Role of Endovascular Therapies in Chronic Mesenteric Ischemia: Current Status and Technical Considerations


Chronic mesenteric ischemia (CMI), commonly referred to as "intestinal angina" is an uncommon vascular condition with an insidious onset that often leads to severe debilitating abdominal symptoms.1 Given its vague presentation, CMI is likely underdiagnosed and undertreated. Consistent with this, CMI currently accounts for <0.5% of all peripheral vascular operations.2

Unlike acute mesenteric ischemia (AMI), which often occurs in the setting of embolic disease or non-occlusive mesenteric ischemia (related to systemic hypoperfusion and diffuse mesenteric vasoconstriction), CMI is mainly attributed to advanced atherosclerotic obstruction or occlusion. Despite the high population prevalence of atherosclerosis of the mesenteric vessels, CMI may not arise until late in the disease course, due to formation of extensive collateral vessels originating from abdominal vasculature. When primary or collateral blood supply becomes threatened as a result of obstructive disease, generally in two or more major abdominal arteries (celiac artery [CA], superior mesenteric artery [SMA], or inferior mesenteric artery [IMA]), clinical symptoms manifest and a decision towards vascular intervention should be considered.

Since its introduction by Shaw et al. in 1958,3 open surgical repair (OSR) has been the standard of treatment for CMI. OSR has been associated with significant morbidity (5-30%) and mortality (5-12%),4-9 perhaps because the CMI patient population is often underweight, malnourished, older, and/or has extensive atherosclerotic co-morbidities.10

In 1980, the first mesenteric artery angioplasty was described.11 In years since, multiple studies have reported that percutaneous endovascular treatment (PVET) of CMI is possible with a high technical success rate and with minimal complications in properly selected patients.12-17 As a result, PEVT has supplanted OSR as the default treatment for CMI in many centers across the United States, especially in patients with severe cardiovascular co-morbitidies.18 As of 2005, PEVT has acquired a Class IB recommendation by the ACC/AHA for the treatment of CMI due to mesenteric stenosis, which is the same level of recommendation as for surgical endarterectomy or bypass grafting. Despite all the above factors, treatment of CMI continues to be underutilized and limited to a few centers.

In this article, we review key pathophysiologic features that are vital for understanding, diagnosing, and treating CMI. In particular, we highlight the clinical aspects as well as technical principles that must be considered to safely perform PEVT in patients with CMI.


The abdominal viscera are supplied by three main arterial branches off the abdominal aorta: the CA, SMA, and IMA.

The CA typically arises at T12 or L1 and branches into the left gastric, splenic, and common hepatic arteries. The CA is thus responsible for the majority of the blood supply to the liver, spleen, stomach, duodenum, and pancreas. The SMA arises 1-2 cm caudal to the CA and supplies parts of pancreas and the intestinal viscera from the jejunum to the splenic flexure. The IMA arises at the level of L3 approximately 3-5 cm above the iliac bifurcation and supplies the remaining intestinal viscera from the splenic flexure to the rectum (Figure 1).

Figure 1: Mesenteric branches of the Aorta

Figure 1
(A) Abdominal CT scan with IV contrast (sagittal view) showing mild disease of the celiac artery (CA), superior mesenteric artery (SMA) and the inferior mesenteric artery (IMA). (B) MRI of the abdomen after the administration of an IV gadolinium-based contrast agent (sagittal view) again showing normal CA and SMA (IMA is not visualized in this reconstruction).

Together, these vessels form a rich and robust vascular supply to the abdominal viscera. Moreover, in the presence of obstructive vascular disease, they are able to compensate for vascular deficiency by forming collaterals. An understanding of collateral anatomy is therefore crucial to delineate for all patients with CMI being considered for revascularization. The most common collateral formation is between the SMA and IMA, and is composed of the meandering artery of Moskowitz (also known as the arc of Riolan) (Figure 2) and the marginal artery of Drummond (Figure 3). If these arteries appear prominent on angiography, it may be an indicator that either the SMA or IMA is occluded. The pancreatico-duodenal arcade is another collateral system between the CA and the SMA, which if prominent on angiography, could represent an occlusion (Figure 4). Similarly, other collateral systems from the esophagus or the rectal arcade (between internal iliac artery and the IMA) may become involved in the event of vascular occlusions. In patients with prior abdominal surgery, or endovascular aneurysmal repair, the source(s) of typical collateral flow may become interrupted. In this scenario, the possibility of atypical compensatory collateral flow via unexpected alternative channels must be appreciated.

