Incidentally detected elevated jugular venous pressure revealing a delayed post-CABG ascending aortic pseudoaneurysm near a saphenous vein graft origin: a case report

Abstract

Background

Ascending aortic pseudoaneurysm is an uncommon but potentially life-threatening delayed postoperative complication of cardiac surgery, arising at previous aortic manipulation sites. It may remain clinically silent until expansion, compressive effects, contained rupture, or catastrophic haemorrhage occurs.

Case presentation

A 72-year-old man with hypertension remained well 30 months after off-pump coronary artery bypass grafting until his general practitioner incidentally detected elevated jugular venous pressure during a consultation for influenza-like symptoms. He denied chest pain, dyspnoea, orthopnoea, syncope, or weight loss. Transthoracic echocardiography showed preserved biventricular systolic function, left ventricular dilatation, moderate aortic regurgitation, proximal ascending aortic dilatation, and an extracardiac mass compressing the right atrium. Electrocardiogram (ECG)-gated computed tomography (CT) angiography of the heart and thoracic aorta demonstrated aneurysmal enlargement of the proximal ascending aorta to approximately 5.6 cm, complicated by a giant partially thrombosed pseudoaneurysm measuring approximately 7.5 cm. The lesion communicated with the aorta through a broad neck and showed contrast leakage into the sac, consistent with an actively leaking pseudoaneurysm or contained rupture. It arose within a few millimetres of a proximal saphenous vein graft origin supplying the right coronary territory, compressed the right atrium and superior vena cava, and lay close to the posterior sternum, indicating substantial redo-entry risk. These findings explained the raised venous pressure despite the absence of florid superior vena cava syndrome. Transoesophageal echocardiography confirmed severe aortic regurgitation. The patient underwent high-risk redo median sternotomy with right axillary arterial cannulation before re-entry, cardiopulmonary bypass with cooling to 17 °C and aortic cross-clamping without circulatory arrest, bioprosthetic aortic valve replacement, supra-coronary ascending aortic replacement, and reimplantation of bypass graft inflow. Postoperative haemorrhagic tendency requiring re-exploration settled with supportive management, and he was discharged on postoperative day 14. At 18-month follow-up, he remained asymptomatic, with echocardiography showing a normally functioning aortic bioprosthesis and preserved biventricular systolic function.

Conclusions

A delayed post-coronary artery bypass grafting ascending aortic pseudoaneurysm may present with minimal symptoms and be uncovered by elevated jugular venous pressure due to right atrial/superior vena cava compression. ECG-gated CT is essential for confirming pseudoaneurysm/contained rupture, defining graft and retrosternal relationships, and guiding safe definitive repair in high-risk redo surgery.

Background

Ascending aortic pseudoaneurysm is an uncommon but potentially life-threatening recognised complication of prior cardiac or aortic surgery, typically developing at sites of previous aortic manipulation [1]. Reported loci include cannulation sites, cross-clamp or aortotomy lines, cardioplegia needle sites, and proximal coronary bypass anastomoses [1]. Because the published literature is dominated by case reports and small surgical series, precise incidence estimates and denominator-based risk quantification remain limited [1].

Although some patients present with pain, haemodynamic compromise, or frank rupture, others remain minimally symptomatic until the lesion enlarges sufficiently to compress adjacent mediastinal structures [1]. Reported postoperative presentations include pseudoaneurysm formation near a proximal saphenous vein graft (SVG) anastomotic site [2] and venous compression with superior vena cava (SVC) or right atrial (RA) involvement [3]. In this setting, cross-sectional imaging is essential not only to establish the diagnosis, but also to define the lesion neck, thrombus burden, retrosternal extent, bypass graft relationships, and operative re-entry risk [1].

We report a delayed post-CABG proximal ascending aortic pseudoaneurysm arising near the proximal SVG origin in a patient whose only trigger for further evaluation was an incidental finding of raised jugular venous pressure. The case is notable for the coexistence of a giant, partially thrombosed, leaking pseudoaneurysm; RA/SVC compression; progressive ascending aortic aneurysmal enlargement with significant aortic regurgitation; and the need for CT-guided planning for high-risk redo sternotomy.

