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Biomedical subjects

Vikram S Kashyap

Publications and source records attributed to Vikram S Kashyap.

At least 19 recordsLinked to original sources
PubMed2007

The management of renal artery atherosclerosis for renal salvage: does stenting help?

OBJECTIVE: The use of endovascular techniques to treat renal artery stenosis (RAS) has increased in recent years but remains controversial. The purpose of this study was to review the outcomes and durability of percutaneous transluminal angioplasty and stenting (PTA/S) for patients with RAS and decreasing renal function. METHODS: Between 1999 and 2004, 125 consecutive patients underwent angiography and intervention for renal salvage and formed the basis of this study. Inclusion criteria for this study included serum creatinine greater than 1.5 mg/dL, ischemic nephropathy, and high-grade RAS perfusing a single functioning kidney. Patients undergoing PTA/S for renovascular hypertension or fibromuscular dysplasia or in conjunction with endovascular stent grafting for aneurysm repair were excluded. The original angiographic imaging was evaluated for lesion grade and parenchymal kidney size. All medical records and noninvasive testing were reviewed. Preoperative and postoperative patient data were standardized and analyzed by using chi(2) tests for nominal values and t tests for continuous variables. The Modification of Diet in Renal Disease equation was used to estimate glomerular filtration rate (GFR), and univariate analysis was performed. RESULTS: Preoperative variables included the presence of coronary artery disease (93%), diabetes (44%), tobacco use (48%), and hypercholesterolemia (70%). RAS was suspected on the basis of preoperative duplex imaging or magnetic resonance angiography. Aortography and PTA/S were performed in 125 patients (mean age, 71 years; 59% male) with a mean baseline creatinine level of 2.2 mg/dL. There were two mortalities (1.6%) in the 30-day postoperative period, but there was no case of acute renal loss. Blood pressure decreased after PTA/S (151/79 mm Hg before vs 139/72 mm Hg after 1 month; P < .03). For all patients, the estimated GFR went from 33 +/- 12 mL . min(-1) . 1.73 m(-2) (mean +/- SD) to 37 +/- 19 mL . min(-1) . 1.73 m(-2) at 6 months (P = .10). Sixty-seven percent of treated patients had improvement (>10% increase in GFR) or stabilization of renal function. A rapid decline in GFR before intervention was correlated with improvement after PTA/S. Responders after PTA/S had a 27% decrease in GFR before intervention (44 +/- 13 mL . min(-1) . 1.73 m(-2) to 32 +/- 13 mL . min(-1) . 1.73 m(-2); P < .001) with a negative to positive slope change in GFR values. Ten patients underwent reintervention for in-stent restenosis. Cases without improvement in GFR after PTA/S were associated with eventual dialysis need (P = .01; mean follow-up, 19 months). Survival at 3 years was 76%, and dialysis-free survival was 63% as estimated by Kaplan-Meier analyses. CONCLUSIONS: Renal artery stenoses causing renal dysfunction can be safely treated via endovascular means. Rapidly decreasing renal function is associated with the response to renal artery angioplasty/stenting and helps identify patients for renal salvage.

Adult↗
PubMed2006

Arginase activity is increased by thrombin: a mechanism for endothelial dysfunction in arterial thrombosis.

