Revised: October 8, 2026
Accepted: October 20, 2026
Published online: October 28, 2026
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Mesenteric ischaemia is a potentially life-threatening vascular disorder caused by impaired intestinal perfusion, with treatment selection requiring consideration of clinical presentation, bowel viability and lesion anatomy. This narrative review examines evidence informing interventional radiology decisions in arterial acute mesenteric ischaemia (AMI) and chronic mesenteric ischaemia (CMI). MED
Core Tip: Mesenteric ischaemia is a potentially life-threatening vascular disorder that remains difficult to diagnose and manage, presenting either as an acute surgical emergency or as a cause of chronic, debilitating abdominal symptoms. Advances in imaging and endovascular therapy have transformed its management, positioning interventional radiology at the centre of diagnosis and treatment. This narrative review examines the evidence informing current interventional radiology practice in the management of both acute and chronic mesenteric ischaemia.
- Citation: Keady C, O’Malley CM, Mohamed SA, Bell J, Crotty C, Patton A, O’Regan D, Keeling A, McGrath A, Given M, Mulholland D, Sheehan M. Endovascular management of acute and chronic arterial mesenteric ischaemia: A narrative review of evidence informing interventional radiology treatment. World J Radiol 2026; 18(10): 125052
- URL: https://www.wjgnet.com/1949-8470/full/v18/i10/125052.htm
- DOI: https://dx.doi.org/10.4329/wjr.125052
Mesenteric ischaemia represents a spectrum of vascular disorders resulting from impaired intestinal perfusion and remains associated with substantial morbidity and mortality despite advances in diagnosis and treatment. Acute mesenteric ischaemia (AMI) constitutes a vascular emergency in which delays in diagnosis may rapidly progress to bowel infarction and death, whereas chronic mesenteric ischaemia (CMI) causes debilitating postprandial symptoms and progressive malnutrition. Over the past two decades, advances in endovascular intervention have fundamentally changed the management of both conditions, establishing interventional radiology as a cornerstone of treatment. Individual endovascular decisions in the management of AMI and CMI are supported by differing combinations of comparative studies, observational evidence, procedural rationale and expert consensus; however, interpretation is complicated by variation in patient selection, lesion anatomy, adjunctive treatments used and definitions of technical and clinical success.
This narrative review examines the evidence supporting key endovascular treatment decisions in arterial AMI including embolic, thrombotic and acute-on-chronic presentations, and CMI. It addresses how society guidance and supporting studies inform treatment selection, and what the available evidence establishes about technical success and comparative patient-centred outcomes. Particular attention is given to patient selection, outcome definitions, lesion anatomy, adjunctive treatments employed and study limitations, distinguishing guideline recommendations and con
Existing comprehensive reviews describe advances in revascularisation strategies for AMI and CMI[1,2], while the European Society for Vascular Surgery (ESVS) clinical practice guidelines provide graded management recommendations[3], and Cardiovascular and Interventional Radiological Society of Europe (CIRSE) Standards of Practice provide con
A structured narrative review was undertaken to identify literature relevant to the diagnosis and endovascular mana
Representative free-text search terms included combinations of “mesenteric ischaemia/ischemia”, “acute mesenteric ischaemia”, “chronic mesenteric ischaemia”, “superior mesenteric artery”, “mesenteric artery stenosis/occlusion”, “computed tomography angiography”, “endovascular revascularisation”, “angioplasty”, “stenting”, “covered stent”, “aspiration thrombectomy”, “mechanical thrombectomy”, and “catheter-directed thrombolysis”. Searches were refined throughout manuscript preparation according to specific diagnostic and therapeutic topics.
Evidence was prioritised according to relevance and methodological strength. International clinical practice guidelines and standards of practice were used to identify management recommendations and consensus-based practice. Supporting evidence was examined through randomised controlled trials, systematic reviews and meta-analyses, prospective and population-based studies, comparative observational cohorts, and larger retrospective series. Technical reports and smaller series were considered where higher-level evidence was unavailable, with their findings interpreted in relation to study design, comparator availability and the outcomes reported.
Peer-reviewed full-text adult studies were preferentially included. The review was restricted to English-language publications. Case reports were generally excluded from efficacy or safety assessments but considered selectively for uncommon techniques or complications. Conference abstracts, preprints and experimental studies were excluded. For overlapping datasets, the largest, most recent or most complete publication was preferentially cited.
Evidence was synthesised qualitatively and organised based on clinically relevant treatment decisions in AMI and CMI. For each treatment decision, formal guideline recommendations and consensus-based practice statements were identified alongside supporting primary studies and evidence syntheses. Appraisal considered study design, patient selection, lesion anatomy, comparator availability, adjunctive treatments, outcome definitions and follow-up. Procedural outcomes, including device deployment, thrombus clearance and vessel patency were distinguished from patient-centred outcomes, including mortality, bowel resection, symptom relief, quality of life and reintervention. Comparative findings were interpreted with respect to potential confounding, selection bias and statistical uncertainty. Society recommendation classes and evidence levels were retained where reported and no new formal evidence grades were assigned. The resulting practice considerations represent an interpretive synthesis of the cited literature rather than independently validated treatment recommendations.
As a narrative review, no prospective protocol, formal PRISMA-based selection process or validated risk-of-bias assessment was undertaken; consequently, citation and selection bias remain inherent limitations.
The three major arteries supplying the splanchnic circulation are the coeliac artery (CA), superior mesenteric artery (SMA) and inferior mesenteric artery (IMA). The CA primarily supplies the foregut structures including the stomach and proximal duodenum. The SMA supplies the midgut territory of the distal duodenum, jejunum, ileum and colon to the proximal one-third of the transverse colon. The IMA supplies the hindgut structures from the distal transverse colon to the upper one-third of the rectum. Significant anatomical variation can exist, with an extensive network of collateral vessels providing a robust compensatory mechanism between these vascular territories during low flow states, or should one vessel become compromised. Consequently, vascular compromise in two or more territories, or in distal end arteries, often leads to mesenteric ischaemia; however, severe single vessel disease, particularly of the SMA, may also cause ischaemia when collateral supply is inadequate[5-8]. Key collateral networks include the anastomoses between the CA and SMA via the superior and inferior pancreaticoduodenal arteries, and the marginal artery of Drummond providing collateral flow between the ileocolic and middle colic arteries arising from the SMA and the left colic artery arising from the IMA. An additional, although anatomically inconsistent collateral network, between the middle colic and left colic arteries, known as the arc of Riolan, provides an important collateral route in proximal SMA occlusion. The IMA has further limited collateral supply from the internal iliac arteries, via the superior and middle rectal arteries. Vulnerable watershed areas with poor collateral blood supply include the splenic flexure of the colon, known as Griffith’s point, an area of susceptibility due to poor collateralisation from the marginal artery of Drummond and the arc of Riolan, and Sudeck’s point at the rectosigmoid junction due to limited collateral supply from the superior and middle rectal arteries. A lesser-known, but vital arcade between the SMA and IMA is the Villemin arcade, serving as a deep anastomosis between the SMA and IMA, arising near the origin of the left colic artery, and is of particular importance in CMI[6-8].
At rest, the bowel receives approximately 20%-25% of cardiac output, which can increase to 35% in the postprandial state[9,10]. Due to its high metabolic demands, blood flow is primarily directed to the bowel mucosa, followed by the muscularis propria, serosa and submucosa. Because of this, initial ischaemia involves the mucosa, with prolonged ischaemia progressing to involve all layers of the bowel wall. Compensatory redistribution of blood flow from the mucosa to the muscularis and serosa, in the setting of acute ischaemia, occurs in an attempt to preserve mural integrity, and is potentially lifesaving[10,11]. However, if ischaemia is prolonged, transmural infarction ensues, resulting in bowel wall necrosis, perforation and potentially fatal intra-abdominal sepsis. Studies have shown remarkable gut resilience under prolonged periods of ischaemia, with the bowel capable of withstanding a 75% reduction in blood flow for up to 12 hours; however, in the setting of an absolute vascular occlusion, irreversible bowel infarction can occur in 6 hours[12].