Case presentation

A 72-year-old man with hypertension had undergone off-pump CABG 30 months earlier for distal left main and multivessel coronary artery disease. Preoperative imaging before CABG had shown only mild ascending aortic dilatation of approximately 35 mm, with a normal-sized aortic root. No relevant family history of thoracic aortic aneurysm, aortic dissection, sudden death, Marfan syndrome, or other heritable thoracic aortic disease was identified, and no syndromic features suggestive of connective tissue disease were documented. The index operation included a left internal mammary artery graft to the left anterior descending artery and multiple SVGs, including grafting to the right coronary territory. His postoperative recovery was reported to be uneventful, and he remained clinically well during subsequent follow-up.

The current problem came to light when his general practitioner noted elevated jugular venous pressure during a consultation for influenza-like symptoms. He denied chest pain, dyspnoea, orthopnoea, syncope, and weight loss. On cardiology review, he was haemodynamically stable. Examination again confirmed raised JVP, but there were no documented focal neurological deficits, overt heart failure syndrome, or peripheral stigmata of infection.

Transthoracic echocardiography showed preserved right and left ventricular systolic function, left ventricular dilatation, moderate aortic regurgitation, and dilatation of the proximal ascending aorta. An extracardiac mass was seen compressing the RA. Because these findings suggested a proximal mediastinal or aortic process rather than isolated right-sided cardiac disease, ECG-gated CT angiography of the heart and thoracic aorta was obtained for further characterisation.

CT demonstrated aneurysmal enlargement of the proximal ascending aorta and arch, with a maximal diameter of approximately 5.6 cm. Adjoining this was a giant pseudoaneurysm arising from the proximal ascending aorta/arch region, in extremely close proximity (about 3 mm) to a proximal SVG origin supplying the right coronary territory. The pseudoaneurysm measured approximately 7.5 cm in maximal dimension and consisted largely of organised thrombus surrounding a contrast-opacified cavity. A broad communication measuring approximately 1.7–1.9 cm connected the lesion to the aortic lumen. Importantly, contrast leakage into the sac was visible, favouring an actively leaking pseudoaneurysm or contained rupture rather than a stable thrombosed cavity alone (Fig. 1).

Fig. 1.

Giant partially thrombosed ascending aortic pseudoaneurysm. ECG-gated axial CT angiography showing a large partially thrombosed pseudoaneurysm adjacent to the proximal ascending aorta, with a contrast-opacified lumen within the sac and surrounding mural thrombus

The pseudoaneurysm/thrombus complex extended cranially and exerted a clear mass effect on right-sided mediastinal structures, with partial compression of both the RA and the SVC (Fig. 2A, B). This provided an anatomic explanation for the elevated JVP despite the absence of florid SVC syndrome. The lesion also lay close to the posterior table of the sternum, making redo sternotomy potentially hazardous (Fig. 3). CT further showed that the bypass grafts were patent, although mild proximal external compression of the RSVG–PDA graft by the adjacent pseudoaneurysm/thrombus complex was present (Fig. 4). Taken together, the CT findings established three clinically important points: the patient had progressive true aneurysmal disease of the ascending aorta, a superimposed focal pseudoaneurysm with active leak/contained rupture, and high-risk retrosternal anatomy that could complicate re-entry.

Fig. 2.

Coronal views of pseudoaneurysm-related RA/SVC compression. Coronal CT angiographic images showing the pseudoaneurysm/thrombus complex and its compressive effects. A Coronal overview of the large pseudoaneurysm adjacent to the ascending aorta. B Coronal image demonstrating partial compression of the right atrium (RA) and superior vena cava (SVC)

Fig. 3.

Retrosternal extent of the pseudoaneurysm. Sagittal CT angiography demonstrating the cranio-caudal extent of the pseudoaneurysm and its close retrosternal location, indicating high risk for redo sternotomy

Fig. 4.

Post-CABG anatomy and graft compression on three-dimensional CT. Three-dimensional volume-rendered CT reconstruction demonstrating postoperative CABG anatomy and the proximal ascending aortic pseudoaneurysm. The arrow indicates mild proximal external compression of the RSVG–PDA graft by the adjacent pseudoaneurysm/thrombus complex

Preoperative transoesophageal echocardiography confirmed severe aortic regurgitation, graded III–IV, with an annular diameter of approximately 21 mm and sinus and sinotubular junction diameters of about 32 mm. The combination of severe aortic regurgitation, progressive ascending aortic enlargement, and a leaking pseudoaneurysm supported the need for urgent operative management rather than observation.