BACKGROUND: Earlier observations implicate arterial thrombosis causing endothelial dysfunction by decreasing nitric oxide (NO) levels. NO levels are restored by regional L-arginine supplementation in animal models. The purpose of this study was to investigate the roles of thrombus components in NO generation. STUDY DESIGN: Human umbilical vein endothelial cells were harvested and cultured. The thrombus components thrombin, thrombin receptor agonist peptide (TRAP), and fibrin were added to a media of confluent human umbilical vein endothelial cells. Endothelial nitric oxide synthase (eNOS) activity was assayed by measuring conversion of L-arginine to L-citrulline. Endothelial NOS mRNA levels were quantitated using real-time polymerase chain reaction. Cellular membrane transport of L-arginine through the y+ channel was assayed with (14)C-labeled L-arginine. Arginase activity was determined as the conversion of (14)C L-arginine to (14)C urea and trapped as Na(2)(14)CO(3) for scintillation counting. Arginase protein amounts were assessed using Western blotting. RESULTS: Endothelial cells exposed to thrombin for 4 hours led to increased arginase activity. Thrombin (10 U/mL) caused a 1.6-fold increase compared with that in controls (320+/-29 microM urea/min versus 194+/-10 microM urea/min, p=0.03), and thrombin (30 U/mL) increased arginase activity 2.1-fold (398+/-27 microM urea/min, p < 0.001, versus controls); thrombin at 1 U/mL and fibrin had no effect. TRAP (50 microM) had an effect similar to that of thrombin 10 U/mL (316+/-21 microM urea/min, p < 0.01, versus controls). Protein amounts of arginase corresponded with activity levels. Neither eNOS nor inducible nitric oxide synthase (iNOS) activities were affected by exposure to thrombin and TRAP for 4 hours. Similarly, quantification of eNOS, iNOS, and endothelin-1 mRNA did not change, although CL-100, a known thrombin-inducible gene, was upregulated. Finally, transport of L-arginine into endothelial cells was unaffected by thrombin, TRAP, and fibrin exposure. CONCLUSIONS: Endothelial cells exposed to thrombin have increased arginase enzymatic activity, and the remainder of NO generation capability is unaffected. L-arginine supplementation or arginase blockade may counteract endothelial dysfunction in the setting of acute arterial thrombosis.

Arginase↗
PubMed2006

Endovascular management of iliac artery occlusions: extending treatment to TransAtlantic Inter-Society Consensus class C and D patients.

OBJECTIVE: The preferential use of endovascular techniques to treat complex aortoiliac disease has increased in recent years. The purpose of this study was to review the outcomes and durability of recanalization, percutaneous transluminal angioplasty, and stenting for iliac occlusions based on the patient's TransAtlantic Inter-Society Consensus (TASC) stratification. METHODS: Between 1998 and 2004, more than 628 patients with a clinical diagnosis of aortoiliac atherosclerotic disease underwent arteriography. The endovascular treatment of 89 consecutive patients (mean age, 66 years; 58% male) with symptomatic iliac occlusions (TASC-B, -C, and -D) was the basis for this study. Original angiographic imaging was evaluated for lesion grade and runoff. Electronic and hard copy medical records were reviewed for demographic data, clinical variables, and noninvasive vascular laboratory testing. Kaplan-Meier estimators were used to determine patency rates according to Society for Vascular Surgery criteria. Univariate and multivariate analyses were performed. P values of <.05 were considered significant. RESULTS: Recanalization and percutaneous transluminal angioplasty/stenting (total, 178 stents) of occluded iliac arteries was technically successful in 84 (91%) of 92 procedures. Patients in the TASC-C and -D groups often required multiple access sites (50%) and femoral artery endarterectomy/patch angioplasty for diffuse disease (24%). The mean ankle-brachial index increased from 0.45 to 0.83. Distal embolization led to major amputation and eventual death in one patient. Two other deaths occurred in the perioperative period secondary to cardiorespiratory causes. Three-year primary patency, secondary patency, and limb salvage rates were 76%, 90%, and 97%, respectively, and progression of infrainguinal disease led to late limb loss in two patients. Diabetes as a risk factor was significantly associated with decreased primary patency (57% vs 83%; P = .049). Critical ischemia at presentation was associated with decreased patency rates as well (P = .002), but TASC classification did not significantly alter patency rates. CONCLUSIONS: Complex long-segment and bilateral iliac occlusions can be safely treated via endovascular means with high rates of symptom resolution. Initial technical success, low morbidity, and mid-term durability are comparable to results with open reconstruction. A liberal posture to open femoral artery reconstruction extends the ability to treat diffuse TASC-C and -D lesions via endovascular means.

