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Review ArticleiMedPub Journals Cardiology JournalISSN 2471-81572017Vol.3 No.1:3DOI: 10.21767/2471-8157.100043How to Approach a Spontaneous Coronary Artery Dissection: An Up-To-DateMartino Pepe1, Annagrazia Cecere1*, Massimo Napodano2, Marco Matteo Ciccone1, FrancescoBartolomucci3, Eliano Pio Navarese4, Fortunato Iacovelli5,6, Domenico Zanna1 and Marco Mele71CardiovascularDiseases Section, Department of Emergency and Organ Transplantation, University of Bari, Italy2Department of Cardiac Thoracic and Vascular Sciences, Cardiac Catheterization Laboratories and Interventional Cardiology, University ofPadova, Padova, Italy3CardiologicUnit, “Lorenzo Bonomo” Hospital, Andria, BT, Italy4Departmentof Internal Medicine, Division of Cardiology, Pulmonology and Vascular Medicine, Heinrich-Heine-University, Düsseldorf, Germany5Interventional6DivisionCardiology Service, Montevergine Clinic, Mercogliano, Italyof Cardiology, Department of Advanced Biomedical Sciences, University of Napoli “Federico II”, Napoli, Italy7CoronaryCare Unit-Cardiology Unit, Teresa Masselli Hospital, San Severo (FG), Italy*Corresponding author: Annagrazia Cecere, Cardiovascular Diseases Section, Department of Emergency and Organ Transplantation (DETO),University of Bari, Italy, Tel: 393934499944, E-mail: agcecere@gmail.comRec Date: Dec 15, 2016, Acc Date: Jan 13, 2017, Pub Date: Jan 15, 2017Citation: Pepe M. How to Approach a Spontaneous Coronary Artery Dissection: An Up-To-Date. Interv Cardiol J 2017, 3:1.AbstarctSpontaneous coronary artery dissection (SCAD) is aseparation of the coronary wall layers, not related to trauma,medical procedures or atherosclerosis. The dissection causesthe blood entry in the vascular wall with the consequentformation of a false lumen and intramural hematoma (IMH).Two pathogenetic mechanisms have been proposed to explainSCAD: a “primary” rupture of coronary endothelium or therupture of the “vasa vasorum”. Clinical presentation andseverity of manifestations are variable, ranging from completeabsence of symptoms to acute coronary syndrome (ACS),cardiogenic shock, cardiac arrest or sudden cardiac death.Despite coronary angiography is the first-line examination, bysupplying two-dimensional images of the lumen, it does notalways allow an incontrovertible diagnosis of SCAD. Newintravascular imaging techniques, such as optical coherencetomography (OCT) and intravascular ultrasound (IVUS), havebeen recently introduced and may be extremely helpful inassessing the coronary wall integrity, thus improving coronaryangiography diagnostic accuracy.Because of the lack of large randomized trials comparingdifferent strategies, the optimal treatment of SCAD is stillcontroversial. The first-line approach is conservative and basedon medical therapy. Nevertheless, in particular situations aninvasive approach is necessary. In the last years, several newstrategies have improved the way to perform percutaneouscoronary interventions (PCI), such as new generation drugeluting stents (DES), bio-resorbable scaffolds (BRS), sirolimusself-expandable stent (SES), drug eluting balloons (DEB), andcutting balloon. Cardiac artery bypass graft (CABG) is an evenmore invasive method to restore coronary flow and should beconsidered in urgent/emergent settings when PCI is notfeasible or has failed.Cause the therapeutic approach of SCAD can besubstantially different from that of atherosclerotic coronaryartery disease, an accurate diagnosis is crucial to set up thebest treatment strategy.Keywords: Spontaneous coronary artery dissection,Iintramural hematoma, Coronary wall, Acute coronarysyndrome, Coronary angiographyAbbreviationsACS: Acute Coronary Syndrome; AMI: Acute MyocardialInfarction; BB: Beta-Blockers; BRS: Bio-Resorbable Scaffolds;CABG: Cardiac Artery Bypass Graft; CCB: Calcium ChannelBlockers; CCTA: Coronary Computed Tomography Angiography;DAPT: Dual Antiplatelet Therapy; DES: Drug Eluting Stents;FMD: Fibromuscular Dysplasia; IMH: Intramural Hematoma;IVUS; Intravascular Ultrasound; OPT: Optical CoherenceTomography; PCI: Percutaneous Coronary Intervention; SCAD:Spontaneous Coronary Artery Dissection; SES: Sirolimus SelfExpandable StentIntroductionDefinitionSpontaneous coronary artery dissection (SCAD) is defined asspontaneous separation of the coronary wall layers, notrelated to trauma, medical procedures, or atherosclerosis. Thedissection causes the blood entry in the vascular wall with theconsequent formation of false lumen and intramuralhematoma (IMH) [1]. Copyright iMedPub This article is available from:

