Abstract
Background
Spontaneous coronary artery dissection (SCAD) is an under-recognized cause of acute coronary syndrome (ACS), particularly in younger patients without conventional cardiovascular risk factors. Accurate differentiation of recanalized thrombi is essential to avoid inappropriate treatment.
Case Summary
Patients with ACS who underwent intracoronary imaging between January 2024 and June 2025 were retrospectively analyzed. Conventional angiography frequently misclassifies lesions. Optical coherence tomography (OCT) provides diagnostic clarity by identifying intramural hematoma and false lumen morphology in true SCAD, confirming recanalized thrombi through multiple intraluminal channels with preserved vessel walls, or ruling out SCAD by demonstrating fibrocalcific atherosclerosis. These findings directly impact therapeutic decisions, ranging from conservative management to revascularization.
Discussion
OCT consistently outperformed angiography in resolving the diagnostic ambiguity in suspected SCAD and thrombus, preventing misdirected interventions, and guiding pathology specific therapies.
Conclusions
OCT is indispensable in suspected SCAD, refining diagnosis, enabling individualized treatment strategies, and improving patient outcomes.
Key words: acute coronary syndrome, coronary angiography, optical coherence tomography, recanalized thrombus, spontaneous coronary artery dissection
Visual Summary
Visual Summary.
Case Series and Review on Differentiating Spontaneous Coronary Artery Dissection From Recanalized Thrombus
OCT clarifies the pathology by revealing hallmark SCAD features vs the channel-like pattern of recanalized thrombi, thereby guiding appropriate conservative or interventional management. ACS = acute coronary syndrome; OCT = optical coherence tomography; SCAD = spontaneous coronary artery dissection.
Spontaneous coronary artery dissection (SCAD) is an increasingly recognized cause of acute coronary syndrome, particularly in young women without conventional atherosclerotic risk factors. It accounts for 0.2% to 4.5% of all acute coronary syndrome presentations1, 2, 3 and up to 35% among women around 50 years of age,4,5 with >90% of cases occurring in females in their fourth and fifth decades.3
Take-Home Messages
-
•
Late-presenting SCAD may mimic thrombus due to false lumen maturation, and can be confused with a recanalized thrombus; here conventional angiography alone is often misleading and OCT becomes indispensable.
-
•
When myocardial compromise is evident, conservative management must be reconsidered, and ischemia-guided PCI strategies, such as distal to proximal stenting, should be used to limit intramural hematoma propagation and achieve optimal outcomes.
SCAD fundamentally differs from atherosclerotic coronary artery disease in terms of its pathophysiology and management. Accurate diagnosis is critical, and misidentification may lead to harmful interventions, such as unnecessary stenting or failure to address thrombotic events. Since the first documented case in a 42-year-old woman in 1931, our understanding of SCAD has evolved considerably6 (Supplemental Table 1).
High-resolution imaging is essential for this purpose. Optical coherence tomography (OCT), with a resolution of 10 to 20 μm, surpasses intravascular ultrasound in visualizing coronary layers and delineating SCAD-specific features such as intramural hematoma (IMH) and intimal disruptions.7 This case series evaluated the diagnostic limitations of angiography in SCAD and highlighted OCTs pivotal role in improving diagnostic precision and guiding therapy.
Case Series
Over the study period, 4 patients with acute coronary syndrome and angiographically ambiguous coronary lesions were analyzed using OCT, each highlighting the unique diagnostic challenges and therapeutic implications of the disease.
Case 1: complex multivessel SCAD in young and intravascular ultrasound inconclusiveness
The first patient was a 38-year-old male bodybuilder who presented with worsening exertional dyspnea. He had a prior inferior wall STEMI in 2018, which was attributed to presumed SCAD involving the right coronary artery (RCA) and left circumflex artery (LCX) (Figures 1A to 1C). His ejection fraction (EF) improved from 20% postinfarct to 55%, and a negative stress test was performed during the 2022 follow-up.
Figure 1.
Case 1: Angiogram
In 2018 at another center, (A) suspected spontaneous coronary artery dissection (SCAD) in the right coronary artery (RCA). (B) Left circumflex artery (LCX) and (C) likely missed SCAD in left anterior descending artery (LAD). In 2024 at our center, interpreted as SCAD of the (D) proximal LAD with (E) extensive SCAD (red arrow) of large nondominant LCX with OMM and (F and G) extensive SCAD (red arrow) of the RCA from the ostium to PDA and PLV. OMM = obtuse marginal - major; PDA = posterior descending artery; PLV = posterior left ventricular artery.
