Abdominal Vascular Disease: Diagnosis and Therapy

  • Johannes Lammer


If acute occlusion of the abdominal aorta or branch vessels occurs, two causes have to be considered:
  • Embolization

  • Dissection.


Magnetic Resonance Angiography Superior Mesenteric Artery Abdominal Aortic Aneurysm Renal Artery Stenosis Autosomal Dominant Polycystic Kidney Disease 
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Acute Arterial Occlusion

If acute occlusion of the abdominal aorta or branch vessels occurs, two causes have to be considered:
  • Embolization

  • Dissection.


Embolization is most common in elderly patients with atrial fibrillation, a history of myocardial infarction, and aortic aneurysm. Embolization from the heart or thoracic aorta may cause acute subtotal or total occlusion of the celiac trunk, superior mesenteric artery (SMA), inferior mesenteric artery (IMA), or renal arteries. The most common causes of embolization are:
  • Atrial fibrillation

  • Thoracic aortic aneurysm

  • Myocardial infarction with mural thrombus formation

  • Left atrial appendage thrombus

  • Advanced aortic arteriosclerosis

  • Penetrating arteriosclerotic ulcer

  • Hypercoagulability syndrome.

Symptoms of acute ischemia are dependent upon the involved vascular territory. Embolization to the liver or spleen may cause acute right or left upper abdominal pain. Acute mesenteric ischemia typically causes severe abdominal pain and bowel paralysis. Embolization to the kidney causes flank pain, hematuria, and hypertension. In any case, severe lactate dehydrogenase (LDH) elevation indicates the ischemic nature of the acute pain. In case of complete ischemia without sufficient collateral circulation, the warm ischemic time tolerated by abdominal organs is <6 h. Therefore, emergent diagnosis and therapy are mandatory.

The primary diagnosis is performed using computed tomography (CT) with contrast enhancement [contrast medium (CM) 300–400 mg/ml; 4 ml/s; total bolus volume 80-120 ml; bolus care technique with 20- to 40-s delay; 2-mm collimation; pitch 2; reconstruction interval 1 mm]. In the arterial phase, the obstructing embolus and the ischemic territory can be visualized. In the delayed phase, residual perfusion through collateral arteries may be demonstrated.

Interventional treatment with a thrombectomy device and/or local intra-arterial fibrinolysis with alteplase (rt-PA) (loading dose 10 mg, infusion dose 5 mg/h) or urokinase (loading dose 250,000 IU, infusion dose 100,000 IU/h), together with a glycoprotein (G) IIb/IIIa antagonist (Abciximab; loading dose 0.25 mg/kg, infusion dose 0.125 mg/kg/h) are one option. The other option is surgery, which may be faster and enables inspection and, if necessary, resection of ischemic organs.


Dissection may occur in patients with chest trauma; chronic severe hypertension; or a connective tissue disease such as Marfan syndrome, Ehlers-Danlos syndrome, Loeys-Dietz syndrome (LDS), and autosomal dominant polycystic kidney disease (ADPKD). Acute types A and B aortic dissection may cause dynamic compression of the true aortic lumen due to pressurized false lumen. This can cause acute ischemia of liver, spleen, bowel, and one or both kidneys. The dissection plane may also involve one of the organ arteries causing obstruction of the true lumen. Options for interventional treatment are:
  • In case of dynamic compression of the true aortic lumen, occlusion of the proximal entry into the false lumen with an aortic stent-graft will cause decompression of the false lumen and result in reopening the true lumen of the aorta and the side branches (Fig. 1).
    Fig. 1 a–f

    Complicated Stanford type B aortic dissection with renal malperfusion. a Computed tomography (CT) demonstrating primary entry tear of type B aortic dissection. b CT demonstrating compression of true lumen of the aorta with left renal ischemia. c Aortic angiogram showing true and false lumen of type B dissection. d Aortography showing compression of true lumen with malperfusion of the renal arteries (“floating visceral sign”). e CT after stent-graft implantation and closure of primary entry tear with false lumen collapse. f Aortography post stent-graft implantation demonstrating spontaneous revascularization of visceral arteries

  • In case of a static compression due to a side-branch dissection, stent placement in the true lumen of the organ artery will cause reconstitution of organ perfusion.