AMI is defined as the sudden interruption in blood flow in a mesenteric artery, resulting in cellular damage, intestinal ischaemia and potential intestinal necrosis in the corresponding bowel segment[13]. Reported mortality rates range between 50% and 80%, primarily due to the non-specific nature of its presentation, often resulting in delayed diagnosis in the absence of a high clinical index of suspicion[14-17]. Acute thromboembolic occlusion of the mesenteric arteries most commonly affects the SMA, with symptomatic occlusion of the CA and IMA rarely clinically apparent due to the ext
AMI is an uncommon condition, with an estimated incidence of 6.2-8.7 cases per 100000 of the population annually, although its frequency increases substantially with advancing age[19-21]. A slight female predominance has been reported, with women accounting for approximately 57% of cases[21]. Several distinct entities can cause AMI, including arterial occlusion, non-occlusive disease in the setting of splanchnic hypoperfusion, and mesenteric venous thrombosis. Arterial occlusion represents the most common aetiology, accounting for approximately 67% of cases, and can be further subcategorised into embolic and thrombotic causes[22-25]. The SMA is the most commonly affected mesenteric vessel, with symptomatic occlusion of either the CA or IMA rarely encountered due to extensive collateralisation from the SMA[18].
Acute arterial thromboembolism and acute arterial thrombosis secondary to underlying atherosclerosis represent the two most frequently identified aetiologies of AMI[4,24]. Emboli originating from the heart, often secondary to untreated atrial fibrillation, left ventricular thrombus or vegetations arising from the cardiac valves, represent the most common source; however, in rare circumstances, emboli can arise from atherosclerosis of the aortic arch. These emboli most commonly migrate to the SMA due to its large calibre and acute take-off angle from the aorta. Emboli typically accumulate more distally in the SMA as it reduces in calibre, generally within a 10 cm segment of the main vessel and usually greater than 3 cm from the vessel ostium, thus often sparing proximal jejunal and colonic branches[26].
AMI may occur in the setting of chronic atherosclerosis, in which acute thrombosis occurs at the site of an atherosclerotic plaque. In the setting of acute-on-CMI, acute thrombosis of either the CA or SMA occurs in association with chronic atherosclerotic stenosis or occlusion of the other, thus markedly limiting collateralisation. Thrombosis, in contrast to embolism, usually occurs proximally in the vessel, often at the origin of the mesenteric arteries, at the site of a chronic atherosclerotic plaque[27,28]. AMI may also occur in the setting of acute aortic dissection with occlusion of a mesenteric vessel secondary to propagation of the dissection flap or acute dissection of a mesenteric vessel, and rarely, due to vas
Early diagnosis of AMI requires a high index of suspicion among both clinicians and radiologists. Classically, embolic AMI presents with the abrupt onset of severe abdominal pain that is disproportionate to the findings on physical examination. This hallmark feature is frequently accompanied by a range of non-specific gastrointestinal symptoms and signs, including nausea and vomiting (39%-93%), abdominal distension (18%-54%), diarrhoea, rectal bleeding (12%-48%), and, in more advanced cases, signs of peritonitis (13%-65%)[30].
Approximately one-third of patients presenting with AMI have concomitant atrial fibrillation, making it a key diagnostic clue. Atrial fibrillation and other cardiac pathologies, including valvular heart disease, infective endocarditis, acute coronary syndromes, and cardiomyopathy, may predispose to intracardiac thrombus formation and subsequent embolisation[31]. Clinicians should also remain vigilant for AMI in patients presenting with abdominal pain in conjunction with acute ischaemic stroke or acute lower limb ischaemia, as these manifestations may reflect a shared embolic source.
AMI secondary to arterial thrombosis is similarly challenging to diagnose and should be suspected in any patient with established atherosclerotic disease presenting with acute abdominal pain. These patients typically have advanced mesenteric atherosclerosis, with superimposed thrombosis occurring at sites of critical stenosis, most commonly at the origins of the SMA or CA[18,31]. Clinical presentation is variable and largely depends on the extent of pre-existing collateralisation. Acute thrombosis of a previously patent mesenteric artery may result in sudden, severe abdominal pain, whereas thrombosis of a chronically stenosed vessel may produce more subtle symptoms due to the presence of well-developed collateral blood flow. This latter scenario represents acute-on-CMI and is often precipitated by factors such as dehydration, reduced cardiac output, or a hypercoagulable state[28]. In retrospect, many of these patients report pre
Duplex ultrasound (DUS) has a negligible role in the diagnosis of AMI and is not recommended for the evaluation of suspected mesenteric arterial occlusion in the emergency setting. Assessment of the mesenteric vasculature is frequently limited by overlying bowel gas, a limitation that is often compounded by the bowel dilatation and ileus commonly encountered in AMI. Furthermore, even under optimal imaging conditions, DUS is generally confined to evaluation of the proximal mesenteric arteries and may fail to identify more distal occlusive lesions. Its operator dependence, limited reproducibility, and restricted availability outside routine working hours further diminish its clinical utility. Con
| Modality | Principal role | Strengths | Limitations and practical considerations | Ref. |
| DUS | Unsuitable as the initial investigation in suspected AMI | May identify proximal mesenteric arterial stenosis or occlusion when technically feasible | Operator dependent; limited by bowel gas, ileus and body habitus. Distal occlusions may be missed. Should not delay CTA | [3] |
| CTA | First-line investigation for urgent diagnosis and treatment planning | Rapidly assesses arterial occlusion, atherosclerosis, collaterals, bowel enhancement and alternative abdominal pathology | Iodinated contrast and radiation exposure. Early bowel changes may be subtle; no individual CT sign definitively establishes bowel viability | [3,36,37,40,41] |
| MRA | Limited role in emergency diagnosis | Vascular imaging without ionising radiation | Longer acquisition, motion sensitivity and limited emergency availability. Should not delay diagnosis or reperfusion | [37] |
| DSA | Primarily used during endovascular treatment | Selective assessment of occlusion, distal perfusion and collateral flow; enables immediate treatment and assessment of reperfusion | Invasive; contrast, radiation and access-site risks. Does not directly establish bowel viability or comprehensively assess alternative abdominal pathology | [3,4] |
CTA is the gold-standard radiological investigation for the diagnosis of AMI, with 24/7 access to high-resolution CTA allowing for rapid assessment of the mesenteric vasculature and identification of secondary signs of bowel ischaemia[33]. The radiologist plays a vital role in the evaluation for and diagnosis of AMI; however, a high index of clinical suspicion is essential in order to appropriately tailor the examination protocol to maximise diagnostic yield, and for the assessment of subtle signs of early intestinal ischaemia[34,35].
Intravenous contrast-enhanced computed tomography (CT) with volumetric slices of ≤ 1 mm, performed in the arterial and portal venous phases, is recommended as the first-line imaging modality for the assessment of AMI and other potential abdominal pathologies[36]. Arterial phase imaging provides excellent visualisation of the mesenteric arterial vasculature, allowing accurate detection of arterial stenoses or occlusions. Portal venous phase imaging is necessary for the detection of mesenteric venous thrombosis, evaluation of bowel wall perfusion and other signs of intestinal ischaemia, and assessment of the other abdominal viscera for other causes of abdominal pain[36,37]. Multiplanar reconstructions in the axial, sagittal and coronal planes should be performed routinely to comprehensively evaluate the mesenteric vas
On arterial phase CT, acute embolic occlusion most commonly involves the SMA and typically appears as a complete intraluminal filling defect or a central ovoid filling defect surrounded by contrast, most often in the mid-to-distal vessel (Figure 1). Synchronous emboli in other vessels may also be present and should be actively sought[38].
