Abstract
We present a case of subclavian artery perforation with mediastinal hematoma following elective percutaneous coronary intervention. A conservative approach was preferred over invasive correction. Although no outcome data exist specifically for subclavian artery injury, registry data in patients with iatrogenic aortic dissection suggest that long-term outcomes are good without vascular repair. (Level of Difficulty: Advanced.)
Key Words: complication, dissection, myocardial revascularization
Abbreviations and Acronyms: CT, computed tomography; ECG, electrocardiogram; PCI, percutaneous coronary intervention
Central Illustration
History of Presentation
A 69-year-old man presented with a 1-day history of chest pain. His initial electrocardiogram (ECG) showed sinus rhythm with first-degree atrioventricular block, and he had raised 0- and 3-hour serum high-sensitivity troponin T levels (23 and 30 ng/L, respectively; reference value <5 ng/L). He was given a diagnosis of non–ST-segment elevation myocardial infarction and was referred for urgent inpatient invasive coronary angiography.
Access was through the right transradial approach. Guidewire progression into the ascending aorta was hindered by tortuosity of the subclavian artery. A hydrophilic wire (RADIFIRST GLIDEWIRE, Terumo; diameter 0.97 mm, total length 150 cm, flexible tip length 3 cm) was therefore used to facilitate catheter advancement into the aortic root. Angiography revealed a heavily calcified stenosis at the ostium of the first obtuse marginal artery, which was successfully revascularized with a single drug-eluting stent (3 × 26 mm Resolute Onyx, Medtronic).
Postprocedurally, the patient developed marked hypotension (brachial blood pressure 70/20 mm Hg in the right arm and 95/40 mm Hg in the left arm), tachycardia (heart rate 120 beats/min), and diaphoresis. He complained of dull, central chest discomfort. Despite aggressive intravenous fluid resuscitation (2,000 mL 0.9% sodium chloride administered immediately through a 16-G peripheral intravenous catheter), he was persistently hypotensive but was alert and orientated. Vasopressor administration for blood pressure support was not deemed necessary.
Learning Objectives
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To recognize procedural factors that may increase the risk of vascular complications during cardiac catheterization and PCI.
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To be able to make a differential diagnosis of complications following PCI that may lead to hemodynamic compromise.
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Appreciate the role of CT in diagnosis and follow-up of vascular injury following PCI.
Past Medical History
The patient’s past medical history included coronary artery disease with previous percutaneous coronary intervention (PCI) to both the left anterior descending and right coronary arteries (more than 10 years before this admission), chronic obstructive pulmonary disease, and obesity. He did not have any history of connective tissue disease or bleeding diathesis.
Differential Diagnosis
Complications following PCI that may lead to hemodynamic compromise include access site bleeding, hematoma or pseudoaneurysm formation, coronary dissection or perforation, air embolism, or large-vessel dissection (1).
Investigations
A 12-lead ECG showed sinus tachycardia, with normal voltage QRS complexes and no ST-T-segment changes. His hemoglobin concentration decreased from 102 g/L preprocedure to 81 g/L. Bedside transthoracic echocardiography did not demonstrate any significant pericardial effusion, left ventricular dysfunction, or dissection of the ascending aorta. A portable chest radiograph showed a widened mediastinum contour (Figures 1A and 1B), and the patient underwent emergency computed tomography (CT) aortography. This imaging revealed right subclavian artery dissection with extension into the brachiocephalic artery and an associated large mediastinal hematoma compressing the superior vena cava (Figures 2A to 2F). A perforation was evident in the distal right subclavian artery just before the origin of the right common carotid artery, with extension of the dissection flap into the proximal vessel (Figure 3).
Figure 1.
Chest Radiographs
(A) Before and (B) immediately after percutaneous coronary intervention. (B) There was new and marked widening of the mediastinal contour. H = head; L = left.
Figure 2.
Contrast-Enhanced Computed Tomography Images
(A to C) Selected coronal and (D to F) axial views are shown. (A and D) Key findings. There is a large mediastinal hematoma (dashed yellow line), which is compressing the superior vena cava (white arrow). Also visible are perforation and dissection of the right subclavian artery (red arrows) extending into its origin from the brachiocephalic artery. Ao = aorta; PA = main pulmonary artery; LV = left ventricle.