Figure 2: Collateral circulation - Meandering artery of Moskowitz (Arc of Riolan)

Figure 2
(A) Abdominal CT scan with IV contrast (3D reconstruction in AP view) showing a prominent arc of Riolan. (B) The same anatomy viewed at an oblique angle reveals an SMA occlusion (white arrow). (C) Selective abdominal angiography of the SMA (AP view) in a different patient. Here a prominent arc of Riolan (blue arrow) is again noted, however in this case, it forms collateral supply to a high-grade lesion in the IMA distribution.

Figure 3: Collateral circulation - Marginal artery of Drummond

Figure 3
Selective injection of the SMA during a conventional abdominal angiography procedure (AP view) showing a prominent marginal artery of Drummond (blue arrows) suggestive of high-grade stenosis in the IMA distribution.

Figure 4: Collateral circulation - Pancreatico-duodenal arcade

Figure 4
(A) Abdominal CT scan with IV contrast showing prominent collateral vessels in the expected location of the pancreatico-duodenal arteries in a patient with an occluded celiac artery. (B) CT scan (3D reconstruction) of prominent pancreatico-duodenal collateral vessels mentioned above.

Figure 5: Mesenteric lesions

Figure 5
3D (A) and sagittal (B) reconstructions from an abdominal CT scan with IV contrast showing occlusions of the CA (arrow) and the SMA (arrowhead). (C) Lateral aortogram in a different patient, showing high-grade stenoses in the CA and SMA.

Knowledge of collateral anatomy is important in understanding the compensatory system that sustains patients with CMI, and may be strategic in pre-procedural planning (particularly with regard to treatment approach and avoidance of further bowel ischemia).


A typical presentation of CMI includes unexplained, chronic abdominal pain (often post-prandial and described as "crampy"), diarrhea, sitophobia (fear of food), and significant weight loss/malnutrition. An epigastric bruit may be present on physical examination in approximately half of patients with CMI.19 Given these non-specific clinical findings, identifying CMI can be particularly challenging.

Patients with CMI are typically older (age >50), and may have coronary artery disease and/or its associated risk factors such as diabetes mellitus, hyperlipidemia, hypertension, renal disease, smoking, obesity, and sedentary lifestyle.20 Other less common non-atherosclerotic etiologies such as fibromuscular dysplasia, median arcuate ligament syndrome, mid-aortic syndrome involving the mesenteric arteries, neurofibromatosis, vasculitis, and post-radiation stenoses have also been implicated in CMI, and must be considered in the differential diagnosis (Table 1).21,22 Lastly, other gastrointestinal conditions that often present with vague symptoms (e.g., pancreatic malignancy) must also be excluded if clinically suspected.

Table 1: Etiologies of Chronic Mesenteric Ischemia



(Associated risk factors)
Diabetes mellitus, hyperlipidemia, hypertension, renal disease, smoking, obesity, sedentary lifestyle

Fibromuscular dysplasia
Median Arcuate Ligament syndrome
Midaortic syndrome
Post radiation stenoses

