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JACC Case Reports logoLink to JACC Case Reports
. 2026 Jun 3;31(32):108733. doi: 10.1016/j.jaccas.2026.108733

Staged Hybrid Rescue With Preoperative PCI via Ascending Aortic Stent in Type A Aortic Dissection

Shota Inoue a,∗, Yukihiro Hayatsu a, Hayate Nomura a, Yoshun Sai a, Naoya Terao a, Akihiro Yamamoto a, Akiko Tanaka b, Masaki Hata a
PMCID: PMC13480211  PMID: 42233905

Abstract

Background

Acute type A aortic dissection (ATAAD) with a completely thrombosed false lumen that causes true lumen collapse and coronary malperfusion is a rare but life-threatening condition.

Case Summary

A 58-year-old man presented with epigastric and back pain. Subsequently, the patient developed shock. An ATAAD with a completely thrombosed false lumen and true lumen collapse was identified in the ascending aorta, resulting in severe ostial stenosis of the left main coronary artery. A bare-metal stent was deployed in the ascending aorta to restore the true lumen patency. Percutaneous coronary intervention (PCI) using stent struts improved coronary perfusion and hemodynamics. The patient subsequently underwent definitive-stage surgical repair.

Discussion

In selected ATAAD cases, ascending aortic stenting enables bridging PCI and hemodynamic stabilization before surgical repair.

Take-Home Message

Ascending aortic stenting may facilitate preoperative bridging PCI for hemodynamic stabilization in selected patients with ATAAD.

Key words: acute type A aortic dissection, ascending aortic bare-metal stent, coronary malperfusion, preoperative PCI, staged hybrid rescue, true lumen collapse

Visual Summary

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Visual Summary.

Visual Summary

Staged Hybrid Rescue Strategy for Acute Type A Aortic Dissection With Coronary Malperfusion

Acute type A aortic dissection with a completely thrombosed false lumen caused severe collapse of the ascending aortic true lumen, resulting in systemic malperfusion and critical ostial stenosis of the left main coronary artery. A staged hybrid rescue strategy was performed using ascending aortic bare-metal stenting to restore true lumen patency, followed by percutaneous coronary intervention through the stent struts to achieve coronary reperfusion and hemodynamic stabilization before definitive surgical repair. LMT = left main trunk; PCI = percutaneous coronary intervention.

History of Presentation

A 58-year-old man presented to the emergency department with sudden-onset epigastric and back pain; the pain radiated caudally toward the lower back and lumbar region. Approximately 1 hour after symptom onset, he developed shock, and he subsequently experienced cardiac arrest shortly after admission to the intensive care unit. Cardiopulmonary resuscitation was initiated immediately, and spontaneous circulation was restored within a few minutes.

Take-Home Message

  • •

    Ascending aortic stenting may facilitate preoperative bridging PCI for hemodynamic stabilization in selected patients with ATAAD.

His vital signs were as follows: heart rate, 99 beats/min; blood pressure, 94/52 mm Hg; and oxygen saturation, 95% on 5 L/min oxygen. A neurological examination revealed paraplegia.

Past Medical History

The patient's medical history included an open Y-graft replacement for an infrarenal abdominal aortic aneurysm, thoracoabdominal aortic replacement for a proximal anastomotic pseudoaneurysm, colonic diverticular bleeding, gastric ulcers, dyslipidemia, type 2 diabetes mellitus, and hypertension.

Differential Diagnosis

Differential diagnoses included acute type A aortic dissection (ATAAD), acute coronary syndrome, rupture of an anastomotic pseudoaneurysm or thoracic aortic aneurysm, pulmonary embolism, and gastrointestinal disorders such as peptic ulcer perforation or bleeding.

Investigations

An initial electrocardiogram revealed ST-segment elevation in leads I, aVR, aVL, and V1-V4. Laboratory findings revealed elevated troponin I (12.7 ng/mL), lactate (6.9 mmol/L), D-dimer (574.9 μg/mL), and leukocytosis (13,300/μL), as well as mild renal dysfunction (creatinine 1.24 mg/dL). Arterial blood gas analysis showed metabolic acidosis with a pH of 7.22 and a base excess of −10.9.

