For this reason, we believe that in the case of suspicion of SCAD, intravascular ultrasound (IVUS) imaging or optical coherence tomography analysis (OCT) becomes of primary importance in order to do a correct diagnosis, and to understand the actual extension of the disease [6,7]. Besides, our case represents an atypical form of SCAD, whose suspicion was not driven by the clinical history of the patients, that was senior, male, without clinical history of vasculitis/autoimmune disease or tortuosity of the coronary artery in the SCAD point. Furthermore, this report clearly shows the importance of using intravascular imaging to confirm the suspicion of intimal flap or intramural hematoma, after the diagnosis of ACS was clear but angiography not diagnostic for obstructive coronary artery disease [6,7]. OCT (spatial resolution of 10–20 μm) compared with IVUS (spatial resolution of 150 μm) is superior for the identification of the intimal rupture site (tear) and to provide a precise visualization of the intimamedia membrane (flap) and intramural hematoma [2,7–9], although OCT analysis always requires an open vessel.
44
Correspondence
Fig. 1. A) Right coronary artery angiography showed a subcritical stenosis at the distal segment (arrow) with instant wave-free ratio™ (iFR®) of 1.00 (box zoomed) confirming the absence of flow-limiting vessel disease. However, second urgent coronarography with optical coherence tomography (OCT) analysis shows the intimal tear at the beginning point of a spontaneous coronary artery dissection (SCAD) (B), with clear intimal flap (thickness 0.10 mm) and false lumen (arrows) (C). D shows good final angiographic result after angioplasty with BVS implantation (arrow). E shows OCT analysis with a well apposed BVS.
Recent data report an in-hospital mortality of SCAD patients ranging from 1 to 5%. The long-term outcome of patients who survived their initial SCAD presentation is good and mortality lower for SCAD patients than for other ACS [8,10]. Appropriate SCAD treatment is, nowadays, strongly debated, and medical therapy is the most widely adapted strategy in western countries [9]. Distal localization of dissections, with TIMI flow grade 2 or 3
is independent predictors for a conservative treatment, whereas more proximal lesions with impaired TIMI flow usually result in revascularization [10]. Despite there are no significant differences in the longterm outcomes between these 2 strategies, revascularization is associated with a procedural success lower than in atherosclerotic lesions, due to a higher rate of complications, probably caused by a mechanical squeeze of the intramural hematoma [10]. Intravascular imaging may
Fig. 2. A–B) 12-month angiographic follow-up with good result of BVS angioplasty (arrow), without further progression of SCAD.
Correspondence Table 1 Diagnostic suspicion and management tools for SCAD. Clinical and angiographic factors suspicion for SCAD. ➢ Clinical/therapeutic characteristics – Female gender/pregnancy (peripartum, history of multiple pregnancy) – Youth/b50 year – No classical coronary risk factors – Estroprogestinic therapy – Connective tissue disorder (Marfan sdr, EDS, cystic medial necrosis)/fibromuscolar dysplasia – Systematic inflammation (SLE, Crohn's disease, sarcoidosis, polyarteritis nodosa) – Cocaine/amphetamines/vasospastic drugs abuse ➢ Angiographic characteristics – One vessel disease (no typical atherosclerotic lesions in other coronary arteries) – Long/tortuous suspected lesion – Diffuse, typically smooth arterial narrowing rather than pathognomonic contrast staining of the arterial wall Intracoronaric images – OCT (first choice), if not available – IVUS Management – BVS (first choice), if not available, – Medical therapy, drug-coated balloon (DCB), cutting balloon, DES, CABG according to the clinic/angiographic situation If there are 3 clinical suspicion factors, according to the angiographic characteristics, in a patient presenting with ECG anomalies (i.e. transitory ST-elevation) or troponin rise/fall, we suggest OCT analysis to exclude SCAD. Abbreviations: sdr = syndrome; EDS = Ehners–Danlos syndrome; SLE = systemic lupus erythematosus; OCT = optical coherence tomography; IVUS = intravascular ultrasonography; BVS = biovascular resorbable scaffold; DES = drug-eluting stent; CABG = coronary-aortic by-pass graft; SCAD = spontaneous coronary artery dissection.
