Femoral artery infections associated with percutaneous arterial closure devices.

Hemostasis obtained by manual compression after femoral artery catheterization results in consistently low rates of major complications. A rare complication of femoral artery catheterization is arterial infection. Its occurrence after diagnostic angiography using manual compression has not been reported. We report two cases of femoral arterial infection after uneventful diagnostic catheterization in nonimmunocompromised patients using the Perclose percutaneous arterial closure device. Our cases are representative of Perclose associated infections, with delayed presentation of a staphylococcal arterial infection requiring arterial debridement and reconstruction. This article indicates that Perclose use carries a risk of severe arterial infection. Surgeons should be aware of the potential infectious complications associated with Perclose use and the need for aggressive treatment.

Ultrasound-guided thrombin injection is a safe and durable treatment for femoral pseudoaneurysms.

Ultrasound-guided percutaneous thrombin injection has recently been described as a treatment for postcatheterization femoral pseudoaneurysms. Although ultrasound guided compression offers another nonoperative treatment option, thrombin injection has shown superior initial success rates. Reports of follow-up for thrombin injection longer than 30 days are currently lacking. The authors reviewed their initial experience with thrombin injection and prospectively evaluated patients for occult late recurrences of pseudoaneurysm and for distal circulatory complications. Records and vascular laboratory data for all patients treated with ultrasound-guided thrombin injection were reviewed for an 18-month period. Tibial vessel Doppler waveforms and ankle/brachial indices were routinely obtained before and after thrombin injection. Follow-up duplex examinations were performed within 24 hours of initial treatment. In the prospective portion of the study, successfully treated patients underwent a repeat femoral duplex scan and lower extremity arterial examination for comparison with the pretreatment studies. Forty-nine of 52 femoral pseudoaneurysms (94%) were successfully treated with ultrasound guided thrombin injection. One immediate failure and 2 early recurrences were treated surgically. There was 1 thrombotic complication of the native circulation identified at the time of injection. Follow-up studies were obtained in 32 of 46 available patients with a mean length of follow-up of 9 months (range 3-17 months). No late recurrences of the pseudoaneurysms or arterial-venous fistulas were observed. No distal circulatory complications were detected by arterial waveform analysis. Three deaths occurred in the interim (cardiac related). Two patients were lost to follow-up. The remaining 12 patients reported no additional limb complications but declined to be restudied. Ultrasound-guided thrombin injection is a safe, effective, and durable treatment for iatrogenic pseudoaneurysms. Thrombin injection should be the therapy of choice for catheter-related femoral false aneurysms.

Elastase is not sufficient to induce experimental abdominal aortic aneurysms.

PURPOSE: Research investigating abdominal aortic aneurysms (AAAs) commonly uses a rat model dependent on aortic infusion of porcine pancreatic elastase to initiate AAA formation. Unfortunately, the sizes of AAAs generated by this model have varied widely among published studies. This may reflect lot-to-lot variations in commercial elastase preparations. This study was undertaken to investigate the ability of different lots of elastase to induce AAAs and explain the variability identified. METHODS: Four lots of elastase were evaluated in the standard rat AAA model. Saline solution was used as a control. Additional groups of rats were treated with higher concentrations of elastase with or without the macrophage activator thioglycollate medium. Aortic diameters were measured in all rats. Inflammation and elastin degradation was examined histologically. Elastase activity and purity were evaluated for all lots. RESULTS: Of the four lots tested, only one was able to consistently generate AAAs at the standard dose (P <.05). Increasing the amount of elastase infused produced AAAs in some ineffective lots. Infusion of thioglycollate medium in combination with otherwise ineffective elastase produced AAAs (P =.02). However, the elastase with the highest purity failed to generate AAAs, even at the highest dose tested or in combination with thyioglycollate medium. Thioglycollate medium alone failed to result in AAA formation. All elastase lots displayed elastolytic activity in vitro and produced elastin degradation in vivo. Elastin degradation did not correlate with AAA size in elastase-treated rats (P = NS). Aneurysm size correlated with extent of inflammation (P =.005). CONCLUSION: Induction of AAAs does not correlate with elastolytic activity. Infusion of pure elastase alone is not sufficient to induce AAA formation in spite of evidence of elastin degradation. Presumed inflammatory modifiers, which contaminate some elastase preparations, enhance AAA formation. Future use of this rat model will need to take the variability of elastase preparations into account with controls for each new elastase lot.

Inhibition of inducible nitric oxide synthase limits nitric oxide production and experimental aneurysm expansion.