In contrast, an acute arterial thrombosis typically appears as an intraluminal filling defect in the vessel at the site of a calcified atherosclerotic plaque, typically occurring at the ostium or proximal portion of the vessel. In the setting of severely stenosed mesenteric vasculature, AMI may still be present without evidence of complete occlusion, due to the critical stenosis resulting in insufficient mesenteric perfusion, particularly in the setting of compromised collateral flow[23,39].
In the early stages of AMI, subtle CT findings of ischaemia may be present, and can be easily overlooked in the absence of a high index of suspicion. Findings such as subtle bowel wall thickening, bowel dilatation secondary to paralytic ileus, mesenteric stranding and peri-intestinal free fluid are all suggestive of underlying pathology such as early bowel ischaemia; however, they are not diagnostic of mesenteric ischaemia in isolation[36,40]. More concerning imaging fea
Without a high clinical suspicion of AMI, subtle findings can be overlooked, particularly if imaging protocols are not optimised for its detection[34,35,38]. Pooled systematic review data suggests that CT has a diagnostic sensitivity of 94% and specificity of 97%; however, in the majority of included studies, AMI was suspected clinically, introducing inherent selection bias that may overestimate real-world diagnostic accuracy[30,33,42]. In practice, AMI is rarely suspected clinically, with portal venous phase imaging typically performed to evaluate for other abdominal pathology, thus the reporting radiologist should maintain a high level of vigilance for the often subtle secondary signs of evolving bowel ischaemia to enable earlier diagnosis of AMI before irreversible bowel infarction occurs.
The management of AMI necessitates a coordinated multidisciplinary approach, with patients ideally managed in specialist centres providing 24/7 access to interventional radiology, vascular and gastrointestinal surgery, intensive care, and hybrid operating facilities, to enable both endovascular and open surgical management as clinically indicated[43]. Definitive treatment selection is directed by a collaborative decision-making process involving interventional radiology, vascular surgery and gastrointestinal surgery, with the principal determination being whether to pursue open surgical repair, endovascular intervention, or a hybrid approach[44]. This decision is informed by both the clinical presentation and CTA findings. Patients exhibiting features of peritonitis or haemodynamic instability, corroborated by radiological appearances highly suspicious for irreversible bowel ischaemia, should be considered candidates for emergency laparotomy with resection of non-viable bowel[26]. In centres with access to hybrid operating facilities, open or endo
In the absence of clinical or radiological features indicative of irreversible ischaemia, endovascular revascularisation is increasingly favoured as an initial treatment strategy[45-48]. Accurate determination of the underlying aetiology of AMI, whether embolic or thrombotic, is essential prior to intervention, as this directly influences the choice of endovascular technique and revascularisation strategy. Successful revascularisation does not exclude the presence of evolving intestinal injury, and patients treated with endovascular intervention alone require close postprocedural monitoring, and a low threshold for urgent laparotomy should be maintained in the event of persistent symptoms, clinical deterioration, or concern for delayed bowel infarction[44]. Supplementary Table 1 links these decisions to society guidance and supporting studies, identifying the limitations that affect interpretation and application of their findings.
Initial resuscitation should prioritise circulatory support through the administration of intravenous crystalloid fluids to optimise mesenteric perfusion and correct underlying metabolic derangements[29,49]. The use of vasopressors should be avoided where clinically feasible, given their propensity to exacerbate splanchnic vasoconstriction and worsen intestinal ischaemia, and their use should be reserved for cases of refractory hypotension[29]. Empirical broad-spectrum antibiotic therapy should be initiated in accordance with local antimicrobial guidelines, as bacterial translocation secondary to ischaemic bowel mucosa represents a frequent and serious complication of AMI, with resultant risk of systemic sepsis[12]. Prompt initiation of systemic anticoagulation with unfractionated heparin, unless contraindicated, is recommended to limit thrombus propagation and facilitate subsequent revascularisation, with a target activated partial thromboplastin time of 1.5-2.5 times the normal range[29]. Close monitoring of serum electrolytes and acid-base status is also essential, as mesenteric ischaemia may result in metabolic acidosis and hyperkalaemia secondary to bowel injury and tissue necrosis[50]. Additional supportive measures should include nasogastric decompression, appropriate analgesia and antiemetic therapy.
Patients with suspected or confirmed AMI should ideally be managed in a hybrid operating theatre environment, where both endovascular and open surgical interventions can be undertaken as required. Prompt revascularisation is critical to maximise bowel salvage and improve survival, with the ESVS stating that endovascular revascularisation should be considered as the initial approach in haemodynamically stable patients without evidence of peritonitis or CT evidence of transmural bowel necrosis (Recommendation 37; Class IIa, level of evidence B)[3]. Expert consensus from the CIRSE Standards of Practice supports this approach[4] (Supplementary Table 1).
The choice between open and endovascular treatment should be guided by the patient’s haemodynamic status, clinical examination, imaging findings, and local expertise[3,4]. In the presence of peritonitis, haemodynamic instability or imaging features strongly suggestive of bowel infarction, urgent surgical exploration is warranted[3,4]. While surgical intervention primarily aims to assess bowel viability and resect infarcted bowel, prompt revascularisation can also be performed. Conversely, endovascular intervention is focused on the rapid restoration of mesenteric perfusion to prevent progression to irreversible bowel infarction, with available options including aspiration thrombectomy, catheter-directed thrombolysis (CDT), and antegrade recanalisation with stenting selected according to the underlying aetiology and vascular anatomy. For consistency throughout this review, thrombectomy is used to describe catheter-based removal of thrombotic material, including emboli; catheter-based procedures termed embolectomy in the original literature are included within this definition.
Endovascular revascularisation should be considered an adjunct to the multidisciplinary management of AMI, rather than a definitive treatment strategy in isolation. ESVS advises considering restoration of arterial flow before bowel resection (Recommendation 35; Class IIa, level of evidence C), allowing reassessment of bowel viability thereafter[3]. Successful endovascular restoration of mesenteric perfusion, however, does not exclude bowel ischaemia, and prompt surgical exploration and bowel resection should be performed if peritonitis develops or clinical deterioration occurs suggesting ongoing ischaemia, as progression to transmural bowel infarction and sepsis can occur rapidly[3,4]. If bowel resection is required before revascularisation, resection should be limited to clearly non-viable bowel, with definitive assessment deferred until mesenteric perfusion has been re-established.
Comparative evidence supporting endovascular vs open revascularisation for arterial AMI remains uncertain, and is derived predominantly from heterogeneous observational studies, with variation in patient selection, aetiology, treatment combinations and outcome definitions[1]. A systematic review by Murphy et al[51] identified seven retrospective com
In patients with acute embolic SMA occlusion, ESVS describes aspiration thrombectomy as an endovascular option in patients without peritonitis, while CIRSE Standards of Practice provide consensus-based guidance supporting aspiration with selective adjunctive treatment[3,4]; however, these statements should be distinguished from evidence establishing comparative patient benefit. Available comparative data does not demonstrate the superiority of either endovascular or open revascularisation; however, several small retrospective single-centre studies support the feasibility of manual syringe aspiration and other mechanical thrombectomy techniques[54-56].