In 2024, he experienced declining EF (35%-40%), new left anterior descending artery (LAD) territory hypokinesia, and a dilated left ventricle (left ventricular end diastolic diameter: 60 mm) with an old RCA scar. Repeat angiography revealed suspected SCAD in the proximal LAD (missed in 2018), proximal LCX extending to the obtuse marginal/obtuse marginal-major, and from the RCA ostium to the posterior left ventricular artery and posterior descending artery (Figures 1D to 1G). Cardiac positron emission tomography computed tomography (PET CT) showed nonviable segments in the basal inferior/inferolateral RCA (2/6 segments), with preserved perfusion/metabolism elsewhere and global hypokinesia (EF: 30%). Autoimmune, prothrombotic, and computed tomography renal angiography findings were unremarkable. Considering the advanced myocardial dysfunction and imaging results, a multidisciplinary heart team recommended cardiac transplantation. However, the patient remained disinclined to undergo transplantation despite structured and repeated counseling.
Given the complex anatomy and reduced EF, percutaneous coronary intervention (PCI) was performed on the RCA under intravascular ultrasound guidance. Intravascular ultrasound (Figure 2) failed to differentiate between SCAD and thrombus. The first stent was placed distally, mainly in the healthy segment, to “jail” the extensive SCAD to prevent its extension and seal the false lumen (proximally). Closure of the PLV false lumen was noted after stenting, likely because of this effect (Video 1).
Figure 2.
Case 1: Pre- and Post-PCI High-Definition Intravascular Ultrasound of the RCA
(A) Multiple blood-filled lumens (yellow arrows) noted from the proximal RCA to the PDA. (B) Post- percutaneous coronary intervention (PCI) intravascular ultrasound, well-expanded stents, and the healthy distal segment of the PDA. Abbreviations as in Figure 1.
Subsequent staged OCT of the LAD (Figure 3A) and LCX (Figure 3B) confirmed SCAD, revealing intimal and internal elastic lamina rupture, IMH, and true lumen compression (subtle or missed on angiography). OCT demonstrated a second lumen in the LCX (Video 2), with a displaced true lumen (3 to 6 o'clock) and clear intimal tears. The patient subsequently underwent PCI of the LCX and the proximal LAD.
Figure 3.
Case 1: Prestenting Optical Coherence Tomography of the LAD and LCX
(A) LAD: intramural hematoma (∗), intimal rupture (blue arrow), and lumen being pushed inward. (B) LCX showing a second lumen forming toward 9 o’clock to 3 o’clock (∗) and the true lumen (#) being pushed toward 3 o’clock to 6 o’clock; clear intimal tears (blue arrow) are noted. Abbreviations as in Figure 1.
At 1-year follow-up, the EF improved to 45%, with patent stents and no new disease. Even after extensive investigation, the etiology of pan coronary SCAD remains elusive. Although the patient presented to us 6 years after the initial presentation, a history review revealed that he was on unknown oral and injectable drugs (likely anabolic steroids), which, along with heavy weight training, could have been the precipitating cause of SCAD.
Case 2: resolving angiographic mimicry: recanalized thrombus misdiagnosed as SCAD
A 45-year-old man with chest pain, initially diagnosed with spontaneous RCA dissection at another center (Figure 4) on medical therapy, remained symptomatic and presented to us. Angiography showed luminal narrowing suggestive of type 1 SCAD, but also multichannel structures raising suspicion for recanalized thrombus, creating a diagnostic dilemma.
Figure 4.
Case 2: Initial Coronary Angiography Image
Projection: LAO cranial (A) and RAO (B) showing luminal irregularities (#) that were initially interpreted as spontaneous right coronary artery dissection. The angiogram depicts an abrupt luminal caliber change, which can be ambiguous and mimicked by an organized thrombus. LAO = left anterior oblique; RAO = right anterior oblique.
Subsequent OCT (Figure 5) revealed multiple small irregular channels within an organized intraluminal mass, consistent with a recanalized thrombus with no SCAD features. This led to the initiation of appropriate antithrombotic treatment and PCI. This case highlights the risk of angiography misdiagnosis and OCT's essential role in achieving diagnostic precision.