Arterial Occlusive Diseases↗
PubMed2006

Infected carotid pseudoaneurysm and carotid-cutaneous fistula as a late complication of carotid artery stenting.

Carotid stenosis after neck irradiation is a well-described entity. A 78-year-old man presented with left eye amaurosis fugax 11 years after radical neck dissection and neck irradiation for mucoepidermoid carcinoma. The patient underwent carotid artery stenting for a high-grade stenosis of the left internal carotid artery. Twenty months after the procedure, a pulsatile neck mass developed with intermittent arterial bleeding. After control of the bleeding, he underwent resection of the left carotid bifurcation, including the indwelling stent and reconstruction with a saphenous vein interposition graft. A pectoralis myocutaneous flap was used for wound closure. In this case, localized infection of the stented carotid artery led to mycotic degeneration, pseudoaneurysm formation, and erosion to the skin surface. As carotid artery stenting becomes more widely used, previously unreported late complications associated with this procedure are likely to become apparent, and continued close follow-up is warranted.

Aged↗
PubMed2006

Emerging drugs in peripheral arterial disease.

Peripheral arterial disease (PAD) is the manifestation of atherosclerotic occlusion within a peripheral vascular bed. This can occur in any noncoronary arterial bed, but PAD most commonly refers to atherosclerosis in the aorto-iliac system and infrainguinal vessels that lead to symptoms in the lower extremities. The disease most often becomes clinically apparent in elderly individuals, commonly presenting as intermittent claudication. More advanced, or multisegmental disease, may present with ischaemic rest pain or tissue loss. Although the limb manifestations of PAD can be disabling, PAD is also a marker of coronary or cerebrovascular atherosclerosis. In fact, approximately 80% of mortality in PAD patients is secondary to a cardiovascular event. In accordance with this, initial medical management of this disease focuses on preventative and risk reduction strategies to minimise the risk of cardiovascular morbidity and mortality. At present, the majority of recommendations with respect to risk reduction therapy in PAD patients are extrapolated from the coronary and cerebrovascular literature. Limb-directed therapy in PAD intends to minimise symptoms and serve as an adjunct to surgical intervention. However, existing data on the efficacy of these agents suggests that they are only partially effective. In addition, the effect of existing nonoperative intervention on the progression of disease has not been completely elucidated. As such, new therapies are under development, which target various goals, including minimising local progression of disease, minimising disability, reducing systemic cardiovascular morbidity/mortality and augmenting the durability of surgical intervention.

Administration, Oral↗
PubMed2006

Combined staged procedures for the treatment of thoracoabdominal aneurysms.

PURPOSE: To examine the efficacy of a staged approach for the treatment of thoracoabdominal aneurysms, with open visceral revascularization followed by aortic endografting, in selected patients not considered candidates for conventional surgical repair. METHODS: A retrospective review was conducted of 13 consecutive patients (8 women; mean age 64 years, range 33-77) who underwent visceral bypass followed by endovascular thoracoabdominal stent-graft implantation since 1999. Three patients presented with symptomatic aneurysms and 2 with rupture. Two patients had connective tissue disorders. All patients were deemed unfit for conventional thoracoabdominal repair due to comorbid conditions. The procedures were tailored to the pathology and specific patient anatomical situation: 5 aortic dissections with aneurysmal degeneration and 8 aneurysms (5 Crawford type II, 2 type III, and 1 type IV). RESULTS: The patients underwent retrograde visceral bypass (11 iliovisceral and 2 infrarenal aortic to visceral artery) followed by endovascular aortic relining with Zenith TX2 devices (n=7), homemade endografts (n=5), or a Talent thoracic endograft (n=1). Six patients required either a proximal or distal direct aortic repair (2 infrarenal reconstructions, 3 arch elephant trunk grafts, and 1 ascending aortic repair), while 3 patients also underwent left carotid-subclavian bypass grafting. Two patients developed paraplegia (1 following a ruptured aneurysm), and 2 patients had transient paraparetic events. Two patients had acute renal failure requiring short-term dialysis. Three patients died within 30 days; 2 late aneurysm-related deaths were noted. Three patients developed endoleaks during follow-up. Mean lengths of stay were 13 days (7-30) for the visceral bypass and 12 (3-25) for the endovascular stent-graft. In addition, remaining procedures in 8 patients required a mean of 7 days (0-14) in hospital. CONCLUSION: Staged endovascular and open procedures are feasible for thoracoabdominal aneurysms in patients at prohibitive risk for open thoracoabdominal reconstruction. However, this approach still carries a significant risk of perioperative mortality and morbidity. The potential for less invasive alternatives should be investigated.