result in a better understanding of the exact extension of disease, therefore allowing for a properly sized device. BVS implantation seems an intriguing choice in this setting, due to the complete restoration of the vessel wall within 2–3 years, an interesting item especially given the young age with low atherosclerotic burden of a typical SCAD patient and avoiding eternal prosthesis in the case of multiple devices needed. On the other hand, our group recently published the results of a study that showed for the first time a pro-healing effect of drugcoated balloons when a dissection was left at the end of PCI in native coronary arteries [11]. In this light, we advance a provocative idea for
45
SCAD treatment with longer balloon inflations using drug-coated balloons, especially for long, distal lesions. This treatment is being studied in a dedicated clinical study. However, if some cases of spontaneous vessel healing at SCAD sites have been described, there are also cases of recurrent SCADs in new segments [2,8,9]. We thus recommend a close follow-up with adequate imaging techniques in such patients [9]. Finally, as previous established, not all SCADs are visible at coronarography [6]. Starting from the description of this case, we here point out a flow-chart (Table 1) with clinical/angiographic criteria for SCAD diagnosis and treatment, following the most modern literature and our own experience. The presence of 3 or more criteria suggests one to perform an endovascular analysis to exclude SCAD.
References [1] K. Najib, S. Boateng, S. Sangodkar, S. Mahmood, H. Whitney, C.E. Wang, et al., Incidence and characteristics of patients presenting with acute myocardial infarction and non-obstructive coronary artery disease, Catheter Cardiovasc Interv (Jun 23 2015), http://dx.doi.org/10.1002/ccd.26043. [2] J. Saw, Spontaneous coronary artery dissection, Can J Cardiol 29 (2013) 1027–1033. [3] D. Giacoppo, D. Capodanno, G. Dangas, C. Tamburino, Spontaneous coronary artery dissection, Int J Cardiol 175 (2014) 8–20. [4] H.N. Rashid, D.T. Wong, H. Wijesekera, S.J. Gutman, V.B. Shanmugam, R. Gulati, et al., Incidence and characterisation of spontaneous coronary artery dissection as a cause of acute coronary syndrome — a single-centre Australian experience, Int J Cardiol 202 (2015) 336–338. [5] J. Saw, Coronary angiogram classification of spontaneous coronary artery dissection, Catheter Cardiovasc Interv 84 (2014) 1115–1122. [6] J. Saw, G.B.J. Mancini, K. Humphries, A. Fung, R. Boone, A. Starovoytov, et al., Angiographic appearance of spontaneous coronary artery dissection with intramural hematoma proven on intracoronary imaging, Catheter Cardiovasc Interv (Jul 21 2015), http://dx.doi.org/10.1002/ccd.26022. [7] F. Alfonso, M. Paulo, N. Gonzalo, J. Dutary, P. Jimenez-Quevedo, V. Lennie, et al., Diagnosis of spontaneous coronary artery dissection by optical coherence tomography, J Am Coll Cardiol 59 (2012) 1073–1079. [8] A. Yip, J. Saw, Spontaneous coronary artery dissection—a review, Cardiovasc. Diagn. Ther. 5 (2015) 37–48. [9] F. Alfonso, T. Bastante, J. Cuesta, D. Rodríguez, A. Benedicto, F. Rivero, Spontaneous coronary artery dissection: novel insights on diagnosis and management, Cardiovasc Diagn Ther 5 (2015) 133–140. [10] C. Lettieri, D. Zavalloni, R. Rossini, N. Morici, F. Ettori, O. Leonzi, et al., Management and long-term prognosis of spontaneous coronary artery dissection, Am J Cardiol 116 (2015) 66–73. [11] B. Cortese, P. Silva Orrego, P. Agostoni, D. Buccheri, D. Piraino, G. Andolina, et al., Effect of drug-coated balloons in native coronary artery disease left with a dissection, J Am Coll Cardiol Intv 8 (2015) 2003–2009.