Figure 5.
Case 2: Prestenting OCT of the Right Coronary Artery
(A) Longitudinal mode optical coherence tomography (OCT) demonstrating the complex channelized nature of the thrombus. (B-G) Magnified OCT view showing clear delineation of the channels (∗) within the thrombus and intact internal elastic lamina (red arrow) and media (open arrows) behind the mass, confirming the intraluminal nature of the lesion rather than dissection within the vessel wall. The intact internal elastic lamina tracing behind the second lumen confirms it is within the vessel cavity, suggesting a thrombus rather than spontaneous coronary artery dissection (SCAD); the edge of the thrombus (#) can be traced back in to a secondary lumen (@) due to recanalization of the thrombus (not to be confused with a false lumen of SCAD).
Case 3: establishing a definitive SCAD diagnosis in a young STEMI patient with ambiguous angiography
A 48-year-old man with STEMI presented with ambiguous angiographic findings (Figures 6A to 6F) in the LAD (thrombotic occlusion or type 1 SCAD) with TIMI flow grade 2 and suspected type 3 SCAD in the mid RCA and OM branches. Given the diagnostic uncertainty, OCT of the LAD (Figures 6G to 6I) revealed inward displacement of the true lumen by an IMH, confirming the diagnosis of SCAD. PCI was performed with a 1:1 cutting balloon and 4-mm drug-eluting stent, achieving TIMI flow grade 3 (Video 3).
Figure 6.
Case 3: Patient Angiogram and OCT of LAD
(A) LAO cranial view with suspected type 3 SCAD of the mid RCA (∗). (B) RAO view with suspected SCAD of the RCA (∗) (C-E). LAD with a suspicious filling defect in the mid LAD (type 1 SCAD/recanalized thrombus) with delayed dye clearance (red arrow) and suspected type 3 SCAD in the LCX/OM (yellow arrow) (F). Final PCI to LAD results (G and H). LAD lumen pushed inward; false lumen indicated with # (I). OCT L-mode: true lumen pushed inward by false lumen (#). Abbreviations as in Figures 1, 4, and 5.
Case 4: woman with Triple Vessel Disease: angiographically SCAD LAD, but is it?
The fourth patient was a 50-year-old woman with no comorbidities, exertional breathlessness, and reduced EF who underwent angiography suggesting triple vessel disease with SCAD in the LAD (Figure 7A). She had been seen at 2 different centers previously and presented to us because of the persistence of symptoms. An angiography review strongly suggested SCAD in the LAD, distal RCA cutoff, and OMM. OCT (Figure 7B) identified a fibrocalcific lesion that was not visible on angiography. The patient subsequently underwent successful angioplasty after lesion preparation using cutting balloon angioplasty (Video 4).
Figure 7.
Case 4: Patient Angiogram and OCT of the LAD
(A) Angiogram showing the LAD, suggestive of a thin tubular lumen with sharp edges, highly suspicious for type 2A/3 SCAD in the LAD. (B) OCT revealing a fibrocalcific plaque with a minimal luminal area of 0.89 mm2 and no features suggestive of an SCAD. Abbreviations as in Figures 1 and 5.
Discussion
The diagnosis of SCAD presents a significant challenge in interventional cardiology. Coronary angiography, although foundational for the initial assessment, often provides “deceptive clarity” because of its lumen only visualization, leading to diagnostic ambiguity or misdiagnosis. This finding has profound implications for patient management and outcomes.
Limitations of angiography and the power of OCT
The inability of angiography to visualize the coronary arterial wall layers limits definitive SCAD diagnosis. Common angiographic features (eg, intimal tears with contrast staining, multiple radiolucent lumens, abrupt caliber changes) are mimicked by other conditions, such as recanalized thrombus or atherosclerosis, leading to misdiagnosis and inappropriate treatment. OCT overcomes this with superior spatial resolution (10-20 μm), directly visualizing SCAD hallmarks: intimal tear, crescent-shaped IMH compressing the true lumen, and precise true/false lumen delineation. IMH is diagnostic, even in the absence of an obvious tear. SCAD typically affects nonatherosclerotic arteries. The core strength of OCT is its ability to differentiate SCAD from recanalized thrombus by revealing irregular channels/lacunae within an organized mass, often overlying an atherosclerotic plaque, with no IMH or dissection flap8 (Tables 1 and 2).