Adult↗
PubMed2005

Endothelial dysfunction after lactated Ringer's solution resuscitation for hemorrhagic shock.

BACKGROUND: Endothelial dysfunction is presumed to occur after hemorrhagic shock and resuscitation. This study uses a novel large-animal model to evaluate the effects of diverse resuscitation regimens on endothelial function. METHODS: Twenty-seven adult domestic pigs (Sus scrofa) were used in this study. Control pigs (n = 3) underwent instrumentation alone. The remaining pigs experienced controlled hemorrhagic shock to a mean arterial blood pressure of 30 +/- 5 mm Hg for 45 minutes. Pigs were resuscitated to their baseline mean arterial blood pressure +/-5 mm Hg with either shed blood (SB; n = 8), lactated Ringers solution (40 mL/kg) followed by shed blood (LRSB; n = 8), or lactated Ringers solution alone (LR; n = 8). At baseline, 1 and 4 hours after resuscitation, acetylcholine (5, 10, and 15 microg/min) was infused into the proximal iliac artery to measure endothelial dependent relaxation (EDR). Sodium nitroprusside was infused to determine endothelial independent relaxation at the end of the study to insure smooth muscle vasomotor integrity. External iliac artery luminal diameter was measured using motion-mode ultrasonography. Statistical analysis was performed using repeated-measures analysis of variance with Tukey's post-hoc analysis. RESULTS: All pigs survived the experiment. Pigs required ninefold more resuscitation with LR (370.58 +/- 29 mL/kg) versus SB (41.45 +/- 3.5 mL/kg) or LRSB (76.4 +/- 1.1 mL/kg) (p < 0.05). EDR for LR pigs 1 hour after initiation of resuscitation (R1) was 70.4 +/- 14.4% compared with 94.2 +/- 13.4% for SB and 106.1 +/- 8.2% for LRSB (p < 0.05). At 4 hours after resuscitation (R4), systolic luminal diameters were larger in the SB (0.45 +/- 0.01 cm) and LRSB (0.51 +/- 0.02 cm) groups compared with LR (0.41 +/- 0.03 cm) (LRSB versus LR; p = 0.01). At R4, EDR for the LR group was 78.3 +/- 10.7% compared with SB (101.4 +/- 8.3%) and LRSB (106.4 +/- 7.4%) (p < 0.05). Infusion of sodium nitroprusside confirmed integrity of smooth muscle vasorelaxation. Analysis of serum nitric oxide levels revealed decreased values after resuscitation with LR (9.44 +/- 0.76 mol/L) compared with SB (26.3 +/- 7.8 mol/L) and LRSB (16.3 +/- 1.0 mol/L) (p = not significant). CONCLUSION: This is the first description of a large-animal model to evaluate EDR after hemorrhagic shock. Resuscitation with LR requires significantly larger volumes than SB or LRSB. LR resuscitation leads to endothelial dysfunction, as determined by decreased EDR, versus SB or LRSB. Resuscitation with blood products may preserve nitric oxide bioactivity when compared with crystalloid resuscitation in the setting of hemorrhagic shock.