Redo median sternotomy was planned as a high-risk procedure because of the substernal position of the pseudoaneurysm and the anticipated dense adhesions from previous CABG. Given the high-risk redo-entry anatomy and combined aortic and valvular pathology, management planning was informed by multidisciplinary discussion involving cardiology, cardiac imaging, cardiothoracic surgery, cardiac anaesthesia, critical care, and nursing teams. To reduce the risk of catastrophic haemorrhage at re-entry, the right axillary artery was cannulated through an 8-mm graft before sternotomy. Femoral vessels were prepared as a contingency, but femoral cannulation was not required. After redo sternotomy and careful adhesiolysis, direct right atrial two-stage venous cannulation was performed, and cardiopulmonary bypass was established. The patient was cooled to 17 °C in anticipation of a possible brief period of circulatory arrest; however, the aortic cross-clamp was repositioned distally in an oblique manner just below the arch, allowing the aortic anastomosis to be performed without circulatory arrest. Cold intermittent antegrade cardioplegia was administered through the coronary ostia and bypass grafts; retrograde cardioplegia was not used. Intraoperatively, the surgeons identified a large thrombosed pseudoaneurysm/contained rupture and extensive organised thrombus. A focal intimal tear was present on the right lateral aspect of the ascending aorta approximately 3 cm above the aortic valve, about 1 cm from the previous proximal graft anastomosis, and did not appear to arise directly from the anastomosis itself. The aortic valve was diseased and severely regurgitant. The operation therefore comprised the evacuation of organised thrombus, aortic valve replacement with a 21-mm bioprosthetic valve, supra-coronary ascending aortic replacement with a 26-mm Dacron graft, and reimplantation of the bypass graft inflow into the prosthetic graft. The PDA/RCA graft and the left-sided SVG graft were reimplanted as two separate buttons into the Dacron graft, while the LIMA–LAD graft was left undisturbed. This strategy addressed both the focal pseudoaneurysm and the background aneurysmal ascending aorta while preserving coronary bypass perfusion.

The early postoperative course was complicated by a severe haemorrhagic tendency requiring multiple transfusions. Ongoing bleeding prompted mediastinal re-exploration on postoperative day 1; however, no focal surgical bleeding source was identified. Coagulopathy was attributed to disseminated intravascular coagulation and was managed supportively. After the haemorrhagic tendency had settled, low-dose low-molecular-weight heparin was used for venous thromboembolism prophylaxis from postoperative day 3, and low-dose aspirin with warfarin, targeting an INR of 2.5, was started on postoperative day 4. Warfarin was continued for 3 months, and aspirin was planned lifelong. The patient subsequently stabilised, improved clinically, and was discharged on postoperative day 14. At the 18-month follow-up, he remained asymptomatic. Transthoracic echocardiography showed a normally appearing and functioning aortic bioprosthesis with preserved biventricular systolic function. Overall, the case illustrates successful treatment of a large, leaking post-CABG proximal ascending aortic pseudoaneurysm with compressive anatomy and a high risk of major redo-entry, in a patient whose disease was discovered because of an incidental physical sign rather than dramatic symptoms.

Discussion and conclusions

This case illustrates an uncommon but clinically important delayed complication after coronary artery bypass grafting: a giant proximal ascending aortic pseudoaneurysm with active leak/contained rupture, substantial thrombus burden, compression of the right atrium and superior vena cava, and close proximity to a proximal saphenous vein graft (SVG) origin. The presentation was particularly instructive because the patient remained minimally symptomatic despite high-risk anatomy, and the diagnostic pathway began with the incidental detection of raised jugular venous pressure during routine primary care review. The case therefore highlights the value of bedside examination in post-cardiac surgery patients and the central role of ECG-gated CT in defining the diagnosis, anatomical relationships, and operative implications of proximal aortic pathology.