Table 1.
SCAD Classification: Saw Classification16
| SCAD Type | Visual Description | Key Characteristics | Angiographic Appearance |
|---|---|---|---|
| Type 1 | Arterial wall contrast staining with multiple radiolucent lumens | Pathognomonic appearance, highly indicative of SCAD. |  |
| Type 2 | Diffuse stenosis of varying severity and length (typically >20 mm) | Appreciable, but often subtle, abrupt changes in arterial caliber. Smooth, diffuse narrowing. |  |
| Type 2A variant | Diffuse narrowing bordered by normal artery segments (proximal and distal to IMH) | The narrowed section is “sandwiched” between healthy vessel. | |
| Type 2B variant | Diffuse narrowing extending to the apical tip of the artery | The narrowing continues to the very end of the affected artery. | |
| Type 3 | Focal or tubular stenosis (typically <20 mm) mimicking atherosclerosis | Looks similar to traditional blockages. Requires intracoronary imaging (eg, OCT, IVUS) for definitive diagnosis. |  |
| Type 4 | Total distal occlusion of the vessel | Rare presentation where the artery is completely blocked at its far end. |
IMH = intramural hematoma; IVUS = intravascular ultrasound; OCT = optical coherence tomography; SCAD = spontaneous coronary artery dissection.
Table 2.
Comparative Angiographic and OCT Features for Differentiating SCAD From Recanalized Thrombus
| Feature | Angiography (Suggestive of SCAD) | Angiography (Suggestive of Recanalized Thrombus) | OCT (Definitive for SCAD) | OCT (Definitive for Recanalized Thrombus) |
|---|---|---|---|---|
| Intimal tear | Contrast staining, faint tear can be missed | Not typically observed | Clearly visualized point of entry/reentry | Absent |
| IMH | Extraluminal contrast staining (subtle, overlooked) | Absent | Crescent-shaped, low signal area compressing true lumen (hallmark) | Absent |
| False lumen | “Double lumen” appearance (can be mimicked) | Can be mimicked by channels within thrombus | Precisely delineated from true lumen, often with web-like structures | Absent; instead, channels within thrombus |
| Underlying atherosclerosis | Typically absent (occurs in healthy arteries) | May be present | Typically absent (occurs in relatively healthy arteries) | Often overlies an atherosclerotic plaque |
| Channels/lacunae | Not characteristic of SCAD | Multiple, tortuous, or serpiginous channels | Absent | Multiple small, irregular channels or lacunae within organized mass |
| Luminal appearance | Abrupt luminal caliber change, “string” sign, diffuse/focal stenosis | Irregular luminal narrowing, filling defects | True lumen compression by IMH, distinct dissection flap | Heterogeneous, organized mass with intraluminal channels |
IMH = intramural hematoma; OCT = optical coherence tomography; SCAD = spontaneous coronary artery dissection.
Implications for clinical practice
An accurate diagnosis of suspected SCAD is paramount. Misdiagnosis of recanalized thrombi as SCAD could lead to undertreatment of thrombotic tendencies, increasing the risk of future thrombotic events. Conversely, misdiagnosing SCAD as thrombus might result in unnecessary stent implantation, which is often detrimental in SCAD due to vessel friability and high risk of dissection propagation.2,9,10
Although conventional wisdom often favors conservative management for SCAD due to its potential for spontaneous healing,8 this dictum of “leaving a SCAD as such” is rightly questioned when there is a compromised myocardium (acute electrocardiographic changes, rest symptoms, and less than TIMI flow grade 3). Physiological imaging, such as PET CT, can provide evidence-based information on the need for intervention. When revascularization is necessary (eg, ongoing ischemia, cardiogenic shock, left main dissection), a properly executed, advanced imaging–guided coronary intervention can be effective.11 Because there is a high degree of SCAD recurrence (even at coronary segments different from the original segment), patients need lifelong follow-up, avoiding exogenous hormonal therapies, intense isometric exercises/sustained Valsalva maneuvers, and limited weight lifting.
