Coronary stenting after aortic root replacement

Abstract

We describe a case of severe coronary artery stenosis in a 29-year-old male 1 month after aortic root replacement (ARR). The patient presented with exertional chest pain that progressed to prolonged resting angina and ventricular arrhythmia. Electrocardiography showed ischemic changes suggestive of left coronary artery involvement, and multislice computed tomography angiography confirmed subtotal stenosis at the left main (LM) bifurcation. Urgent percutaneous coronary intervention (PCI) with drug-eluting stent implantation from the LM to the left anterior descending artery was performed using a provisional technique, resulting in improvement of left ventricular ejection fraction from 23% to 55%. The patient was discharged without complications and remained event-free at 6-month follow-up. This case highlights a rare but potentially life-threatening coronary complication after ARR, which may be related to perfusion cannula placement, technical factors during coronary ostial reimplantation, or proliferative reactions to the aortic prosthesis or gelatin–resorcinol–formaldehyde glue. It underscores the need for early recognition and vigilance for coronary ischemia after ARR − even in young patients without prior coronary artery disease − and emphasizes the efficacy of emergency PCI. A multidisciplinary approach is recommended to optimize outcomes in complex postsurgical cardiovascular patients.

Introduction

Aortic root replacement (ARR) is often the only viable surgical option for patients with complex aortic root pathology. Over the years, ARR has undergone significant refinements, overcoming early complications to achieve the high standards seen today. Pioneering surgeons such as Bentall, De Bono, Carrel, Kouchoukos, Cabrol, David, Ross, and others have been crucial in developing and perfecting surgical techniques and demonstrating their efficacy. In parallel, improvements in prosthetic materials have significantly lowered the incidence of complications such as false aneurysms of the coronary and distal aortic anastomoses and paraprosthetic hematomas caused by graft porosity.

Despite significant advances in ARR techniques, de novo ostial coronary artery stenosis remains 1 of the most serious and well-recognized complications, yet its precise incidence is unclear. Large-scale studies of ARR outcomes generally do not report specific rates for these lesions, likely due to their low incidence and inclusion under broader categories such as myocardial infarction (MI), sudden death, and life-threatening arrhythmias. In a systematic review by Mookhoek A, et al. [1] (46 studies, 7,629 patients), early hospital mortality was 5.6%. Within this cohort, MI accounted for 5.9% of early deaths, arrhythmias for 5.9%, and low cardiac output for 20.4%. Coronary obstruction may be embedded in these fatal events and may also manifest later. Regarding long-term outcomes after ARR, the authors reported that 9% of late deaths were attributed to low cardiac output, 3.3% to arrhythmias, and 9.6% to other cardiac-related causes.

Nevertheless, several single-centre studies, case reports, and small series provide evidence for the occurrence of these de novo lesions. Guilmet D et al. [2] reported an incidence of ostial left coronary artery (LCA) stenosis after Bentall surgery (using the button reimplantation technique) in 2 of 150 patients (1.33%). A similar rate was observed by Gordeev M.L. et al. [3], who described a 5-year single-centre experience involving patients who developed coronary stenosis following ARR: 5 of 302 individuals (1.66%). Likewise, Ramarathnam A. et al. [4] reported a rate of intraoperative or immediate postoperative ischaemia in 4 of 271 ARR cases (1.5%). According to Won K. et al. [5], significant stenosis, kinking, or occlusion of the coronary interposition graft was detected by MSCT angiography in 4 of 25 patients (16%) who underwent ARR using the Cabrol technique. Meanwhile, Kincaid E. et al. [6], in a retrospective single-centre study of ARR using stentless porcine valves, reported an intraoperative incidence of coronary insufficiency at the time of cardiopulmonary bypass weaning of 2.6% (13 of 503 patients). Notably, none of these patients experienced late coronary occlusion; hence, the authors attributed the complication primarily to technical factors related to coronary attachment. These publications confirm that, although rare, ostial lesions remain a serious concern after ARR.

Such complications can be life-threatening and may manifest at varying intervals after surgery, depending on the underlying aetiological factors. The pathogenesis of these lesions is likely multifactorial.