Contents lists available at ScienceDirect
International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard
Correspondence
Intravascular imaging as a tool for definite diagnosis of acute coronary syndrome caused by spontaneous coronary artery dissection Dario Buccheri a,b, Davide Piraino a,b, Bernardo Cortese a,⁎ a b
Interventional cardiology, A.O. Fatebenefratelli, Milano, Italy Interventional cardiology, A.O.U.P. Paolo Giaccone, Palermo, Italy
a r t i c l e
i n f o
Article history: Received 12 February 2016 Accepted 19 March 2016 Available online 26 March 2016
A number of patients presenting with acute coronary syndrome (ACS)/myocardial infarction (MI) show angiographic non-obstructive coronary artery disease (NOCAD) [1]. Among the causes of this event, spontaneous coronary artery dissection (SCAD) is a rare and often misdiagnosed phenomenon that represents 0.1%–4% of all ACSs [2,3] and 3% of all NOCADs [1]. A 70-year-old male with arterial hypertension, type II diabetes and a history of myocardial infarction (2008) due to left circumflex coronary artery spasm treated with calcium-channel blockers was admitted at our department for an ACS with dynamic shift of the ST segment in the inferior leads at the ECG. Coronary angiography showed a moderate stenosis of the distal segment of the right coronary artery. Instant wavefree ratio™ (iFR®) for assessment of coronary artery stenosis severity was 1.00, confirming that the lesion was not hemodynamically significant (Fig. 1A), thus medical treatment was prescribed. The following day the patient experienced a sudden chest pain with transient STsegment elevation in the inferior leads. Urgent coronary angiography confirmed previous findings; optical coherence tomography analysis (OCT) was thus performed, and showed clear signs of right coronary artery spontaneous dissection with an intimal tear at the entry point (Fig. 1B) and a clear image of intimal flap and false lumen downstream (Fig. 1C). Notably, the atherosclerotic burden was low in that segment. We thus treated the lesion with a 3.00/18 mm Absorb bioresorbable vascular scaffold (BVS, Abbott Vascular, Santa Clara, US) implantation obtaining good angiographic result confirmed by the OCT (Fig. 1D–E). At 12 month follow-up, the patient was in good clinical condition and the coronarography confirmed good angiographic result without signs of dissection (Fig. 2A–B).
⁎ Corresponding author at: Interventional Cardiology, A.O. Fatebenefratelli Milano, Bastioni di Porta Nuova 21, 20100 Milano, Italy. E-mail address: [email protected] (B. Cortese).
http://dx.doi.org/10.1016/j.ijcard.2016.03.114 0167-5273/© 2016 Elsevier Ireland Ltd. All rights reserved.
Here we present a case of SCAD causing an ACS in a senior man in which coronary angiography was not useful for the diagnosis (or even suspicion) of dissection, with normal iFR®. Only the OCT analysis, performed during the second urgent coronarography, allowed us to diagnose the SCAD. SCAD etiopathogenesis often remains unclear but some evidences correlate it with connective/collagen tissue alterations, arteritis with or without an intimal damage caused by higher vessel wall shear stress finally determining the separation of tunica intima and media or media and adventitia, due to an intramural hematoma that determines the creation of a false lumen, sometimes with impairment of the anterograde coronary blood flow and subsequent myocardial ischemia/infarction [2]. Renown risk factors for this entity are: 1) female gender, especially b50 years; 2) peripartum period or with multiple prior pregnancies; 3) coronary artery tortuosity and extracoronary vascular abnormalities, especially fibromuscular dysplasia; 4) a common angiographic presentation with diffuse, typically smooth arterial narrowing rather than pathognomonic contrast staining in the arterial wall; and 5) frequent recurrences [2,4]. Its clinical presentation may consist in angina pectoris, any type of ACS, cardiogenic shock or even sudden cardiac death [3], and a number of patients show mild lumen obstruction (often b50%) at coronary angiography without the pathognomonic appearance of multiple radiolucent lumen [5,6]. For this reason, we believe that in the case of suspicion of SCAD, intravascular ultrasound (IVUS) imaging or optical coherence tomography analysis (OCT) becomes of primary importance in order to do a correct diagnosis, and to understand the actual extension of the disease [6,7]. Besides, our case represents an atypical form of SCAD, whose suspicion was not driven by the clinical history of the patients, that was senior, male, without clinical history of vasculitis/autoimmune disease or tortuosity of the coronary artery in the SCAD point. Furthermore, this report clearly shows the importance of using intravascular imaging to confirm the suspicion of intimal flap or intramural hematoma, after the diagnosis of ACS was clear but angiography not diagnostic for obstructive coronary artery disease [6,7]. OCT (spatial resolution of 10–20 μm) compared with IVUS (spatial resolution of 150 μm) is superior for the identification of the intimal rupture site (tear) and to provide a precise visualization of the intimamedia membrane (flap) and intramural hematoma [2,7–9], although OCT analysis always requires an open vessel.
