Chronic mesenteric ischemia: clinical practice guidelines from the Society for Vascular Surgery

Chronic mesenteric ischemia (CMI) results from the inability to achieve adequate postprandial intestinal blood flow, usually from atherosclerotic occlusive disease at the origins of the mesenteric vessels. Patients typically present with postprandial pain, food fear, and weight loss, although they can present with acute mesenteric ischemia and bowel infarction. The diagnosis requires a combination of the appropriate clinical symptoms and significant mesenteric artery occlusive disease, although it is often delayed given the spectrum of gastrointestinal disorders associated with abdominal pain and weight loss. The treatment goals include relieving the presenting symptoms, preventing progression to acute mesenteric ischemia, and improving overall quality of life. These practice guidelines were developed to provide the best possible evidence for the diagnosis and treatment of patients with CMI from atherosclerosis. The Society for Vascular Surgery established a committee composed of vascular surgeons and individuals experienced with evidence-based reviews. The committee focused on six specific areas, including the diagnostic evaluation, indications for treatment, choice of treatment, perioperative evaluation, endovascular/open revascularization, and surveillance/remediation. A formal systematic review was performed by the evidence team to identify the optimal technique for revascularization. Specific practice recommendations were developed using the Grading of Recommendations Assessment, Development, and Evaluation system based on review of literature, the strength of the data, and consensus. Patients with symptoms consistent with CMI should undergo an expedited workup, including a computed tomography arteriogram, to exclude other potential causes. The diagnosis is supported by significant arterial occlusive disease in the mesenteric vessels, particularly the superior mesenteric artery. Treatment requires revascularization with the primary target being the superior mesenteric artery. Endovascular revascularization with a balloon-expandable covered intraluminal stent is the recommended initial treatment with open repair reserved for select younger patients and those who are not endovascular candidates. Long-term follow-up and surveillance are recommended after revascularization and for asymptomatic patients with severe mesenteric occlusive disease. Patient with recurrent symptoms after revascularization owing to recurrent stenoses should be treated with an endovascular-first approach, similar to the de novo lesion. These practice guidelines were developed based on the best available evidence. They should help to optimize the care of patients with CMI. Multiple areas for future research were identified.

Shear level influences resistance artery remodeling: wall dimensions, cell density, and eNOS expression.

The magnitude of shear stimulus has been shown to determine the level of growth factor expression in cell culture. However, little is known regarding what effect shear level has on specific arterial wall remodeling events in vivo. We have hypothesized that the rate of luminal diameter change and specific remodeling events within the arterial wall layers are dependent on shear level. Selective ligations were made to alter the number of microvascular perfusion units of mesenteric arteries within the same animal to approximately 50%, 200%, and 400% of control. Arterial blood flow and wall shear rate were correlated with the degree of alteration in perfusion units. Luminal diameters were decreased in 50% arteries by day 2 and increased approximately 17% and 33% respectively, in 200% and 400% arteries at day 7. The rate of diameter change was greatest in 50% and 400% arteries. Wall areas (medial +37%; intimal +18% at day 2) and cell densities (intimal +26%; adventitial +44% at day 2) were altered only in the 400% arteries. A positive correlation existed by day 2 between endothelial staining for endothelial nitric oxide synthase and shear level. The results demonstrate that shear level influences the rate of luminal expansion, specific remodeling events within each wall layer, and the degree of endothelial gene expression. A greater understanding of how shear level influences specific remodeling events within each wall layer should aid in the development of targeted therapies to manipulate the remodeling process in health and disease.

Stent grafting of abdominal aortic aneurysms: pre-and postoperative evaluation with multislice helical CT.

Endovascular stent grafting of abdominal aortic aneurysms is a new technique that may replace open surgery in selected cases. Pre-and postoperative angiography can be replaced by helical CT. This pictorial essay describes and illustrates the use of multislice helical CT where maximum intensity projection and multiplanar reformats play a central role in the evaluation.

A multicenter, phase I evaluation of cryopreserved venous valve allografts for the treatment of chronic deep venous insufficiency.

