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J J Alexander

Publications and source records attributed to J J Alexander.

At least 37 records · Page 2Linked to original sources
PubMed1997

Production of the rat complement regulator, Crry, as an active soluble protein in Pichia pastoris.

In this report, we describe the use of the methylotrophic yeast Pichia pastoris for the production of the rat complement regulator, Crry. Crry normally exists as an intrinsic membrane protein containing six to seven short consensus repeats (SCRs), a transmembrane region, and a cytoplasmic tail. To produce Crry as a soluble recombinant protein, nucleotides encoding the five N-terminal SCRs from the rat Crry cDNA were amplified by PCR, and cloned into the P. pastoris expression vector, pPIC9. This vector contains the yeast alpha-factor signal sequence, thereby leading to secretion of recombinant protein. This construct was subsequently integrated into P. pastoris strain GS115 genomic DNA. Secreted soluble Crry was produced by induction of the AOX1 promoter with methanol. Recombinant Crry protein was purified to homogeneity by sequential Mono Q and Mono P chromatography. The protein was highly active toward the alternative and classical pathways of complement, inhibiting the latter by approximately 90% at a concentration of 15 nM. The P. pastoris system offers an efficient method for the production of soluble recombinant Crry. Production of active rat Crry offers opportunities to study long-term models of disease in rats, which has not been possible with available heterologous complement inhibitors.

Animals↗
PubMed1997

Transmembrane calcium flux regulates LDL oxidation by arterial smooth muscle cells.

Although clinical and experimental studies have supported a role of calcium in atherogenesis, the nature of this relationship has not been determined. The following investigation was performed to examine the effect of transmembrane calcium flux on the oxidative modification of low-density lipoprotein (LDL) by arterial smooth muscle cells (SMC). Confluent SMC were incubated in basal medium alone or in medium containing either nifedipine (0.25 microM), a calcium channel blocker, or dantrolene (10 microM), a blocker of calcium release from the endoplasmic reticulum. Cells were then suspended in medium with either physiologic (1.25 mM) or supraphysiologic (2.5 mM) calcium concentrations ([Ca2+]e) and were exposed to oxidized LDL (20 micrograms/protein/ml; 4.96 +/- 0.76 nmole malondialdehyde/mg LDL protein). Changes in cytosolic calcium ([Ca2+]i) were measured by spectrofluorometric analysis using a Fura 2-AM indicator. In similar studies, the cellular oxidation of native LDL was determined by fluorometric measurement of thiobarbituric acid-reactive substances in the media. Nifedipine and, to a lesser extent, dantrolene lowered steady-state [Ca2+]i at supraphysiologic [Ca2+]e (2.5 mM; P < 0.0002). Exposure of SMC to Ox-LDL increased [Ca2+]i (P < 10(7), which was further augmented by increasing [Ca2+]e (P < 10(-7). Nifedipine significantly reduced the calcium response to Ox-LDL proportionate to [Ca2+]e (P < 0.0002). A similar reduction in [Ca2+]i vs control was seen with dantrolene, but was independent of [Ca2+]e. TBARS assays revealed a significantly greater degree of cellular oxidation of native LDL following preincubation of SMC with Ox-LDL (P < 10(8). This effect was markedly inhibited by both nifedipine (P < 10(-8) and dantrolene (P < 10(-8), which showed some degree of synergism. These results indicate that the increase in cytosolic calcium in SMC exposed to Ox-LDL may occur through both membrane channels and reticular release. Inhibition of transmembrane calcium flux severely limits the cellular oxidation of low-density lipoprotein. These alternate means of calcium signal generation may allow a more varied response of the SMC to atherogenic stimuli and provide an opportunity for specific therapeutic intervention.

Arteriosclerosis↗
PubMed1997

Flexible sigmoidoscopy. A reliable determinant of colonic ischemia following ruptured abdominal aortic aneurysm.