PURPOSE: Nitric oxide (NO), frequently cited for its protective role, can also generate toxic metabolites known to degrade elastin. Both abdominal aortic aneurysms (AAAs) and inducible nitric oxide synthase (iNOS) are associated with inflammatory states, yet the relationship between NO production by iNOS and AAA development is unknown. The current study examines iNOS expression, NO production, and the effects of selective inhibition of iNOS by aminoguanidine in experimental AAA. METHODS: An intra-aortic elastase infusion model was used. Control rats received intra-aortic saline infusion and postoperative intraperitoneal saline injections (Group 1). In the remaining groups, intra-aortic elastase infusion was used to induce aneurysm formation. These rats were treated with intraperitoneal injections of saline postoperatively (Group 2), aminoguanidine postoperatively (Group 3), or aminoguanidine preoperatively and postoperatively (Group 4). Aortic diameter and plasma nitrite/nitrate levels were measured on the day of surgery and postoperative day 7. Aortas were harvested for biochemical and histologic analysis on postoperative day 7. RESULTS: Infusion of elastase produced AAAs (P <.001) with significant production of iNOS (P <.05) and nitrite/nitrate (P <.003) compared with controls. Selective inhibition of iNOS with aminoguanidine in elastase-infused aortas significantly reduced aneurysm size (P <.01) compared with elastase infusion alone. Aminoguanidine-treated rats displayed suppression of iNOS expression and plasma nitrite/nitrate production not significantly different from the control group. Histologic evaluation revealed equivalent inflammatory infiltrates in elastase-infused groups. CONCLUSION: Expression of iNOS is induced and plasma nitrite/nitrate levels are increased in experimental AAA. Inhibition of iNOS limits NO production and iNOS expression, resulting in smaller aneurysm size. NO production by iNOS plays an important role with detrimental effects during experimental aneurysm development.

Carotid endarterectomy: the financial impact of practice changes.

PURPOSE: New techniques in the management of extracranial carotid occlusive disease have focused attention on the outcome and economics of carotid endarterectomy (CEA). Changing practice patterns for CEA must be assessed to allow accurate comparisons. The purpose of this study was to evaluate the effect of practice modifications related to CEA on patient outcome and cost data. METHODS: Data on patients undergoing CEAs at a single institution from fiscal year 1992 to 1998 were prospectively collected and entered into a computerized database. Records were reviewed for patient demographics and outcome with regard to stroke and death. Selected years that corresponded to transitions in perioperative management were audited for complete hospital financial information from. RESULTS: We performed 960 CEAs during the study period, with a combined stroke and death rate of 1.1%. Inflation-adjusted hospital costs per patient in 1998 dollars for the years 1992, 1996, and 1998 were $5494, $4476, and $3350, respectively. In 1998, costs for patients who required arteriography were $1825 greater than those operated on during duplex scan examination alone in 1998. Statistically significant differences occurred in the year-to-year comparisons in the use of arteriography, intensive care unit monitoring, same day admissions, and length of stay. There were no statistically significant differences in the stroke and death rate between years. CONCLUSION: Practice changes related to CEA have resulted in significant savings without detriment in patient outcome. Comparisons between CEA and endovascular techniques will need to be evaluated within this context. Given these advances in perioperative management, it will be difficult to justify carotid stenting on the basis of current economic considerations.

Use of limited color-flow duplex for a carotid screening project.

BACKGROUND: Although the efficacy of carotid endarterectomy for asymptomatic carotid stenosis has been established, no cost-effective approach for identification of these patients has yet been devised. The purpose of this study was to develop a limited carotid duplex screening examination to be utilized for the detection of asymptomatic carotid stenoses. METHODS: Carotid screening examinations employed rapid identification of the carotid bifurcation using color-flow duplex imaging and an immediate Doppler-derived velocity of the segment of the internal carotid artery with the most turbulent flow. Complete examinations were then finished using well-established protocols in our accredited vascular laboratory. A total of 512 patients were referred for complete studies based upon standard indications. Criteria for at least a 50% internal carotid artery stenosis on the complete examination was defined as a peak systolic velocity (PSV) of at least 125 cm/sec. Receiver operator characteristic (ROC) curves were then constructed to identify the optimal screening velocity criteria as compared with the final results on the complete examination. RESULTS: Five screening examinations were technically limited yielding a total of 507 patients with 1,014 carotid arteries available for analysis. Comparison of screening examinations versus complete examinations for a PSV of 125 cm/sec yielded sensitivity 86%, specificity 98%, positive predictive value (PPV) 95%, and a negative predictive value (NPV) 93%. ROC analysis identified a "cut point" of 115 cm/sec on the screening examinations to achieve sensitivity 91%, specificity 95%, PPV 89%, and NPV 96%. Time to perform screening examinations averaged 3.2 minutes per patient. Three patients had common carotid lesions not identified on the limited internal carotid screening examinations. CONCLUSIONS: Screening carotid examinations are a rapid, reliable, and relatively inexpensive method for detection of patients with asymptomatic internal carotid artery stenosis. Limited screening examinations should be developed in each vascular laboratory and utilized in high-risk patients.