Figure 3.
Volume-Rendered Computed Tomography Image of the Aortic Arch and Branch Vessels
There is a distal right (Rt) subclavian artery perforation (blue arrow) with extension of a dissection flap proximally (red arrow). Lt = left.
Management
The proximity of the dissection flap to the right common carotid artery (Figure 3) precluded any percutaneous closure, given the associated risk of graft-induced occlusion of the carotid artery. After discussion with both cardiothoracic and vascular surgery, a conservative management approach was agreed on. The patient was treated with a blood transfusion comprising 2 U of packed red blood cells, with gradual and sustained improvement in his clinical condition and hemodynamic parameters. Serial CT aortograms (Figure 4) did not show extension of the dissection flap or expansion of the mediastinal hematoma. After 1 week the patient was discharged home, and he has remained well on subsequent follow-up.
Figure 4.
Follow-Up Contrast-Enhanced Computed Tomography
A single axial computed tomography slice is shown, demonstrating nearly complete resolution of the previous mediastinal hematoma (dashed yellow line).
Discussion
Large-vessel perforation with mediastinal hematoma formation is an extremely rare complication of PCI. Clues to the underlying cause of the patient’s hemodynamic collapse were the fall in hemoglobin concentration indicative of significant bleeding, the absence of new ST-T-segment changes suggestive of ischemia or infarction on his ECG, an unremarkable bedside echocardiogram, and a widened mediastinal contour on his chest radiograph. In this case, rapid CT aortography confirmed the diagnosis of large-artery perforation and dissection. This was likely the result of artery wall insult by guidewire advancement, with the tortuous subclavian artery being a patient-specific factor that heightened the risk of this particular complication.
Vascular complications following PCI are not infrequent and occur more commonly when the femoral rather than the radial artery is the access site. The transradial approach has significantly reduced the incidence of vascular access site–related complications (particularly rates of major bleeding) (2). Nevertheless, complications may occur and include arterial perforation or dissection, radial spasm, radial artery pseudoaneurysm, and radial occlusion (3). Furthermore, the risk of dissection or perforation is higher with hydrophilic wires because of their design with a coated, stiffer tip. Typically, vascular complications involve the peripheral arteries rather than the central arteries. Central vascular complications are extremely rare (incidence of iatrogenic aortic dissection estimated to be <0.1% globally) (4), and to our knowledge there is only 1 similar report of brachiocephalic artery dissection following right transradial cardiac catheterization (5). No studies have specifically addressed long-term outcomes or management strategies following subclavian artery dissection or perforation with or without mediastinal hematoma, given the rarity of this complication. However, in a small (n = 74, mean age 67 years, 68% male, median follow-up duration 51 months) retrospective analysis of iatrogenic aortic dissections following cardiac catheterization, 2 patients died after developing cardiogenic shock, 2 required aortic surgery, and percutaneous intervention was performed only in cases with coronary artery involvement. The remainder of patients had excellent long-term outcomes with conservative management (6). Similar to our own approach, it appears that the combination of watchful waiting and serial imaging is the preferred strategy in patients who are hemodynamically stable after adequate resuscitation. Spontaneous remodeling of the aorta and restoration to normal aortic anatomy have been reported 30 days after catheter-induced aortic dissection in 1 case report, thus supporting a conservative approach (7).
Follow-up
The patient was followed up in an outpatient setting 12 weeks after discharge. His chest pain had entirely resolved, and he was independent with all activities of daily living. He is planned for routine follow-up in 12 months. No further imaging has since been performed.
Conclusions
Central vascular injury involving the subclavian artery is an extremely rare complication of PCI. A conservative approach using serial imaging to monitor disease resolution is likely to be the preferred management strategy. Although no outcome data exist specifically for subclavian artery dissection, registry data in patients with iatrogenic aortic dissection suggest that long-term outcomes are good without vascular repair.
Funding Support and Author Disclosures
Dr Gulsin is supported by a British Heart Foundation Travel Fellowship (FS/TF/21/33008). All other 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.
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