BACKGROUND: The development of colonic ischemia following repair of ruptured abdominal aortic aneurysm (AAA) is associated with significant morbidity and timely diagnosis is essential. The purpose of this study was to determine the efficacy of endoscopy in the diagnosis of colonic ischemia and in prediction of need for resection. METHODS: Patients who underwent postoperative lower endoscopy after ruptured AAA from 1986 to 1995 were reviewed for endoscopic findings, clinical course, and patient outcome. RESULTS: A total of 80 patients had ruptured AAA during the study period, of which 56 survived for longer than 24 h postoperatively. Flexible lower endoscopy was done in 18 patients (32%) on an average of 4.4 days following AAA repair (range 1-16). Indications for initial endoscopy included early or bloody stools in 12 (67%), hemodynamic instability or sepsis in eight (44%), and acidosis in four (22%). The extent of the examination was sigmoid or descending colon in 13, cecum in four, and transverse colon in one. Endoscopic findings were normal in four patients. Five examinations showed only areas of hemorrhagic mucosa. Absence of full-thickness ischemia was confirmed by clinical course or autopsy in these nine patients. Two examinations demonstrated full-thickness necrosis which was confirmed at subsequent laparotomy. In six examinations, ischemia was noted but judged to be limited to mucosa only. Absence of full-thickness disease was demonstrated by laparotomy in three and subsequent course in three. Eight patients (57%) with initial abnormal examinations underwent repeat endoscopy showing improved interval appearance in seven cases and progression to full-thickness ischemia in one patient. CONCLUSIONS: Flexible sigmoidoscopy reliably predicts full-thickness colonic ischemia following repair of ruptured aortic aneurysms. Patients with non-confluent ischemia limited to the mucosa can be safely followed by serial endoscopic examinations.

Aged↗
PubMed1997

Characterization of C3 receptors on cultured rat glomerular endothelial cells.

In this study we characterized C3 receptors on cultured rat glomerular endothelial cells (GEnC), using immunochemical and molecular techniques. GEnC membrane proteins were immunoprecipitated with a polyclonal antibody directed towards mouse complement receptor 2 (CR2). This anti-MCR2 immunoprecipitated GEnC proteins of 120 and 150 kDa. By immunohistochemistry, anti-MCR2 stained GEnC in rat glomeruli in vivo. Given the presence of CR2-like proteins on GEnC, subsequent studies were done to determine whether GEnC had C3-binding proteins. GEnC proteins of 80, 200, and 300 kDa specifically bound to columns of rat C3d-Sepharose and C3b-Sepharose, illustrating that these proteins were binding to the C3d portion of C3. The 80, 200, and 300 kDa C3d-binding proteins were distinct from the 120 and 150 kDa anti-MCR2 reactive proteins, as shown by immunoabsorption studies. Next, a specific cDNA probe for rat CR2 was generated by RT-PCR. Oligonucleotides were chosen from highly conserved regions in mouse and human CR2 spanning 224 bases, with the rationale that these would also be conserved in the rat. A 224 bp PCR product was generated from both rat GEnC and rat kidney cDNA, illustrating the presence of CR2 mRNA in these tissues. By Northern analysis, the CR2 PCR product hybridized to mRNA of 2 and 5 kb from GEnC. The 5 kb transcript was also identified in rat kidney mRNA. Therefore, proteins immunologically related to mouse CR2 are present in GEnC in vitro and in vivo. C3d-binding proteins of 80, 200, and 300 kDa are also present on rat GEnC, yet these appear to be immunologically distinct from the proteins identified by anti-MCR2. Whether the GEnC CR2 mRNA transcripts of 2 and 5 kb are translated into the 80 and 200 kDa C3d-binding proteins or the 120 and 150 kDa mouse CR2-like proteins remains to be defined.

Animals↗
PubMed1996

Sex hormones affect the calcium signaling response of human arterial cells to LDL.