Pathophysiological mechanisms can be categorised into 5 principal groups:

• 1.Technical factors during coronary reimplantation that lead to haemodynamic alterations and disturbed flow. These include misalignment of the coronary buttons or excessive tension, twisting, or kinking of the arteries, which may cause acute or delayed ostial obstruction [5,7]. Size mismatch between the interposed coronary graft and the native coronary artery may also promote turbulent flow and intimal hyperplasia, thereby increasing the risk of stenosis.
• 2.Ischaemic and mechanical coronary artery injury during surgery. Direct trauma to the coronary ostia during antegrade cardioplegia can result in intimal damage, micro-injuries, and local pressure necrosis, predisposing to fibrosis and late stenosis. Over-dilatation of the coronary artery due to the perfusion cannula or excessive infusion pressure during cardioplegia has also been implicated in ostial injury. This aetiology has been reported even in patients undergoing aortic valve replacement without coronary reimplantation, with an incidence of approximately 0.3% in a series of 2158 operations performed at the Montreal Heart Institute [8].
• 3.Tissue reaction and inflammatory responses, including immunological reactions to prosthetic and suturing materials, as well as local tissue irritation induced by aggressive adhesives such as GRF glue [[9], [10], [11], [12], [13], [14]]. These adhesives can provoke a local inflammatory response or cause external compression if the glue mass deforms, particularly when used extensively.
• 4.External compression from a tense paraprosthetic haematoma [15].
• 5.Genetic predisposition in patients with the apolipoprotein-E genotype 4 (ApoE-ε4), which has been identified as a potential risk factor for coronary ostial stenosis and for multiple lesions in other vascular territories [16,17].

This case report describes a patient who developed de novo left main (LM) stenosis after ARR and underwent percutaneous coronary intervention (PCI) as the selected revascularization strategy. It underscores the importance of timely recognition, the role of multimodal imaging for accurate diagnosis, and an interventional approach to managing post-ARR coronary complications.

Case presentation

Patient information. A 29-year-old male patient was transported to the hospital by ambulance with complaints of pain in his left shoulder, radiating to the left arm and lower jaw. He reported that, 2 weeks prior to admission, he had experienced similar pain triggered by minimal exertion (eg, dressing), which resolved spontaneously at rest. Two days before hospitalization, the symptoms worsened, with increased pain intensity and more pronounced radiation to the left upper limb and lower jaw. On the day of admission, the pain occurred at rest and lasted for more than 30 minutes, prompting him to call an ambulance.

Upon admission, during the transfer from the ambulance stretcher to the hospital bed, the patient developed recurrent life-threatening ventricular arrhythmia. Resuscitation was performed, and sinus rhythm was restored after multiple shocks delivered by an automated external defibrillator (AED).

One month earlier, he had undergone ARR with an “On-X” (ARTIVION™) 23 mm prosthetic mechanical valve conduit (Bentall-De Bono technique modified by Kouchoukos) due to severe aortic regurgitation. Since then, he has been on anticoagulant therapy with a vitamin K antagonist (VKA), specifically warfarin at a dosage of 4.5 mg q.d.

The timeline of the patient’s clinical progression and treatment milestones is summarized in Table 1.

Table 1.

Patient history and treatment chronology leading to PCI.

Date	Age, years	Event
2018	23	Diagnosis of PFO, BAV, aortic root dilatation, and moderate AR. Surveillance and routine follow-up were recommended.
2022	27	Progression of aortic root dilatation and moderate-to-severe AR. Surgery was recommended.
2023	28	Diagnosed with UCTD based on comprehensive clinical and genetic tests.
2024, 1 Jul	29	Underwent ARR surgery with an “On-X” (ARTIVION) prosthetic valve conduit (Bentall-De Bono in Kouchoukos modification) and PFO closure via J-shaped mini-sternotomy. Anticoagulant therapy with VKA therapy initiated (warfarin).
2024, 25 Jul		Presented with pain in the left shoulder triggered by minimal exertion (e.g., dressing).
2024, 7 Aug		Worsening of symptoms, including pain radiating to the left arm and lower jaw.
2024, 9 Aug		Chest pain at rest lasting longer than 30 minutes. Called an ambulance and was admitted to the emergency department.