The initial work-up for CMI includes radiographic imaging such as abdominal ultrasonography (US), computed tomography angiography (CTA), or magnetic resonance angiography (MRA). Abdominal US acquisition may vary due to operator expertise, bowel gas, or body habitus. However, if a fasting peak systolic velocity of ≥275 cm/s is detected, it is predictive of a ≥70% SMA stenosis (sensitivity 92%, specificity 96%). Similarly, a peak systolic velocity of ≥200 cm/s is predictive of ≥70% CA stenosis (sensitivity 87%, specificity 80%).23 Detection of vessel calcification on CTA may also lend a diagnostic clue towards CMI. Moreover, modern digital processing and volumetric reconstruction of 3D data makes CT a useful tool during pre-procedural planning of a percutaneous approach to the vessel in question (i.e., brachial vs. femoral, choice of catheter, etc.). MRA has also been utilized in the diagnosis of CMI. It has the advantage of high resolution imaging without exposure to radiation. MRA utilizing gadolinium-based contrast agents has been reported to have diagnostic sensitivity and specificity for detecting proximal mesenteric disease greater than 90%.24 Selective mesenteric angiography remains the gold standard test for diagnosing CMI, especially for detection of distal vessel disease, or when a concurrent intervention is planned.


Initial therapy of CMI should be directed towards controlling underlying risk factors such as diabetes, hypertension, and hypercholesterolemia. Moreover, smoking cessation should be strongly advised. Any excessive increase in intestinal demand (e.g., large meals) or decrease in intestinal supply (e.g., hypovolemia) must also be avoided. Vasodilator agents such as oral nitrates may provide episodic relief. In patients with CMI due to thrombosis, or non-occlusive thrombotic stenosis, systemic anticoagulation therapy is beneficial in the absence of contraindications. Ultimately, most patients with CMI require revascularization, and medical management alone is usually reserved for patients who are too high risk for any revascularization options (surgical or percutaneous), or who have refractory symptoms despite failed previous revascularization attempts.

In patients with severe symptoms and nutritional deficiency, total parenteral nutrition may be considered on a supportive basis. Vasopressors agents, if needed, must be carefully selected and dosed so as to avoid excessive bowel vasoconstriction. Lastly, broad-spectrum antibiotics against Gram-negative organisms are recommended in patients who progress to acute mesenteric ischemia or ischemic colitis.25,26

Percutaneous Revascularization

As mentioned above, PEVT currently has a Class IB ACC/AHA recommendation for the treatment of CMI. Due to the associated lower morbidity and mortality compared to OSR, PEVT is gaining popularity especially in high surgical risk patients. Despite this, several considerations must be undertaken before directing a patient towards PEVT (over OSR).

First, the center at which PEVT is to be performed must have adequate operator experience, with surgical backup to rescue acute treatment failure. Second, the specific anatomy of the culprit lesion(s) (e.g., the angle of vessel branching from the aorta, presence of flush ostial occlusion, occluded stent, etc.) must be amenable to a percutaneous approach. Other anatomic factors such as prior vascular complications, luminal calcifications/tortuosity, or presence of dialysis fistulas must also be taken into consideration. Third, although patients undergoing PEVT have a high initial success rate (88-100%), patency rates at 1 year may decrease to 70-80%.19 Some authors have reported restenosis rates as high as 25-50%.27,28 Furthermore, in a recent retrospective study of patients undergoing surgery versus PEVT, those undergoing PEVT were five times more likely to require re-intervention.29 Knowledge of such outcomes must be weighed against the risk of OSR. Finally, certain patients are better surgical candidates despite being amenable to PEVT, based on CMI due to non-atherosclerotic causes (Table 1) or occurrence of restenoses despite multiple PEVT attempts.

Once a decision towards revascularization is made, careful consideration must be made towards selecting which vessel(s) to revascularize in situations where more than one vessel is significantly stenosed. As a general rule, the single artery that supplies a major collateral vessel is given preference. Studies have shown that recanalization of the SMA has the highest likelihood of providing lasting benefit. However, if the SMA cannot be treated by endovascular means (e.g., due to calcification or presence of an ostial or long occlusion), an attempt at celiac angioplasty can be beneficial.30,31 Therapeutic benefit from IMA angioplasty has also been reported, as would be expected in patients with a stenosis at the origin of an IMA that provides the major blood supply to the midgut via a hypertrophied marginal artery when both the SMA and celiac arteries are occluded.32 Multi-vessel PVET is conducted less frequently, often not needed, and sometimes due to the presence of an ostial occlusion in at least one vessel in CMI patients. However, a report by Kougias et al. suggested that symptomatic recurrence was significantly greater in patients undergoing single-vessel over two-vessel angioplasty,33 which is likely a function of higher disease burden in patients undergoing multivessel PVET.