The present study was designed to examine the role of calcium-dependent signal transduction as a common link between the atherogenic effect of LDL and the mitigating influence of sex hormones in aortic endothelial (EC) and smooth muscle cells (SMC). Human aortic EC and SMC were pre-incubated for 48 hr in media containing no hormone, 17-beta-estradiol (20 ng/ml) or testosterone (300 ng/ml). Low density lipoprotein (N-LDL) or its minimally oxidized species (Ox-LDL) was added to the media at different concentrations (0, 2, 5, 10, 20, and 40 micrograms protein/ml), and changes in cytosolic calcium [Ca+2]i were measured by spectrofluorometric analysis using a Fura 2-AM indicator. Cell viability was determined with a 51chromium release assay. In EC, exposure to N-LDL resulted in a weak and unsustained increase in [Ca+2]i, (max. 21.9 +/- 4.6%) while a more marked rise was seen in SMC (max. 79.1 +/- 11.5%; P < 0.005). There was an amplified response to the more atherogenic Ox-LDL in both EC (max. 130.9 +/- 22.9%) and SMC (max. 240.5 +/- 14.2%; P < 0.0002). Estrogen was associated with a lower resting level of [Ca+2]i in both cell types, and resulted in a significant, dose-dependent inhibition of cytosolic calcium mobilization in SMC exposed to Ox-LDL (P < 0.05). Alternatively, testosterone increased cytosolic calcium response in SMC exposed to either N-LDL (P < 0.05) or Ox-LDL (P < 0.05). Similar trends were seen in EC, but failed to reach statistical significance. These changes could not be attributed to cell toxicity. Sex hormones may modulate the atherogenic potential of LDL by influencing intracellular, calcium-dependent signaling mechanisms.

Analysis of Variance↗
PubMed1996

Mature human atherosclerotic plaque contains peroxidized phosphatidylcholine as a major lipid peroxide.

The initial stage of atherosclerotic plaque formation involves oxidation of the phosphatidyl-choline moiety of low density lipoprotein (LDL) and subsequent uptake by macrophages. Ongoing uptake in developing plaque also may involve oxidized LDL and would require an oxidizing environment in plaque lipids. Atherosclerotic plaque lipids from 12 patients undergoing peripheral vascular procedures were extracted in chloroform: methanol (2:1). This extract was applied to a 25 cm 5 micron silica HPLC column and eluted with a ternary gradient mobile phase utilizing a laser light scattering (ELSD) mass detector. Individual lipid fractions were then analyzed. Cholesterol, both free and esterified, was the most prominent lipid in plaque (104 +/- 74 mg/gm tissue. However, lipid peroxides were present in much higher concentrations (3.52 +/- 2.84 FU X 10(4)/mg phospholipid) and overall level (21.27 +/- 10.10 FU X 10(4)/gm plaque) in the phospholipid component (*p< 0.05). Phosphatidyl-choline (PC) accounted for 63% of the total phospholipid peroxides recovered (6.31 +/- 5.09 mg/gm plaque; *p<0.05). PC and phosphatidylinositol (PI) content were linearly related to lipid peroxide fluorescence (PC; r=0.696; p=0.01) (PI; r=0.809; p=0.001). Lipid peroxides in human atherosclerotic plaque are present primarily in the phospholipid component and phosphatidyl-choline forms the bulk of these peroxides. PC may play an important role in ongoing plaque lipid accumulation.

Analysis of Variance↗
PubMed1996

The role of composite sequential bypass in the treatment of multilevel infrainguinal arterial occlusive disease.

BACKGROUND: In this study, the efficacy of composite sequential bypass is compared to that of standard in situ bypass, and to alternate prosthetic graft systems which have been used for the treatment of multilevel infrainguinal arterial occlusive disease in the absence of suitable autogenous vein. PATIENTS AND METHODS: A retrospective review of graft patency and limb salvage included 197 patients undergoing 211 bypass procedures consisting of in situ femoral-tibial (IS; n = 119); composite sequential (CS; n = 35), prosthetic femoropopliteal with single (PFP-1; n = 30) or no vessel runoff (PFP-O; n = 9), and prosthetic femoral-tibial (PFT; n = 18) bypass. RESULTS: By life-table analysis, IS bypass provided superior primary (P < 0.005) and secondary (P < 0.0005) patency over the other groups. CS bypass was similar to PFP-1, with a 2-two year primary patency of 35% and 44% (NS), respectively, and limb salvage rates of 60% and 80% (P = 0.01). PFP-O and PFT bypass procedures did considerably worse, with a 1-year patency of 19% and 22%, respectively, and associated limb salvage rates of 25% and 41% (NS). CONCLUSIONS: Composite sequential bypass is an acceptable procedure for infrainguinal arterial reconstruction when absence of autogenous vein prevents either in situ or secondary vein graft bypass procedures.