Ascending aortic pseudoaneurysm after cardiac surgery is an uncommon but recognised potentially life-threatening complication. The published evidence is dominated by case reports, small series, and systematic reviews of reported cases rather than large-denominator-based epidemiological studies, so the true frequency in specific postoperative subgroups remains difficult to determine [1]. Precise incidence estimates, particularly for lesions arising after CABG near proximal graft anastomoses, are therefore limited. However, the available literature consistently describes postoperative pseudoaneurysm formation at sites of previous aortic manipulation, including cannulation sites, aortotomy or clamp sites, cardioplegia needle sites, and proximal coronary bypass anastomoses [1]. CABG is therefore best regarded as a recognised postoperative context in which ascending aortic pseudoaneurysm can occur, rather than an independently proven population-level causal risk factor. In this patient, the anatomical relationship between the pseudoaneurysm and the proximal SVG origin supports a plausible graft-related or aortic-manipulation-related mechanism but does not establish the exact site of origin. The lesion arose close to a proximal SVG origin supplying the right coronary territory, and intraoperative inspection identified a focal intimal tear on the right lateral aspect of the ascending aorta close to a previous graft origin. Further operative clarification indicated that the tear was approximately 1 cm from the proximal SVG anastomosis and did not arise directly from the anastomosis itself. Thus, anatomical proximity should be interpreted as supportive of a plausible mechanistic association, rather than as direct proof that the pseudoaneurysm originated from the proximal SVG anastomosis.

Similar CABG-associated cases of ascending aortic pseudoaneurysm arising from or near proximal SVG anastomoses have been reported, with local intimal injury or late disruption at the anastomotic site proposed as a possible mechanism [2]. Although the original operation was performed off-pump, which reduces mechanisms related to aortic cannulation or full cross-clamping, it does not eliminate aortic manipulation during proximal SVG construction. Several mechanisms therefore remain possible, including focal aortic wall injury related to prior aortic manipulation, side-biting clamp-related injury during construction of the proximal anastomosis, progressive disease of the ascending aortic wall, or, less likely, direct anastomotic disruption. A reasonable interpretation is therefore that local wall injury or weakness near, but not directly at, the proximal graft origin contributed to pseudoaneurysm formation in a susceptible aorta. An infectious or mycotic pseudoaneurysm was considered but was not supported by the available clinical, laboratory, echocardiographic, microbiological, or intraoperative findings. There were no clinical features of sepsis or infective endocarditis; transthoracic and transoesophageal echocardiography showed no evidence of infective endocarditis; no intraoperative vegetations, abscess, pus, infected thrombus, or friable infected tissue were seen; and both thrombus culture and postoperative blood cultures were negative. However, histopathological examination was unavailable; therefore, an infectious aetiology cannot be excluded with absolute certainty.

The background aortic disease is also relevant. Before CABG, the ascending aorta was only mildly dilated, whereas at presentation it had enlarged to approximately 5.6 cm and was associated with severe aortic regurgitation. This suggests a combined-pathology model in which progressive aneurysmal degeneration of the ascending aorta provided a vulnerable substrate, while a focal area of prior manipulation served as the site of wall disruption. Current ACC/AHA guidance supports surgery for a sporadic ascending aortic aneurysm measuring 5.5 cm and also recognises rapid growth and lower thresholds in experienced centres [4]. ESC guidance similarly supports consideration of concomitant aortic replacement at lower diameters when aortic valve surgery is indicated [5]. In this case, aneurysm size, interval enlargement, severe aortic regurgitation, active leak/contained rupture, and compressive anatomy together supported definitive operative repair.

A key diagnostic issue is the distinction between pseudoaneurysm/contained rupture and classic propagating aortic dissection. Classic aortic dissection is characterised by an intimal tear with formation of an intimal flap separating true and false lumens, usually extending longitudinally along the aorta [6]. In contrast, this lesion showed a sac-like contour external to the expected aortic lumen, a broad but discrete communication with the aorta, extensive mural thrombus, and contrast leakage into a contained cavity. These CT features favour a pseudoaneurysm or a contained rupture rather than a long-segment classic dissection. The intraoperative description of a focal intimal tear and contained dissection is not contradictory; rather, it can be reconciled by describing the lesion as a pseudoaneurysm/contained rupture arising from a focal tear in the ascending aorta.

The raised jugular venous pressure was the sentinel clinical clue. CT demonstrated partial compression of both the right atrium and superior vena cava, providing a clear anatomical explanation for venous congestion despite the absence of florid superior vena cava syndrome. Previous reports have described ascending aortic pseudoaneurysm presenting with superior vena cava syndrome, illustrating that venous compression can dominate presentation [3]. The present case extends that observation to a subtler clinical scenario: isolated raised jugular venous pressure in an otherwise stable post-CABG patient. In such patients, unexplained venous congestion should prompt consideration not only of heart failure, pulmonary hypertension, tricuspid valve disease, or pericardial pathology, but also of extrinsic right atrial or caval compression from mediastinal vascular disease.