In a retrospective single-centre series, Raupach et al[54] reported complete SMA main-stem recanalisation in 34/37 patients (91.9%) following aspiration thrombectomy, with adjunctive thrombolysis and stenting used in two patients each. Subsequent laparotomy was performed in 27/37 (73.0%), bowel resection in 15/37 (40.5%), and in-hospital mortality was 10/37 (27.0%), with one fatal haemorrhagic complication reported. These figures demonstrate the feasibility within a combined endovascular and surgical pathway, rather than the efficacy of aspiration thrombectomy alone. Li et al[56] retrospectively compared endovascular treatment in 14 patients with open surgery in 27 patients with acute embolic mesenteric ischaemia. Endovascular success was achieved in 13/14 (93%), but neither bowel resection nor in-hospital mortality differed significantly, and significant selection bias limits conclusions regarding comparative benefit. In a separate retrospective cohort, Shi et al[55] compared stent-retriever thrombectomy plus aspiration (n = 14) with aspiration alone (n = 27). Combined treatment was associated with greater complete SMA main-trunk thrombus clearance [11/14 (78.6%) vs 12/27 (44.4%); P = 0.04], less adjunctive thrombolysis [2/14 (14.3%) vs 13/27 (48.1%); P = 0.03], and shorter mean hospital stay (5.7 days vs 10.7 days; P = 0.03). The study defined “clinical success” as clot retrieval and flow restoration, and this did not differ significantly between groups [11/14 (78.6%) vs 21/27 (77.8%); P = 1.00], nor did bowel resection or 30-day mortality. Operator-selected treatment and adjunctive therapies limit causal interpretation, with findings suggesting procedural feasibility, but not establishing superior bowel preservation or survival. Endo
The CA and SMA may be accessed via femoral, brachial, or radial arterial approaches[57,58]. In cases of acute downward angulation of the mesenteric vessel origin or significant ostial calcification, upper limb access-preferably via the left radial or brachial artery-may provide more favourable catheter and sheath alignment. Following insertion of a short 5-6 French (Fr) sheath and diagnostic aortography, a stiff guidewire is used to exchange for a longer working sheath, with sheath length selected according to the access site-typically 45 cm for femoral access, 90 cm for brachial access, and 100-110 cm for radial access[58,59]. Flush aortography is performed to identify the origins of the CA and SMA using a 5-Fr pigtail catheter positioned within the supracoeliac abdominal aorta, followed by selective catheterisation using a catheter-wire combination selected according to the access route and mesenteric anatomy[4]. Cobra and Simmons catheters are commonly employed via femoral access, whereas angled Bernstein or multipurpose catheters are often preferred for radial or brachial approaches[4]. Subsequent selective angiography in anteroposterior and lateral projections allows detailed assessment of the occlusive lesion and facilitates procedural planning.
Embolic AMI: In appropriately selected patients with embolic proximal SMA occlusion, aspiration thrombectomy may be performed with manual syringe aspiration or a dedicated mechanical aspiration system[3,4]. These techniques can facilitate rapid mesenteric revascularisation; however, successful restoration of arterial flow should be distinguished from demonstrated benefit in bowel preservation or survival[60]. Potential procedural complications include vessel dissection and distal embolisation[61]. Residual thrombus or underlying stenosis may require adjunctive thrombolysis, angioplasty or stenting[3,4] (Supplementary Table 1).
Manual syringe aspiration involves positioning an aspiration catheter at or beyond the embolus and applying negative pressure with a syringe whilst withdrawing the catheter. Multiple aspiration passes may be undertaken until satisfactory angiographic recanalisation and restoration of distal perfusion are achieved[4,59]. Mechanical aspiration thrombectomy is performed in a similar manner, using a suction system to extract thrombus through the catheter[4,62]. Stent-retriever, rheolytic and rotational thrombectomy are distinct mechanical techniques and should be considered separately when interpreting device-specific evidence[4,63,64]. Following aspiration, residual thrombus and distal perfusion should be reassessed angiographically. If flow remains inadequate, further aspiration, selective CDT or another thrombectomy technique may be considered according to clot location, vascular anatomy and the patient’s clinical condition[3,4].
Comparative evidence evaluating manual syringe aspiration and mechanical aspiration in arterial AMI remains limited. Garzelli et al[62] retrospectively compared 31 patients who underwent manual aspiration (n = 16) or mechanical aspiration using the Indigo aspiration system (Penumbra Inc, Alameda, California) (n = 15). Reported technical success was 13/16 (81.3%) vs 11/15 (73.3%), respectively. Bowel resection occurred in 7/16 (43.8%) vs 6/15 (40.0%; P = 0.99), and 30-day survival was 15/16 (93.8%) vs 12/15 (80.0%; adjusted P = 0.14). Adjunctive thrombolysis or stenting was used in 8/16 and 10/15 patients, respectively. The small sample, operator-selected treatment allocation and adjunctive therapies limit attribution of the outcomes to the aspiration technique, and the descriptive findings do not establish superiority or equivalence and should not be extrapolated to other mechanical thrombectomy devices.
In an additional uncontrolled retrospective series of 15 patients with acute SMA embolism, Li et al reported complete thrombus removal in all patients using the Indigo aspiration system, with additional distal-branch aspiration using the CAT RX system (Penumbra Inc, Alameda, California) used in five patients. No adjunctive thrombolysis or stenting was performed[65]. Despite angiographic success, bowel resection was required in 3/15 (20.0%), and in-hospital mortality was 1/15 (6.7%). No intraoperative vessel perforation or dissection was reported and no recurrent SMA embolism or further mortality was reported during follow-up (range 3-12 months). Again, the small sample and absence of a comparator sup
Stent-retriever thrombectomy has also been described in combination with manual aspiration for arterial AMI. In a retrospective series containing 9 patients, Shi et al[63] reported successful Solitaire AB stent retriever (Medtronic, Irvine, CA, United States) deployment and retrieval in all patients, but successful thrombus retrieval and SMA flow restoration in 7/9 (77.8%). Adjunctive stenting was performed in 3/9 (33.3%), with final SMA recanalisation reported in all nine patients. No patient underwent bowel resection, no device-related complications or distal embolisation were reported, and in-hospital mortality was 1/9 (11.1%). This uncontrolled series demonstrates feasibility of the combined strategy but does not establish comparative efficacy or reliably characterise safety.
CDT: CDT involves placement of a catheter within or immediately proximal to the thrombus, facilitating high local concentrations of thrombolytic agent, whilst minimising systemic exposure. ESVS describes the use of local thrombolysis as an option in patients without peritonitis, following incomplete aspiration thrombectomy or distal embolisation[3]. CIRSE Standards of Practice provide consensus-based technical guidance supporting selective CDT for residual thromboembolic material, inadequate blood flow or thrombus lodged within distal branch vessels[4]. These statements describe the role of CDT in treatment pathways; however, they do not establish comparative benefit in bowel preservation or survival. Although CDT can facilitate further thrombus resolution and improve distal vessel patency, its use requires careful patient selection owing to the risks of major haemorrhage, access-site bleeding, and catheter-related vessel injury. Local administration does not eliminate bleeding risk, and treatment requires assessment of contraindications and continued monitoring of bowel viability[3,4]. Furthermore, successful revascularisation does not eliminate the risk of subsequent complications, as bowel reperfusion injury or persistent intestinal ischaemia following delayed or incomplete reperfusion may still progress to bowel necrosis and necessitate urgent surgical intervention[60,66] (Figures 2, 3, and 4; Supplementary Table 1).
Prior to commencing CDT, contraindications and bleeding risk should be assessed, including active bleeding, recent cerebrovascular haemorrhage, major surgery or trauma, and uncontrolled hypertension. Treatment should be undertaken in a monitored setting, with frequent assessment of haemodynamic status, abdominal findings, vascular access sites and neurological status, supported by serial haemoglobin levels, platelet count, coagulation studies and lactate measu
Catheter selection varies depending on thrombus location and vessel calibre. CIRSE describes multiple side-hole infusion catheters positioned within the thrombus, end-hole catheters placed immediately proximal to the occlusion and microcatheters for distal branch vessel emboli[4]. CDT regimens vary between centres. ESVS and CIRSE describe infusion regimens including recombinant tissue plasminogen activator at 0.5-1 mg/h or urokinase at doses such as 120000 IU/h[3,4]. These represent examples of technical practice rather than evidence establishing an optimal regimen, with most centres following their own local protocols. Bolus administration, concomitant anticoagulation and measures to maintain sheath patency should follow an institution-specific protocol, rationalised against individual patient bleeding risk.