Interventional Cardiology JournalISSN 2471-8157EpidemiologyThe first case of SCAD was an autopsy report described in1931 by Pretty [2]. A better awareness of the disease and theimprovement of coronary diagnostic imaging has over time ledto an increased number of diagnoses. In the coronaryangiography era SCAD prevalence has risen from 0.2% to 1.1%[3,4] to 1.7% to 4% according to more recent reports [5,6]. Theprevalent occurrence of SCAD in women has also been welldocumented: Vanzetto reported a 8.7% prevalence of SCAD inwomen younger than 50 years in a series of more than 10000acute coronary syndrome (ACS) patients [7].Same prevalence (9%) has been recently confirmed by aCanadian study, conducted in a population of young women( 50 years) who underwent coronary angiography [8].Moreover, Nakashima et al. recognized SCAD as the cause ofacute myocardial infarction (AMI) in 35% of women under 50years, while Elkayam et al. showed that SCAD is the mostcommon cause of pregnancy-related AMI (mean age 34 years),especially in the third trimester of pregnancy or in postpartumperiod [9,10]. A gender preference seems thusunquestionable: women cover about 90% of the diagnosedSCAD with a mean age of 44-55 years and similar involvementof all races [5,9,11].PathogenesisSCAD can affect any layer of the vascular wall: intima, mediaor adventitia. Two pathogenetic mechanisms have beenproposed to explain the spontaneous separation of thevascular wall layers: the “primary” laceration of coronaryendothelium and the rupture of the vasa vasorum, bothleading to IMH; the consequence of blood accumulation insidethe vascular wall is the reduction of coronary flow within thetrue lumen and an impaired myocardial perfusion [12].Many non-atherosclerotic conditions can promote orprecipitate SCAD, as documented in literature. Fibromusculardysplasia (FMD) is an inflammatory non-atheroscleroticvascular disease strongly associated with SCAD and should bealways investigated [13-16]. Pregnancy is also considered acondition predisposing to SCAD; this association may be due tothe drastic hemodynamic changes and the increase of severalhormone levels [17,18]. In particular, progesterone levelselevation alters the fibro-elastic composition and collagenproduction of the vascular wall, while the increase of estrogendrives a pro-thrombotic state [19,20]. Pregnancy and chronicuse of hormonal therapies are indeed considered contributorycauses of SCAD [21,22].Chronic inflammatory diseases, such as polyarteritis nodosa,Crohn’s disease, ulcerative colitis, sarcoidosis, Churg-Strausssyndrome, Wegener’s, granulomatosis, rheumatoid arthritis,giant cell arteritis, celiac disease could cause SCAD through along term vasculitic process [1,23,24].Also, some connective tissue disorders, such as EhlersDanlos syndrome, systemic lupus erythematosus, Marfan22017Vol.3 No.1:3syndrome, cystic medial necrosis, alpha-1 antitrypsindeficiency, polycystic kidney disease, seem to contributesignificantly to the development of SCAD because of analteration of the elastic fibers composition of coronary wall[1,25,26].In addition to the over-exposed conditions favoring thedevelopment of SCAD, numerous stressful events, such asintense physical exercise and use of sympathetic-mimeticsubstances, could represent precipitating factors [27-31]. Theunderlying pathogenetic mechanisms include the intenserelease of catecholamines and the increase of intra-abdominalpressure, due to prolonged Valsalva-like activities, leading toan increase of coronary arteries shear stress and amplified riskof rupture of intimal wall or vasa vasorum.Clinical Aspects and DiagnosisClinical aspectsClinical presentation and severity of manifestations isvariable in patients with SCAD, depending on the degree ofreduction of the true lumen, and the number and extension ofthe involved vessels [32]. For this reason, patients affected bySCAD could be either completely asymptomatic or presentwith ACS, cardiogenic shock, cardiac arrest or