Animals↗
PubMed2005

Bilateral brachial artery occlusion decreases internal carotid artery volume flow: a simple adjunct for cerebral protection?

PURPOSE: To investigate if a decrease in internal carotid artery (ICA) blood flow occurs with bilateral brachial artery occlusion (BBO), which may improve the effectiveness of cerebral protection devices during carotid interventions. METHODS: Thirty-two asymptomatic patients (21 men; mean age 67 years) with carotid atherosclerosis between 15% and 79% were enrolled in the study. Carotid duplex ultrasound was followed by volume flow rate (VF) determination in the right ICA, external carotid (ECA), and vertebral arteries. After baseline values were obtained, BBO was induced by bilateral arm pressure cuff inflation to 30 mmHg over the systolic pressure for no more than 3 minutes. VF measurements were repeated. RESULTS: Seventeen patients (responders) had an ICA VF decrease from 406+/-109 mL/min (+/-SD) to 303+/-90 mL/min (p=0.005), while 15 patients (nonresponders) had no significant change in their ICA VF (340+/-192 versus 447+/-267 mL/min, p=0.22). In responders, ECA VF increased (190+/-65 to 232+/-125 mL/min), as did vertebral VF (77+/-53 to 95+/-60 mL/min; p>0.05). The ratio of ICA/ECA VF dropped from 2.13 to 1.31 in responders, but did not change in nonresponders. No patient exhibited any neurological symptoms during the study. Post cuff volume flows approximated baseline values. Cerebral magnetic resonance angiograms obtained in 10 responders revealed a complete circle of Willis in 8 (80%), while only 1 (16%) of 6 nonresponders had a complete pathway. CONCLUSIONS: A transient decrease in ICA VF, with concomitant elevations of the ECA and vertebral VFs, occurs with occlusion of the brachial arteries in the setting of a complete circle of Willis. Since no flow reversal occurs, this maneuver is insufficient to provide complete cerebral protection, but it may improve the effectiveness of cerebral protection devices and serve as an adjunctive maneuver in selected cases. Furthermore, changes in ICA VF may prove to be a noninvasive test for evaluating the integrity of the circle of Willis.

Adult↗
PubMed2005

Carotid revascularization in the presence of contralateral carotid artery occlusion is safe and durable.

OBJECTIVE: Complete occlusion of the contralateral carotid artery has been thought to increase the risk of carotid endarterectomy (CEA). This study was conducted to determine whether contralateral occlusion (CO) leads to a higher rate of complications among patients undergoing CEA or alters long-term outcomes. METHODS: All CEAs (N = 221) performed at our institution between September 1997 and June 2002 were reviewed. Patients were divided into two groups, i.e., CO and contralateral patency. Statistical analyses were performed using Fisher's exact test for nominal values and the t test for continuous variables. Life-table analyses were performed for patency and survival. RESULTS: Complete data and follow-up results were available for 170 of the 221 operations performed during the study period. CO was present in 16 cases (9.4%). Preoperative demographic features, indications for surgery, and operative techniques did not vary between study groups; there was increased use of general anesthesia (p = 0.05) in the CO group. No surgical deaths occurred. The perioperative stroke rates were not statistically different between groups (CO group, 6.3%; contralateral patency group, 2.6%; p = 0.39). Long-term patency and stroke-free survival rates at 5 years exceeded 90% and did not vary significantly between groups. CONCLUSION: Patients undergoing CEA with occlusion of the contralateral carotid artery do not have unique preoperative demographic features or indications. Contralateral carotid artery occlusion does not increase risk or alter long-term outcomes after CEA. Carotid revascularization can be safely performed in tertiary military centers.

Aged↗
PubMed2004

Resuscitation with a blood substitute causes vasoconstriction without nitric oxide scavenging in a model of arterial hemorrhage.