Once a vessel is identified for revascularization, the decision to conduct plain balloon angioplasty versus primary stenting must be made. This decision remains a controversial one; however, results from small series suggest that primary stenting may improve patency over plain balloon angioplasty.34 Despite the lack of definite supporting evidence, primary stenting is the preferred option in many centers.35 Moreover, stents are undoubtedly useful as a rescue procedure for dissection, acute occlusion, or failure to maintain adequate dilatation following angioplasty of a tight stenosis of the SMA or CA. A residual stenosis of >30% or a persistent pressure gradient of >15 mmHg after angioplasty has been cited as indication for inserting a stent.33

PVET is technically more challenging in totally occluded vessels compared to treatment of stenosed mesenteric arteries. Such interventions theoretically carry a higher risk of embolization and bowel infarction, and therefore distal embolic protection devices should be considered in these cases. Nonetheless, equivalent results have been reported for angioplasty or stenting of occluded and stenosed vessels (though the number of patients with treated occluded vessels was comparatively small).36 Endovascular recanalization of an occluded mesenteric vessel usually requires a short stump of patent artery to allow engagement of the guide wire. However, retrograde angioplasty via collaterals from the celiac artery has been reported in the literature with ostial occlusions of the mesenteric arteries.37 Overall, one should carefully consider all these factors and weigh procedural risks and benefits before attempting PVET.

Technical Aspects of Endovascular Intervention

The majority of PEVT for CMI are conducted using a femoral approach under local anesthesia and conscious sedation. A left upper extremity (brachial or radial artery) approach may sometimes be required in patients with downward pointing mesenteric arteries, a narrow abdominal aorta, or downstream aorto-iliac obstructive disease precluding femoral access.

Pre-procedural non-invasive imaging with CTA or MRA often helps identify the culprit mesenteric artery as well as optimal views during selective angiography. Diagnostic selective angiography is used to confirm the culprit stenosis severity in orthogonal views. Often, a non-selective abdominal aortogram is performed first to visualize the CA, SMA, and IMA ostia. The mesenteric artery of interest is then selectively cannulated and angiography is performed using digital subtraction in orthogonal views. The choice of guiding catheter depends on the visualized anatomy. Pre-shaped reverse curved catheters such as Cobra, Simmons, or SoS are often utilized to selectively engage mesenteric vessels. Sometimes a shorter reverse-curve catheter such as the visceral selective 1 is used, allowing for easier technical manipulation. After selective cannulation, diluted contrast should be injected through the catheter to exclude the possibility of dissection prior to any further manipulation.

In patients with underlying renal insufficiency, CO2 angiography may be utilized for the initial non-selective angiogram and selective engagement. Contrast dye is used only for selective injections once optimal cannulation is confirmed on CO2 angiography. This strategy often allows for minimal contrast use without affecting the diagnostic image quality on the angiogram.

Once a culprit stenosis is identified on selective angiography, anticoagulation with intravenous unfractionated heparin boluses is used with an activated clotting time goal of 250-300. Aspirin 325 mg and clopidogrel 300 mg is routinely given before the procedure and dual anti-platelet maintenance therapy is typically continued for a minimum of 3 months thereafter.

A conventional short-tipped atraumatic wire such as a 0.035" Magic Torque or Wholey may be used as a "working guidewire" for lesion crossing. If difficulty is encountered, 0.014" or 0.018" wires may be used instead. Hydrophilic wires such as the Roadrunner (Cook Medical Inc., Bloomington, IN, USA), or the Radifocus-stiff/angled glide wires (Terumo) may also be chosen to negotiate past high-grade lesions.