ESVS and CIRSE describe repeat angiography once or twice daily during CDT to assess thrombus resolution and arterial patency[3,4]. Angiographic findings should be interpreted alongside the patient’s clinical condition, with inadequate reperfusion or deterioration prompting reassessment of the revascularisation strategy and bowel viability. ESVS also describes anticoagulation with heparin as an option for small residual emboli in peripheral marginal branches of the SMA where collateral circulation provides sufficient perfusion[3]. Supporting observational experience includes Acosta et al[67], who reported residual emboli after satisfactory aspiration thrombectomy, with or without adjunctive thrombolysis, in seven patients, one of whom required bowel resection. These findings support selective management according to residual thrombus, with the authors considering collateral perfusion a possible explanation for bowel preservation despite residual emboli; however, no comparative benefit with respect to bowel preservation or survival has been determined.
Najdawi et al[46] retrospectively analysed prospectively collected data from 58 patients undergoing endovascular treatment for arterial AMI, including 19 treated with intra-arterial thrombolysis. CDT technical success was reported as 89%, defined as partial or total arterial recanalisation assessed at 24 hours. However, bowel resection and mortality were reported for the overall cohort rather than separately for CDT, and one SMA perforation during thrombolysis caused haemorrhagic shock. These findings support technical feasibility within a multidisciplinary treatment strategy; however, selection bias, heterogeneous treatment strategies and the absence of a direct comparator group prevent conclusions being drawn regarding comparative safety, bowel preservation or survival benefit.
In a multicentre observational cohort of 34 patients with acute SMA occlusion without peritonitis at admission, Björnsson et al[68] reported technically successful thrombolysis in 30/34 (88.2%), defined as complete lysis with restored flow or partial lysis with improved flow, with complete lysis occurring in 14/34 (41.2%).
Adjunctive endovascular procedures were performed in 16/34 (47.1%), including aspiration thrombectomy in 10/34 (29.4%). Subsequent exploratory laparotomy was performed in 13/34 (38.2%), bowel resection in 8/34 (23.5%), and in-hospital mortality was 9/34 (26.5%). Six self-limiting bleeding events occurred in five patients (14.7%), with none requiring transfusion, cessation of thrombolysis or surgery[68]. These findings support the feasibility of a treatment strategy incorporating local thrombolysis in selected patients, but the absence of an alternative-treatment comparator, frequent adjunctive procedures and variation in treatment across centres limit attribution of outcomes to CDT alone, and preclude conclusions regarding comparative safety, bowel preservation or survival.
Shi et al[60] retrospectively compared 47 patients with arterial AMI who underwent mechanical thrombectomy treatment (n = 29) or CDT (n = 18) as their initial treatment strategy. Final angiographic success, defined as complete or partial recanalisation after adjunctive treatment, occurred in 26/29 (89.7%) vs 16/18 (88.9%). There were no significant differences in bowel resection [3/29 (10.3%) vs 3/18 (16.7%); P = 0.66] or 30-day mortality [9/29 (31.0%) vs 6/18 (33.3%); P = 0.87], although minor bleeding occurred only with CDT [0/29 vs 2/18 (11.1%); P = 0.14][60]. Seven thrombectomy patients received adjunctive CDT. Operator-selected treatment, heterogeneous thrombectomy techniques, additional adjunctive procedures and differing symptom duration again limit causal interpretation, with findings representing the success of the overall treatment strategy rather than individual techniques, thus findings do not establish equivalence or superior bowel preservation, survival or safety.
Acute thrombotic/acute-on-CMI: Acute thrombotic mesenteric ischaemia typically results from in situ thrombosis of a pre-existing atherosclerotic stenosis, most commonly involving the vessel origin[3,4]. CIRSE Standards of Practice provide consensus-based guidance prioritising SMA recanalisation in atherosclerotic AMI or acute-on-chronic disease involving both the SMA and CA, with CA revascularisation considered when SMA recanalisation is unsuccessful or not feasible[4]. Treatment may involve aspiration thrombectomy or selective CDT for acute thrombus, as well as angioplasty and stenting of the underlying atherosclerotic lesion[3,4]. ESVS guidance also describes treatment of the underlying atherosclerotic lesion during the same procedure as thrombus removal, with the clinical rationale being the restoration of arterial inflow; however, this technical guidance should be distinguished from a demonstrable comparative benefit in bowel preservation or survival[3]. If percutaneous antegrade stenting is not possible, ESVS states that retrograde open mesenteric artery stenting may be considered (Recommendation 38; Class IIb, Level C)[3].
Pedersoli et al[69] reported a retrospective single-centre series of 40 patients undergoing angioplasty and stenting for AMI caused by proximal SMA and/or CA thrombosis in the setting of atherosclerotic disease. Technical success, defined as restoration of target-vessel patency with peripheral branch flow and residual stenosis below 30%, was achieved in 36/40 patients (90.0%). Following revascularisation, 25/40 (62.5%) patients underwent surgical exploration, with bowel resection performed in 12/25 (48%). Thirty-day mortality was 25/40 (62.5%). Again, these findings support the technical feasibility of angioplasty and stenting of the underlying atherosclerotic lesion in AMI; however, the absence of a com
CMI is characterised by haemodynamically significant stenosis or occlusion of the mesenteric arteries, resulting in the classic clinical triad of postprandial abdominal pain, unintentional weight loss, and a fear of eating. The underlying pathological process is mesenteric artery occlusive disease (MAOD), which most commonly results from atherosclerosis of the ostia of the mesenteric arteries. Importantly, MAOD itself is a relatively common incidental finding, particularly in the elderly population, and does not necessarily produce the clinical syndrome of CMI, in which symptoms do not typically manifest until at least two of the three mesenteric arteries are significantly stenosed or occluded. Notably, severe single-vessel disease, particularly of the SMA may also cause ischaemia when collateral supply is inadequate. Non-atherosclerotic causes of MAOD include median arcuate ligament syndrome, vasculitis, and fibromuscular dysplasia[70]. The diagnosis of CMI requires the combination of a characteristic clinical presentation, radiological or haemodynamic evidence of MAOD, and the exclusion of alternative causes of abdominal pain and weight loss, particularly gastro
CMI itself remains a relatively rare clinical entity, with its incidence reported at approximately 9.0 per 100000 of the population[72], demonstrating an increasing prevalence with advancing age and exhibiting a slight female predilection[73,74]. Given that CMI is predominantly atherosclerotic in aetiology, its risk factor profile mirrors that of systemic atherosclerotic disease and includes hypertension, smoking, diabetes mellitus, and hyperlipidaemia. As detailed above, atherosclerosis of the mesenteric vasculature is common, with population-based studies demonstrating single-vessel mesenteric stenosis in up to 17.5% of individuals, further underscoring that anatomical stenosis alone does not defi
CMI most commonly results from atherosclerotic disease of the mesenteric arteries. Traditionally, symptomatic disease was thought to require haemodynamically significant stenosis or occlusion of at least two of the three major mesenteric vessels; however, it is now recognised that isolated single-vessel disease, particularly involving the SMA, may produce symptoms when collateral circulation is inadequate[76,77]. Mesenteric blood flow may increase to approximately 35% of cardiac output in the postprandial state to meet the metabolic demands of digestion; however, in the setting of CMI, fixed atherosclerotic stenoses limit this physiological augmentation in blood flow, resulting in a mismatch between intestinal oxygen supply and metabolic demand. This supply-demand mismatch leads to intestinal ischaemia, stimulating afferent pain fibres, producing the characteristic postprandial pain of CMI. This phenomenon is analogous to exertional angina in the setting of coronary artery disease, and from which the historical term “mesenteric angina” is derived[9,71]. Atherosclerotic plaque formation tends to occur proximally in the mesenteric vessels, typically originating at the ostia and extending distally. Critical stenosis or occlusion of the SMA represents the most prevalent pattern of disease, and due to its anatomical and haemodynamic significance, renders it the primary target vessel in endovascular revascularisation strategies[78,79].