BACKGROUND: The purpose of this study was to determine if a hemoglobin-based oxygen carrier, HBOC-201 (Hemopure, Biopure Corp), alters endothelial function and nitric oxide physiology when used for hemorrhagic shock. STUDY DESIGN: Female swine (Sus scrofa) underwent catheterization of the femoral, circumflex iliac, and pulmonary arteries. Control animals (n = 3) underwent instrumentation only. Study animals underwent hemorrhage to mean arterial pressure of 30 +/- 5 mmHg, were maintained for 45 minutes, and resuscitated to the baseline mean arterial pressure for 4 hours. Resuscitation fluids included: shed blood (SB) (n = 8), lactated Ringers plus shed blood (LRSB) (n = 8), and HBOC (n = 8). At baseline, 1, and 4 hours after resuscitation, acetylcholine was infused into the proximal iliac artery and endothelial-dependent relaxation was measured with M-mode ultrasonography. Nitric oxide levels were determined using a chemiluminescent assay. RESULTS: HBOC, SB, and LRSB provided equivalent survival and resuscitation as measured by mean arterial pressures (65.3 +/- 2.48 mmHg); pulmonary artery mean pressures (15.8 +/- 0.84 mmHg); and lactate levels (1.22 +/- 0.19 mmol/L). HBOC group animals required the lowest resuscitation volume (SB, 41.5 +/- 3.5 mL/kg; LRSB, 76.4 +/- 1.1 mL/kg, HBOC, 14.6 +/- 2.1 mL/kg, p < 0.001). Response to acetylcholine was normal in the SB and LRSB groups, but the HBOC group had diminished acetylcholine response (29.5% endothelial-dependent relaxation end resuscitation, p < 0.001). Arterial nitric oxide levels did not differ between study groups (p = 0.69). CONCLUSIONS: HBOC might be an alternative resuscitation agent in patients with hemorrhagic shock. Resuscitation with HBOC requires less volume than blood or crystalloid. These data suggest HBOC-201 has a vasoconstrictive effect that cannot be attributed soley to nitric oxide scavenging.

Animals↗
PubMed2004

Thrombus-induced endothelial dysfunction: Hemoglobin and fibrin decrease nitric oxide bioactivity without altering eNOS.

BACKGROUND: Arterial thrombosis is associated with endothelial dysfunction. The purpose of this study was to determine which components of thrombus induce endothelial dysfunction and to determine their effect on endothelial nitric oxide synthase (eNOS) activity and expression. MATERIALS AND METHODS: Human aortic endothelial cells were grown to confluence. Group 1 consisted of control cells exposed to media. Group 2 was exposed to cellular components of thrombus, including erythrocytes (RBCs) (1.5, 3, and 6 x 10(4) cells/ml) and platelets (0.5, 1, and 2 x 10(5) platelets/ml). Group 3 was exposed to extracellular thrombus components, including hemoglobin (1.25, 2.5, and 5.0 g/dl), thrombin (0.4, 4.0, and 10.0 units/ml), and fibrin. The exposure time was 20 h. Nitric oxide (NO) levels were measured following exposure. Global cellular integrity was evaluated by MTS (3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium) conversion. eNOS mRNA expression was measured using semiquantitative PCR and eNOS protein activity evaluated via a l-citrulline conversion assay. Studies were done in replicates of six and expressed as percentages of controls. RESULTS: NO levels decreased following exposure to hemoglobin (1.25 g/dl = 59 +/- 5%, 2.5 g/dl = 38 +/- 3%, 5 g/dl = 37 +/- 6%, P < 0.001). MTS metabolism was likewise suppressed (1.25 g/dl = 57 +/- 2%, 2.5 g/dl = 55 +/- 3%, 5 g/dl = 44 +/- 6%, P < 0.001). Fibrin diminished NO levels (37 +/- 5%, P < 0.01) and MTS metabolism (49 +/- 5%, P < 0.01). RBCs and platelets had no effect on NO production or MTS metabolism (P > 0.05). Thrombin's effect was concentration dependent, inhibiting nitric oxide production at low doses while stimulating it at high doses (P < 0.01). All thrombin doses enhanced MTS metabolism (P < 0.05). eNOS activity was not altered by fibrin, thrombin, or hemoglobin exposure (P > 0.05). Moreover, eNOS mRNA expression was unaffected (P > 0.05). CONCLUSIONS: Intact cellular components of thrombus do not cause endothelial dysfunction in vitro. However, free hemoglobin and fibrin diminish NO bioactivity, likely via scavenging. Thrombin affects NO levels in a concentration-dependent manner. Neither eNOS expression nor eNOS activity is diminished, indicating that thrombus does not cause permanent changes in NO generation capability.