  • In case of organ perfusion through the false lumen, balloon fenestration of the intimal flap will reestablish flow into the malperfused territory.

Chronic Arterial Occlusive Disease

In young patients, causes of chronic arterial occlusion may be:
  • Fibromuscular disease (FMD)

  • Takayasu arteritis

  • Neurofibromatosis Recklinghausen.

In elderly patients, the primary cause of chronic arterial occlusive disease is arteriosclerosis.

Mesenteric Artery Stenosis

Between the three large mesenteric arteries (celiac artery, SMA, IMA), many collateral pathways exist:
  • Pancreaticoduodenal arteries

  • Arc of Buehler between celiac artery and SMA

  • Arc of Riolan

  • Marginal artery of Drummond between SMA and IMA.

Usually, an obstruction of more than one mesenteric artery is necessary to cause ischemic symptoms. The typical clinical symptom is “abdominal angina,” with:
  • Abdominal pain (94%)

  • Postprandial cramps (86%)

  • Weight loss (74%)

  • Abdominal bruit (70%)

  • Diarrhea.

The primary diagnosis is made by CT angiography, magnetic resonance angiography (MRA), or intra- arterial catheter angiography of the abdominal aorta in a lateral projection. Interventional treatment is percutaneous transluminal angioplasty (PTA) with or without secondary stent placement of the obstructed arteries.

Celiac Trunk Stenosis

Chronic obstruction may remain asymptomatic because of the collateral pathways through gastroduodenal and pancreatic arteries from the SMA. Causes are arteriosclerotic plaque, compression by the arcuate ligament, and carcinoma of the pancreas.

Superior Mesenteric Artery Stenosis

Postprandial abdominal pain, called “abdominal angina,” is the leading symptom. Causes for SMA obstruction are arteriosclerosis, FMD, Takayasu arteritis, pancreatic carcinoma, and chronic pancreatitis.

Inferior Mesenteric Artery Stenosis

Obstruction of the IMA is most commonly observed in patients with advanced atheromatosis or partially thrombosed abdominal aortic aneurysm. Due to the collateral circulation through the arc of Riolan and the marginal artery, IMA obstruction normally remains asymptomatic.

Renal Artery Stenosis

Renal artery stenosis (RAS) may cause hypertension and/or renal insufficiency. Acute onset of clinical symptoms and repeated flash pulmonary edema are suggestive for RAS. Etiology can be
  • Arteriosclerosis in 65–75%
    • Patients >50 years

    • Male >female

    • Proximal 2 cm of renal artery

    • Atherosclerotic changes of aorta

    • Bilateral in 30%.

  • FMD in 20–30%
    • Patients <50 years

    • Female:male ratio 5:1

    • Middle to distal renal artery, including branches

    • Bilateral involvement in 50–70%

    • “String of beads” appearance, aneurysms, dissections

    • No aortic disease.

  • Takayasu arteritis

  • Midaortic syndrome

  • Morbus Recklinghausen

  • Postradiation therapy.

RAS Diagnosis

The most appropriate algorithm for diagnosing RAS is not yet established.

Color Duplex Ultrasound

Color duplex ultrasound (US) is a noninvasive test but is a complex procedure that requires operator experience. An increased peak systolic velocity of >250 cm/s, a renal-to-aortic ratio of peak systolic velocity of >3.5, intrastenotic turbulence, and a flattened pulse wave in the periphery (pulsus tardus) are diagnostic criteria for RAS. The sensitivity of color duplex sonography for detecting RAS >70% is 72–92%. Color duplex US with an angiotensin- converting enzyme (ACE) inhibitor provides a positive predictive value (PPV) of 67–95% for cure or improvement after revascularization.

