Mycotic aneurysm of the superior mesenteric artery: a delayed complication from a neglected septic embolus-a case report.

Mycotic aneurysm formation in a visceral artery carries a significant risk of mortality and morbidity. The authors present a case of a symptomatic superior mesenteric artery aneurysm secondary to a septic embolus in a patient who had undergone aortic valve replacement. The patient initially presented with evidence of acute intestinal ischemia from a presumed embolic source. Although an extensive bowel resection was performed, an adequate search for the embolus was not carried out. Prompt diagnosis and removal of suspected septic emboli must be performed to avoid the formation of delayed mycotic aneurysms.

Matrix metalloproteinase-specific inhibition of Ca2+ entry mechanisms of vascular contraction.

OBJECTIVE: Abdominal aortic aneurysm (AAA) is a common disease with as yet unclear cause. Increased matrix metalloproteinase (MMP) levels in the plasma and aorta are a consistent finding in AAA. Although the role of MMPs in AAA has largely been attributed to degradation of the extracellular matrix proteins, the effects of MMPs on the mechanisms of aortic contraction are unclear. The purpose of this study was to test the hypothesis that MMPs promote aortic dilation by inhibiting the Ca2+ mobilization mechanisms of smooth muscle contraction. METHODS: Isometric contraction and 45Ca2+ influx were measured in aortic strips isolated from male Sprague-Dawley rats treated or not treated with MMP-2 and MMP-9. RESULTS: In normal Krebs solution (2.5 mmol/L Ca2+ ) phenylephrine (10-5 mol/L) caused contraction of the aortic strips, which was significantly inhibited (P < .05) by MMP-2 (maximum, 48.9% +/- 5.0%) and to a greater extent by MMP-9 (maximum, 69.8% +/- 6.2%). The MMP-induced inhibition of phenylephrine contraction depended on concentration and time. The inhibitory effects of MMPs on phenylephrine contraction were reversible. In Ca2+ -free (2 mmol/L ethylene glycol bis[beta-aminoethyl ether]-N,N,N',N'-tetraacetic acid) Krebs solution phenylephrine caused a small contraction that was not inhibited by MMP-2 or MMP-9, which suggests that MMPs do not inhibit Ca2+ release from the intracellular stores. Membrane depolarization with 96 mmol/L of potassium chloride, which stimulates Ca2+ entry from the extracellular space, caused a time-dependent and reversible contraction, which was inhibited by MMP-2 and MMP-9. Histologic studies of MMP-treated tissues stained with hematoxylin-eosin or Verhoeff stain for elastin confirmed the absence of degradation of the extracellular matrix. MMP-2 and MMP-9 also caused significant inhibition of 45Ca2+ influx induced by phenylephrine and potassium chloride. CONCLUSIONS: These data suggest that MMP-2 and MMP-9 promote aortic dilation by inhibiting the Ca2+ entry mechanism of vascular smooth muscle contraction. CLINICAL RELEVANCE: Abdominal aortic aneurysm (AAA) is a slow and progressive disease. The late stages of AAA are characterized by degenerative changes in the extracellular matrix and smooth muscle components of the aortic wall. The present study describes novel inhibitory effects of matrix metalloproteinase (MMP) on the Ca2+ entry mechanisms of aortic smooth muscle contraction, even in the absence of extracellular matrix degradation. The MMP-induced inhibition of aortic contraction may further explain the role of increased MMP activity particularly during the early development of AAA. Chronic exposure to MMPs may lead to protracted inhibition of aortic contraction, progressive aortic dilation, and aneurysm formation. MMP-9 is a more potent inhibitor of aortic contraction than MMP-2, consistent with a more dominant role in AAA. Restoration and preservation of smooth muscle contractile function by specific inhibitors of MMPs may represent a new strategy in preventing the progression of small AAA.

Thoracovisceral segment aneurysm repair after previous infrarenal abdominal aortic aneurysm surgery.