OCT provides a granular understanding of lesion activity, distinguishing healing from active dissections, and guiding management. PCI in SCAD is challenging, but specific strategies, such as stenting the distal edge first and then the proximal and middle segments, can prevent IMH propagation by further false lumen progression. This emphasizes the need for a nuanced, individualized approach to SCAD management.12
Role of OCT in SCAD management and pathophysiological understanding
Beyond diagnosis, OCT directs clinical interventions and enhances the understanding of SCAD pathophysiology (Figure 8). It guides PCI by sizing stents and confirming true lumen wire placement, which is crucial in fragile vessels.11 OCT also monitors SCAD healing, vascular remodeling, and neovascularization in the false lumen, providing prognostic information.13
Figure 8.
Evidence-Based Diagnostic Workflow
ACS = acute coronary syndrome; other abbreviations as in Figures 1 and 5.
OCT has deepened our insight into SCAD, revealing how absent fenestrations affect false lumen pressure and the heterogeneous composition of its contents. The data support the “outside to in” hypothesis, where intramural hemorrhage from the vasa vasorum initiates false lumen formation, with neovascularization aiding healing, informing disease progression, and targeted therapies.13, 14, 15
Limitations, future directions, and therapeutic considerations
Safety considerations for OCT in SCAD include the risk of dissection propagation,9 impaired flow, iatrogenic dissection, catheter-induced occlusion, and hydraulic extension. OCT should be judiciously applied, with decisions integrating echocardiography, fractional flow reserve, and cardiac positron emission tomography findings, especially if a “no intervention” strategy is being considered.13
Future directions highlight OCT's value as a high-resolution modality that minimizes misdiagnosis and inappropriate treatment. Although cardiac computed tomography angiograph may be useful for follow-up, its limited resolution restricts diagnostic accuracy at initial presentation.
Conclusions
The diagnostic discrepancy between coronary angiography and OCT has been highlighted in cases in which chronic or healed SCAD lesions resemble thrombotic lesions. OCT revealed IMH and false lumen organization (cases 1 and 3), clarifying the underlying pathology of the dissection. In contrast, in case 4, a fibrocalcific tight lesion was treated as SCAD even after the patient was symptomatic. Late-presenting SCAD can mimic thrombus due to organizing hematoma or false lumen maturation; PET CT can guide therapy at this stage by revealing ischemic/hibernating myocardium. The dictum of “leaving a SCAD as such” is questioned when there's existing proof of compromised myocardium. OCT is essential for diagnosing SCAD and differentiating it from recanalized thrombi, thus forming the backbone for successful management in complex cases.
Funding Support and Author Disclosures
The authors have reported that they have no relationships relevant to the contents of this paper to disclose.
Footnotes
The authors attest they are in compliance with human studies committees and animal welfare regulations of the authors’ institutions and Food and Drug Administration guidelines, including patient consent where appropriate. For more information, visit the Author Center.
Appendix
For supplemental videos and tables, please see the online version of this paper.
Appendix
– Case 1: Angiography of Severe Spontaneous Coronary Artery Dissection of Right Coronary Artery and Intravascular Ultrasound–Guided Percutaneous Coronary Intervention
– Case 1: Optical Coherence Tomography of Spontaneous Coronary Artery Dissection Left Circumflex Artery
– Case 3: Angiography of Left Anterior Descending Artery Spontaneous Coronary Artery Dissection, Optical Coherence Tomography Left Anterior Descending Artery, and Post-Percutaneous Coronary Intervention Result
Case 4: Angiographically Spontaneous Coronary Artery Dissection Left Anterior Descending Artery Optical Coherence Tomography Shows A Fibrocalcific Tubular Lesion
References
- 1.Alfonso F., Bastante T., García-Guimaraes M., et al. Spontaneous coronary artery dissection: new insights into the diagnosis and treatment. Coron Artery Dis. 2016;27(8):696–706. doi: 10.1097/MCA.0000000000000412. [DOI] [PubMed] [Google Scholar]