Nuclear Scan

A nuclear scan [renal scintigraphy with technetium-99m mercaptoacetyltriglycine (99mTc-MAG-3) or technetium- 99m diethylenetriaminepentaacetic acid (99mTc-DTPA)] with an angiotensin-converting enzyme (ACE) inhibitor (captopril 25 mg) shows delayed tracer washout within the poststenotic kidney. However, in bilateral disease and in chronic ischemic nephropathy, tracer lateralization is less evident. In a selected population with a clinically high risk for RAS, sensitivity for detection of a unilateral RAS >70% is 51–96% (mean 82%). Its PPV, with improvement of hypertension after revascularization, is 51– 100% (mean 85%). However, scintigraphy is much less sensitive in unselected patients, bilateral disease, impaired renal function, urinary obstruction, and chronic ACE inhibitor intake.

Newer Tests

Newer tests are gadolinium (Gd)-enhanced MRA and spiral CT angiography (CTA).

Gd-Enhanced MRA

For state-of-art MRA, high-field-strength systems with high-performance gradients are necessary for breath-hold 3D T1-weighted spoiled-gradient-echo imaging with short TR and TE. Intravenous administration of Gd contrast material (0.1 mmol/kg; flow rate 2 ml/s), a central k-space readout, and background subtraction are additional techniques to improve signal-to-noise ratio (SNR) and spatial resolution. Sensitivity for detecting RAS >50% is >95% with MRA (Fig. 2). The main limitations of renal MRA are evaluation of small, accessory renal arteries and branch vessels, presence of stents, and a tendency to overestimate moderate stenoses.
Fig. 2 a–d

Imaging and intervention in a patient with hypertension due to renal artery stenosis. a Magnetic resonance angiography (MRA) showing stenosis of right renal artery. b Computed tomography angiography (CTA) showing stenosis of right renal artery. c Arteriography showing stenosis of right renal artery. d Arteriography of right renal artery after stent placement


CTA of the renal arteries has a >95% sensitivity to detect RAS and accessory renal arteries. For high-quality opacification of renal arteries and to avoid renal vein overlap, accurate bolus planning is mandatory: density measurement during bolus rise, flow 4 ml/s, total volume 80–120 ml; multidetector (MD) scanners need less contrast. A short breath-hold acquisition, collimation (1–2 mm), pitch (1.5–6 depending on single or MD technology), reconstruction overlap (0.5–0.75) are important parameters for spatial resolution. Curved planar reconstruction (CPR, most useful for stents), volume rendering, and maximum intensity projection (MIP) are used for 3D imaging (Fig. 2).

Intra-Arterial Catheter Arteriography

Intra-arterial catheter arteriography together with pressure-gradient measurement is still the “gold standard“ for RAS evaluation.

RAS Revascularization

The revascularization technique of choice is renal PTA with or without stent placement (Fig. 2). Aortorenal bypass surgery is indicated only if PTA fails. In a recently published meta-analysis, stent placement proved to be technically superior and clinically comparable with renal PTA alone. The technical success rate of stent vs. PTA was 98% vs. 77%, and the restenosis rate was 17% vs. 26%, respectively (p<0.001). In hypertension, the cure rate of PTA vs. stent was 10% vs. 20% and improvement rate was 53% vs. 49%, respectively. In renal insufficiency, the improvement rate was 38% vs. 30% and stabilization 41% vs. 38%, respectively. Complication rate was 11–13% [95% confidence interval (CI) 6–19] and inhospital mortality rate 1%. In a randomized study comparing stents vs. PTA in ostial stenoses, the technical success rate was 88% vs. 57% and the 6-month primary patency rate 75% vs. 29%, respectively. Surprisingly, randomized trials comparing the effect of PTA and drug therapy on renal hypertension did not reveal a significant benefit of PTA and stenting over continuous drug therapy. However, in a Dutch study, PTA patients required only 2.1 vs. 3.2 daily drug doses (p<0.001); 22/53 patients in the drug group had to be switched to the PTA group because of persistent hypertension or deterioration of renal function.