PURPOSE: A phase I feasibility study was conducted to determine whether cryopreserved venous valved segments would remain patent/competent in a short-term period (6 months). METHODS: The target group consisted of 10 patients (C(4-6), E, A(D), P(R)). The exclusion criteria included untreated superficial/perforator venous disease, significant venous or arterial obstruction, hypercoagulability or coagulopathy, and significant preexisting medical conditions. Required preoperative tests were venous duplex, ascending/descending venography, and a physiologic study (eg, APG, blood typing, an ankle/brachial index, and if post-thrombotic, a hypercoagulability work-up). A single-valve transplant was placed below all reflux, aided by anticoagulation with or without a distal arteriovenous fistula. Postoperative assessment included duplex scanning/clinical examination (at 1, 3, and 6 months), descending venogram (at 1 month), and physiologic study (at 1 and 6 months). The primary end point was valve patency/competence, with clinical outcome as a secondary end point. Adverse events were recorded. RESULTS: After eliminating protocol violations, nine patients with superficial femoral (5) or popliteal (4) vein valve transplants were studied. Six-month actuarial results show a patency rate of 67% +/- 16% and 78% +/- 13%, respectively, a primary and secondary competency rate of 56% +/- 17% and 67% +/- 16%, respectively, and a 100% patient survival rate. Clinical outcome averaged 1.1, with healing and/or freedom from ulcer recurrence, in six of nine patients. A postoperative risk of seroma formation (3) and cellulitis (1) exists. CONCLUSION: In patients with few remaining therapeutic options, one can achieve a 6-month assisted patency and competency rate of 78% and 67%, respectively, with an improved clinical outcome.

The value of acetazolamide single photon emission computed tomography scans in the preoperative evaluation of asymptomatic critical carotid stenosis.

PURPOSE: Acetazolamide (ACZ)-enhanced single photon emission computed tomography (SPECT) scans can assess both cerebral perfusion and vascular reactivity. Patients with asymptomatic critical carotid artery stenosis were evaluated for cerebral vascular reactivity to determine the effect of extracranial occlusive disease and the effect of carotid endarterectomy (CEA) on intracerebral reactivity. METHODS: In 44 patients with asymptomatic critical carotid artery stenosis, cerebral perfusion and vascular reactivity were assessed before CEA with resting and ACZ-enhanced SPECT scans. All patients had a 70% or greater ipsilateral internal carotid artery stenosis. Preoperative ACZ-enhanced SPECT scans were obtained, usually 5 days before CEA. Postoperative ACZ-enhanced SPECT scans were obtained in 30 patients. RESULTS: Preoperative SPECT scans were asymmetric, revealing focal (n = 19) or global (n = 15) decreased reactivity in 34 patients (77%). Ten patients had symmetric or normal reactivity. After CEA, 23 patients demonstrated an improvement in reactivity ipsilateral to the side of surgery. The remaining seven patients failed to improve after surgery. CONCLUSION: Although all patients had a high-grade internal carotid stenosis, nearly a quarter of the patients had excellent intracerebral collateral flow. Only 71% of patients demonstrated improved intracerebral vasoreactivity after CEA. The lack of improvement in the other patients may have resulted from intracerebral pathology or lack of improvement in the extracranial carotid hemodynamics.

Drag reducing polymers may decrease atherosclerosis by increasing shear in areas normally exposed to low shear stress.

PURPOSE: Drag reducing polymers (DRPs) have been shown to decrease plaque formation. Their mechanism of action is unknown. Atherosclerosis tends to develop in areas of low shear stress. This study investigates whether DRPs increase shear stress in areas normally exposed to low shear stress. METHODS: Six dogs underwent surgical plication of the left half of the aorta. A specially modified 20-MHz Doppler ultrasound probe mounted at a 45-degree angle on a micromanipulator was used to measure blood flow velocity at six 4-mm intervals along both lateral sides of the aorta starting at the aortic wall and then at subsequent 0.1-mm depths moving into the lumen before and after administering DRP. Shear rates were calculated using linear regression and then compared using the paired t test. The blood viscosity remained constant at 0.04 poise during infusions of this amount of DRP. RESULTS: The maximum shear rate occurring during the cardiac cycle on the side of the aortic stenosis (plication) was 9.96 +/- 1.52/sec before the administration of the DRP and 14.27 +/- 2.01/sec after the administration of the DRP (P =.0240). The maximum shear rate on the side of the unstenosed aortic wall was 57.25 +/- 7.93/sec before the administration of the DRP and 44.80 +/- 6.23/sec after the administration of the DRP (P =. 0081). CONCLUSION: One of the ways that DRPs inhibit the development of atherosclerosis appears to be by increasing shear stress in areas normally exposed to low shear stress. Understanding this mechanism may lead to the development of pharmaceutical agents that inhibit the development of atherosclerosis.