Transesophageal echocardiography revealed reduced left ventricular ejection fraction, no significant aortic regurgitation, and no pericardial effusion. A completely thrombosed false lumen was observed in the ascending aorta (Figure 1A).

Figure 1.

Figure 1

Preoperative Transesophageal Echocardiography and Contrast-Enhanced Computed Tomography

(A) Transesophageal echocardiography showing an acute type A aortic dissection with a completely thrombosed false lumen in the ascending aorta (arrow). (B) Contrast-enhanced computed tomography showing severe compression and collapse of the true lumen in the ascending aorta due to the thrombosed false lumen, which was considered the cause of the patient's hemodynamic instability.

Contrast-enhanced computed tomography revealed an ATAAD extending from the aortic root to the descending thoracic aorta with complete thrombosis of the false lumen and collapse of the true lumen in the ascending aorta (Figure 1B). The location of the entry tear was unclear. The origin of the left main coronary artery was severely narrowed.

Coronary angiography revealed 90% ostial stenosis of the left main coronary artery, which may have been caused by the dynamic compression of the dissected aortic wall (Figure 2A).

Figure 2.

Figure 2

Percutaneous Coronary Intervention Findings

(A) After deployment of a bare-metal stent in the ascending aorta, selective cannulation of the left main coronary artery was achieved through the stent struts. A 90% ostial stenosis of the left main coronary artery was identified, which was believed to have contributed to the lethal arrhythmia and cardiac arrest. (B) Coronary perfusion markedly improved after stent implantation in the left main coronary artery. The patient was subsequently transferred to the operating room for definitive surgical repair.

Management

We considered proceeding directly to surgery without prior hemodynamic stabilization to be excessively risky, given the preceding cardiac arrest and persistent hypotension. We hypothesized that the primary cause of hemodynamic instability was severe true lumen collapse with a completely thrombosed false lumen in the ascending aorta. Consequently, we planned a bridging approach involving the insertion of a bare-metal stent into the ascending aorta, followed by percutaneous coronary intervention (PCI) to stabilize circulation before definitive aortic repair.

At the initiation of catheter intervention, the patient's systolic blood pressure was 60 mm Hg. A 14 × 60 mm Luminexx bare-metal stent (C.R. Bard) was deployed in the ascending aorta via the left radial artery to expand the collapsed true lumen. After stent deployment, systolic blood pressure improved to 90 mm Hg, indicating resolution of shock. Although the true lumen had successfully expanded, severe stenosis of the left main coronary artery persisted. Immediately after deployment, access to the left main coronary artery was achieved through the stent struts. PCI using a 4.5 × 23 mm Xience Skypoint stent (Abbott Vascular) (Figure 2B) restored coronary perfusion. Emergency surgical repair was performed via median sternotomy.

The ascending aorta and proximal arch (zone 1) were replaced using a 24-mm 2-branch J-graft (Japan Lifeline), with reconstruction of the brachiocephalic artery and fenestrations created for the left common carotid and subclavian arteries. A 29 × 120 mm Frozenix stent graft (Japan Lifeline) was deployed into the descending thoracic aorta. The ascending aortic stent was removed after completion of the anatomical repair, as it was no longer required (Figure 3). Intraoperative inspection revealed no residual stenosis at the left main coronary artery ostium, suggesting that the coronary malperfusion was primarily caused by dynamic obstruction rather than by static extension of the dissection into the coronary artery. A coronary stent was deemed unnecessary and was removed. No entry tears were identified in the visualized aortic segments. A frozen elephant trunk procedure was selected to expand the narrowed descending aorta and to facilitate potential future interventions. The total operative time was 5 hours 47 minutes, the cardiopulmonary bypass time was 3 hours 5 minutes, the aortic cross-clamp time was 1 hour 50 minutes, and the circulatory arrest time was 1 hour 2 minutes.