The matrix metalloproteinase inhibitor BB-94 limits expansion of experimental abdominal aortic aneurysms.

PURPOSE: Matrix metalloproteinases (MMPs) are proteolytic enzymes that can degrade the extracellular matrix of the aortic wall and lead to the formation of abdominal aortic aneurysms (AAAs). MMP inhibitors are a class of drugs that were developed to inhibit the activity of these proteolytic enzymes and are currently being studied as a way to control inflammatory diseases and cancer metastases. In this project, BB-94 (also known as batimastat), a specific inhibitor of MMPs, was evaluated for its ability to control aneurysmal growth in an experimental AAA model. METHODS: Experimental AAAs were created in a standard rat model by perfusing elastase into an isolated segment of aorta. The rats then were randomized to postoperatively undergo treatment daily with the MMP inhibitor BB-94 or the carrier control solution. Measurements of the aortic diameter were made at the time of initial surgery and at the time of death on postoperative day 7. Aortic tissue was obtained for histologic examination, elastin evaluation, and MAC 1-alpha antibody staining to evaluate the inflammatory response. RESULTS: The rats that underwent treatment with BB-94 had significantly less aneurysmal dilatation and a 113% increase in aortic size, as compared with the control rats that had a 157% increase (P =.026). Histologic examination of the harvested aortas and grading of the elastin content showed a significantly greater elastin preservation in those rats that were treated with BB-94 as compared with the control rats (P =.036). MAC 1-alpha antibody staining showed an attenuation of the inflammatory response in the group of rats that underwent treatment with BB-94. Morphologic examination also revealed that the control of the inflammatory response correlated with the areas of elastin preservation. CONCLUSION: MMP inhibition with BB-94 limited the expansion of AAAs in this rat model. BB-94 appears to work not only as a direct pharmacologic inhibitor of MMPs but also as an interference with the inflammatory response seen in AAAs. Control of the inflammatory response was an unexpected result and may be related to the alterations in feedback mechanisms that are related to extracellular matrix degradation. Because this class of drugs is presently being developed to control the MMP inflammatory response seen with arthritis, these drugs also may ultimately serve as a pharmacologic treatment for patients with AAAs.

Dobutamine stress echocardiography prior to aortic surgery: long-term cardiac outcome.

This study was undertaken to evaluate the efficacy of dobutamine stress echocardiography (DSE) in predicting not only perioperative but also long-term cardiac events. One hundred fifty-nine patients who were evaluated for elective abdominal aortic surgery were screened preoperatively with DSE from January 1, 1992 to December 31, 1993. We concluded that DSE is useful for preoperative assessment of cardiac risk prior to elective aortic surgery to minimize the need for cardiac intervention and still maintain acceptable perioperative MI and death rates. A selective approach for coronary revascularization is justified by the higher mortality in the subgroup requiring sequential procedures. DSE also allowed us to identify those high-risk patients who are best excluded from aortic surgery. Patients with abnormal DSE results are at higher risk for late cardiac events, require cardiology follow-up, and may require late coronary intervention.

Normothermia is protective during infrarenal aortic surgery.