Abdominal Aortic Aneurysm (AAA)

The incidence of AAA in European adults ⩾60 years is 2.5%. Up to 10% of patients with symptomatic peripheral arterial disease (PAD) die from aneurysm rupture. Standard treatment is open surgery. However, endovascular implantation of stent-grafts is a new, emerging technique that may replace open surgery. Since the first clinical implant of a tube stent-graft in 1990, many different designs have been developed and tested in feasibility studies. Most recently, randomized studies [Endovascular Aneurysm Repair (EVAR) 1 trial; Dutch Randomized Endovascular Aneurysm Repair (DREAM) trial] compared results of open vs. endovascular repair. In the EVAR trial, the 30-day mortality in the EVAR group was 1.7% (9/531) vs. 4.7% (24/516) in the open repair group (p=0.009). Four years after randomization, all-cause mortality was similar between groups (~28%; p=0.46), although there was a persistent reduction in aneurysm-related deaths in the EVAR group (4% vs 7%; p=0.04). Meanwhile, 60–80% of patients are treated by EVAR with stent-grafts.


Indications for endovascular treatment of AAA are the same as for open surgery:
  • Diameter of the aneurysm >5.5 cm (Fig. 3)
    Fig. 3 a–g

    Patient with abdominal aortic aneurysm (AAA). a Axial computed tomography (CT) showing partially thrombosed AAA 5.5 cm in diameter. b CT angiography (CTA) of AAA with coronal reconstruction showing long infrarenal neck. c CTA of AAA with maximum intensity projection (MIP) reconstruction. d Aortography before stent-graft placement. e Aortography after stent-graft placement. f CTA of AAA with coronal reconstruction showing stent-graft in place. g CTA of AAA with coronal reconstruction after stent-graft implantation showing complete thrombosis of AAA

  • Documented growth >0.5 mm/year

  • Symptomatic aneurysm (i.e., embolization, pain, ureteral compression)

  • Rupture.

Specific clinical indications for the endovascular approach may be:
  • Patients >75 years old

  • American Society of Anesthesiologists (ASA) 3 and 4

  • Hostile abdomen

  • Inflammatory aneurysm, horseshoe kidney

  • Severe chronic obstructive pulmonary disease (COPD).

Anatomic indications for stent-graft treatment are:
  • Infrarenal neck ⩾15 mm in length

  • Infrarenal neck without thrombus or severe calcification

  • Angulation of the infrarenal neck <65°

  • Patent celiac trunk and SMA

  • Stent-graft diameter ⩾10% than neck diameter

  • Iliac artery angulation <90°

  • Iliac artery without thrombus or severe calcification

  • More than 15-mm overlap within iliac arteries.


Endovascular implantation of stent-grafts can be performed under general, epidural, or local anesthesia. The use of epidural anesthesia is a major advantage in elderly and high-risk patients.

Stent-Graft Designs

Stent-grafts have a self-expandable stent structure covered by an ultrathin polyester or expanded polytetrafluoroethylene (ePTFE) fabric. Only bifurcated stent-grafts are used for AAA treatment.

Imaging Before Stent-Graft Implantation

Contrast-enhanced spiral CT with multiplanar (MPR) or MIP reconstruction is the most important examination before stent-graft implantation (Fig. 3). The diameter of the landing zones (infrarenal neck, iliac arteries), maximum diameter of the aneurysm, thrombus, and calcifications can be well depicted from CT.

The most common complication is incomplete exclusion of the aneurysm with remaining pressurization of the aneurysm sack through an endoleak. White and May proposed a classification of endoleaks: primary (<30 days) and secondary (>30 days) endoleaks.
  • Type 1: direct perfusion through the proximal (infrarenal) or distal (iliac) anastomosis

  • Type 2: retrograde perfusion through branch vessels (lumbar arteries, IMA, accessory renal artery)

  • Type 3: midgraft leak due to disintegration of the stentgraft (disconnection of the second iliac limb, fabric erosion)

  • Type 4: fabric porosity

  • Type 5: endotension.