Arterial Occlusive Diseases↗
PubMed1996

Is deep vein thrombosis surveillance warranted in high-risk trauma patients?

BACKGROUND: Deep vein thrombosis (DVT) has been reported to occur in 20% to 40% of high-risk trauma patients if no prophylaxis is used. The purpose of this study was to determine the incidence of DVT and utility of a screening program in a high-risk group of trauma patients for whom routine DVT prophylaxis was utilized. PATIENTS AND METHODS: Of 3,154 trauma admissions over a 20-month period, 343 patients (10.9%) identified as high risk based on established criteria (prolonged bed rest, Glasgow coma score (GCS) of 7, spinal injury, lower extremity or pelvic fracture) were placed on a prospective surveillance protocol using color-flow duplex scanning and received thromboembolic prophylaxis. RESULTS: Twenty-three thromboembolic complications occurred, including 20 DVTs (5.8%) and 3 pulmonary emboli ([PE] 1%). Univariate analysis showed that the risk of DVT was related to age (52.6 + 19.9 years versus 38.1 + 18.5; P = 0.001), a longer hospital stay (31.4 versus 17.8 days; P = 0.001), or the presence of spinal fracture (12.6% versus 3.5%; P = 0.01). Discriminant function analysis revealed that length of stay, intensive care unit days, age, and GCS allowed correct classification of those who did not develop DVT in 97% of cases but was only correct in 15% of cases in predicting those who would develop DVT. Injury severity score (ISS) was not predictive in this multivariate analysis. Seventeen (85%) DVTs were unsuspected clinically. Study patients received an average of 3.5 studies at an overall charge of $313,330 to detect 17 clinically unsuspected DVTs (5%). This represents about 5% of the total bed charges for these patients, or $18,000 per DVT. CONCLUSIONS: These results suggest that standard use of DVT prophylaxis in a high-risk trauma population leads to a low incidence of DVT and that a screening protocol is effective in detecting unsuspected DVTs. Use of a surveillance protocol, however, may reduce but will not eliminate the incidence of pulmonary emboli in this patient population.

Adult↗
PubMed1996

Calcium-dependent second-messenger regulation of low-density lipoprotein oxidation by human aortic smooth muscle cells.

BACKGROUND: We postulated that the response of vascular smooth muscle cells (SMCs) to oxidized low-density lipoprotein (LDL) may be modulated through calcium and 3', 5' cyclic adenosine monophosphate (Ca+2-cAMP) second-messenger activity. METHODS: Changes in cytosolic calcium [Ca+2]i in aortic SMCs exposed to native (N-) and oxidized (Ox-) LDL were measured with a Fura 2-AM indicator. The influence of cAMP on this response was determined by incubating the cells with either forskolin or 8-bromo-cAMP (stimulatory) or galanin (inhibitory). The cells were then activated by an initial preincubation with N- or Ox-LDL, and the subsequent cellular oxidation of N-LDL was measured. The effect of cAMP mediators alone or in conjunction with calcium antagonism was studied. RESULTS: Exposure of SMCs to Ox-LDL resulted in a marked elevation of [Ca+2]i(306 +/- 12 nmol/L) compared with that in the control group (192 +/- 15 nmol/Liter; p < 10(-6)). This response was augmented by cAMP stimulation (406 +/- 8 nmol/L; p < 10(-6)) but reduced by cAMP inhibition (247 +/- 8 nmol/L; p < 10(-6)). The activation of intracellular signaling by initial Ox-LDL priming increased the subsequent oxidation of N-LDL (0.40 +/- 0.02 nmol malondialdehyde versus 0.24 +/- 0.02 nmol MDA control; p < 10(-4)). This response was enhanced by cAMP (0.45 +/- 0.03 nmol MDA; p < 10(-4)) and inhibited by galanin (0.26 +/- 0.02; p < 10(-4)). The cAMP effect was reversed by the blockade of calcium mobilization via membrane channels and reticular release. CONCLUSIONS: Oxidized LDL-induced Ca+2-cAMP signaling modulates the cellular oxidation of N-LDL. This finding suggests a mechanism through which the scavenger uptake of modified LDL may potentially be regulated.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1996