ECG-gated CT was decisive for both diagnosis and operative planning. Echocardiography identified an extracardiac compressive mass, but CT defined the pseudoaneurysm neck, thrombus burden, active leak, relationship to the proximal SVG origin, compression of right-sided mediastinal structures, bypass graft patency, and close retrosternal position. ECG gating is particularly valuable in the ascending aorta because cardiac motion artefact can reduce diagnostic confidence and may simulate or obscure dissection-related findings; Budeanu et al. showed higher diagnostic performance, inter- and intra-reader agreement, and observer confidence with ECG-gated CTA compared with non-gated CTA for ascending aortic dissection [7]. These findings directly influenced operative strategy. A substernal pseudoaneurysm in a reoperative chest carries a major risk of catastrophic haemorrhage if the sac is entered during sternal re-entry [8]. Prior reports and reviews support careful preoperative mapping, peripheral arterial cannulation, and hypothermic circulatory protection in selected high-risk cases [1, 3, 8] The use of right axillary arterial cannulation before sternotomy, contingency preparation for femoral cannulation, direct right atrial two-stage venous cannulation after adhesiolysis, cooling with distal aortic cross-clamping, ascending aortic replacement, aortic valve replacement, and graft inflow reimplantation was therefore anatomically rational and consistent with principles of safe reoperative aortic surgery. Myocardial protection was achieved using cold intermittent antegrade cardioplegia delivered through the coronary ostia and bypass grafts, without retrograde cardioplegia.

This report has limitations. The mechanistic link between the proximal SVG origin and pseudoaneurysm formation cannot be proven definitively from a single case, and the literature on post-CABG ascending aortic pseudoaneurysm near graft origins remains sparse and largely case-based. Histopathological examination was not available because no specimen was submitted for pathology; however, thrombus culture and postoperative blood cultures were negative. No intraoperative photographs or videos were taken for publication. Nevertheless, the close anatomical relationship to the graft origin, the operative finding of a focal tear, the coexistence of progressive ascending aortic aneurysmal disease, and relevant published experience support a coherent and clinically plausible explanation.

In conclusion, delayed post-CABG ascending aortic pseudoaneurysm may remain minimally symptomatic despite active leak, thrombus burden, and compression of the right atrium and superior vena cava. Raised jugular venous pressure may be the sentinel bedside sign of a dangerous mediastinal vascular complication. ECG-gated CT is essential for confirming pseudoaneurysm/contained rupture, distinguishing it from classic dissection morphology, defining graft and retrosternal relationships, and guiding safe definitive repair in high-risk redo surgery.

Abbreviations

ACC/AHA

American College of Cardiology/American Heart Association

CABG

Coronary artery bypass grafting

CT

Computed tomography

ECG

Electrocardiogram

ESC

European Society of Cardiology

JVP

Jugular venous pressure

PDA

Posterior descending artery

RA

Right atrium

RSVG

Reversed saphenous vein graft

SVG

Saphenous vein graft

SVC

Superior vena cava

Authors’ contributions

NL and NP conceptualised and designed the case report, acquired and interpreted clinical data, reviewed the literature, and drafted the manuscript. NL also contributed to cardiac CT interpretation. SP, SS, and DS contributed to data acquisition, literature review, data interpretation, and manuscript revision. WS and KD contributed to the patient’s clinical and surgical care, operative data interpretation, and critical revision of the manuscript for important intellectual content. All authors read and approved the final manuscript and agree to be accountable for all aspects of the work. Niroshan Chandrajith Lokunarangoda (NL), Nadhee Peries (NP), Senaka Devendra Pilapitiya (SP), Sucheera Samarasinghe (SS), Indika Deepani Siriwardhana (DS)‬, K. Kesava Dev (KD), Wijeyasingam Samuel Santharaj (WS).

Funding

No specific funding was received for this work.

Data availability

No datasets were generated or analysed during the current study.

Declarations

Ethics approval and consent to participate

Ethics approval was not required for this single-patient case report according to local institutional policy. The patient provided written informed consent for publication of the case details and accompanying images.

Consent for publication

Written informed consent was obtained from the patient for publication of this case report and the accompanying images.

Competing interests

The authors declare no competing interests.