Visceral Artery Aneurysm

Aneurysms of the celiac trunk and splenic, hepatic, gastroduodenal, and SM arteries are caused by arteriosclerosis, arteritis, periarterial inflammation such as pancreatitis, trauma, and soft tissue diseases such as Marfan, Ehlers-Danlos, and LDS. An aneurysm >2.5 cm in diameter should be considered for treatment to prevent rupture. Meticulous imaging, including selective catheter angiography and 3D imaging with CTA or MRA, is necessary before surgery or endovascular treatment. Endovascular options are embolization and exclusion with a stentgraft.

Renal Artery Aneurysm

Causes of renal artery aneurysms are arteriosclerosis, systemic vasculitis such as polyarteritis nodosa or lupus erythematosus, FMD, soft tissue disorders, and trauma. Arteriosclerotic and large aneurysms are usually calcified. The risk of rupture and chronic embolization are indications for treatment. Bypass surgery, coil embolization, and stent-graft implantation are therapeutic options.

Therapeutic Embolization of Gastrointestinal Bleeding

Upper Gastrointestinal (GI) Bleeding

Causes of Upper-GI Bleeding

  • Gastroduodenal ulcer

  • Proximal jejunal tumors [endocrine carcinomas, angiofibroma, melanoma metastases, arteriovenous (AV) malformation, etc.]

  • Pseudoaneurysm of the gastroduodenal, pancreaticoduodenal, intrapancreatic, and splenic arteries after pancreatitis or trauma; bleeding through the ductus Wirsungianus

  • Pseudoaneurysm of the hepatic artery, bleeding through the common bile duct (triad of hemobilia: abdominal colic followed by jaundice; hematemesis; melena).

Treating Upper-GI Bleeding

Upper GI bleedings are usually treated by endoscopic coagulation therapy. However, if endoscopic therapy fails or the bleeding source is inaccessible to endoscopy, angiographic embolization is indicated. Patients after gastric resection, with bilioenteric anastomoses, and with bleeding from hepatobiliary and pancreatic pathologies (i.e., pseudoaneurysms) should be treated primarily by angiographic techniques. Because of the extensive collateral circulation in the upper abdomen, a detailed angiographic evaluation followed by embolization of all feeding arteries is required.

Lower-GI Bleeding

In lower-GI bleeding, diagnosis and treatment is preferentially done by colonoscopy. However, in selected cases, embolization is required. For the primary diagnosis, a contrast-enhanced CT of the abdomen (CM 400 mg/ml, flow 4 ml, volume 100 ml) in arterial and delayed phases usually demonstrates nicely the area of bleeding. This helps identify the bleeding source during catheter angiography. Superselective catheterization, and bowel paralysis induced with Buscopan are mandatory when investigating a bleeding angiogram.

Causes of Lower-GI Bleeding
  • Small-bowel tumors (endocrine carcinomas, angiofibroma, melanoma metastases, AV-malformation, etc.)

  • Meckel’s diverticulum

  • Large-bowel diverticulum bleeding (most common cause in elderly patients)

  • Hemangiomatosis and AV malformation of the colon

  • Colon cancer.

Rectal bleeding due to hemorrhoidal disease has to be ruled out primarily.

Treatment for Lower-GI Bleeding

Lower-GI bleedings are preferentially embolized by coils.

Treatment for Bleeding Complications after Surgery, Trauma, and Postpartum

Bleeding in the abdomen may occur from iatrogenic causes, particularly in the kidneys and liver after percutaneous interventions, trauma, and tumour. Frequent and typical locations are renal AV fistulas due to nephrostomy (Fig. 4) or biopsy, laceration of the hepatic arteries by percutaneous manipulations, psoas, and pelvic bleeding due to traumatic arterial injury and uterine artery bleeding postpartum. Temporary occlusion of the uterine artery can then be a valid alternative to emergency hysterectomy in patients with intractable bleeding due to an atonic uterus. In other locations, type, source, and area of bleeding determine the method used to safely interrupt extravasations.
Fig. 4 a–c

Hematuria, shock due to renal bleeding after nephrostomy. a Computed tomography (CT) showing large perirenal hematoma and active bleeding. b Selective angiography demonstrating bleeding site. c Control angiography after selective coil embolization

Venous Interventions

Transjugular Intrahepatic Portocaval Shunt

Transjugular intrahepatic portocaval shunt (TIPS) was introduced into clinical medicine at the end of the 1980s. In the meantime, a standardized technique allows safe application of this artificial connection between portal and hepatic veins to depressurize the portal venous system. The introduction of stent-grafts instead of bare stents led to improved patency of the shunt tract. TIPS is indicated in patients symptomatic of portal hypertension with:
  • Acute or chronic bleeding of esophageal or gastric varices

  • Intractable ascites.