Colonic ischemia: the Achilles heel of ruptured aortic aneurysm repair.

Colonic ischemia is an often fatal complication of abdominal aortic aneurysm (AAA) repair. In elective AAA repair, patency of the inferior mesenteric artery (IMA) has been shown to be an important contributing factor. The purpose of this study was to determine which clinical and operative factors are important in the development of colonic ischemia in ruptured AAA repair. A retrospective review of all patients treated for ruptured AAA over a 7-year period was performed. Of 101 patients who were treated for ruptured AAA, 71 (70 per cent) survived for longer than 24 hours postoperatively, and these patients are the basis for this study. Colonic ischemia, primarily left sided, was a common perioperative complication (n = 24; 35 per cent) requiring colectomy in 11 patients (44 per cent). It carried a 44 per cent mortality compared to 20 per cent in patients without this complication (P = 0.07). Colonic ischemia occurred more frequently in patients with preoperative shock (P = 0.01) and a greater intraoperative blood loss (P = 0.003), but showed no correlation with patient age, co-morbid medical conditions, laboratory values, time to operation, or treatment of the IMA. Most patients with postoperative bowel ischemia were found to have chronic IMA occlusion, including 8 of the 11 patients requiring colectomy. Revascularization would not be feasible in this group. Revascularization of patent IMAs had little effect on outcome. Of the 17 patent IMAs, 9 were reimplanted and 5 (55 per cent) developed bowel ischemia, two of which required colectomy. Eight were ligated and 3 (38 per cent) developed bowel ischemia, one requiring colectomy. The presence of preoperative shock is the most important factor predicting the development of colonic ischemia following ruptured AAA. The incidence of ischemia is not altered by the presence of a patent IMA or with attempts at IMA revascularization. Colonic ischemia remains a significant source of morbidity and mortality in these patients.

Aged↗
PubMed1995

Hyperammonemia increases serotonin 1A receptor expression in both rat hippocampus and a transfected hippocampal cell line, HN2-5.

Hyperammonemia is an important cause of cerebral dysfunction in liver failure. We used two well-established models to induce hyperammonemia in rats, injection of urease and injection of methionine sulfoximine (MSO). Urease gave a 10-fold increase in blood ammonia while MSO, a glutamine synthetase inhibitor, gave a 4-fold increase in blood ammonia with no increase in brain glutamine levels. We observed a 2-fold increase in 5-HT1A receptor (5-HT1A-R) expression ([3H] 8-OH-DPAT binding) in hippocampus, and little change elsewhere, including thalamus in both models, thus eliminating a role for increased glutamine in the receptor induction. In contrast, a 4 to 8-fold increase in 5-HT1A-R mRNA was observed both in hippocampus and thalamus, suggesting some post-transcriptional regulation. In the absence of glutamine, ammonium acetate treatment of a hippocampal cell line which had been engineered to stably express the 5-HT1A-R (HN2-5) gave a 1.5-fold increase in [3H] 8-OH-DPAT binding and a 4-fold increase in the mRNA levels for the 5-HT1A-R. We conclude that the cell line HN2-5 is a good model for studying some of the biochemical sequelae of hyperammonemia and that changes in brain function are not only at the metabolic level, as thought earlier, but can also occur at the transcriptional level.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1995

Calcium regulation of endothelial permeability to low-density lipoprotein.