PURPOSE: Mild hypothermia has been suggested to be protective against tissue ischemia during aortic operations. However, recent studies have documented detrimental cardiac effects of hypothermia during a variety of operative procedures. The influence of different warming methods and the impact of hypothermia during standard aortic procedures was assessed. METHODS: One hundred patients who underwent repair of infrarenal aortic aneurysms or aortoiliac occlusive disease were prospectively randomized into 2 groups, receiving either a circulating water mattress or a forced air warming blanket. Adjuvant warming methods were standardized. The day before surgery, 48-hour Holter monitors were applied and interpreted by a cardiologist blinded to the treatment. Randomization resulted in equivalent groups with regard to patient history, indications for surgery, body mass index, length of surgery, and fluid requirements. RESULTS: Core temperatures were significantly warmer during surgery (36.3 degrees C +/- 0.7 degrees C vs 35.4 +/- 0.8 degrees C) and after surgery (36.4 degrees C +/- 0.7 degrees C vs 35.6 degrees C +/- 0.9 degrees C) in patients with forced air warming (P <.001). The circulating water mattress group had significantly more metabolic acidosis perioperatively (P =.03). Postoperative length of stay, cardiac complications, and death rates were not significantly different. Subgroup analysis of 83 aneurysm patients comparing normothermia with hypothermia (temperature less than 36 degrees C) on arrival to the recovery room identified decreased cardiac output (P =.02), thrombocytopenia (P =.02), elevated prothrombin time (P =.04), and inferior Acute Physiology and Chronic Health Evaluation (APACHE) II scores (P <.001) in the hypothermic group. Holter analysis revealed more sinus tachycardia (ST) segment changes and ventricular tachycardia in hypothermic aneurysm patients (P =.05). CONCLUSION: Patients treated with forced air blankets had significantly less metabolic acidosis and were kept significantly warmer than those treated with circulating water mattresses. Patients with aneurysms that were kept normothermic had a significantly improved clinical profile, with fewer cardiac events on the Holter recordings. We therefore conclude that (1) normothermia is protective for infrarenal aortic surgical patients; and (2) forced air warming blankets provide improved temperature maintenance compared with circulating water mattresses.

A Salmonella typhimurium mutant unable to utilize fatty acids and citrate is avirulent and immunogenic in mice.

Salmonella typhimurium SR-11 is extremely virulent at a dose as low as 10(5) colony forming units (cfu) when administered perorally to BALB/c mice. Utilizing mini-transposon mutagenesis, a mutant of S. typhimurium SR-11 was isolated that was unable to utilize oleate and citrate as carbon sources. This mutant, designated S. typhimurium SR-11 Fad- (Fatty acid), was found to utilize sugars under cya/crp control as sole carbon sources, suggesting that the mutation is not in either of these genes. In addition, SR-11 Fad- utilized pyruvate and succinate, but was unable to utilize either acetate or isocitrate as sole carbon source. In contrast to SR-11, SR-11 Fad- was found to be avirulent, i.e. BALB/c mice were completely healthy after oral infection with 10(9) S. typhimurium SR-11 Fad- cells. Moreover, 21 days after SR-11 Fad- infection, BALB/c mice were found to be protected against an oral challenge with 10(9) cells of S. typhimurium SR-11.

Expression of matrix metalloproteinases and TIMPs in human abdominal aortic aneurysms.

Degradation of extracellular matrix, especially elastin, within the aortic wall is a hallmark of abdominal aortic aneurysms (AAAs). Normal turnover of matrix proteins is mediated by a family of enzymes called matrix metalloproteinases (MMPs). MMP activity is regulated by proteins called tissue inhibitors of metalloproteinases (TIMPs). We analyzed the expression of all known MMPs with established elastolytic activity and TIMPs in human AAA and control tissue. mRNA coding for MMP-9, MMP-2, human macrophage metalloelastase, MMP-7, TIMP-1, and TIMP-2 were amplified by reverse transcriptase-PCR in control and AAA tissue. A Northern blot assay was used to measure the levels of mRNA coding for MMP-2, MMP-9, TIMP-1, and TIMP-2. Control aortic tissue was obtained from patients with occlusive disease and from organ donors. The expression of MMP-7 and human macrophage metalloelastase was not detected in any aortic specimens. By Northern blot analysis the mean level of MMP-2 mRNA was not significantly different between control groups and AAAs (normalized values: occlusive, 1.5 +/- 0.8, n = 3; donor, 4.5 +/- 2.2, n = 6; AAA, 4.0 +/- 0.95, n = 15). There was a significant increase in the level of MMP-9 mRNA in AAA specimens (occlusive, 16.8 +/- 3, n = 3; donor, 5.7 +/- 1.2, n = 6; AAA, 56.7 +/- 11, n = 15, p = 0.0069). The levels of mRNA coding for TIMP-1 were not significantly different. There was a small but statistically significant increase in TIMP-2 mRNA in AAA tissue. These data support the hypothesis that increased activity of MMP-9, but not MMP-2, is an important factor in the etiology of AAAs. This enhanced MMP-9 activity could then result in degradation of the ECM, leading to aneurysmal dilatation.

Carotid endarterectomy: the mandate for high quality duplex.