Typically, all significant ostial lesions are stented. With the use of premounted stents, the pre-dilation step is omitted. This may reduce distal plaque embolization. However, in certain severe and/or calcified lesions, pre-dilation may be required. Balloon expandable stents (BES) can improve the immediate success of the procedure. Low-profile balloons or stents, such as the Express 0.014-inch Monorail stent (Boston Scientific, Natick, MA, USA) may track and cross a lesion more easily than conventional systems. Typically, a 6-8 mm stent is used and positioned such that 2-3 mm of the stent is protruding into the aorta. Covered BES (CBES) is another potential option but the iCAST CBES is currently restricted for use in the United States. Self-expanding stents can also be considered for more distal lesions or to treat post-stenting dissections. Confirmatory angiography is performed upon completion of the intervention to document the final result.


The overall complication rate of PEVT is low (0-10%), and is mostly attributed to access site complications, including access site hematoma, AV fistula, pseudoaneurysm, etc.38 Other possible complications include iatrogenic dissection, rupture, or distal embolization in the mesenteric circulation.

Acute intestinal ischemia secondary to embolization, thrombosis, or dissection is the most feared complication of mesenteric endovascular intervention. With prompt recognition, this complication can often be salvaged using endovascular techniques. Distal embolization and thrombosis may require thromboaspiration or thrombolytic therapy. Arterial dissection may be treated by placing a stent at the proximal dissection flap, thus "tacking" the origin or the flap against the vessel wall. In the event of vessel rupture, covered balloon expandable stents may be required to control vessel hemorrhage. Other techniques using snares or grasping forceps are rarely needed to retrieve dislodged stents.

If the situation cannot be rescued by endovascular methods, the patient must promptly be sent for emergent mesenteric bypass surgery. Any delay in reaching the operating theater may, despite the administration of intravenous heparin, allow the propagation of clot into the jejunal and ileal arcades. Such propagated clot is very challenging to extract with balloon catheters and often results in patchy intestinal infarction. Isolated splenic infarction has also been reported after stenting of the celiac artery.39 Intestinal reperfusion hemorrhage is rare, but has been successfully treated by endovascular embolization.40

Manipulation of the catheter or guide wire within a diseased aorta may result in distal embolization into the legs or the renal arteries, resulting in an ischemic foot or acute renal failure. Similarly, catheter manipulation in close proximity to the vertebral artery within the subclavian artery (with brachial approach) may result in embolic stroke. Acute renal failure may also result from contrast administration, which should be minimized by ensuring adequate hydration and stopping metformin for 24 hours prior to the procedure.

Outcomes of Endovascular Revascularization

Outcomes data comparing PEVT to OSR are largely limited to observational cohorts. In a nationwide United States inpatient sample of 5583 medicare beneficiaries (1988-2006) undergoing revascularization for CMI, PEVT was performed in 62% patients.18 The remaining 32% underwent OSR. In this study, mortality was significantly higher with OSR (surgical bypass) compared to PEVT (13% vs. 3.7%, p<0.001). After multivariate adjustment increasing age, atrial fibrillation, congestive heart failure, and OSR were independently predictive of increased mortality in CMI patients. These authors did not report data on primary patency and need for repeat revascularization, but others have suggested decreased primary patency and increased need for repeat procedures with PEVT compared to OSR.

In a multi-center analysis from the United Kingdom comparing OSR to PEVT in 76 patients,27 cumulative mean primary patency following OSR was 126 months (95% CI, 92-159 months) and 51 months (95% CI, 20-80 months) after PEVT. In another report, PEVT group was also noted to have a higher incidence of recurrent symptoms (p=0.001).41 In most cases, symptomatic recurrence corresponds to the demonstration of restenosis on duplex ultrasonography or angiography, although asymptomatic restenosis has been reported in several patients as well.42,43 In patients needing repeat intervention after PEVT, OSR may be preferred but repeat PEVT is also an option especially in those who are poor surgical candidates. These choices are largely driven by individual clinical scenarios and overall center expertise.

