SCAD is characterized by the separation of coronary artery wall layers due to intramural hemorrhage, with or without associated intimal tear. This condition is unrelated to atherosclerosis, iatrogenic injury, or trauma [2]. Women account for 87–95% of SCAD patients, with an average age of onset ranging from 44 to 53 years [7], In women under 50, SCAD accounts for 25–33% of myocardial infarctions and it is responsible for approximately 15–20% of myocardial infarctions during pregnancy or the perinatal period [2]. Type 2 SCAD is the most common form, accounting for approximately 60–75% of cases diagnosed via coronary angiography, characterized by the absence of an intimal tear and presenting as diffuse arterial narrowing due to intramural hematoma-induced stenosis [2]. Treatment decisions for SCAD are influenced by key differences from atherosclerotic coronary artery disease. First, the underlying pathophysiology of SCAD involves intramural dissection rather than plaque rupture or erosion in an inflammatory and thrombotic milieu [8]. Second, PCI for SCAD is more challenging and associated with inferior short-term and long-term outcomes compared to PCI for atherosclerotic lesions. Most conservatively managed SCAD lesions demonstrate improved coronary flow and reduced stenosis over time, with approximately 95% showing vascular healing within 30 days post-SCAD [9]. Therefore, expert consensuses recommend conservative management for clinically stable SCAD patients over immediate revascularization [3, 10]. For high-risk SCAD patients, several factors must be considered in choosing between medical management and revascularization. High-risk clinical features include persistent chest pain with ongoing or worsening ischemia, hemodynamic instability, shock, or malignant arrhythmias. High-risk anatomical features encompass severe proximal dissection of multiple vessels or dissection involving the left main or LAD ostium [3, 10]. When high-risk features are present, immediate revascularization should be contemplated. A retrospective study categorized left main or proximal coronary artery involvement as high-risk SCAD, while mid, distal, or collateral artery involvement was classified as low-risk SCAD. PCI was predominantly performed in high-risk patients (68.4%), while conservative management was more prevalent in low-risk patients (62.8%). One-year follow-up indicated similar rates of major adverse cardiac events between the two groups; however, the healing rate was higher in the low-risk group compared to the high-risk group (86.4% vs. 33.3%, p < 0.05), suggesting that lesion anatomy plays a critical role in treatment decision-making [11]. Factors that can elevate the risk of PCI include longer lesions requiring multiple stents [12], T guidewire entry into the false lumen causing vessel occlusion, hematoma extension [13] and poor stent apposition due to hematoma absorption [14]. Techniques to mitigate iatrogenic complications during PCI include preferring femoral access [15], utilizing hydrophilic guidewires [16], initiating with soft guidewires and progressing to stiffer wires as necessary [16], employing intravascular imaging for diagnosis and stent optimization [17], using smaller diameter balloons, considering cutting balloons to create windows in the hematoma to reduce false lumen pressure, using multiple stents, starting with the distal segment, then proximal, and finally mid-segment to prevent hematoma expansion [18], considering longer stents with an additional 5–10 mm coverage at the proximal and distal edges of the dissection [3, 10, 18], avoiding a 1:1 vessel-to-stent size ratio, and opting for optimal apposition and self-expanding stents [18]. The European Society of Cardiology recommends drug-eluting stents for SCAD patients, cautioning against the use of bioresorbable vascular scaffolds due to potentially elevated event rates [3]. Dual antiplatelet therapy (DAPT) is typically recommended for SCAD patients undergoing PCI for one year, followed by single antiplatelet therapy. The role of statins in SCAD remains inadequately supported by evidence [3, 10].

This case report first presents a patient with SCAD exhibiting a more severe clinical presentation than typical SCAD cases. The patient, a middle-aged woman with hypertension and depression, initially presented with chest discomfort and was diagnosed with proximal LAD stenosis via coronary computed tomography angiography. Three months later, coronary angiography revealed Type 2 SCAD-like lesions in the LAD and diagonal branch with no self-healing noted in the literature. The lesions were more severe than classic Type 2 SCAD, with IVUS showing intimal dissection and thrombus extending into the media. Despite high-risk features, the patient did not experience acute myocardial infarction. During the PCI procedure, although a soft guidewire was initially used, the insufficient understanding of SCAD lesions resulted in the absence of low-pressure dilation balloons or cutting balloons to relieve false lumen pressure. This led to the expansion of the dissection, causing no-reflow, which rapidly progressed to left main thrombosis and hemodynamic collapse. Rapid placement of a long stent, along with supportive medications, restored blood flow and improved the patient’s condition. Follow-up angiography showed no abnormalities in the stented area, though the diagonal branch remained stenosed. PCI for the distal lesion was successful, but without IVUS, atherosclerosis could not be completely excluded. At 8 months follow-up, coronary angiography showed stable stent placement and no new SCAD or complications. Although IVUS after the initial PCI indicated satisfactory stent expansion and apposition, the patient’s large coronary false lumen at baseline posed higher long-term risks of stent malapposition, in-stent thrombosis or in-stent restenosis. Regular follow-up with intravascular imaging would have been warranted to monitor this risk, however, the absence of such follow-up in this case represents a limitation. The patient received DAPT following the initial coronary intervention and transitioned to aspirin monotherapy after one year, which continues to date. The patient has since remained asymptomatic.