Excellent correlation between carotid angiography and duplex scanning has made it possible to perform carotid endarterectomy without angiography. The accuracy of scans from practices without a dedicated vascular laboratory must be validated prior to their use for clinical decisions. Seventy six patients had a carotid duplex performed at an outside institution and were referred for vascular surgery. All patients underwent a repeat study at our dedicated vascular lab. The overall accuracy of our lab was 93.8% for all carotid categories as demonstrated by angiography. Outside carotid duplex reports correlated with repeat exams as follows: occlusions: 10/13 carotids (76.9%); 80%-99% stenoses: 15/39 carotids (38.5%); 50%-79% stenoses: 28/44 carotids (63.6%). If a surgeon's practice is to operate for asymptomatic 80%-99% stenoses by report, then unnecessary surgery might have been performed in 61.5% of these carotids and appropriate surgery denied in 3.6%. Outside duplex velocities consistent with a 60%-99% stenosis correlated in 13/17 carotids (76.5%). If a surgeon's practice is to operate for asymptomatic 60%-99% stenoses based on velocity criteria, then unnecessary surgery might have been performed in 23.5% of these carotids, and appropriate surgery denied in 7.6% placing these patients at increased risk of stroke. Outside scans significantly overestimated the severity of carotid disease (p = 0.003). The weighted kappa analysis for agreement between scans was only 60.2%. Failure to have validated high-quality duplex in labs performing carotid studies can lead to unnecessary angiography or surgery. Carotid endarterectomy without angiography should be performed only when duplex accuracy has been previously validated by angiographic correlation studies. Poor agreement with studies from practices without a dedicated vascular lab makes it mandatory to repeat the duplex on all patients prior to clinical decision making. Reimbursement for such repeat studies should not be denied.

Physician work effort and reimbursement for ruptured abdominal aortic aneurysms.

BACKGROUND: Two major flaws have been previously identified in the resource-based relative value scale (RBRVS): (1) inaccurate estimation of physician work effort; and (2) RBRVS compression, which results in undervaluation of major surgical procedures. The impact of RBRVS for physicians treating patients with ruptured abdominal aortic aneurysms (RAAAs) has not been previously reported and is important owing to the severity of the illness, the potential to quantitate actual work effort, and the high percentage of these patients covered by Medicare. PATIENTS AND METHODS: All patients were studied who underwent surgery for RAAAs during a 5-year period encompassing the implementation of RBRVS. Analysis included all physician services including vascular surgeons, anesthesiologists, and all other medical specialists. Total work effort was quantitated for each specialty in minutes/patient. The financial data were obtained by reviewing all professional bills and reimbursements. Cost of service was calculated to include physician compensation, practice overhead costs, and malpractice expenses. RESULTS: In all, 84 patients underwent repair of a RAAA with a mortality rate of 42%. Medicare was the primary insurance for 87% of patients. The cost of service exceeded the reimbursement by 50% for vascular surgeons, resulting in an average loss of $1,593/patient. Actual operative time represented only 24% of total surgical work effort. Early death and a length of stay (LOS) < or = 1 day for 24 patients resulted in a reimbursement rate of $5.98/minute for surgeons. This gain was significantly offset by 30 patients with a LOS > or = 14 days, resulting in a reimbursement rate of $1.94/minute for vascular surgeons. Over the 5-year period there was a trend of decreasing reimbursement for vascular surgeons (P <0.005) but not other physicians. Vascular surgeons incurred a 28% decrease in reimbursement over the study period. CONCLUSIONS: Physician reimbursement under RBRVS for the treatment of patients with RAAAs is inadequate to cover the costs of providing this care. Reimbursement trends and potential changes to the practice component of the RBRVS will further aggravate the losses involved in caring for these very ill patients. Vascular surgeons must continue to provide input to the Health Care Financing Administration to help correct inequities built into RBRVS.

Carotid duplex overestimation of stenosis due to severe contralateral disease.