Abbreviations: AR, aortic regurgitation; ARR, aortic root replacement; BAV, bicuspid aortic valve; PFO, patent foramen ovale; UCTD, undifferentiated connective tissue disorder; VKA, Vitamin K antagonist.

Physical examination findings. Following resuscitation, the patient was conscious and alert, with an asthenic body habitus and adequate nutritional status. The skin and mucous membranes appeared pale, without cyanosis or oedema. A well-healed J-shaped sternotomy scar was noted. The respiratory rate was 19 breaths per minute, and oxygen saturation (SpO₂) was 96% on oxygen via mask. Breath sounds were harsh, with no wheezes or rales. Blood pressure measured 108/63 mmHg. Heart auscultation revealed an audible mechanical prosthetic aortic valve click without additional murmurs. The abdomen was soft and nontender. Pupils were equal and reactive to light.

Diagnostic assessment. After resuscitation, an electrocardiogram (ECG) was recorded. As shown in Fig. 1, the ECG demonstrates signs of myocardial ischaemia, including sinus rhythm with a heart rate (HR) of 75 beats per minute, ST-segment depression in leads I, II, aVL, and V4–V6, and ST-segment elevation in lead aVR, accompanied by features of incomplete right bundle branch block.

Fig. 1.

ECG on admission showing sinus rhythm with a heart rate of 75 beats per minute, incomplete right bundle branch block, ST-segment depression in leads I, II, aVL, and V4–V6, and ST-segment elevation in lead aVR. The red dotted line indicates the isoelectric line.

The initial troponin I level was 0.01 ng/mL.

Transthoracic echocardiography (TTE) revealed a reduced left ventricular ejection fraction (LVEF) of 23%, with akinesis of all apical segments, the entire anterior wall, and the medial segment of the interventricular septum. The calculated left ventricular stroke volume (LV SV) was 30 mL. Additionally, trace mitral regurgitation and trace transvalvular regurgitation of the prosthetic aortic valve were noted, without signs of prosthetic dysfunction.

Given the patient’s recent major cardiac surgery, ECG-gated MSCT angiography was performed. Centreline reconstructions of the coronary arteries revealed an ostial stenosis of the right coronary artery (RCA), estimated at 40%, as shown in Fig. 2.

Fig. 2.

Centreline reconstruction of the RCA from admission MSCT angiography. AO, aorta; RCA, right coronary artery.

The LCA exhibited a subtotal bifurcation lesion involving the trunk and distal segment of the LM, classified as Medina 1,0,0, as shown in Fig. 3. The proximal LM diameter measured 3.58 mm, with a lesion length of 4 mm. Notably, radiodensity measurements within the LM ostium lumen were 388 Hounsfield units (HU), 75 HU within the identified lesion, and 290 HU within the LCA bifurcation lumen.

Fig. 3.

Centreline reconstruction from the LM to the LAD from admission MSCT angiography, showing subtotal occlusion of the terminal LM. AO, aorta; HU, hounsfield units; LM, left main; LAD, left anterior descending; LCX, left circumflex.

Intervention. Given the recent sternotomy, the emergent nature of the clinical presentation, and imaging findings, the local heart team, in consultation with the patient, decided to proceed with coronary angiography and PCI. The patient received a loading dose of dual antiplatelet therapy consisting of 600 mg clopidogrel and 300 mg acetylsalicylic acid (ASA).

Emergency coronary angiography was performed via transfemoral access with administration of 5,000 IU of unfractionated heparin intravenously, achieving an activated clotting time (ACT) of 301 seconds.

Selective RCA angiography confirmed a solitary ostial 40% lesion with Thrombolysis in Myocardial Infarction (TIMI) grade 3 flow. Well-developed septal collaterals supplying the mid-segment of the left anterior descending (LAD) artery and proximal third of the diagonal branch were identified, along with collateral filling of the terminal branches of the left circumflex (LCX) artery, as shown in Fig. 4.

Fig. 4.

RCA angiography revealing 40% ostial stenosis and collaterals from the RCA system to the LAD. DB, diagonal branch; LAD, left anterior descending artery; RCA, right coronary artery; SB, septal branch.