Figure 3.

Figure 3

Intraoperative Findings

The bare-metal stent in the ascending aorta and the coronary stent at the origin of the left main coronary artery were identified and removed. No intimal tear (entry) was observed in the accessible aortic segments.

Outcome and Follow-Up

The patient was extubated on postoperative day 9, and he was transferred from the intensive care unit to the general ward on postoperative day 16. Cerebrospinal fluid drainage was initiated immediately after surgery and continued until postoperative day 3. However, the patient showed no neurological improvement. Follow-up contrast-enhanced computed tomography revealed an enlarged descending aorta with partial reperfusion of the false lumen. Therefore, additional thoracic endovascular aortic repair was performed on postoperative day 28, after which no further aortic enlargement was observed. At the time of transfer, the patient remained paraplegic with a Frankel grade B status. Although he was able to maintain a seated position on the bed, he was unable to ambulate.

Discussion

Acute aortic dissection with complete thrombosis of the false lumen is relatively rare, accounting for approximately 5.7% of all cases.1 When the false lumen is completely thrombosed, organ perfusion depends entirely on blood flow through the true lumen. If the compression of the true lumen is severe, hypotension and subsequent organ malperfusion may occur.

The standard treatment for ATAAD is an open surgical repair. A clinical trial has described endovascular approaches for the ascending aorta.2 Several studies have also reported endovascular treatment of the ascending aorta, including in patients with type A aortic dissection.3,4 However, serious complications such as stroke, stent migration, redissection, and coronary artery stenosis have been documented. Therefore, indications for endovascular treatment of the ascending aorta in ATAAD remain limited. However, in this case, severe true lumen collapse with a completely thrombosed false lumen in the ascending aorta, along with coronary malperfusion, made it difficult to maintain adequate systemic perfusion. Therefore, an initial bare-metal stent in the ascending aorta was selected. This technique carries a risk of intimal injury in the ascending aorta and potential aortic rupture; therefore, careful stent sizing is essential to avoid oversizing.

Even when coronary perfusion is not fully restored, as in the present case, the use of a bare-metal stent permits catheter access through stent struts for subsequent PCI. In addition, the expansion of the ascending true lumen may provide sufficient anatomical space for catheter manipulation, potentially reducing technical difficulties during PCI. In the present case, PCI was completed within 18 minutes of ascending stent deployment, suggesting procedural feasibility even under hemodynamically unstable conditions. In contrast, when an entry tear is clearly identified in the ascending aorta on preoperative imaging and PCI is not planned, a covered stent to seal the entry tear may be a reasonable option.5

Coronary artery involvement occurs in approximately 15% of ATAAD cases and is associated with poor prognosis, particularly when the left main coronary artery is affected.6 PCI bridging has been reported as a strategy to restore coronary perfusion before definitive aortic repair in such critical situations.7 A surgical single-stage strategy aimed at restoring coronary perfusion before aortic cross-clamping has also been reported.8 Accordingly, 2 main treatment strategies have been described for ATAAD with coronary malperfusion: PCI followed by surgery and upfront surgical repair. However, in cases with severe true lumen collapse and a completely thrombosed false lumen in the ascending aorta, as in the present case, PCI may be technically challenging and insufficiently hemodynamically beneficial. Additionally, given the presence of hypotension, a surgical single-stage strategy may also be associated with increased risk. In such situations, a staged strategy consisting of ascending aortic stenting followed by PCI and subsequent surgical repair may provide an alternative approach to achieve rapid and effective hemodynamic stabilization and coronary perfusion restoration.

Conclusions

ATAAD with complete false lumen thrombosis, severe true lumen collapse, and coronary malperfusion can lead to profound hemodynamic instability. In such patients, a staged hybrid strategy combining ascending aortic bare-metal stenting and PCI may enable rapid stabilization before definitive surgical repair. To our knowledge, PCI performed through the struts of an ascending aortic bare-metal stent in ATAAD has not been previously documented and may broaden therapeutic options in this critical context setting.

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.

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