OBJECTIVE: Repair of thoracovisceral aortic aneurysms (TVAA) after previous open repair of an infrarenal abdominal aortic aneurysm (AAA) poses significant challenges. We sought to better characterize such recurrent aneurysms and to evaluate their operative outcome. METHODS: We reviewed the records and radiographs of 49 patients who underwent repair of TVAAs between 1988 and 2002 after previous repair of an AAA. Visceral artery reconstructions were completed with combinations of beveled anastomoses, inclusion patches, and side arm grafts. In 14 patients visceral endarterectomy was required to treat associated occlusive disease. Sixteen patients had cerebrospinal fluid drainage, and 10 patients had distal perfusion during cross-clamping. RESULTS: Patient mean age was 72 years, and 80% were men. Fifty-one percent of patients had symptomatic disease, and average TVAA diameter was 6.2 cm. Mean time between AAA and TVAA repair was 77 months. Twenty-six percent of aneurysms were restricted to the lower visceral aortic segment, 35% extended to the diaphragm, another 35% extended to the distal or middle thoracic aorta, and 4% involved the entire remaining visceral and thoracic aorta. The 30-day operative mortality rate was 4.1% in patients with nonruptured aneurysms and 50% in patients with ruptured aneurysms, for an overall mortality rate of 8.2%. Fifteen patients (30.6%) had major morbidity, including paresis in two patients and dialysis-dependent renal failure in five patients. At late follow-up, three patients required further aortic operations to treat additional aneurysms, and four patients had fatal aortic ruptures. Two-year and 5-year cumulative survival rates were 61% (+/-7.5%) and 37% (+/-7.8%), respectively. At univariate analysis, operative blood loss was the sole significant predictor of major morbidity (P <.023), and rupture (P <.030, P <.0001) and aneurysm extent (P <.0007, P <.0001) correlated with both operative death and long-term survival. Only aneurysm extent (P <.010, relative risk 37.3) remained a significant predictor of long-term survival at multivariate analysis. CONCLUSION: Elective repair of TVAAs after previous AAA repair can be performed with an acceptable level of operative mortality, though with considerable operative morbidity. Limited long-term survival mandates careful patient selection, and the high mortality associated with ruptured TVAA underscores the need for post-AAA surveillance.

Elastase promotes aortic dilation by inhibiting Ca2+ influx into vascular smooth muscle.

Abdominal aortic aneurysm (AAA) is a common vascular disease with, as of yet, unclear mechanism. Increased elastase activity and elastin degradation in the aorta are consistent findings in human AAA. Also, elastase perfusion of the aorta promotes aortic dilation in animal models of AAA. Although elastase-induced degradation of extracellular matrix proteins and the ensuing inflammation of the aortic wall have been implicated as possible causes of the aortic dilation in AAA, little is known regarding the effects of elastase on the mechanisms of aortic smooth muscle contraction. The purpose of this study was to test the hypothesis that elastase promotes aortic dilation by inhibiting the Ca2+ mobilization mechanisms of smooth muscle contraction. Isometric contraction and 45Ca2+ influx were measured in aortic strips isolated from male Sprague-Dawley rats non-treated or treated with elastase. Initial experiments suggested that elastase alone caused matrix degradation. To avoid potential degradation of the extracellular matrix proteins by elastase, the same experiments were repeated in the presence of saturating concentrations of elastin (10 mg/ml). In normal Krebs (2.5 mM Ca2+), phenylephrine (Phe, 10(-5) M) caused contraction of the aortic strips that was significantly inhibited by elastase. The elastase-induced inhibition of Phe contraction was concentration- and time-dependent. At 5 U/ml elastase, the inhibition of Phe contraction was rapid in onset (2.4 +/- 0.3 minutes) and complete in 32 +/- 4 minutes. The inhibitory effects of elastase on Phe contraction were partially reversible. In Ca2+-free (2 mM EGTA) Krebs, Phe caused a small contraction that was not inhibited by elastase, suggesting that elastase does not inhibit Ca2+ release from the intracellular stores. Membrane depolarization by 96 mM KCl, which stimulates Ca2+ entry from the extracellular space, caused a contraction that was inhibited by elastase in a time-dependent and reversible fashion. The reversible inhibitory effects of elastase, particularly in the presence of saturating concentrations of elastin, suggest that they are not due to dissolution of the extracellular matrix or permanent damage to the smooth muscle contractile proteins. Elastase also caused significant inhibition of Phe- and KCl-induced 45Ca2+ influx. These data suggest that elastase promotes aortic relaxation by inhibiting the Ca2+ entry mechanism of vascular smooth muscle contraction, and thus further explain the role of increased elastase activity during the early development of AAA.

The role of a putative microfibrillar protein (80 kDa) in abdominal aortic aneurysm disease.