Selective angiography of the LCA demonstrated a subtotal lesion involving the trunk and distal portion of the LM artery, as shown in Fig. 5. The LAD artery exhibited TIMI grade 2 flow, with evidence of reversed blood flow originating from the major septal branch, interrupting LAD contrast filling. Blood flow in the LCX artery was assessed as TIMI grade 3, accompanied by collateral circulation at the level of its terminal branches.

Fig. 5.

Left coronary artery angiography showing a subtotal lesion in the terminal LM. LM, left main coronary artery; LAD, left anterior descending artery; LCX, left circumflex artery.

A JL 3.5 guide catheter was used to introduce two 0.014″ coronary wires sequentially across the lesion, advancing into the LCX and LAD distal ends. A DES measuring 4 × 18 mm (Resolute Integrity™, Medtronic) was directly deployed from the LM ostium into the proximal LAD, with minimal protrusion into the aorta, as shown in Fig. 6.

Fig. 6.

Coronary wires positioned in the distal LAD and distal LCX, with a DES placed through the LM lesion to the LAD; arrows mark the proximal and distal ends of the DES delivery balloon catheter (4 × 18 mm). DES, drug-eluting stent; LAD, left anterior descending artery; LCX, left circumflex artery; LM, left main.

The delivery balloon was inflated to 16 atmospheres and maintained for 10 seconds. Subsequently, the jailed LCX wire was recrossed, followed by ‘kissing balloon’ postdilatation using a 3.5 × 12 mm balloon catheter for the LM to LAD artery and a 2.5 × 20 mm balloon catheter for the LM to LCX, both inflated to 16 atmospheres. The procedure was completed with the proximal optimization technique (POT) by inflating the stent delivery balloon catheter (4 × 18 mm) to 20 atmospheres. Completion angiography revealed no evidence of coronary embolism or dissection, and final blood flow was graded as TIMI 3, as shown in Fig. 7.

Fig. 7.

Final left coronary artery angiography after DES implantation, demonstrating restored antegrade TIMI 3 flow with no residual stenosis, signs of blood flow limitation, or distal embolism. LM, left main coronary artery; LAD, left anterior descending artery; LCX, left circumflex artery.

Considering the high risk of puncture site bleeding, VKA therapy was resumed with bridging anticoagulation using subcutaneous low molecular weight heparin (enoxaparin 40 mg b.i.d. for 4 days). During the post-PCI intensive care unit (ICU) stay, no symptoms of myocardial ischaemia or additional rhythm or conduction abnormalities were observed. A follow-up troponin I test performed 5 hours after PCI revealed a significant increase to 0.9 ng/mL, confirming the diagnosis of non-ST-elevation myocardial infarction (NSTEMI). One hour after PCI, TTE demonstrated positive functional improvement, with LVEF increasing to 34%, persistent akinesis of all apical segments, and hypokinesis of the anterior, lateral, and septal walls. LV SV also improved, rising to 42 mL. Three days post-PCI, repeat TTE showed a further increase in LVEF to 55%, with no wall motion abnormalities or areas of asynergy.

During his hospital stay, the patient developed suspected aspiration pneumonia attributed to prior resuscitation efforts. MSCT revealed bilateral, predominantly central, multisegmental ground-glass opacities and areas of pulmonary consolidation, with a small amount of material identified in the segments 9 and 10 bronchi of the right lung. Treatment with intravenous cefepime 1 g and sulbactam 1 g administered b.i.d. for 9 days resulted in a positive clinical response. Follow-up imaging demonstrated reduced volume and density of the affected lung regions and confirmed a patent DES in the LM artery with minimal protrusion into the aorta, as shown in Fig. 8.

Fig. 8.

Control MSCT angiography at discharge, 18 days post-PCI, with arrowheads marking the ends of the implanted coronary stent; AO, aorta; PA, pulmonary artery; PV, pulmonary vein; SVC, superior vena cava; RA, right atrium.

On the 18th day postintervention, the patient was discharged from the hospital in stable condition on maintenance therapy with acetylsalicylic acid (ASA) 75 mg q.d. for 1 month, clopidogrel 75 mg q.d. for 12 months, and warfarin 6.25 mg q.d. lifelong, targeting an international normalized ratio (INR) between 2.0 and 3.0. Additional medications included a β-blocker (metoprolol 25 mg b.i.d.) and a proton pump inhibitor (pantoprazole 20 mg q.d. for 30 days).