44
Correspondence
Fig. 1. A) Right coronary artery angiography showed a subcritical stenosis at the distal segment (arrow) with instant wave-free ratio™ (iFR®) of 1.00 (box zoomed) confirming the absence of flow-limiting vessel disease. However, second urgent coronarography with optical coherence tomography (OCT) analysis shows the intimal tear at the beginning point of a spontaneous coronary artery dissection (SCAD) (B), with clear intimal flap (thickness 0.10 mm) and false lumen (arrows) (C). D shows good final angiographic result after angioplasty with BVS implantation (arrow). E shows OCT analysis with a well apposed BVS.
Recent data report an in-hospital mortality of SCAD patients ranging from 1 to 5%. The long-term outcome of patients who survived their initial SCAD presentation is good and mortality lower for SCAD patients than for other ACS [8,10]. Appropriate SCAD treatment is, nowadays, strongly debated, and medical therapy is the most widely adapted strategy in western countries [9]. Distal localization of dissections, with TIMI flow grade 2 or 3
is independent predictors for a conservative treatment, whereas more proximal lesions with impaired TIMI flow usually result in revascularization [10]. Despite there are no significant differences in the longterm outcomes between these 2 strategies, revascularization is associated with a procedural success lower than in atherosclerotic lesions, due to a higher rate of complications, probably caused by a mechanical squeeze of the intramural hematoma [10]. Intravascular imaging may
Fig. 2. A–B) 12-month angiographic follow-up with good result of BVS angioplasty (arrow), without further progression of SCAD.
Correspondence Table 1 Diagnostic suspicion and management tools for SCAD. Clinical and angiographic factors suspicion for SCAD. ➢ Clinical/therapeutic characteristics – Female gender/pregnancy (peripartum, history of multiple pregnancy) – Youth/b50 year – No classical coronary risk factors – Estroprogestinic therapy – Connective tissue disorder (Marfan sdr, EDS, cystic medial necrosis)/fibromuscolar dysplasia – Systematic inflammation (SLE, Crohn's disease, sarcoidosis, polyarteritis nodosa) – Cocaine/amphetamines/vasospastic drugs abuse ➢ Angiographic characteristics – One vessel disease (no typical atherosclerotic lesions in other coronary arteries) – Long/tortuous suspected lesion – Diffuse, typically smooth arterial narrowing rather than pathognomonic contrast staining of the arterial wall Intracoronaric images – OCT (first choice), if not available – IVUS Management – BVS (first choice), if not available, – Medical therapy, drug-coated balloon (DCB), cutting balloon, DES, CABG according to the clinic/angiographic situation If there are 3 clinical suspicion factors, according to the angiographic characteristics, in a patient presenting with ECG anomalies (i.e. transitory ST-elevation) or troponin rise/fall, we suggest OCT analysis to exclude SCAD. Abbreviations: sdr = syndrome; EDS = Ehners–Danlos syndrome; SLE = systemic lupus erythematosus; OCT = optical coherence tomography; IVUS = intravascular ultrasonography; BVS = biovascular resorbable scaffold; DES = drug-eluting stent; CABG = coronary-aortic by-pass graft; SCAD = spontaneous coronary artery dissection.