Data on comparative effectiveness of various treatment options with in PEVT is also limited to observational series. In a study of 107 patients undergoing primary PEVT for CMI,43 technical success was reported in 100%. At one year, the primary patency for bare-metal stent, PTA, and polytetrafluoroethylene (PTFE)-covered stents was 54%, 67%, and 100% respectively, but primary-assisted patency did not differ based on treatment type. For patients undergoing PEVT following prior failed PEVT and/or OSR, some have suggested similar treatment efficacy with PTFE-covered stents (provided proximal branch occlusion can be avoided).44 However, given restriction on use of iCAST PTFE-covered stents in the United States, revascularization options for PEVT in the US are largely limited to BMS or PTA alone.

Lastly, in a mesenteric stent series of 140 patients, Dahl et al. noted a significant difference in 1-year primary patency for SMA (55%) versus CA (17%) stenting based on ultrasound duplex criteria, indicating that outcomes may also be influenced by the primary anatomical target, as well as lesion complexity and number of vessels treated.45 Interestingly, however, Schoch et al. reported no difference primary patency between SMA and CA.43


The clinical recognition of CMI can be challenging due to its vague symptoms and insidious clinical presentation. Because of this, physicians must regard this condition with a higher clinical index of suspicion, especially in patients with atherosclerotic co-morbidities. Once diagnosed, treatment options include PEVT and OSR. OSR has been traditional treatment of choice in CMI, and still remains so for low risk patients, for certain lesion types (e.g., flush occlusions), for patients with recurrence despite multiple PEVT attempts, or for patients with non-atherosclerotic CMI. However, for many high surgical risk patients, PEVT is becoming the preferred treatment in atherosclerotic CMI due to reduced peri-operative morbidity and mortality compared to OSR. In the era of rising atherosclerosis incidence and prevalence, greater knowledge of CMI and PEVT amongst practitioners is necessary to advance minimally invasive therapies as alternatives to open surgery in selected patients.