BACKGROUND: We previously have reported the partial amino acid sequence of a putative aortic autoantigen in patients with abdominal aortic aneurysm (AAA) disease that has homologies with an elastin-associated microfibrillar protein found in aorta of pigs. This study was conducted to further define the role that microfibrillar proteins may play as autoantigens in AAA disease. MATERIALS AND METHODS: An extraction procedure was performed on AAA tissue using high concentrations of guanidinium hydrochloride (GuHCl) under reducing conditions. The microfibrillar extract was then probed with immunoglobulin (Ig) G isolated with Protein A from phosphate-buffered saline (PBS) extracts of 10 AAA specimens and 6 atherosclerotic, nonaneurysmal aortas. Immunoblotting was also performed with serum IgG from 9 AAA patients and 9 normal control patients. Immunohistochemistry using goat anti-human IgG (Fc-specific) on AAA tissue and AAA wall IgG on normal aorta were also performed. RESULTS: Eight of 10 AAA wall IgG reacted with an 80-kDa protein from the aortic microfibrillar extract, compared to 0 out of 6 atherosclerotic wall IgG (P = 0.0035, Fischer's Exact Test). Staining of the 80-kDa band appeared to increase with progressive additions of GuHCl, up to extract SKGCGC. Immunoblotting using serum IgG from 9 AAA patients and 9 normal control patients on the aneurysm microfibrillar extracts revealed no reactive bands. Immunohistochemistry using IgG from AAA wall showed the localization of the antibodies to the adventitial connective tissue matrix, mainly collagen fibers. CONCLUSIONS: These observations suggest that a collagen-associated protein, extractable by a microfibrillar extraction procedure from aortic aneurysm tissue, may be among the targets of an autoimmune response in AAA disease.

Elastase-induced suppression of endothelin-mediated Ca2+ entry mechanisms of vascular contraction.

Abdominal aortic aneurysm (AAA) is associated with increased endothelin (ET-1), both systemically and locally in the aorta. Also, elastase activity is increased in human AAA, and elastase perfusion of the aorta induces aneurysm formation in animal models of AAA. However, whether elastase directly affects the ET-1-induced mechanisms of aortic smooth muscle contraction is unclear. Isometric contraction and 45Ca2+ influx were measured in aortic strips isolated from male Sprague-Dawley rats and treated with elastase (5 U/mL). To avoid degradation of the extracellular matrix proteins by elastase, experiments were performed in the presence of elastin (10 mg/mL). In normal Krebs solution (2.5 mmol/L Ca2+), ET-1 (10(-7) mol/L) caused contraction of aortic strips that was inhibited by elastase (5 U/mL). The elastase-induced inhibition of ET-1 contraction was slow in onset (4.6+/-0.4 minutes), time-dependent, complete in 34+/-3 minutes, and reversible. In Ca2+-free Krebs solution, caffeine (25 mmol/L) caused a small contraction that was not inhibited by elastase, suggesting that elastase does not inhibit Ca2+ release from the intracellular stores. Membrane depolarization by 96 mmol/L KCl, which stimulates Ca2+ entry from the extracellular space, caused a contraction that was inhibited by elastase in a concentration-dependent, time-dependent, and reversible fashion. The reversible inhibitory effects of elastase, particularly in the presence of elastin, suggest that they are not due to dissolution of the extracellular matrix or smooth muscle contractile proteins. Elastase also inhibited ET-1 and KCl-induced 45Ca2+ influx. Thus, elastase directly inhibits ET-1-induced Ca2+ entry mechanisms of vascular smooth muscle contraction, which may explain the role of elastase and ET-1 during the development of AAA.

Splenic rupture from metastatic granulosa cell tumor 29 years after curative resection: case report and review of the literature.

Granulosa cell tumors account for 2 to 3 per cent of all ovarian neoplasms. This case report describes a patient with splenic rupture from a bulky metastatic deposit 29 years after her initial surgery. A review of the literature regarding the patterns and timing of recurrence is also discussed.

Outcome in patients at high risk after open surgical repair of abdominal aortic aneurysm.

OBJECTIVE: Outcomes after surgical repair of abdominal aortic aneurysm (AAA) in patients at high risk remain poorly defined. We investigated the short-term and long-term results of open repair of infrarenal AAA in a high-risk and comparison low-risk patient population. METHODS: Conventional open surgical repair of nonruptured infrarenal AAA was performed in 572 consecutive patients from 1990 to 2000. Patients were considered at high risk if they had one or more of the following criteria: age 80 years or more, creatinine level 3.0 mg/dL or higher, severe pulmonary insufficiency, severe cardiac dysfunction, or hepatic failure. A retrospective review was carried out to determine relative risks, perioperative morbidity and mortality, and long-term survival. A P value of less than.05 was considered statistically significant. RESULTS: One hundred twenty-eight of the study patients (22%) were at high risk and 444 were at low risk. Patients at high risk were older (77 versus 69 years; P <.001), were more likely female (26% versus 16%; P <.009), and had larger (mean, 5.9 versus 5.6 cm; P <.024), more symptomatic (20% versus 13%; P <.001) aneurysms. The 30-day operative mortality rate for the high-risk group was 4.7%, compared with 0.0% (P <.001) in the low-risk group. Overall and major morbidity rates were 29% and 14% in the high-risk cohort versus 17% (P <.003) and 5% in the low-risk cohort, respectively. The 5-year survival rate was 46% (standard deviation, 5.2%) in the high-risk group versus 74% (standard deviation, 2.6%) in the low-risk group (P <.001). On multivariate analysis, age 80 years or more (P <.046), creatinine level 3.0 mg/dL or higher (P <.022), prior stroke (P <.012), and pulmonary dysfunction were significant predictors of poor operative outcome (30-day mortality and major morbidity), and female gender (P <.035), cardiac dysfunction (P <.004), creatinine level 3.0 mg/dL or higher (P <.0001), prior stroke (P <.005), and pulmonary dysfunction (P <.0001) negatively impacted long-term survival rates. CONCLUSION: This study shows that open repair of infrarenal AAA in patients at high risk can be performed with relative safety and with results that offer a benchmark with which endovascular repair can be compared. Poor long-term survival in this population, however, highlights the importance of patient selection and raises the question of whether repair of many patients at high risk is warranted.