sudden cardiacdeath, although this fatal presentation seems to beunderestimated [33,34]. Most patients presenting to medicalattention manifested typical symptoms of ACS (chest pain,nausea, vomiting, diaphoresis, dyspnea) sometimesaccompanied by the increase of cardiac enzymes [35].The increase of cardiac necrosis markers is often mild, asdemonstrated by a Japanese study that emphasizes a lessextensive myocardial damage in the presence of SCAD ratherthan of atherosclerotic lesions; as a supporting evidence, leftventricle ejection fraction during hospitalization for SCAD isbetter preserved and likely to rise in the follow-up [9,36].DiagnosisCoronary angiographyCoronary angiography is the first-line examination in orderto identify and type a SCAD; classic angiographic featuresinclude extraluminal contrast spreading, multiple lumens andreduced intraluminal filling [37-40] (Figure 1a and 1b). Saw etal. recognized and classified three different subtypes of SCADon the basis of coronary angiography: type 1 detects thepathognomonic lesion of SCAD characterized by intimal lesionwith false lumen evidence; type 2 describes the presence ofwidespread and long stenosis (typically 20 mm) limited eitherto the area of IMH (type 2A) or involving the coronary in toto(type 2B); type 3 concerns a focal stenosis ( 20 mm) similar toan atherosclerotic lesion and, therefore, worthy of furtherinvestigations such as intracoronary imaging [1].This article is available from:

Interventional Cardiology JournalISSN 2471-81572017Vol.3 No.1:3Figure 1 Long dissection of the second obtuse marginal branch in a right-caudal view (Figure 1a) and a caudal view (Figure 1b)evident as a radiolucent linear defect at coronary angiography.In consideration of this angiographic classification, Sawproposed a diagnostic algorithm for suspected SCAD includingboth clinical and anamnestic elements: absence ofatherosclerotic risk factors, ACS in young women ( 50 years),history of FMD, chronic inflammatory or connective tissuediseases, recent physical or emotional stress [41]. Ifangiographic evidence of false lumen allows an easy diagnosisof type 1 SCAD, in absence of this pathognomonic sign acareful assessment of the angiographic lesion is needed: a type2 SCAD should be considered if coronary stenosis length is 20mm and can be confirmed by intracoronary nitroglycerininjection, and a possible repeated angiography after 4-6weeks; if coronary stenosis is conversely shorter than 20 mm,the distinction from the classical atherosclerosis stenosisbecomes challenging and an intracoronary imaging examshould be performed, especially if the suspicion is supportedby the absence of atherosclerotic disease in other coronaryarteries, and in presence of long (11 mm to 20 mm) and linearstenosis. The most frequent angiographic subtype is type 2 in67.5% of cases, followed by type 1 in 29.1% and type 3 in 3.4%of cases.Every coronary segment may be potentially involved butVirmani et al. documented a significantly higher involvementof left anterior descendent (70% to 75% of cases) followed bythe right coronary artery (20% of cases); a remarkablepredilection for distal and smaller tracts has been alsodescribed [42-44]. A gender difference has moreover beenreported with left anterior descendent more frequentlyinvolved in females, while right coronary artery in males[45,46] (Figure 2). Copyright iMedPubFigure 2 Right coronary artery with angiographic evidenceof caliber reduction at the distal tract (Figure 2a), IVUSimage shows the presence of a false lumen at the same site(Figure 2b).Intravascular imaging: As stated above a two-dimensionalimage of the lumen, supplied by the coronary angiography, issometimes not exhaustive if SCAD is suspected; newintravascular imaging techniques, such as optical coherencetomography (OCT) and intravascular ultrasound (IVUS), areable to improve the diagnostic accuracy of coronaryangiography by providing direct and detailed visualization ofthe coronary wall [47-49].OCT utilizes the effects of the light for the evaluation ofintracoronary structures. However, since the blood distortsOCT images, the injection of a iodinated contrast agent isnecessary during the acquisition. OCT has a considerablespatial image resolution (10 μm to 20 μm) and is thereforeable to distinguish all the anatomic features of a SCAD: intimalflap, intraluminal thrombus, false lumen and IMH.Nevertheless, OCT is limited in the ability to observe the entire3