Follow-up and outcomes. At follow-up visits, the patient reported no chest pain, dyspnoea, or other signs of heart failure or angina while performing his daily activities. Serial TTEs confirmed stable LV function without mechanical complications. He remains compliant with the prescribed therapy, maintaining INR values within the target range and exhibiting no signs of bleeding. The patient continues regular follow-up with both a cardiologist and an aortic surgeon, with ongoing focus on secondary prevention.

Patient perspective

The patient provided informed consent for the publication of anonymized clinical materials related to his case.

Upon our request, the patient offered a brief reflection on his experience: “When I first felt chest pain, I didn’t think it was a big deal—just something minor that would pass. However, the pain worsened and persisted. My mother insisted on calling an ambulance. At the hospital, I was informed that the arteries of my heart were blocked following my recent surgery. I found this confusing and frightening. When they told me I required emergency stenting, I was fearful that the situation might be fatal. Subsequently, I felt anxious, and then pneumonia hit, which complicated my recovery. Nevertheless, the quality of medical care reassured me. I now visit a cardiologist regularly, and so far, no further surgeries have been necessary. It has been a lot, but I am more aware of my health today. However, I still experience some minor limitations in my daily life.”

Discussion

This case illustrates an early presentation of LM stenosis following ARR. De novo coronary lesions after ARR may manifest at varying intervals and are likely to have differing aetiologias depending on the timing of onset. Early presentation, within 1–3 months post-ARR, aligns with several previously reported cases of coronary obstruction occurring during this period [11,[18], [19], [20]].

Laimoud M. [21] reported a series of intraoperative and early postoperative cases of coronary insufficiency. The etiology is likely multifactorial, primarily related to surgical technique factors such as external compression from surgical glue use, early thrombosis of interposed grafts, tension, kinking, and angulation. Additional contributing factors include cardiopulmonary bypass-related effects and in situ complications such as arterial dissection and spasm [4,22,23].

Coronary lesions occurring later, typically several months after ARR, are often attributed to neointimal proliferation. Numerous reported cases of ostial stenosis have manifested within the 4-10-month postoperative period. This timeframe suggests that intimal hyperplasia and fibrosis are the primary pathological processes, likely resulting from endothelial injury caused by antegrade cardioplegia cannulation or suture trauma at the ostial buttons. Additionally, tissue reactions to foreign materials – such as the aortic conduit, interposed coronary grafts, suture materials, and GRF glue – may contribute to lesion development [12,14,[24], [25], [26], [27]].

In contrast, ischaemic events occurring 10 years or more after ARR, as documented in other cases, are more likely driven by atherosclerotic plaque progression rather than surgical factors [28]. Park T. et al. [29] reported a case of bilateral coronary artery involvement characterized by subtotal LCA stenosis and RCA occlusion. Both lesions were successfully treated with stenting, including retrograde RCA recanalisation, performed in a single procedure. These observations underscore the importance of considering the time elapsed since surgery when evaluating post-ARR coronary lesions, as it helps distinguish between primary causes related to surgical factors and those due to atherosclerosis progression.

MSCT angiography played a crucial role in the diagnostic process of this case by enabling detailed evaluation of the aortic root reconstruction, coronary ostial reattachment sites, and coronary artery lesions. Thorough assessment of these structures is essential for planning selective angiography and PCI, as 3-dimensional (3D) reconstructions facilitate identification of optimal angiographic projections [30,31]. In this instance, preprocedural MSCT may facilitate uncomplicated coronary catheterization during PCI. However, interpreting MSCT images post-ARR can be challenging, as benign surgical changes may mimic pathological findings. Accurate differentiation requires specialized expertise to distinguish expected anatomical alterations – such as graft materials and their configuration, surgical clips, and Teflon felt – from true complications [32].