Developments in diagnosis and classification of venous disorders: non-invasive diagnosis.

PURPOSE: This review examines the many techniques that have been used for the non-invasive diagnosis of acute and chronic venous disease and was conducted by members of the Committee on Research of the American Venous Forum. It proposes to identify those techniques with the greatest clinical potential, to suggest algorithms for the clinical application of non-invasive techniques in the identification of acute deep venous thrombosis and chronic venous insufficiency, and to identify areas of deficient knowledge and potential areas for future research initiatives. METHODS: Review of pertinent clinical and research material. RESULTS: Impedance plethysmography and ultrasonic imaging are the primary non-invasive tools used in the diagnosis of acute deep venous thrombosis. At present, ultrasonic imaging techniques are recommended on the basis of greater diagnostic accuracy in recent comparative clinical trials. Data would suggest that serial evaluation should probably be viewed as the preferred option for symptomatic patients with a negative initial examination and the presence of risk factors or physical findings suggesting a proximal deep venous obstruction/thrombosis. Chronic venous disease is the result of valvular incompetence, with or without associated venous obstruction. Duplex imaging can be used to determine the location and extent of reflux; however, there are reported procedural variations in the performance and interpretation of such studies. Recent innovations in air plethysmography may provide a means of quantifying volume changes, and permit an objective characterization of venous reflux and calf pump efficiency. CONCLUSIONS: There are still significant questions that need to be answered by well-designed research initiatives. Research applications that incorporate non-invasive diagnostic techniques may involve the diagnosis, treatment and natural history of acute deep venous obstruction/thrombosis and chronic venous insufficiency, assessment prior to and following venous reconstruction, and the basic science aspects of acute and chronic venous disease. At present, a lack of common standards is, by far, the greatest impediment to an organized research approach to venous disease.

Primary aortic mural thrombus: presentation and treatment.

The clinical presentation of patients with acute lower-limb ischemia and primary aortic thrombus prompted this review. Following recognition of the first case in early 1994, relevant patients (n = 6) were kept in a database and were reviewed for presentation, treatment, and follow-up. The median age was 41 and five patients were male. Angiography, computed tomography, and/or magnetic resonance angiography demonstrated one or more aortic sessile or pedunculated thrombus(i) without associated atherosclerotic disease. In two cases, a retropancreatic intraaortic mural thrombus was associated with severe pancreatitis. All other cases presented with acute lower-limb emboli requiring limb salvage embolectomy. Because of significant patient illness, systemic anticoagulation was chosen acutely to prevent recurrent emboli. Interestingly, serial studies demonstrated aortic thrombus resolution. Failure to continue warfarin therapy resulted in recurrent problems (n = 1) unless the instigating event had resolved (n = 3). There were no deaths or amputations. We concluded that surgical embolectomy, when required, with subsequent anticoagulation, results in limb salvage and allows for eventual resolution of the primary aortic thrombus. Long-term anticoagulation is required unless the etiologic process resolves. The literature describes patients with atherosclerosis and overlying thrombus but fails to describe the approach to patients with primary thrombus formation.

Lower-extremity arterial endovascular stenting.