Aorta↗
PubMed2004

Initial management and outcome of aortic endograft limb occlusion.

OBJECTIVE: The purpose of this study was to determine the differences in outcome related to initial management of aortic endograft limb occlusion (ELO). METHODS: During a 7-year period, 823 endovascular aneurysm repairs (EVARs) resulted in 25 ELOs in 22 patients. The initial management and outcome of these ELOs were reviewed. Median follow-up after ELO was 24.2 +/- 16.8 months. RESULTS: Initial EVARs included both unsupported unibody (n = 5) and supported modular (n = 17) devices. ELO was significantly more common in the unsupported unibody graft design (P <.024) and with extension of the graft limb to the external iliac artery (P <.001). ELO was managed with an endovascular approach (EVA), including some combination of mechanical thrombectomy (n = 8), angioplasty with or without stenting (n = 8), and thrombolysis (n = 2) in 12 patients and bypass procedures (femoral-femoral bypass, n = 11; axillofemoral bypass, n = 1; and aortofemoral bypass, n = 1) in 13. At 12-month follow-up, freedom from secondary procedures with EVA was 80.2 +/- 17.7% versus 53.2 +/-17.1% with extra-anatomic bypass (EB) (P = NS). Secondary patency was 100% with EVA and 80.6 +/- 14.4% with EB (P = NS). Of the 12 EVAs, there was 1 (8.3%) perioperative mortality with EVA and none with EB. EB failure was directly attributed to donor limb occlusion in 4 of 6 EVAs (67%), and when this occurred it resulted in bilateral lower extremity ischemia. Amputation was required in 2 of 12 (16.7%) EBs versus none of the 12 EVAs (P = NS). EVA never resulted in graft dislodgement or endoleak but did identify an underlying treatable cause in 8 of 12 (67%). CONCLUSION: Both EVA and EB are acceptable management strategies for ELO. The potential risk of graft dislodgement was not observed with an EVA. If EB is employed, assessment of the donor limb and treatment of any underlying lesions is advisable in an attempt to minimize future donor limb occlusion.

Angioplasty↗
PubMed2003

Caval and ureteral obstruction secondary to an inflammatory abdominal aortic aneurysm.

Inflammatory abdominal aortic aneurysms (IAAA) represent 3% to 10% of all abdominal aortic aneurysms. Obstructive uropathy is a well-described feature of IAAAs, but venous complications are unusual secondary to IAAA. The authors report a patient presenting with acute renal failure and deep venous thrombosis secondary to an IAAA. We believe this represents the first case of an IAAA manifesting as combined inferior vena cava compression and associated obstructive uropathy. Successful operative repair was performed. With resolution of the retroperitoneal inflammation, long-term follow-up revealed spontaneous release of both ureteral and caval compression.

Aged↗
PubMed2003

Graft patency is not the only clinical predictor of success after exclusion and bypass of popliteal artery aneurysms.