- 2.Nishiguchi T., Tanaka A., Ozaki Y., et al. Prevalence of spontaneous coronary artery dissection in patients with acute coronary syndrome. Eur Heart J Acute Cardiovasc Care. 2016;5(3):263–270. doi: 10.1177/2048872613504310. [DOI] [PubMed] [Google Scholar]
- 3.Saw J., Mancini G.B.J., Humphries K.H. Contemporary review on spontaneous coronary artery dissection. J Am Coll Cardiol. 2016;68(3):297–312. doi: 10.1016/j.jacc.2016.05.034. [DOI] [PubMed] [Google Scholar]
- 4.Nakashima T., Noguchi T., Haruta S., et al. Prognostic impact of spontaneous coronary artery dissection in young female patients with acute myocardial infarction: a report from the Angina Pectoris-Myocardial Infarction Multicenter Investigators in Japan. Int J Cardiol. 2016;207:341–348. doi: 10.1016/j.ijcard.2016.01.188. [DOI] [PubMed] [Google Scholar]
- 5.Rashid H.N.Z., Wong D.T.L., Wijesekera H., 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. 2016;202:336–338. doi: 10.1016/j.ijcard.2015.09.072. [DOI] [PubMed] [Google Scholar]
- 6.Pretty H. Dissecting aneurysm of coronary artery in a woman aged 42: rupture. BMJ. 1931;1:667. [Google Scholar]
- 7.Barbieri L., D’Errico A., Avallone C., et al. Optical coherence tomography and coronary dissection: precious tool or useless surplus? Front Cardiovasc Med. 2022;9 doi: 10.3389/fcvm.2022.822998. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 8.Hassan S., Prakash R., Starovoytov A., Saw J. Natural history of spontaneous coronary artery dissection with spontaneous angiographic healing. JACC Cardiovasc Interv. 2019;12(6):518–527. doi: 10.1016/j.jcin.2018.12.011. [DOI] [PubMed] [Google Scholar]
- 9.Yang C., Offen S., Saw J. What is new in spontaneous coronary artery dissection? CJC Open. 2024;6(2Part B):417–424. doi: 10.1016/j.cjco.2023.10.007. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 10.Rawala M.S., Naqvi S.T.S., Yasin M., Rizvi S.B. Spontaneous coronary artery dissection masquerading as coronary artery stenosis in a young patient. Am J Case Rep. 2019;20:159–162. doi: 10.12659/AJCR.913522. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 11.Main A., Saw J. Percutaneous coronary intervention for the treatment of spontaneous coronary artery dissection. Interv Cardiol Clin. 2019;8(2):199–208. doi: 10.1016/j.iccl.2018.11.008. [DOI] [PubMed] [Google Scholar]
- 12.Walsh S.J., Jokhi P.P., Saw J. Successful percutaneous management of coronary dissection and extensive intramural haematoma associated with ST elevation MI. Acute Card Care. 2008;10(4):231–233. doi: 10.1080/17482940701802348. [DOI] [PubMed] [Google Scholar]
- 13.Jackson R., Al-Hussaini A., Joseph S., et al. Spontaneous coronary artery dissection: pathophysiological insights from optical coherence tomography. JACC Cardiovasc Imaging. 2019;12(12):2475–2488. doi: 10.1016/j.jcmg.2019.01.015. [DOI] [PubMed] [Google Scholar]
- 14.Nepal S., Chauhan S., Bishop M.A. StatPearls. StatPearls Publishing; 2025. Spontaneous coronary artery dissection. [PubMed] [Google Scholar]
- 15.Maqableh G.M.Y., Khan K.A., Shahid F., Khan S.Q. Role of optical coherence tomography in chronic spontaneous coronary artery dissection-diagnosis and management. Heart Views. 2023;24(2):119–121. doi: 10.4103/heartviews.heartviews_101_22. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 16.Saw J. Coronary angiogram classification of spontaneous coronary artery dissection. Catheter Cardiovasc Interv. 2014;84(7):1115–1122. doi: 10.1002/ccd.25293. [DOI] [PubMed] [Google Scholar]
Associated Data
This section collects any data citations, data availability statements, or supplementary materials included in this article.
Supplementary Materials
– Case 1: Angiography of Severe Spontaneous Coronary Artery Dissection of Right Coronary Artery and Intravascular Ultrasound–Guided Percutaneous Coronary Intervention
– Case 1: Optical Coherence Tomography of Spontaneous Coronary Artery Dissection Left Circumflex Artery
– Case 3: Angiography of Left Anterior Descending Artery Spontaneous Coronary Artery Dissection, Optical Coherence Tomography Left Anterior Descending Artery, and Post-Percutaneous Coronary Intervention Result
Case 4: Angiographically Spontaneous Coronary Artery Dissection Left Anterior Descending Artery Optical Coherence Tomography Shows A Fibrocalcific Tubular Lesion