Although endoscopic techniques to treat varices are competitive techniques in bleeders, in some patients with ascites, there are few alternatives. Randomized trials, meta-analyses, and Cochrane data review analyses demonstrate that TIPS is superior to endoscopic therapy to prevent rebleeding and superior to paracenteses to remove ascites. In patients with acute or subacute Budd- Chiari syndrome, TIPS can be a life-saving procedure and help overcome the acute phase but is burdened by a relatively high rethrombosis rate. Risks after TIPS procedure are liver failure from shunted blood volume and encephalopathy.

Embolization of Portal Vein Collaterals

In liver cirrhosis with portal hypertension, collateral pathways may develop. Pathways to the superior vena cava (SVC) are from the left gastric vein (coronary vein) and the short gastric veins to the esophageal venous plexus. This pathway may cause esophageal and gastric varices with bleeding. Pathways to the inferior vena cava (IVC) are splenorenal and mesenteric-renal shunts and umbilical and hemorrhoidal collaterals. Embolization indications are bleeding and hepatic encephalopathy.

Suggested Reading

  1. ASTRAL Investigators, Wheatley K, Ives N, Gray R et al (2009) Revascularization vs. medical therapy for renal artery stenosis. N Engl J Med 361:1953–1962.PubMedCrossRefGoogle Scholar
  2. Bax L, Woittiez AJ, Kouwenberg HJ et al (2009) Stent placement in patients with atherosclerotic renal artery stenosis and impaired renal function: a randomized trial. Ann Intern Med 2009 150:840–848.Google Scholar
  3. Blankensteijn JD, de Jong SE, Prinssen M; Dutch Randomized Endovascular Aneurysm Management (DREAM) Trial Group (2005) Two-year outcomes after conventional or endovascular repair of abdominal aortic aneurysms. N Engl J Med 352:2398–2405.Google Scholar
  4. Blum U, Voshage G, Lammer J et al (1997) Endoluminal stentgrafts for infrarenal abdominal aortic aneurysms. N Engl J Med 336:13–20.PubMedCrossRefGoogle Scholar
  5. D’Amico G, Luca A, Morabito A et al (2005) Uncovered transjugular intrahepatic portosystemic shunt for refractory ascites: a metaanalysis. Gastroenterology 129:1282–1293.CrossRefGoogle Scholar
  6. EVAR trial participants (2005) Endovascular aneurysm repair vs. open repair in patients with abdominal aortic aneurysm (EVAR trial 1): randomised controlled trial. Lancet 365:2179–2186.CrossRefGoogle Scholar
  7. Greenhalgh RM, Brown LC, Kwong GP et al; EVAR trial participants (2004) Comparison of endovascular aneurysm repair with open repair in patients with abdominal aortic aneurysm (EVAR trial 1), 30-day operative mortality results: randomised controlled trial. Lancet 364:843–848.PubMedCrossRefGoogle Scholar
  8. Kaatee R, Beek FJ, de Lange EE et al (1997) Renal artery stenosis: detection and quantification with spiral CT angiography vs. optimized digital subtraction angiography. Radiology 205:121–127.PubMedCrossRefGoogle Scholar
  9. Kasirajan K, O’Hara PJ, Gray BH et al (2001) Chronic mesenteric ischemia: open surgery vs. percutaneous angioplasty and stenting. J Vasc Surg 33:63–71.PubMedCrossRefGoogle Scholar
  10. Khan S, Tudur Smith C, Williamson P, Sutton R (2006) Portosystemic shunts vs. endoscopic therapy for variceal rebleeding in patients with cirrhosis. Cochrane Database Syst Rev 18:CD000553.Google Scholar