CMI classically presents with a triad comprising postprandial abdominal pain, unintentional weight loss, and a fear of eating. The abdominal pain is typically crampy in nature, localising to the mid-abdomen or epigastric region, and deve
DUS is frequently the first imaging modality employed in the screening of patients with clinically suspected CMI, and should ideally be performed after a minimum of 4 hours of fasting[81,82]. Peak systolic velocity and end-diastolic velocity are the principal haemodynamic parameters utilised to quantify the degree of mesenteric vascular stenosis; however, variation exists between international guidelines regarding the appropriate diagnostic threshold values. These diagnostic thresholds must, however, be interpreted in light of the well-recognised limitations of DUS in this clinical context. Validated cut-off values have not been definitively established due to a paucity of rigorous validation studies, and dia
| Modality | Principal role | Strengths | Limitations and practical considerations | Ref. |
| DUS | Initial screening in experienced centres | Non-invasive assessment of proximal CA and SMA anatomy and flow velocities without radiation or intravenous contrast | Requires fasting and expertise; affected by bowel gas, body habitus and respiration. Positive or inconclusive results require CTA or MRA confirmation | [3,81,82,85] |
| CTA | Preferred examination for anatomical confirmation and treatment planning | Defines stenosis, lesion length, calcification, vessel origins and collaterals; evaluates alternative causes of symptoms | Iodinated contrast and radiation exposure. Anatomical stenosis alone does not establish symptomatic CMI | [3,84,85,87] |
| MRA | Alternative when CTA is contraindicated | Contrast-enhanced assessment of proximal mesenteric stenoses without radiation; specialised techniques permit flow assessment | Longer acquisition and motion artefact; smaller vessels less reliably assessed and stenosis may be overestimated. Gadolinium suitability requires individual assessment | [3,85,87,90,91] |
| DSA | Generally reserved for endovascular intervention | Detailed vascular and collateral assessment with concurrent treatment; selective pressure measurements may help assess uncertain lesions | Invasive; contrast, radiation and access-site risks. Pressure measurements are adjunctive and do not independently establish CMI | [3,85,92,93] |
CTA is the imaging modality of choice in the evaluation of patients with suspected CMI. Thin-section volumetric acquisition (≤ 1 mm slices) enables high-resolution multiplanar and three-dimensional reconstruction of the mesenteric arterial circulation and collateral networks, with reported sensitivity and specificity approaching 100% for the detection of MAOD. The threshold for haemodynamically significant mesenteric stenosis remains a topic of debate. The Society of Interventional Radiology and the Society for Vascular Surgery (SVS) define significant stenosis as greater than 70% stenosis of any major mesenteric artery, whereas European guidelines adopt both an anatomical cross-sectional area and postprandial flow-based approach, defining greater than 50% stenosis of the SMA as haemodynamically relevant in the context of multivessel disease and appropriate symptoms[81,84-86]. Beyond assessment of the mesenteric vasculature, CTA can provide comprehensive evaluation of the abdominal viscera, facilitating the exclusion of alternative causes of abdominal pain and weight loss[37,84,87]. Whilst DUS is an effective screening tool, CTA provides the anatomical detail necessary for procedural planning and remains essential for confirming the diagnosis. Compared with DUS, magnetic resonance angiography (MRA), and catheter-directed angiography, CTA offers superior spatial resolution, greater acc
Contrast-enhanced MRA is a useful alternative when CTA is contraindicated, demonstrating sensitivities and specificities exceeding 95% for the detection of haemodynamically significant mesenteric artery stenosis. Notable advantages of MRA when compared with CTA include the potential for haemodynamic flow quantification, superior soft tissue characterisation, and the absence of ionising radiation exposure[84,89]. MRA, however, has several limitations. Its lower spatial resolution may lead to overestimation of luminal stenosis, while visualisation of smaller-calibre vessels, particularly the IMA, is often suboptimal. In addition, longer acquisition times and greater susceptibility to respiratory and bowel motion artefact limit its utility in routine clinical practice[89-91].
Digital subtraction angiography provides high-resolution visualisation of the mesenteric vasculature and collateral networks, with the additional advantage of enabling concurrent endovascular intervention at the time of diagnosis. The procedure involves selective catheterisation of the mesenteric arteries and contrast injection in both anteroposterior and lateral projections, generating detailed fluoroscopic images. Furthermore, it permits haemodynamic flow assessment via trans-stenotic pressure gradient measurement, to determine the functional significance of identified lesions, and guide the need for synchronous revascularisation. Haemodynamically significant SMA stenosis is defined as a mean arterial pressure gradient across the lesion of ≥ 10 mmHg, a systolic pressure gradient ≥ 20 mmHg, or a distal-to-proximal pre
For patients with CMI requiring revascularisation, with suitable anatomy, ESVS recommends an endovascular approach in the first instance (Recommendation 14; Class I, Level B), and that open revascularisation should be considered in fit patients, after failed endovascular intervention, or when endovascular treatment is not feasible or contraindicated (Recommendation 19; Class IIa, Level C)[3]. CIRSE Standards of Practice provide consensus-based guidance also sup
A systematic review and meta-analysis by Alahdab et al[73] synthesised 100 observational studies comprising 18726 patients with CMI, including 22 studies directly comparing endovascular and open revascularisation, demonstrating that open surgery was associated with more in-hospital complications (15 studies; RR = 2.19, 95%CI: 1.84-2.60), but less symptom recurrence within three years (13 studies; RR = 0.47, 95%CI: 0.34-0.66)[73]. No significant difference in 30-day mortality (18 studies; RR = 1.57, 95%CI: 0.84-2.93) or three-year survival (13 studies; RR = 0.96, 95%CI: 0.86-1.07) was identified, suggesting a trade-off between perioperative morbidity and subsequent symptom recurrence, rather than superiority across all patient-centred outcomes. The authors rated certainty as low for complications and symptom recurrence, and very low for mortality outcomes, with non-randomised treatment allocation, differences in anatomy and comorbidity and a heterogeneous mix of procedures limiting causal interpretation.
Erben et al[95] retrospectively analysed United States National Inpatient Sample data from 2000-2014, reporting 10920 endovascular and 4555 open revascularisation admissions for CMI. Endovascular treatment was associated with lower unadjusted in-hospital mortality (2.4% vs 8.7%) and shorter mean hospital stay (6.3 days vs 14.0 days; both P < 0.0001). Following adjustment for age, sex, comorbidity and hospital factors, open treatment remained associated with higher in-hospital mortality (OR = 7.2, 95%CI: 4.9-10.6) and longer admission by 9.7 days. These associations support the perioperative rationale for a primary endovascular approach; however, factors such as an absence of post-discharge follow-up and unmeasured differences in anatomy and treatment selection limit interpretation and assessment of long-term benefit.
In an attempt to assess long term survival comparison between endovascular and open intervention, Tallarita et al[96] retrospectively evaluated 343 patients undergoing open (n = 187) or endovascular (n = 156) revascularisation for atherosclerotic CMI between 1991 and 2010. A propensity matched analysis of 127 patients per group was performed, demonstrating that five-year survival did not differ significantly between open and endovascular treatment (60% vs 57%; P = 0.7). Retrospective evaluation, exclusion of unmatched patients and longer follow-up in the open group limit inter
ESVS recommends revascularisation for patients with multivessel occlusive mesenteric artery disease and CMI (Recommendation 9; Class I, Level B), including at least the SMA (Recommendation 10; Class I, Level C)[3]. In single vessel disease, revascularisation should be considered for CMI attributable to the SMA, if stenosis is > 70% (Recom
Observational evidence from Terlouw et al[72] reported higher rates of clinical success after revascularisation in patients with multivessel atherosclerotic disease than in those with single-vessel disease, with clinical success reflecting symptom improvement or resolution, assessed three months after treatment, which also informed confirmation of the CMI diagnosis. These findings support careful patient selection but do not establish that treating multiple vessels provides greater benefit than treating a single target vessel.