Radiodensity analysis using MSCT imaging provided valuable insight into the lesion’s composition. The LM lesion demonstrated a uniform density of 75 HU, which falls within the 65–260 HU range typically associated with fibrous plaques, as described by Obaid D. et al. [33]. This finding suggests a fibrotic aetiology, consistent with a case reported by Funada A. et al. [18], in which intravascular ultrasound (IVUS) with virtual histology confirmed the presence of fibrotic plaques post- ARR, exhibiting radiodensity values of 59.5 HU and 71.7 HU. However, attenuation values can vary depending on the type of examination, vessel type, body region, MSCT vendor, and technical settings, as highlighted in a meta-analysis by Kristanto W. et al. [34]. Thus, although the 75 HU value observed in our case is consistent with a fibrotic origin, such findings should be interpreted cautiously and adjusted according to local imaging protocols.

One potential factor contributing to post-ARR stenosis development is the use of surgical adhesives. When GRF glue is applied to secure the coronary buttons, it may cause external compression or provoke a pronounced inflammatory response, leading to stenosis. Trivi M. et al. [11] reported a case in which PCI for a GRF glue-related lesion failed to resolve myocardial ischaemia 3 months later. Nuclear perfusion imaging demonstrated widespread ischaemia, and IVUS revealed a hypoechoic mass prolapsing through the stent struts without evidence of external compression or in-stent neointimal growth. Consequently, the patient required coronary artery bypass grafting (CABG). Although GRF glue use was not confirmed in our case, this example highlights the significance of surgical adhesives on PCI outcomes and underscores the consideration of CABG as a viable alternative when appropriate.

CABG performed after ARR surgery is associated with several technical challenges, including anatomical alterations resulting from the initial procedure. Given that the patient was receiving VKA therapy, emergency resternotomy posed a high risk of bleeding due to the presence of mature scar tissue and adhesions, thereby increasing operative risks. Considering the urgency of the clinical situation alongside these risks, PCI was deemed the safest revascularisation strategy for this patient.

Thus, the choice of revascularization modality depends on multiple factors, including the clinical presentation (urgent and life-threatening conditions such as acute MI or arrhythmia versus stable scenarios such as exertional angina or ischaemia detected on stress testing or nuclear imaging), concomitant anticoagulation therapy (for example, when ARR is performed with a stentless bioprosthetic valve, VKA therapy may be discontinued 3 to 6 months postoperatively), the type of coronary lesion identified, comorbidities, and specific details of the primary surgical technique.

Conclusion

Proximal coronary artery stenosis is a rare but serious complication following ARR. This case demonstrates that, even in a young patient, acute LM coronary occlusion can arise shortly after surgery, constituting a life-threatening emergency. Prompt recognition and management of this complication are critical. Multimodal imaging modalities – such as MSCT angiography and intravascular visualization – facilitate accurate diagnosis and guide therapeutic intervention. Emergency PCI, performed by an experienced team, can effectively restore myocardial perfusion and result in significant recovery of cardiac function. Finally, a multidisciplinary Heart Team approach combined with meticulous long-term follow-up is essential to optimize outcomes in patients experiencing post-ARR coronary complications.

Declaration of generative AI and AI-assisted technologies in the writing process

Statement: During the preparation of the manuscript, authors used AI tool (OpenAI, GPT-5) to assist in language editing, enhance the readability, coherence, and overall flow of the text. The authors reviewed, verified, and fully assume responsibility for all content presented in the final manuscript.

Author contributions

Alexey Viktorovich Kudrinskiy: Project administration, Conceptualization, Writing – Original Draft, Writing – Review & Editing, Visualization, Diagnostic Imaging Interpretation, Approval of the Final Manuscript. Artem Vladimirovich Snitsar: Conceptualization, Diagnostic Imaging Interpretation, Approval of the Final Manuscript. Marat Amayakovich Sedgaryan: Clinical Management of the Patient, Conceptualization, Data Curation, Writing – Original Draft, Writing – Review & Editing, Diagnostic Imaging Interpretation, Approval of the Final Manuscript. Maxim Valentinovich Patlachuk: Clinical Management of the Patient, Supervision of Clinical Care, Conceptualization, Diagnostic Imaging Interpretation, Approval of the Final Manuscript.

Patient consent

Complete written informed consent was obtained from the patient for the publication of this study and accompanying images.