Increasing clinical and experimental evidence suggests a multifunctional role of calcium in determining the response of the arterial intima to atherogenic stimuli. In this study, an endothelial cell (EC)-smooth muscle cell (SMC) bilayer model of the arterial wall was used to investigate the effect of calcium manipulation on the sequestration of 125I-labeled LDL within the subendothelial space. Bilayer cell cultures were exposed to EGTA (0.25-2.0 mM), ionophore A23187 (5 x 10(-6) M), lanthanum chloride (0.1 mM), and trifluoperazine (TFP; 0.25 microM). The movement of 125I-labeled LDL (10 micrograms/ml) through the endothelial barrier was measured, as was the binding and cellular uptake of 125I-labeled LDL by each cell type. Extracellular Ca2+ chelation with EGTA and intracellular Ca2+ mobilization with A23187 both increased EC permeability to LDL (P < 0.05; P = 0.0001, respectively), while not significantly affecting EC binding or uptake of lipoprotein. Conversely, these agents increased SMC uptake of LDL (P < 10(-7); P < 10(-8), respectively). Calcium blockade with lanthanum chloride had the opposite effect, reducing EC permeability (P = 0.011) and SMC uptake (P < 10(-5)), while increasing EC uptake (P = 0.016). TFP, a calmodulin inhibitor, had an effect similar to A23187, although reducing SMC uptake of LDL (P = 0.015). Alteration of the calcium gradient across the plasma membrane appears to influence EC permeability. This effect may be stabilized by Ca2+ blockade or calmodulin regulation of cytoplasmic Ca2+. Additional anti-atherogenic effects of calcium blockade may include a reduction in SMC uptake by the SMC.

Animals↗
PubMed1995

Molecular characterization of rat Crry: widespread distribution of two alternative forms of Crry mRNA.

The rat complement regulator 5I2 antigen/Crry is present in a widespread distribution as at least two discrete proteins of Mr 65000-70000 and 75000-85000. The molecular basis for the different proteins has not been determined. We screened a cDNA library derived from cultured rat glomerular epithelial cells with a polymerase chain reaction (PCR)-generated nucleotide probe for CR1 and Crry. Two identical clones with 1.8 kilobase inserts were obtained. Clone 6.1 consisted of 1811 nucleotides. The sequence was identical to nucleotides 42-1666 of the cDNA for rat 5I2 antigen/Crry except for 11 nucleotides at the extreme 5' and 3' ends and an exact duplication of 186 bases that would encode an additional complete short consensus repeat (SCR). By reverse transcription PCR, we show that the two forms of Crry mRNA exist in all rat cells/tissues examined. It is likely that these two Crry mRNA species differ by the absence or presence of a 186 base repeat that encodes a complete SCR. These are translated into Crry proteins, containing six and seven SCRs, respectively, which explains the different sizes of Crry proteins. The role of the SCR duplication remains to be defined.

Alternative Splicing↗
PubMed1995

Infrainguinal bypass in patients with end-stage renal disease.

BACKGROUND: This study was undertaken to evaluate the outcome of infrainguinal arterial reconstruction in a high-risk subset of patients with end-stage renal disease. METHODS: We reviewed the medical records of 44 patients requiring maintenance dialysis and undergoing 57 infrainguinal bypass procedures for limb salvage from 1986 to 1992. These included 16 (28%) femoropopliteal and 41 (72%) tibial or pedal bypasses with autogenous (82%), prosthetic (12%), or composite (6%) graft materials. The principal indications for operation were ischemic ulceration or gangrene (79%) and rest pain (21%). Angiographic evaluation most frequently showed single-vessel runoff (56%). Risk factors included age (mean, 63 years), diabetes (75%), hypertension (93%), coronary artery disease (52%), smoking (39%), previous myocardial infarction (20%), and contralateral amputation (18%). Infection was present in 22 limbs (39%). RESULTS: Early (30-day) surgical morbidity rate was 39%, including wound breakdown (19%), graft thrombosis (9%), and major amputation (4%). Perioperative mortality rate was 9%. Cumulative primary graft patency rates were 71% and 63%, secondary patency rates were 80% and 66%, and limb salvage rates were 70% and 52% at 1 and 2 years, respectively. Limb loss correlated most highly with the presence of preoperative infection (p = 0.036; log-rank method). Patient survival rate was 52% at 2 years. CONCLUSIONS: Life-table analysis confirms a poor life expectancy for this population but indicates that an acceptable level of limb salvage may be achieved with arterial reconstruction in properly selected patients.