Intraluminal arterial stenting for the management of arterial occlusive disease of the lower extremities has evolved over the years. Most stents are used to correct inadequacies of PTA or to correct a PTA complication. These include (1) restenosis within 90 days of PTA, (2) chronic iliac occlusion, (3) acute occlusions during PTA, (4) a significant residual gradient following PTA, (5) dissections longer than the angioplasty site, and (6) a 30% or greater residual stenosis after PTA. Both the Palmaz stent and the Wallstent have performed well in the iliac artery system. Their use in the femoropopliteal system has not been as successful and should be reserved for selected cases. Long-term anticoagulation is generally required for femoropopliteal stent patency. Placement in the lower superficial femoral or popliteal artery is best avoided. Re-angioplasty or additional stenting may be used to prolong patency, although with the risk of a second intervention. Progression of arteriosclerosis is a factor to consider when choosing an endoluminal treatment versus standard bypass.

Animal models for the study of lower extremity chronic venous disease: lessons learned and future needs.

The purpose of this review is to define animal models of chronic venous disease and to demonstrate how animal studies can impact our understanding and treatment of this disorder. To this end an extensive literature search was conducted highlighting potential animal models of chronic lower extremity venous disease. Scientific investigations using animals to study particular aspects of this disease are also reviewed. This review was conducted by members of the Committee on Research of the American Venous Forum to help provide direction for future venous research endeavors. Useful models of chronic venous occlusive disease involve controlled ligation of a major lower limb vein and multiple tributaries. Such a model can provide sustained venous hypertension and studies using this model have confirmed that an isodiametric graft can provide early hemodynamic relief. Models of primary, postphlebitic, and isolated chronic deep venous insufficiency are available for study. Valve repair or transplantation can positively impact the insufficiency observed in these models. Investigations into valve substitutes have generally been disappointing or are undergoing early evaluation. In conclusion, animal models for the study of some aspects of chronic venous disease do exist and have already affected our clinical approach to patients. The scientific study of basic pathophysiology, diagnostics, end-organ response, and long-term surgical treatments of this disorder in well-controlled animal experiments have not been conducted.

Wall remodeling after wall shear rate normalization in rat mesenteric arterial collaterals.

Previous studies have demonstrated endothelial and smooth muscle hyperplasia occur during arterial luminal expansion associated with elevation of arterial wall shear rates. The current study investigated whether remodeling induced by elevated wall shear would ultimately result in a vessel with intimal and medial cell densities and other wall characteristics similar to control arteries. A rat mesenteric model was used in which collateral wall shear is restored to normal 4 weeks after arterial occlusion. Twelve weeks after shear elevation, paired in vivo measurements indicated that the maximum collateral inner diameter was increased 27-75%. Morphometric evaluation of collateral cross sections indicated that, relative to control arteries, luminal and medial areas were increased 79 +/- 22 and 56 +/- 15%. Collateral medial cell density was decreased (1.12 +/- 0.044 vs. 1.35 +/- 0.005 nuclei/1,000 micrometer(2) but intimal cell density was similar (2.86 +/- 0.166 vs. 2.49 +/- 0.102 nuclei/100 micrometer luminal perimeter). Medial thickness to radius ratio was also similar between control and collateral arteries. Thus, for the wall characteristics evaluated, there are many similarities between enlarged collaterals and control arteries. Comparison of nuclear numbers in arterial cross sections of the current and previous studies suggest that intimal and medial cellular regression is correlated with a decrease in wall shear force toward normal levels.

Aggressive management of vascular injuries of the thoracic outlet.

PURPOSE: We present a review of 35 patients who underwent an operation for subclavian (n = 18) or axillary (n = 17) vessel injury. In some patients, both an artery and a vein were damaged, resulting in a total of 30 arterial and 16 venous injuries. METHODS: The wounding source included a gunshot (n = 19), a stab wound (n = 9,) and blunt trauma (n = 7). Seven patients had hypotension and were taken immediately to the operating room. Seventeen patients had diminished or absent pulses, whereas 13 patients had normal pulses despite an arterial injury. Associated injuries included nerve injury (n = 15), pneumohemothorax (n = 5), and fractures (n = 7). Angiography in 21 patients demonstrated an intimal flap (n = 8), extravasation (n = 5), a pseudoaneurysm (n = 3), an arteriovenous fistula (n = 2), and occlusion (n = 1). Two angiograms were normal. Arterial repair was accomplished by interposition graft (n = 17), primary repair (n = 9), patch angioplasty (n = 3,) and ligation (n = 1). RESULTS: No functional deficits occurred in patients with an isolated vascular injury. Seven patients with associated brachial plexus injuries experienced severe disability. One arm of a patient was amputated. Two patients died. CONCLUSIONS: The use of angiography helps to confirm and localize injuries. Prompt correction of the vascular injury avoids disability resulting from ischemia. Although the amputation rate is low with vascular repair, the functional disability resulting from associated nerve injuries can be devastating.