PURPOSE: The traditional measure of success after exclusion and bypass of popliteal artery aneurysm (PAA) is graft patency. In addition to fate of the bypass, we hypothesize that late outcome after surgical treatment of PAA is influenced by completeness of exclusion. METHODS: Thirty patients who underwent 41 reconstructions for PAA over a 10-year period were reviewed. RESULTS: Excluded PAAs were examined with duplex ultrasound scan for size, patency, and patent feeding branches; bypass grafts and native inflow and outflow arteries were examined for patency and size. Thirty-six limbs were available for follow-up (mean follow-up period, 46 +/- 42 months). Only two aneurysms (5.6%) appeared patent on duplex ultrasound scan, but five limbs had patent arterial branches communicating with thrombosed excluded PAAs. PAA diameter decreased from 2.5 +/- 0.8 cm to 1.7 +/- 0.5 cm (P <.0001) in most. However, 12 excluded PAAs (33%) showed significant enlargement from 2.2 +/- 0.9 cm to 2.8 +/- 1.0 cm (P =.002). A quarter of enlarging excluded PAA were associated with new compressive symptoms. Three methods of PAA exclusion were used: proximal and distal ligation with short segment isolation (type 1), proximal and distal ligation with long segment isolation (type 2), and single ligature (type 3). In univariate analysis, type of exclusion significantly influenced late size of excluded PAA (P =.004). Type 1 exclusion was superior to both type 2 and 3 exclusions in producing aneurysm diameter reduction. Type 3 exclusion resulted in aneurysm growth. In addition, excluded aneurysms with visualized feeding branches were associated with significant growth compared with PAAs without feeding branches (P =.006). Graft primary and assisted primary patency rates at 5 years were 86% +/- 9.4% and 92% +/- 7.4%, respectively. Although graft diameter and native donor artery diameter significantly increased, this did not adversely affect graft patency. CONCLUSION: Enlargement of excluded PAA after surgical treatment can cause compressive symptoms. Exclusion requires adequate vascular isolation to prevent late PAA enlargement, with proximal and distal arterial ligation best performed adjacent to the aneurysm. Vein graft enlargement occurs, but this enlargement does not adversely influence patency.

Aged↗
PubMed2003

Endothelial dysfunction after arterial thrombosis is ameliorated by L-arginine in combination with thrombolysis.

PURPOSE: To assess endothelial function after arterial thrombosis creation and after administration of a novel thrombolytic regimen in a new porcine model. MATERIALS AND METHODS: Untreated arteries that had undergone thrombosis for 90 minutes were compared to arteries treated with tissue plasminogen activator (tPA, 4 mg) and a combination of tPA and L-arginine (L-arg; 600 mmol/L). External iliac artery luminal diameter was measured with use of duplex ultrasonography. Endothelial-dependent relaxation (EDR) and endothelial-independent relaxation (EIR) were measured with use of acetylcholine chloride (ACh) and sodium nitroprusside (NTP), respectively. Endothelial integrity was confirmed by scanning electron microscopy (SEM). Nitric oxide (NO) levels were determined with use of a chemiluminescent assay of its nitrite/nitrate metabolites (NO(x)). RESULTS: After thrombosis, EDR was decreased (69% +/- 9.5; ACh = 15 micro g/min; n = 6). EDR remained unchanged after thrombolysis with tPA despite complete dissolution of thrombus (67% +/- 5.7; ACh = 15 micro g/min; n = 5). Thrombolysis with use of tPA coupled with L-arg resulted in an increase in EDR (95% +/- 4.9; ACh = 15 micro g/min; n = 5; P =.007). EIR was preserved in all groups, with uniform response to NTP. SEM analysis revealed intact endothelium in all groups. Local NO(x) levels were diminished after 90 minutes of thrombosis (49.3 micro mol/L vs 40.8 micro mol/L; P =.0002), but increased to 55.7 micro mol/L after thrombolysis with tPA and L-arg (P = NS). CONCLUSIONS: Thrombus induces arterial dysfunction acutely without altering endothelial integrity. This dysfunction is ameliorated through regional administration of L-arg in combination with standard thrombolytic therapy, which increases local NO levels. This model allows the in-vivo study of thrombosis and alternative thrombolytic regimens. Regional enhancement of NO levels may prove to be an attractive adjunct in thrombolytic therapy.

Animals↗