  1. Moawad J, Gewertz BL. Chronic mesenteric ischemia: clinical presentation and diagnosis. Surg Clin North Am 1997;77:357-69.
  2. Foley MI, Moneta GL, Abou-Zamzam AM, et al. Revascularization of the superior mesenteric artery alone for treatment of intestinal ischemia. J Vasc Surg 2000;32:37-47.
  3. Shaw RS, Maynard EP. Acute and chronic thrombosis of the mesenteric arteries associated with malabsorption. N Engl J Med 1958;258:874-8.
  4. Cho J, Carr JA, Jacobsen G, Shepard AD, Nypaver TJ, Reddy DJ. Long-term outcome after mesenteric artery reconstruction: a 37-year experience. J Vasc Surg 2002;35:453-60.
  5. Park WM, Cherry KJ, Chua HK, et al. Current results of open revascularization for chronic mesenteric ischemia: a standard for comparison. J Vasc Surg 2002;35(5):853-9.
  6. Kihara TK, Blebea J, Anderson KM, Friedman D, Atnip RG. Risk factors and outcomes following revascularization for chronic mesenteric ischemia. Ann Vasc Surg 1999;13:37-44.
  7. Johnston KW, Lindsay TF, Walker PM, Kalman PG. Mesenteric arterial bypass grafts: early and late results and suggested surgical approach for chronic and acute mesenteric ischemia. Surgery 1995;118:1-7.
  8. Mateo RB, O'Hara PJ, Hertzer NR, Mascha EJ, Beven EG, Krajewski LP. Elective surgical treatment of symptomatic chronic mesenteric occlusive disease: early results and late outcomes. J Vasc Surg 1999;29:821-31.
  9. Moawad J, McKinsey JF, Wyble CW, Bassiouny HS, Schwartz LB, Gewertz BL. Current results of surgical therapy for chronic mesenteric ischemia. Arch Surg 1997;132:613-9.
  10. Brown DJ, Schermerhorn ML, Powell RJ, et al. Mesenteric stenting for chronic mesenteric ischemia. J Vasc Surg 2005;42:268-74.
  11. Uflacker R, Goldany MA, Constant S. Resolution of mesenteric angina with percutaneous transluminal angioplasty of a superior mesenteric artery stenosis using a balloon catheter. Gastrointest Radiol 1980;5:367-9.
  12. McShane M, Proctor A, Spencer P, Cumberland DC, Welsh CL. Mesenteric angioplasty for chronic intestinal ischaemia. Eur J Vasc Surg 1992;6:333-6.
  13. Allen RC, Martin GH, Rees CR, et al. Mesenteric angioplasty in the treatment of chronic intestinal ischemia. J Vasc Surg 1996;24:415-23.
  14. Levy PJ, Haskell L, Gordon RL. Percutaneous transluminal angioplasty of splanchnic arteries: an alternative method to elective revascularisation in chronic visceral ischaemia. Eur J Radiol 1987;7:239-42.
  15. Roberts L, Wertman DA, Mills SR, Moore AV, Heaston DK. Transluminal angioplasty of the superior mesenteric artery: an alternative to surgical revascularization. AJR Am J Roentgenol 1983;141:1039-42.
  16. Odurny A, Sniderman KW, Colapinto RF. Intestinal angina: percutaneous transluminal angioplasty of the celiac and superior mesenteric arteries. Radiology 1988;167:59-62.
  17. Golden DA, Ring EJ, McLean GK, Freiman DB. Percutaneous transluminal angioplasty in the treatment of abdominal angina. AJR Am J Roentgenol 1982;139:247-9.
  18. Schermerhorn ML, Giles KA, Hamdan AD, Wyers MC, Pomposelli FB. Mesenteric revascularization: management and outcomes in the United States, 1988-2006. J Vasc Surg 2009;50:341-8.
  19. Herbert GS, Steele SR. Acute and chronic mesenteric ischemia. Surg Clin North Am 2007;87:1115-34.
  20. Casserly IP, Sachar R, Yadav JS. Practical Peripheral Vascular Intervention. 2nd ed. Philadelphia: Lippincott Williams & Wilkins; 2012.
  21. Cognet F, Salem DB, Dranssart M, et al. Chronic mesenteric ischemia: imaging and percutaneous treatment. Radiographics 2002;22:863-79.
  22. Escárcega RO, Mathur M, Franco JJ, et al. Nonatherosclerotic obstructive vascular diseases of the mesenteric and renal arteries. Clin Cardiol 2014;37:700-6.
  23. Moneta GL. Screening for mesenteric vascular insufficiency and follow-up of mesenteric artery bypass procedures. 2001;14:186-92.
  24. Meaney JF, Prince MR, Nostrant TT, Stanley JC. Gadolinium-enhanced MR angiography of visceral arteries in patients with suspected chronic mesenteric ischemia. J Magn Reson Imaging 1997;7:171-6.
  25. Hohenwalter EJ. Chronic mesenteric ischemia: diagnosis and treatment. Semin Intervent Radiol 2009;26:345-51.