Direct in vivo measurement of flow-dependent nitric oxide production in mesenteric resistance arteries.

PURPOSE: To determine whether the concentration of nitric oxide (NO) at the arterial wall is increased subsequent to the abrupt elevation of blood flow in resistance arteries. METHODS: Eight dogs underwent laparotomy with anesthesia, and their small bowels were exteriorized. NO concentration was measured with NO-specific electrodes (200-micro-tip diameter) at the outer wall of the mesenteric arteries. Flow was increased by occlusion of the adjacent mesenteric arteries. In four animals, flow and NO concentration were measured after the administration of Nomega-nitro-L-arginine-methyl ester (L-NAME) to inhibit NO production. RESULTS: As arterial flow was increased from a baseline of 5.4 +/- 1.3 ml/min to 10.9 +/- 1.8 ml/min (p = 0.001), NO electrode current was elevated in every animal. With repetition of the flow stimulus, the response tended to be attenuated. In the first experimental trial, NO electrode current measured at the arterial wall increased from 2.86 +/- 0.56 to 3.00 +/- 0.60 nA (p = 0.02). L-NAME (10 mg/kg intravenous) effectively inhibited NO synthase as indicated by the elevation of mean arterial pressure (11 +/- 1.7 mm Hg; p = 0.04). After administration of L-NAME, NO electrode current measured at the outer arterial wall fell 0.23 +/- 0.05 nA (p = 0.02). CONCLUSIONS: The data indicate that a doubling of blood flow in the canine mesenteric resistance arteries is associated with an increase in NO concentration of at least 100 nm at the outer arterial wall. This association is probably a substantial underestimation of the actual concentration because of the geometry of the electrode tip. To our knowledge, ours is the first report of direct in vivo measurement of flow-dependent NO release in resistance arteries.

Experimental repair of venous valvular insufficiency using a cryopreserved venous valve allograft aided by a distal arteriovenous fistula.

PURPOSE: To evaluate the patency and hemodynamic impact of a cryopreserved allograft venous valve transplanted to the superficial femoral vein (SFV) of a canine insufficiency model aided by a distal arteriovenous fistula (dAVF). METHODS: Eight greyhounds had intravenous hemodynamic parameters measured (venous filling time [VFT], 90% of venous refilling time [VRT90], and simulated ambulatory venous pressure [AVP]) before (T0) and after complete hindlimb venous valvulotomy (T1) to produce venous insufficiency. Simultaneously, a valve-containing vein segment was harvested from the opposite SFV or external jugular vein (n = 1) and cryopreserved. Three weeks later a blood type-matched cryopreserved valve was transplanted to the insufficient SFV aided by a low-flow (n = 4) or high-flow (n = 4) dAVF. The fistula was ligated in 3 to 6 weeks, and venous indexes (T2) were obtained 3 weeks later. Analysis of variances compared the venous indexes at T0, T1, and T2 for statistical significance. Gross and histologic inspection assessed valve integrity. RESULTS: Two valves aided by a low-flow dAVF exhibited thrombosis and scarring. The hemodynamics of the six remaining valves demonstrated normalization of the VRT90, an AVP consistent with insufficiency, and a VFT between normal and total venous insufficiency. The patent valves were normal on gross examination and by histologic examination with signs of normal external healing. CONCLUSIONS: A cryopreserved venous valve allograft transplanted to the SFV of an incompetent hindlimb partially corrects venous hemodynamics. A high-flow arteriovenous fistula most consistently preserves transplant patency.

Cerebral vascular reactivity assessed with acetazolamide single photon emission computer tomography scans before and after carotid endarterectomy.