Adult↗
PubMed1995

Rupture of known abdominal aortic aneurysms: an ethical dilemma.

Elderly patients with abdominal aortic aneurysms (AAA) may be deemed inoperable due to the presence of comorbid conditions. Presentation of these patients with acute rupture can then result in difficult ethical decisions regarding surgical treatment. Over six years, 80 patients were treated emergently for ruptured AAA. Of these patients, 26 (32.5%) had known aneurysms. This study was performed to determine outcome and factors affecting mortality in patients with known AAAs. There were no significant differences between known and unknown AAA groups with regard to operative risk. In the overall group (n = 80), patient delay in seeking treatment averaged 20.4 hours with a trend towards shorter times in those with known AAAs (13.8 hours) compared with the unknown group (23.6 hours; p = 0.09). Medical transport delay, however, was significantly shorter for patients with known AAA (124 minutes versus 230 minutes; p = 0.04). Overall mortality was 56 per cent (n = 45). Those patients with known AAAs had a higher mortality (69%; n = 18) than those with unknown AAAs (50%, n = 27) but this was not statistically significant (P = 0.10). In patients with known AAAs, operative death was related to patient delay, with an average delay in seeking medical advice of 21.3 hours in nonsurvivors compared with 8.6 hours in survivors (P = 0.04). No other risk or demographic factors correlated with mortality. Despite a known AAA, significant delay in seeking medical advice occurred, and this delay resulted in decreased survival. Patient education is imperative if nonoperative treatment is chosen.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1994

Atherosclerotic aneurysm formation in an in situ saphenous vein graft.

Nonanastomotic aneurysm formation in autogenous vein grafts, although rarely described, has been uniformly associated with advanced atherosclerotic change of the vein wall. In the case reported, histologic examination of an in situ vein graft aneurysm demonstrates obliteration of normal vessel wall architecture by penetrating atherosclerotic plaque. Although these findings do not prove a causal relationship, they do provide additional support for atherosclerosis as an etiologic factor in aneurysm disease.

Aged↗
PubMed1994

Is the increasing use of prophylactic percutaneous IVC filters justified?

To determine whether the ease of percutaneous inferior vena cava (IVC) filter placement has led to an alteration of procedural indications, we reviewed the medical records of 150 patients who underwent 156 filter insertions from January 1986 through June 1993. Thirty-nine Greenfield filters were surgically inserted, while 117 percutaneous devices were placed in 111 patients. A comparison of these two groups showed that they had similar thromboembolic risks. Indications for surgical filter placement included pulmonary embolism (PE) prophylaxis (23%), PE with a contraindication to anticoagulation therapy (28%), and complication (26%) or failure (20%) of anticoagulation therapy. Indications for initial percutaneous placement included PE prophylaxis (56%), PE with a contraindication to anticoagulation therapy (27%), and complication (7%) or failure (9%) of anticoagulation therapy. Early mortality in the surgical and percutaneous groups was 26% and 27%, respectively. Ten percent of early deaths in the surgical group and 50% in the percutaneous group were associated with prophylactic insertions (P = 0.032). Associated morbidity was 8% in the surgical versus 24% in the percutaneous group (P = 0.036). The unrestricted use of prophylactic percutaneous IVC filters appears to have resulted in an increased procedure-related morbidity with no clear benefit in early patient survival. These findings suggest a need for improved patient selection.

Adolescent↗