Interventional Cardiology JournalISSN 2471-81572017Vol.3 No.1:3extension of IMH by the poor optical tissue penetration (1 mmto 2.5 mm) [50,51].The currently most accessible alternative to OCT isrepresented by IVUS, that is based on the ability of apiezoelectric crystal to emit ultrasounds which interact withtissues and adjacent structures and are reflected to atransducer with production of images. IVUS has a discreteimage resolution (100 μm to 200 μm) but a greater tissuepenetration (about 5 mm): when compared to OCT, it allows abetter assessment of the false lumen and of the IMH extensionbut is less effective in evaluating the intima interface [52](Figure 2a and 2b).For these reasons, OCT is the intravascular imagingtechnique of choice in the evaluation of SCAD for its ability toidentify the IMH and the double lumen, also considering thelimited clinical benefit of assessing the exact transverseextension of IMH [53]. Moreover, these techniques are alsohelpful in evaluating the proper deployment of either the stentor the bioresorbable scaffold (BRS) if a percutaneous coronaryintervention is chosen (Figure 3a-3d). Conversely, althoughthese intracoronary imaging techniques can definite thediagnosis of SCAD, facilitate and guide the correct placementof coronary devices, confirm adequate coverage of thecoronary dissection, they are not riskless. The introduction ofIVUS or OCT catheters and the injection of a contrast agent forOCT may indeed cause the extension of the dissection and acomplete catheter-induced occlusion of the vessel. About theuse of these extremely advanced diagnostic tools a carefulevaluation of the case by case risk/benefit ratio is thusadvocated.Non-invasive imaging: Coronary computed tomographyangiography (CCTA) is the only non-invasive diagnostic examfor coronary arteries evaluation [54,55]. In SCAD setting CCTAmay demonstrate the spreading of contrast within the falselumen, coronary stenosis, and presence of IMH. However, inconsideration of the low diagnostic power of this test inevaluating distal and small-caliber coronary arteries (diameter 2.5 mm) and of the high prevalence of SCAD in this type ofvessels, often occurring without extraluminal contrastspreading, the diagnostic usefulness of CCTA in SCAD settingappears limited. For this reason, CCTA is not recommended asfirst-choice examination in patients with SCAD; converselyCCTA may be useful in the non-invasive follow-up of patientswith proximal-to-middle tracts SCAD, as recently demonstratedby Roura [56,57].TreatmentRandomized trials comparing different treatment strategieshave not been carried out and the optimal treatment of SCADis still uncertain. In general, the first-line approach consists of aconservative medical therapy [1]. This widespread opiniondepends on the evidence that angiographic healing occurs inthe majority of cases, varying from 73% to 90% and reaching100% if the control angiography is performed 26 days afterSCAD onset [42,58].4Figure 3 Left anterior descending coronary artery withdishomogeneous caliber reduction at the distal tract (Figure3a). IVUS shows the presence of a false lumen at the samesite (Figure 3b). Coronary angiography after stenting (Figure3c). IVUS confirms good immediate result after stenting(Figure 3d).The preference for medical therapy is also motivated by thelow procedural success rate and long-term results of bothpercutaneous coronary intervention (PCI) and cardiac arterybypass grafting (CABG) [11]. The need for revascularization isdriven by angiographic and clinical aspects: in case of ongoingmyocardial ischemia, persistent ST elevation, hemodynamicinstability, complicated ventricular arrhythmias, an invasiveapproach is advocated, particularly when left main or theproximal tracts of the major coronary arteries are involved [1].On the basis of observational studies only 17% to 20% ofpatients with a definite diagnosis of SCAD are treatedinvasively, including the 3.5% to 10% of patients initiallytreated conservatively and subsequently undergoing aninvasive in-hospital revascularization for recurrent ischemia[41,58,59].Medical therapy: As stated above there is no full consensusabout medical therapy and current recommendations derivefrom observational studies, cause therapy for ACS (SCAD mostfrequent presentation) has not been specifically tested in thesubset of patients with SCAD [19,56].This article is available from:

Interventional Cardiology JournalISSN 2471-8157Despite the lack of evidence, beta-blockers (BBs) areconsidered a cornerstone of medical treatment. Similarly, toaortic dissection, BBs could lessen the risk of propagation ofthe dissection by reducing systemic arterial pressure and heartrate; several studies have indeed demonstrated that BBsreduce arterial shear stress. Moreover, BBs reduce myocardialoxygen consumption, exert an important anti-arrhythmicaction and are known to be associated to a significantreduction in mortality in the setting of AMI [60].A recent observational study in the specific setting of SCADpatients has suggested that BBs is associated with a significantreduction of recurrent AMI [61].Though in absence of data, antiplatelet therapy is commonlyused for management of SCAD: the rationale for single or dualantiplatelet therapy is the risk of thrombosis of thecompressed true lumen; on the other hand, antiplatelettherapy increases the bleeding risk and could theoreticallydetermine the expansion of the IMH and extension of thedissection [56,62]. Aspirin is commonly used, while clopidogrelseems to be the preferred choice when a dual antiplatelettherapy (DAPT) regimen is chosen [61]. The duration of DAPTusually varies from 1 month to 1 year [56]. The role ofticagrelor and prasugrel has not been evaluated and isprobably restrained to the cases of stent implantation [1].There are no data supporting the use of glycoprotein IIb/IIIainhibitors.Anticoagulant therapy is mandatory in the setting of ACS butthe clinical benefit in SCAD is uncertain; similarly, toantiplatelet agents, the positive anti-thrombotic effect isantagonized by the risk of propagation of the IMH so that themajority of evidences discourage heparin continuation onceSCAD diagnosis is assessed [19].Thrombolysis is potentially harmful because of a significantrisk of extension of IMH and has to be avoided when clinicaland anamnestic data suggest a SCAD [63]. In a retrospectivestudy Shamloo pointed out as, among 87 patients with SCADtreated with thrombolysis, about 60% required a subsequenturgent revascularization [64].The use of calcium channel blockers (CCB) and nitrates couldbe beneficial in alleviating symptoms related to a concomitantcoronary spasm, but could contribute to increase the arterialwall stress; the use of CCB has been also recently associated toa higher recurrence of myocardial infarction at long termfollow-up in patients admitted for SCAD [32,61].The role of statins in the setting of SCAD is poorly evaluatedand controversial. A small retrospective study pointed outsafety concerns in a higher SCAD recurrence associated withthe use of statins. This finding has not been confirmed bysubsequent evidences and a small ongoing randomized study(SAFER-SCAD) is currently investigating the hypotheses ofbeneficial effects of statins and angiotensin-convertingenzyme inhibitors in SCAD [11,36,65].Percutaneous coronary intervention: In the setting of SCAD,the rate of procedural success of PCI is low: in a largeretrospective analysis of 189 patients presented with SCAD a Copyright iMedPub2017Vol.3 No.1:353% of technical failure of PCI was reported and 13% ofpatients initially treated with PCI underwent an emergentCABG [58]. In this cohort, PCI failed to protect against repeatedrevascularization or recurrent SCAD. On the basis of, thesefindings, a conservative approach and a prolonged observationis currently recommended [58].In a prospective observational study, Saw described a 64%procedural success rate for PCI; among the patients facingunsuccessful PCI 57% had extension of SCAD, 6% definite stentthrombosis, and 12% underwent urgent CABG [42].Lettieri described a more encouraging PCI success rate of73%, but also in this series the conservative approach wascharacterized by a lower rate of in-hospital cardiac adverseevents, when compared to the invasive strategy; moreover 9%of PCI patients required an urgent CABG and 5% of themexperienced a stent thrombosis [33].The poor