In patients with single-vessel atherosclerosis of either the SMA or CA, van Dijk et al[97] retrospectively evaluated 59 symptomatic patients, of whom 37 underwent revascularisation following multidisciplinary diagnosis supported by functional testing for mucosal ischaemia. Thirty-five patients underwent endovascular treatment and two underwent surgical management, with patients reporting sustained symptom relief in 27/37 (73%) after a mean follow-up of 5.0 years. Symptom response did not differ significantly between CA and SMA disease (22/30 vs 5/7; P = 0.919). Six patients required repeat revascularisation for symptomatic restenosis, with renewed symptom relief reported in all six. The retrospective design, however, and the absence of an untreated comparator group limits assessment of comparative benefit and the attribution of symptom relief to the procedure alone.
Anatomical assessment may also inform patient selection, with Omran et al[98] developing a mesenteric artery scoring model in a retrospective cohort of 242 patients with suspected CMI, which incorporated the severity and extent of disease in the CA, SMA and IMA. The scoring system, however, lacked external validation and therefore only provided exp
In selected asymptomatic patients undergoing abdominal aortic aneurysm repair, SVS guidelines suggest prophylactic treatment of high-grade SMA stenosis when mesenteric perfusion depends on a dominant mesenteric artery/arc supplied by a large IMA that will be sacrificed during repair, representing concern about loss of collateral perfusion (Grade 2C)[99].
Long-segment occlusions, extensive calcification, tandem lesions and flush ostial occlusions may complicate endovascular revascularisation, although these features do not definitively preclude successful treatment[71]. ESVS advises considering open revascularisation in fit patients after failed endovascular intervention, or when endovascular treatment is not feasible or contraindicated (Recommendation 19; Class IIa, Level C)[3]. Median arcuate ligament syndrome requires separate consideration, as primary CA stenting does not address the underlying extrinsic com
In a study describing endovascular outcomes alone, Nana et al[94] synthesised 16 retrospective studies comprising 1224 patients with atherosclerotic CMI and 1368 target vessels, demonstrating pooled technical success of 95% (95%CI: 93%-97%), immediate symptom relief of 87% (95%CI: 80%-92%) and 30-day mortality of 2%. During a mean follow-up of 28 months, pooled symptom recurrence and reintervention rates were 25% and 26%, respectively. These estimates do not demonstrate comparative superiority, and their retrospective design, heterogeneous outcome definitions and follow-up, led the authors to ascribe a low to very low level of certainty to the data.
A retrospective single-centre analysis by Bulut et al[100] evaluated 185 bare-metal-stented CA/SMA vessels in 141 patients, including 128 with CMI and 13 with acute presentations. Primary patency was 77.0% at 12 months and 45.0% at 60 months, compared with secondary patency of 98.3% and 93.6%, respectively. The exclusion of patients without avai
Altintas et al[101] reported outcomes from a Danish national cohort of 245 patients undergoing endovascular treatment, including 178 with CMI and 67 with acute-on-CMI. Among patients with CMI, complete symptom improvement at discharge was reported in 127/178 (71.3%) and partial improvement in a further 24/178 (13.5%); 30-day mortality was 3/178 (1.7%). Again, the absence of a surgical comparator prevents conclusions being drawn about com
For patients with atherosclerotic CMI requiring endovascular treatment, ESVS recommends routine mesenteric artery stenting rather than plain balloon angioplasty (Recommendation 15; Class I, Level C)[3]. Similarly, consensus opinion from CIRSE describes stenting as the standard endovascular approach[4]. Technical rationale includes maintaining luminal expansion and limiting elastic recoil in ostial lesions; however, this should be distinguished from evidence of superior patient-centred outcomes. Nana et al’s systematic review and meta-analysis included 16 retrospective studies comprising 1224 patients and 1368 treated vessels; however, only 90 procedures were performed using angioplasty alone, reflecting the widespread preference for primary stent placement[94]. This study principally described endovascular outcomes rather than a comparison of stenting vs angioplasty, and pooled endovascular outcomes therefore do not establish greater symptom relief, fewer reinterventions or improved survival with primary stenting vs with angioplasty alone (Figures 5, 6 and 7; Supplementary Table 2).
The SMA remains the principal revascularisation target in multivessel CMI, with ESVS recommending treatment of at least the SMA (Recommendation 10; Class I, Level C)[3]. CA revascularisation may be considered when SMA recanalisation is unsuccessful or deemed unlikely to succeed because of extensive calcification or long-segment occlusion[3,4]. Additional CA treatment may also be considered in selected patients with severe gastric ischaemia and inadequate CA-SMA collateralisation, although this introduces further procedural risks[3]. These considerations inform individualised target-vessel selection; however, they do not establish superior outcomes from routine two-vessel stenting.
Malgor et al[102] retrospectively compared 101 patients undergoing stenting for atherosclerotic CMI, with the SMA alone treated in 61, combined SMA/CA treatment in 24, and only the CA treatment in 16. During a mean follow-up of 41 ± 17 months, no significant differences in freedom from recurrent symptoms or reintervention were identified between treatment groups. Two-vessel treatment was undertaken because of operator preference in 18/24 patients, with the remaining six receiving additional CA stenting for residual SMA stenosis or dissection, or severe gastric ischaemia. The small, non-randomised groups and differing indications for treatment limit causal interpretation, and findings did not establish equivalence between treatment of the SMA alone, combined treatment of the SMA and CA or additional CA treatment in selected patients.
A retrospective series by Flis et al[103] of 27 patients with SMA and CA disease considered unsuitable for endovascular treatment, who underwent retrograde aortomesenteric bypass of the SMA supports surgical experience. Symptom improvement was reported in 25/27 patients (92.6%), with one early death occurring 31 days after surgery. Mean follow-up was 71 months, with no graft occlusion or reintervention reported. This study provides supporting evidence of the feasibility of SMA surgical revascularisation in two-vessel disease; however, it does not provide evidence of equivalence to multi-vessel reconstruction or comparative benefit of endovascular SMA treatment.
IMA stenting may be considered to improve collateral perfusion in selected patients when SMA or CA revascularisation is unsuccessful or unsuitable. CIRSE provides consensus-based guidance supporting this approach, while ESVS discusses the limited supporting evidence without assigning a separate graded recommendation for IMA intervention[3,4]. Wohlauer et al[104] described four patients with initial symptom relief after IMA stenting, although one subsequently required treatment of in-stent restenosis and another underwent multivessel surgical bypass for recurrent symptoms despite a patent IMA stent. Feldman et al[105] reported five salvage IMA revascularisations, including four endovascular procedures and one open repair, in patients with chronic or acute-on-CMI; however, subsequent CA/SMA revascularisation in some patients makes it difficult to attribute clinical outcomes solely to IMA treatment. Nair et al[106] reported attempted IMA stenting in eight patients, with one technical failure and two procedure-related complications. Four patients achieved complete symptomatic improvement, while three developed recurrent symptoms during a median follow-up of 18 months. These small, uncontrolled series support technical feasibility and possible symptom relief in selected patients, but do not establish comparative benefit or justify routine IMA intervention.
Endovascular approach: The general endovascular approach to accessing the target mesenteric vessel is similar to that described for AMI, with the access route and equipment selected according to mesenteric anatomy. The target stenotic lesion may be crossed using a hydrophilic 0.035″ or 0.018″ guidewire and an appropriate catheter (Figure 6). If there is difficulty crossing the lesion using a standard system, a 0.014’’ microwire and microcatheter combination can be used[69], and angiography should confirm intraluminal catheter position distal to the lesion before further treatment[4,69]. Translesional pressure measurements may complement angiographic assessment, particularly when the severity of a stenosis is uncertain[4,107,108]. Catheter-based methods and thresholds vary between studies, with AbuRahma et al[107] using a 4-Fr catheter, where they considered a systolic gradient of 20 mmHg significant, whereas Landis et al[108] obtained simu
Following target vessel assessment, a long 6-Fr or 7-Fr sheath is advanced towards the ostium over a support wire (Figure 6). Systemic unfractionated heparin is administered before angioplasty or stenting, with balloon dilatation of the ostium used selectively to assist sheath advancement or prepare the lesion[4,107]. Monorail and over-the-wire balloon system selection are both acceptable depending on operator preference, lesion characteristics and the support required[4]. Balloon-expandable stents are commonly used for ostial lesions, with sizing based on vessel calibre and lesion extent[107,108]. CIRSE describes proximal aortic protrusion and flaring of the stent to ensure ostial coverage, while avoiding excessive extension into the aortic lumen[4]. In the proximal SMA, covered stents are preferred in selected cases, provided no side-branches are occluded[109]. Completion angiography is performed to assess vessel and branch patency and residual stenosis (Figure 7), with further dilatation considered for residual narrowing > 30%[4]. Angiographic success should be distinguished from symptom relief. For selected complex lesions, the use of an embolic-protection filter wire has also been described[110].