  11. Khuroo MS, Al-Suhabani H, Al-Sebayel M et al (2005) Budd-Chiari syndrome: long-term effect on outcome with transjugular intrahepatic portosystemic shunt. J Gastroenterol Hepatol 20:1494–1502.PubMedCrossRefGoogle Scholar
  12. Laheij RJF, J Buth for the European Collaborators. Participants report. Overview of the overall patients cohort of the EUROSTAR data registry 2000.Google Scholar
  13. Leertouwer TC, Gussenhoven EJ, Bosch JL et al (2000) Stent placement for renal artery stenosis: where do we stand? A meta-analysis Radiology 216:78–85.Google Scholar
  14. Mann SJ, Pickering TG (1992) Detection of renovascular hypertension: state of the art 1992. Ann Intern Med 117:845–853.PubMedCrossRefGoogle Scholar
  15. Perler AB, Becker GJ (1998) Vascular intervention — a clinical approach. Visceral vascular disease. Thieme, New York Stuttgart, pp 517–637.Google Scholar
  16. Prinssen M, Verhoeven EL, Buth J et al; Dutch Randomized En-dovascular Aneurysm Management (DREAM) Trial Group (2004) A randomized trial comparing conventional and endovascular repair of abdominal aortic aneurysms. N Engl J Med 351:1607–1618.PubMedCrossRefGoogle Scholar
  17. Rose SC, Quigley TM, Raker EJ (1995) Revascularization for chronic mesenteric ischemia: comparison of operative arterial bypass grafting and percutaneous transluminal angioplasty. J Vasc Interv Radiol 6:339–349.PubMedCrossRefGoogle Scholar
  18. Saab S, Nieto JM, Lewis SK, Runyon BA (2006) TIPS vs. paracentesis for cirrhotic patients with refractory ascites. Cochrane Database Syst Rev 18:CD004889.Google Scholar
  19. Salerno F, Cammà C, Enea M et al (2007) TIPS for refractory as-cites: a meta-analysis of individual patient data. Gastroen-terology 133:825–834.CrossRefGoogle Scholar
  20. Soulez G, Oliva VL, Turpin S et al (2000) Imaging of renovascular hypertension: respective values of renal scintigraphy, renal Doppler US, and MR angiography. Radiographics 20:1355–1368.PubMedCrossRefGoogle Scholar
  21. van de Ven PJ, Kaatee R, Beutler JJ et al (1999) Arterial stenting and balloon angioplasty in ostial arteriosclerotic renovascular disease: a randomized trial. Lancet 353:282–286.PubMedCrossRefGoogle Scholar
  22. Van Jaarsveld BC, Krijen P, Pieterman H et al (2000) The effect of balloon angioplasty on hypertension in atherosclerotic renal-artery stenosis. Dutch Renal Artery Stenosis Intervention Cooperative Study Group. N Engl J Med 342:1007–1014.PubMedCrossRefGoogle Scholar
  23. Webster J, Marshall F, Abdalla M et al (1998) Randomized comparison of percutaneous angioplasty vs continued medical therapy for hypertensive patients with atheromatous renal artery stenosis. Scottish and Newcastle Renal Artery Stenosis Collaborative Group. J Hum hypertens 12:329–335.PubMedCrossRefGoogle Scholar
  24. Williams DM, Lee DY (1997) Dissected aorta, parts I-III. Radiology 203:23–44.PubMedCrossRefGoogle Scholar
  25. Zheng M, Chen Y, Bai J et al (2008) TIPS vs. endoscopic therapy in the secondary prophylaxis of variceal rebleeding in cirrhotic patients: meta-analysis update. J Clin Gastroenterol 42:507–516.PubMedCrossRefGoogle Scholar

Copyright information

© Springer-Verlag Italia 2014

Authors and Affiliations

  • Johannes Lammer
    • 1
  1. 1.Cardiovascular and Interventional Radiology and Biomedical Imaging and Image-Guided TherapyMedical University Vienna, University ClinicsViennaAustria

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