results of PCI recognize several reasons that makethe setting of SCAD nowadays still challenging.Firstly, in most cases a predisposing pathology of arterialwall tissues is present and can favor a iatrogenic coronarydissection during intracoronary devices maneuvering; in arecent report a 3.4% rate of catheter-induced dissection wasobserved in patients with SCAD who underwent coronaryangiography [66].Coronary wiring is probably the most crucial proceduralthreat: the guide wire may fail to enter the true lumen and thefalse lumen engagement can potentially extend the dissectionand worsening the arterial flow; the collateral vessels wiringdistally to the stenosis probably represents the only “trick” toconfirm the correct position of the guidewire.The choice of stent dimension could represent a furtherissue; interventional cardiologists usually prefer long and/oroverlapped stents to be sure to cover the whole dissectedsegment, but this strategy predisposes to stent thrombosis andrestenosis. The device diameter choice may also beproblematic, as the real arterial caliber, especially in case oftype 2 and 3 SCAD, could be difficult to perceived atangiography. Nevertheless, an optimal sizing of stent diameteris crucial because after IMH reabsorption an undersized stentstrongly favors late or very late malapposition and the relatedincreased risk of stent thrombosis [67]. Intravascular imagingcould be in this scenario extremely helpful though the use ofIVUS and OCT, as described before, is potentially harmful and aroutine utilization is currently not recommended [48].Other reasons for high PCI failure rate are the prevalentinvolvement of distal coronary segments and the moretortuous pathway of coronary arteries in patients with SCAD,as compared with non-SCAD patients [41,68]. Distal sites andtortuosity are well-known unfavorable factors during PCIbecause of higher risk of arterial wall damage and thedifficulties to reach the target segments with stents orballoons [42].In the last years, several strategies and tricks have beenproposed to reduce PCI complications and improve long-termresults (Table 1); for example, unlike general ACS5

Interventional Cardiology JournalISSN 2471-8157recommendations, the femoral access should be preferred,even though associated with an increased bleeding risk,because the rate of radial access site failure is significantlyhigher in patients with SCAD [42,66]. In order to avoid IMHextension and eventual stent malapposition, many authorssuggest to carefully assess the length of dissected segment andthe true caliber of the vessel with intravascular imagingsupport (OCT or IVUS) [67].Table 1 Percutaneous interventions in SCAD: issues andcorresponding helpful strategies.Tendency to vascular accessartery dissectionFemoral approachCatheter-induced coronarydissectionCareful manipulation of guide catheterWiring the false lumenCheck for collateral vesselengagementRisk of extension of IMHLength of stent exceeding 5 mm to 10mm the dissectionMultiple stentsSESDEBRisk of late/very latemalappositionAdequate stent diameter selection(IVUS, OCT)BRSSESOCT/IVUS confirmation of goodimmediate appositionContinuing DAPT to prevent stentthrombosisBRS: Bio-resorbable scaffold; DAPT: Dual antiplatelet therapy; DEB: drugeluting balloons; IMH: Intramural hematoma; IVUS: Intravascular ultrasound;OCT: Optical Coherence Tomography; SES: Self-expandable stentTo adequately cover the edges of IMH, the stent bordersshould exceed by 5-10 mm the dissection edges. In casemultiple stents are needed, it is preferable to start coveringthe two edges of the dissection (the distal first) and to finallyimplant a third overlapped stent in the mid-segment; thisapproach reduces the risk of a “squeezing-induced”propagation of IMH [1]. An alternative and “more minimalist”procedure consists in stenting only the intimal tear [67].As regards device selection in PCI, drug eluting stents (DES)have dramatically improved patients outcome; despite in ACStreatment DES are considered the standard of care, no dataare available in the specific setting of SCAD. The main issues ofDES are the risk of late malapposition after IMH reabsorptionand the theoretical harm for IMH propagation if accuratesizing of the dissected segment is lacking [19].Bio-resorbable scaffolds (BRS) are recently introduceddevices for percutaneous treatment of coronary arterydisease; BRS provide a temporary support to the arterial wall,release an anti-proliferative drug to limit the inflammatoryreaction and the restenosis phenomenon, and allow vessel62017Vol.3 No.1:3healing and its physiological function restoration. BRS probablyrepresent the most revolutionary approach of the last twodecades, born to overcome the limitations of DES, especiallythe long-term risk of neo-atherosclerosis [69]. In the setting ofSCAD, BRS would eliminate the issue related to late or very latemalapposition after IMH reabsorption because the scaffoldcompletely reabsorbs. Moreover, the complete long-termanatomical and functional healing is a further major advantageas SCAD usually affect young patients. It has been reported thesuccessful use of BRS for treatment of SCAD even fortreatment of very long dissected segments [70-72].However, the use of BRS presents nonetheless somelimitations: Procedural success and long-term results strictlydepend on an accurate evaluation of the coronary lesion basedon the systematic use of IVUS or OCT to determine length ofthe SCAD and caliber of the vessel, but also to check thecorrect expansion and apposition of the scaffold afterdeployment [73]. The risk of early thrombosis after BRSimplantation is strongly related to insufficient lesionpreparation and post-dilatation, nevertheless the routinely useof intravascular imaging techniques is conversely known to beharmful [1,74]. In the setting of SCAD it is often necessary tostent long coronary segments and overlap 2 or more BRS witha consequent additional theoretical risk of thrombosis andrestenosis [75]. Furthermore, BRS should be avoided when thevessel diameter is less than 2.5 mm because of an increasedrisk of device thrombosis [76] and we know that, mostly inyoung female patients, SCAD affects mid-distal segments;another limit is the frequent coronary tortuosity that couldchallenge BRS deliverability, because of higher profile andworse trackability of BRS when compared to conventionalstents.The use of cutting balloon for treatment of SCAD is even lessevaluated and is limited to case reports [77]. The rationale ofthe use of cutting balloon is the attempt to reduce thepressure of false lumen by fenestrating the IMH, avoidingpropagation of dissection and facilitating the healing.However, the use of cutting balloon is associated to the risk ofcoronary rupture, especially in SCAD patients who have highprobability of arterial wall disease [1,77].A recent Italian registry suggests the intriguing possibility toavoid any stent or scaffold implantation and to achieve a TIMI3 flow using drug eluting balloons, allowing a spontaneousdelayed healing [78]. In contrast with this hypothesis, there isa concrete risk of extension of IMH for the increase of pressurein the false lumen during balloon inflation. Moreover, even ifcoronary arteries in SCAD patients are often notatherosclerotic, an acute recoil cannot be ruled out.The use of sirolimus self-expandable stent (SES) has beenalso proposed [79]. The theoretical advantage of SES, knownthat post-dilation is not required, is driven by its ability toadapt softly to the arterial wall, avoiding the risk of IMHpropagation and minimizing struts malapposition due tounderestimation of vessel caliber.Coronary artery bypass graft (CABG): Emergent CABG is anoption after PCI failure, or when coronary anatomy is notThis article is available from:

Interventional Cardiology JournalISSN 2471-8157favourable to PCI or if left main is involved. Procedural successis high because of the relatively young age of patients, theusual absence of comorbidity and of coronary atherosclerosisand calcification. In a small cohort of patients Tweet et al.observed only a 6% unsuccessful grafting in the setting ofSCAD [58]. The long-term results are less encouraging, as at amedian 3.5 years follow-up a consistent part of grafts wereclosed and CABG did not demonstrate to protect agains

intravascular imaging techniques, such as optical coherence tomography (OC T) and intravascular ultrasound (IVUS), have been recently introduced and may be ex tremely helpful in assessing the coronar y wall integrity,

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