  26. Reinus JF, Brandt LJ, Boley SJ. Ischemic diseases of the bowel. Gastroenterol Clin North Am 1990;19:319-43.
  27. Rawat N, Gibbons CP, Joint Vascular Research Group. Surgical or endovascular treatment for chronic mesenteric ischemia: a multicenter study. Ann Vasc Surg 2010;24:935-45.
  28. Kougias P, El Sayed HF, Zhou W, Lin PH. Management of chronic mesenteric ischemia. the role of endovascular therapy. J Endovasc Ther 2007;14:395-405.
  29. Oderich GS, Bower TC, Sullivan TM, Bjarnason H, Cha S, Gloviczki P. Open versus endovascular revascularization for chronic mesenteric ischemia: risk-stratified outcomes. J Vasc Surg 2009;49:1472-9.
  30. Landis MS, Rajan DK, Simons ME, Hayeems EB, Kachura JR, Sniderman KW. Percutaneous management of chronic mesenteric ischemia: outcomes after intervention. J Vasc Interv Radiol 2005;16:1319-25.
  31. Gotsman I, Verstandig A. Intravascular stent implantation of the celiac artery in the treatment of chronic mesenteric ischemia. J Clin Gastroenterol 2001;32:164-6.
  32. Alam A, Uberoi R. Chronic mesenteric ischemia treated by isolated angioplasty of the inferior mesenteric artery. Cardiovasc Intervent Radiol 2005;28:536-8.
  33. Kougias P, Huynh TT, Lin PH. Clinical outcomes of mesenteric artery stenting versus surgical revascularization in chronic mesenteric ischemia. Int Angiol 2009;28:132-7.
  34. Matsumoto AH, Angle JF, Spinosa DJ, et al. Percutaneous transluminal angioplasty and stenting in the treatment of chronic mesenteric ischemia: results and longterm followup. J Am Coll Surg 2002;194:S22-31.
  35. Silva JA, White CJ, Collins TJ, et al. Endovascular therapy for chronic mesenteric ischemia. J Am Coll Cardiol 2006;47:944-50.
  36. Sarac TP, Altinel O, Kashyap V, et al. Endovascular treatment of stenotic and occluded visceral arteries for chronic mesenteric ischemia. J Vasc Surg 2008;47:485-91.
  37. Robken J, Shammas NW. Treatment of a totally occluded superior mesenteric artery facilitated by retrograde crossing via collaterals from the celiac artery. J Endovasc Ther 2007;14:745-7.
  38. Schaefer PJ, Schaefer FK, Mueller-Huelsbeck S, Jahnke T. Chronic mesenteric ischemia: stenting of mesenteric arteries. Abdom Imaging 2007;32:304-9.
  39. Almeida JA, Riordan SM. Splenic infarction complicating percutaneous transluminal coeliac artery stenting for chronic mesenteric ischaemia: a case report. J Med Case Rep 2008;2:261.
  40. Moore M, McSweeney S, Fulton G, Buckley J, Maher M, Guiney M. Reperfusion hemorrhage following superior mesenteric artery stenting. Cardiovasc Intervent Radiol 2008;31:S57-61.
  41. Kasirajan K, O'Hara PJ, Gray BH, et al. Chronic mesenteric ischemia: open surgery versus percutaneous angioplasty and stenting. J Vasc Surg 2001;33:63-71.
  42. Fenwick JL, Wright IA, Buckenham TM. Endovascular repair of chronic mesenteric occlusive disease: the role of duplex surveillance. ANZ J Surg 2007;77:60-3.
  43. Schoch DM, LeSar CJ, Joels CS, et al. Management of chronic mesenteric vascular insufficiency: an endovascular approach. J Am Coll Surg 2011;212:668-75.
  44. Horesh L. Recanalization of an occluded celiac artery: PTFE-covered stenting in the mesenteric arteries after previous failed endovascular and open mesenteric revascularizations. Endovascular Today 2010:33-8.
  45. Dahl TJ, Stout CL, Veale WN, et al. Our experience with 140 visceral artery stents: Should celiac artery stenting be abandoned? J Vasc Surg 2010;51:1071.

Clinical Topics: Anticoagulation Management, Arrhythmias and Clinical EP, Diabetes and Cardiometabolic Disease, Dyslipidemia, Heart Failure and Cardiomyopathies, Invasive Cardiovascular Angiography and Intervention, Noninvasive Imaging, Prevention, Atherosclerotic Disease (CAD/PAD), Anticoagulation Management and Atrial Fibrillation, Atrial Fibrillation/Supraventricular Arrhythmias, Homozygous Familial Hypercholesterolemia, Acute Heart Failure, Interventions and Coronary Artery Disease, Interventions and Imaging, Interventions and Vascular Medicine, Angiography, Magnetic Resonance Imaging, Nuclear Imaging, Hypertension, Smoking

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