BACKGROUND AND METHODS: In 64 patients, cerebral perfusion and vascular reactivity were assessed before and after carotid endarterectomy (CEA) using acetazolamide (ACZ)-enhanced single photon emission computer tomography (SPECT). Twenty-five patients were asymptomatic, whereas the remainder were symptomatic. Sixty-one patients had a > or = 70% ipsilateral internal carotid artery stenosis. RESULTS: Fifty SPECT scans revealed decreased vascular reactivity. Twenty-three showed infarcts. Fourteen patients had normal studies. Twenty of the SPECT scans of asymptomatic patients demonstrated poor vascular reactivity. After CEA, 39 patients had improved ipsilateral vasoreactivity. In 12 patients, contralateral improvement was also found. CONCLUSION: ACZ-enhanced SPECT scans, by assessing cerebral perfusion and vascular reactivity, may help to identify patients at risk of stroke should perfusion further diminish. Postoperative studies confirm improvement in vascular reactivity. ACZ-enhanced SPECT scans may provide objective evidence for the selection of patients with a high-grade asymptomatic carotid stenosis for CEA.

Research and clinical issues in chronic venous disease.

The purpose of this study was to summarize the current issues in chronic venous disease by reviewing of the literature relating to the condition. The review was conducted by members of the Committee on Research of the American Venous Forum and includes the Committee's venous disease and current/future directions. Progress in the understanding and management of chronic venous problems has lagged behind that in arterial disease, despite the large number of patients affected. The complex pathophysiology of venous problems, lack of accepted evaluation standards and lack of prosthetic conduits are some of the factors which contribute to this. New information in these areas has laid the foundation for advances in both operations and non-operative therapy. In conclusion, many opportunities for clinical and basic research in the area of chronic venous disease are available. Application of basic science techniques, including those of molecular biology, will lead to new insights into pathophysiology of chronic venous syndrome. Developments in technology, classification and basic science suggest multiple new potentials therapeutic approaches in the next decade.

Median arcuate ligament syndrome with multivessel involvement: diagnosis with spiral CT angiography.

Intestinal angina may be caused by compression of the celiac artery by the median arcuate ligament of the diaphragm. Aortography can suggest the diagnosis, but the diaphragm cannot be visualized by this examination. We report a symptomatic woman in whom spiral computed tomography-guided angiography demonstrated stenosis of the celiac artery, superior mesenteric artery, and both renal arteries due to diaphragmatic compression. Surgery was beneficial.

Wall remodeling during luminal expansion of mesenteric arterial collaterals in the rat.

Wall remodeling associated with rapid luminal enlargement of collateral mesenteric arteries in rats was investigated 1 and 4 weeks after creation of a collateral pathway by ligating three to four sequential arteries. Paired observations were made of inner diameters of collateral and normal arteries in the same animals. Arterial blood flow was measured at the final observation. Sections of arteries were processed for morphological measurements. After 4 weeks, inner arterial diameter was increased more at the beginning (63 +/- 6%) than the end (25 +/- 9%) of the collateral pathway. At 1 and 4 weeks, respectively, cross-sectional areas of collateral relative to normal arteries were increased by 46 +/- 5% and 59 +/- 13% (lumen), 55 +/- 8% and 65 +/- 14% (media), and 89 +/- 18% and 60 +/- 31% (intima). The wall expansion during luminal enlargement resulted in a normal medial thickness:luminal radius relationship. At 1 week postligation, wall shear rate remained elevated and endothelial but not smooth muscle hyperplasia had occurred (intimal nuclei: 40 +/- 1.7 collateral versus 24 +/- 3.0 normal; medial nuclei: 42 +/- 6.8 collateral versus 37 +/- 2.1 normal). At 4 weeks, wall shear rate in collaterals was similar to normal arteries, and smooth muscle hyperplasia had taken place (medial nuclei: 84 +/- 9.4 collateral versus 44 +/- 4.7 normal). The data demonstrate that wall expansion associated with rapid luminal enlargement of these collaterals involves hyperplasia of both endothelial and smooth muscle cells; however, smooth muscle proliferation does not occur until after wall shear rate is reduced. The specific cellular adaptations that occur during collateral development may depend on the level of wall shear and shear-dependent modulation of endothelial growth factors.