Bypass in the absence of ipsilateral greater saphenous vein: safety and superiority of the contralateral greater saphenous vein.

PURPOSE: The purposes of this study were to evaluate the long-term results of different autogenous conduits used for infrainguinal bypass when ipsilateral greater saphenous vein (IGSV) is absent or inadequate and to determine the impact on the contralateral lower extremity. METHODS: The study was performed as a retrospective evaluation of a prospective vascular registry together with review of patient records and telephone follow-up. RESULTS: From January 1990 to June 2000, 226 autogenous infrainguinal reconstructions were performed in 203 patients without adequate IGSV. The patients consisted of 128 men and 98 women, with a mean age of 69 years. Prevalent risk factors included diabetes (51%) and prior coronary bypass (46%). Limb salvage was the predominant indication (93%), and 59% of the procedures were secondary reconstructions. All bypasses were completed with autogenous vein, which included contralateral greater saphenous vein (CGSV; 31%), single-segment lesser saphenous vein (5%), single-segment arm vein (19%), and autogenous composite vein (45%). Bypasses were performed to the tibial and pedal arteries in 84% of the cases. The 30-day mortality and graft occlusion rates were 1% and 9%, respectively. The overall postoperative morbidity rate was 24%, with a 7% rate of major complications. Follow-up was complete in 95% of patients over a mean period of 24 months (range, 0.1 to 106 months). The 5-year primary patency rates were significantly better for CGSV compared with autogenous composite vein grafts (61% +/- 7% versus 39% +/- 6%; P <.009). The 5-year secondary patency (60% to 73%) and limb salvage (78% to 81%) rates did not differ significantly between the three groups. Follow-up of the contralateral lower limb revealed that nine of 226 limbs (4%) were amputated at a mean of 36 months after the ipsilateral bypass. The overall 5-year contralateral limb preservation rate was 90% +/- 3%. Contralateral vein harvest and the presence of diabetes did not affect the need for bypass or amputation of the contralateral limb. CONCLUSION: For most patients with inadequate IGSV, the CGSV is the alternative conduit of choice because of its length, superior performance, ease of harvest, and minimal risk to the donor limb.

Initial experience with minimally invasive in situ bypass procedure with blind valvulotomy.

OBJECTIVE: The in situ vein (ISV) bypass is uniquely suited to technical modifications designed to reduce the wound morbidity of infrainguinal revascularization. A technique of "blind" valvulotomy and selective vein branch ligation was used, and a preliminary study was performed to assess safety and efficacy. METHODS: From November 1998 to July 2001, all patients for infrainguinal bypass procedures underwent evaluation for inclusion in the study. Thirty-five patients underwent ISV bypass procedures with an expandable, self-centering valvulotome (ESV). Intraoperative selection of veins suitable for the study was assisted with venography and duplex scanning. The ISV bypass procedures were performed with initial groin and distal incisions, with smaller incisions to ligate significant arteriovenous fistulae (AVF). Duplex graft scanning was performed at routine intervals after surgery. RESULTS: Thirty-seven ISV grafts were performed from the common femoral artery to the popliteal (n = 14), tibial (n = 20), and dorsalis pedis (n = 3) arteries. In 35 cases (95%), a full-length incision was avoided. With ESV, all valves in 34 cases (92%) were effectively lysed. Proximal extension of the distal incision was performed in four cases (10.8%). The mean number of incisions per case was 3.1 +/- 1.7. One graft failed within 30 days (2.7%), with successful revision. During the early follow-up period (9.9 +/- 7.3 months; range, 1 to 33 months), 44% of residual AVF closed spontaneously (15 of 34 AVF; 16 patients) and two anastomotic stenoses and two symptomatic AVF were corrected surgically. Four late graft occlusions occurred, with a 1-year cumulative primary patency rate of 77% and a secondary patency rate of 92%. CONCLUSION: Blind valvulotomy with ESV facilitates safe and effective minimally invasive ISV bypass. Resultant graft patency rates appear comparable with results with open techniques. This preliminary experience warrants further study to refine patient selection criteria and operative technique and to better clarify the natural history of residual AVF.