result in a better understanding of the exact extension of disease, therefore allowing for a properly sized device. BVS implantation seems an intriguing choice in this setting, due to the complete restoration of the vessel wall within 2–3 years, an interesting item especially given the young age with low atherosclerotic burden of a typical SCAD patient and avoiding eternal prosthesis in the case of multiple devices needed. On the other hand, our group recently published the results of a study that showed for the first time a pro-healing effect of drugcoated balloons when a dissection was left at the end of PCI in native coronary arteries [11]. In this light, we advance a provocative idea for
45
SCAD treatment with longer balloon inflations using drug-coated balloons, especially for long, distal lesions. This treatment is being studied in a dedicated clinical study. However, if some cases of spontaneous vessel healing at SCAD sites have been described, there are also cases of recurrent SCADs in new segments [2,8,9]. We thus recommend a close follow-up with adequate imaging techniques in such patients [9]. Finally, as previous established, not all SCADs are visible at coronarography [6]. Starting from the description of this case, we here point out a flow-chart (Table 1) with clinical/angiographic criteria for SCAD diagnosis and treatment, following the most modern literature and our own experience. The presence of 3 or more criteria suggests one to perform an endovascular analysis to exclude SCAD.
References [1] K. Najib, S. Boateng, S. Sangodkar, S. Mahmood, H. Whitney, C.E. Wang, et al., Incidence and characteristics of patients presenting with acute myocardial infarction and non-obstructive coronary artery disease, Catheter Cardiovasc Interv (Jun 23 2015), http://dx.doi.org/10.1002/ccd.26043. [2] J. Saw, Spontaneous coronary artery dissection, Can J Cardiol 29 (2013) 1027–1033. [3] D. Giacoppo, D. Capodanno, G. Dangas, C. Tamburino, Spontaneous coronary artery dissection, Int J Cardiol 175 (2014) 8–20. [4] H.N. Rashid, D.T. Wong, H. Wijesekera, S.J. Gutman, V.B. Shanmugam, R. Gulati, et al., Incidence and characterisation of spontaneous coronary artery dissection as a cause of acute coronary syndrome — a single-centre Australian experience, Int J Cardiol 202 (2015) 336–338. [5] J. Saw, Coronary angiogram classification of spontaneous coronary artery dissection, Catheter Cardiovasc Interv 84 (2014) 1115–1122. [6] J. Saw, G.B.J. Mancini, K. Humphries, A. Fung, R. Boone, A. Starovoytov, et al., Angiographic appearance of spontaneous coronary artery dissection with intramural hematoma proven on intracoronary imaging, Catheter Cardiovasc Interv (Jul 21 2015), http://dx.doi.org/10.1002/ccd.26022. [7] F. Alfonso, M. Paulo, N. Gonzalo, J. Dutary, P. Jimenez-Quevedo, V. Lennie, et al., Diagnosis of spontaneous coronary artery dissection by optical coherence tomography, J Am Coll Cardiol 59 (2012) 1073–1079. [8] A. Yip, J. Saw, Spontaneous coronary artery dissection—a review, Cardiovasc. Diagn. Ther. 5 (2015) 37–48. [9] F. Alfonso, T. Bastante, J. Cuesta, D. Rodríguez, A. Benedicto, F. Rivero, Spontaneous coronary artery dissection: novel insights on diagnosis and management, Cardiovasc Diagn Ther 5 (2015) 133–140. [10] C. Lettieri, D. Zavalloni, R. Rossini, N. Morici, F. Ettori, O. Leonzi, et al., Management and long-term prognosis of spontaneous coronary artery dissection, Am J Cardiol 116 (2015) 66–73. [11] B. Cortese, P. Silva Orrego, P. Agostoni, D. Buccheri, D. Piraino, G. Andolina, et al., Effect of drug-coated balloons in native coronary artery disease left with a dissection, J Am Coll Cardiol Intv 8 (2015) 2003–2009.