Covered vs bare-metal stents: ESVS advises considering covered stents for lesions shorter than 25 mm when no signi
In a retrospective two-centre study, Oderich et al[111] evaluated 225 patients with CMI, analysing primary inter
Further to this, in the multicentre CoBaGI randomised trial, 94 patients were allocated equally to covered or bare-metal stenting, with 47 patients receiving 62 stents in the covered-stent group, and 47 receiving 66 stents in the bare-metal group[109]. At 24 months, primary patency was assessed in 52 covered and 53 bare-metal stents after excluding missing observations. Patency was greater with covered stents [42/52 (81%) vs 26/53 (49%); OR = 4.4, 95%CI: 1.8-10.5; P < 0.0001]. Reintervention was also analysed per stent and occurred in 11/62 covered vs 22/66 bare-metal stents by 24 months (18% vs 33%; P = 0.041). Procedure-related adverse events were assessed per patient and occurred in 17/47 (covered stent group) vs 9/47 patients (bare-metal stent group) respectively (36% vs 19%; P = 0.065). These findings support improved two-year patency and a lower reintervention rate at 24 months in selected short lesions, but do not establish a survival benefit.
In patients undergoing revascularisation for CMI, the evidence base remains limited with respect to the efficacy and risk-benefit profile of dual antiplatelet therapy (DAPT). ESVS states that aspirin and clopidogrel may be considered for a short course of at least one month to reduce stent thrombosis risk (Recommendation 18; Class IIb, Level C; consensus), in the absence of contraindications and with an acceptable bleeding risk, to mitigate the risk of stent thrombosis[3]. CIRSE describes one month of DAPT followed by lifelong antiplatelet monotherapy, reflecting practice extrapolated from established practice in endovascular revascularisation for coronary artery and peripheral arterial disease, and is acknowledged as an interim position pending higher-quality evidence to define the optimal antiplatelet strategy[4]. Nana et al’s study-level meta-regression did not identify significant differences in reported outcomes between single antiplatelet therapy and DAPT, but retrospective data and under-reporting of bleeding and treatment adherence preclude conclusions of equivalence[94]. The optimal regimen and duration therefore remain uncertain, with treatment individualised according to bleeding risk and other antithrombotic indications, and there is currently insufficient evidence to support the routine use of direct oral anticoagulants following mesenteric stenting[3].
The principal complications of mesenteric angioplasty and stenting are access-site related (haematoma and pseudoaneurysm), arterial dissection or perforation, distal embolisation, stent displacement and stent thrombosis[4].
An imaging finding of recurrent narrowing should be distinguished from recurrent symptoms or the need for reintervention. In a retrospective cohort of 121 patients with multivessel mesenteric disease, Ahanchi et al[112] compared 92 SMA and 40 CA stents, with a mean follow-up of 12.8 months. Estimated one-year primary patency was higher for SMA than CA stents (55% vs 18%; P < 0.0001), but one-year survival free from symptom recurrence did not differ significantly (63% vs 53%; P = 0.07). Factors such as non-randomised vessel selection and surveillance using duplex sonography limit interpretation, as well as the inclusion of early follow-up angiograms as reintervention, which may have influenced reported patency rates.
For symptomatic restenosis, ESVS advises considering endovascular treatment first (Recommendation 24; Class IIa, Level C)[3]. Treatment may also be considered in selected patients with asymptomatic > 70% restenosis (Recom
Tallarita et al[113] retrospectively evaluated 30 patients undergoing reintervention for mesenteric in-stent restenosis, 24 of whom had recurrent symptoms, including three acute presentations, and six had asymptomatic preocclusive lesions. Treatment was endovascular in 26 patients and open bypass in four patients. Symptoms improved in 22/24 symptomatic patients (91.7%), while complications occurred in 7/26 patients undergoing endovascular reintervention (26.9%). One procedure-related death occurred 57 days after repeat stenting for AMI. During mean follow-up of 29 months, 15/30 patients developed further restenosis and 7/30 required another intervention. The heterogeneous treatment population, non-randomised treatment allocation and heterogeneous interventions precluded the identification of a preferred reintervention technique.
Reported outcomes generally appear to be more favourable following SMA stenting than CA stenting. Additionally, covered stents have demonstrated superior long-term patency and lower rates of restenosis and reintervention compared with bare-metal stents, and are increasingly regarded as the preferred option for mesenteric revascularisation where side-branch preservation is not a limiting consideration[111].
Endovascular revascularisation is a feasible option for selected patients with arterial AMI, and is recommended as the initial approach for CMI with suitable anatomy[3,4]. In arterial AMI, studies demonstrate that the restoration of mesenteric perfusion is feasible; however, comparative effects on bowel preservation and survival remain uncertain. In CMI, comparative evidence identifies differences in perioperative morbidity, symptom recurrence and stent patency that inform treatment selection. Treatment selection should therefore balance the expected clinical benefit against procedural risk, with consideration of lesion anatomy, bowel viability and patient outcomes.
In arterial AMI, aspiration and other thrombectomy techniques have been demonstrated to achieve high rates of angiographic recanalisation, although frequently within treatment pathways that include adjunctive interventions such as thrombolysis, stenting or surgery. Small comparative cohorts have identified differences in thrombus clearance and adjunctive treatment requirements, but have not established corresponding improvements in bowel preservation or survival. Observational comparisons of endovascular and open revascularisation suggest favourable early outcomes with endovascular treatment, although differences in patient presentation, bowel viability and treatment selection limit causal interpretation. Further research should determine which patients benefit from an initial endovascular strategy, whether specific thrombectomy techniques improve patient outcomes, and when incomplete reperfusion should prompt alter
In CMI, the evidence supports a clinically important trade-off between the lower perioperative morbidity associated with endovascular treatment and the lower subsequent symptom recurrence associated with open surgery[73]. Long-term survival comparisons have not established superiority or equivalence between these approaches[96]; however, these findings inform the ESVS recommendation for initial endovascular treatment in patients with suitable anatomy and CIRSE consensus-based guidance supporting this strategy[3,4]. Randomised evidence demonstrates better 24-month primary patency with covered stents in comparison to bare-metal stents in selected lesions[109], while observational studies show that symptom relief can persist despite a substantial burden of restenosis and repeat intervention[94,97,100,113]. Further studies should establish how stent selection affects sustained symptom relief, quality of life and repeat intervention across different lesion anatomies, and whether additional vessel revascularisation improves outcomes beyond SMA treatment alone.
Important uncertainties also remain regarding the prevention and management of restenosis. Selected cohorts report renewed symptom relief after reintervention, but recurrent restenosis and procedural complications remain relevant[113]. Comparative studies are needed to define the preferred reintervention strategy, identify which asymptomatic restenoses warrant treatment, and determine whether surveillance improves patient outcomes. The optimal antithrombotic regimen and duration after mesenteric stenting also require direct investigation.
This review complements existing reviews and society guidance by relating individual endovascular treatment decisions to the populations studied, outcomes measured and limitations of the supporting evidence. It identifies where formal recommendations, consensus-based practice and evidence of technical feasibility inform treatment, and where comparative patient benefit has been demonstrated or remains uncertain.
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