BACKGROUND: In the quest to use carotid duplex to assess carotid occlusive disease, it has been reported that the current velocity criteria to calculate stenosis tends to overestimate the severity when there is a contralateral highly stenotic or occluded carotid artery. METHODS: Patient records were reviewed for 592 consecutive carotid endarterectomies performed from 1987 to 1994. Preoperative and postoperative duplex scan results were compared in a subset of patients in whom duplex overestimated the degree of stenosis, as compared to preoperative angiography. RESULTS: A total of 146 patients were identified in whom duplex overestimated the degree of stenosis contralateral to a high grade stenosis or an occlusion. Of 76 arteries, 18 (23.7%) contralateral to an occluded artery were overestimated by duplex, and 128 (27.0%) of 474 arteries contralateral to a high grade stenosis were overestimated. Following endarterectomy 44 (51.8%) of 128 nonoperated contralateral stenoses decreased by at least one duplex category. The average peak systolic frequency (PSF) decreased by 1175 Hz (P = 0.0018), and the average end diastolic frequency (EDF) decreased by 475 Hz (P = 0.011). CONCLUSIONS: Patients with high grade stenosis have a significant decrease in PSF and EDF in the unoperated carotid after endarterectomy, supporting a compensatory flow phenomenon. This often results in a decrease in the postoperative duplex defined stenosis by at least one category. The clinical significance of these findings is of increasing importance as carotid surgery is being performed more frequently without angiography.

Phorbol ester treatment inhibits phosphatidylinositol 3-kinase activation by, and association with, CD28, a T-lymphocyte surface receptor.

CD28 is a costimulatory receptor found on the surface of most T lymphocytes. Engagement of CD28 induces interleukin 2 (IL-2) production and cell proliferation when combined with an additional signal such as treatment with phorbol ester, an activator of protein kinase C. Recent studies have established that after CD28 ligation, the cytoplasmic domain of CD28 can bind to the 85-kDa subunit of phosphatidylinositol 3-kinase (PI3 kinase). There is a concomitant increase in PI3 lipid kinase activity that may be important in CD28 signaling. Despite the requirement of phorbol 12-myristate 13-acetate (PMA) for effector function, we have found, however, that treatment of Jurkat T cells with the phorbol ester PMA dramatically inhibits (i) the association of PI3 kinase with CD28, (ii) the ability of p85 PI3 kinase to be immunoprecipitated by anti-phosphotyrosine antibodies, and (iii) the induction of PI3 kinase activity after stimulation of the cells with the anti-CD28 monoclonal antibody 9.3. These changes occur within minutes of PMA treatment and are persistent. In addition, we have found that wortmannin, a potent inhibitor of PI3 kinase, does not interfere with the induction of IL-2 after stimulation of Jurkat T cells with anti-CD28 monoclonal antibody and PMA. We conclude that PI3 kinase activity may not be required for CD28-dependent IL-2 production from Jurkat T cells in the presence of PMA.

Peter B. Samuels Award. Ruptured abdominal aortic aneurysm repair: the financial analysis.

BACKGROUND: Denial of ruptured abdominal aortic aneurysm (RAAA) repair has been advocated based upon historically poor surgical outcome and a perceived lack of cost effectiveness. Although the repair intuitively seems expensive, the actual cost of care, adequacy of reimbursement, and cost per additional life-year gained for RAAA repair are poorly defined. PATIENTS AND METHODS: Retrospective clinical and financial chart review of 119 consecutive patients undergoing operation for RAAA from 1986 to 1993. RESULTS: Overall in-hospital mortality was 45%. Mean institutional charge per patient in 1993 dollars was $40,763 (range $4,473 to $284,374), with an actual mean cost for service of $22,420 and an average reimbursement of $21,360, resulting in a loss of $1,060 per patient. Losses were higher in Medicare patients. Survivors (n = 65) had an average length of stay of 20 days, cost $41,045 each, and incurred an institutional loss of $298,405. Mean cost per additional (adjusted) life-year was $3,953. One-, 3-, and 5-year survival rates following hospital discharge were 97%, 85%, and 77%, respectively. CONCLUSIONS: Emergency repair of RAAA is relatively inexpensive when compared to other commonly used health maintenance protocols and effectively restores survivors to their former health. Since no clinical or physiologic parameter can predict poor outcome, operative intervention should not be denied.

Regulation of MAP kinase activity by growth stimuli in vascular smooth muscle.

Intracellular signaling pathways regulating vascular smooth muscle (VSM) cell growth and hypertrophy can be initiated by activation of receptor tyrosine kinases and/or protein kinase C (PKC). Mitogen-activated protein kinases (MAP kinases) are cytosolic serine/threonine kinases, proposed to act as a point of convergence for diverse growth factors utilizing these signaling pathways. The goals of this study were (1) to determine whether MAP kinase is expressed in cultured rat aortic VSM, (2) to assess the activation of MAP kinase by known proliferative and hypertrophic stimuli, and (3) to determine if stimulation of a PKC-dependent signaling pathway in these cells results in MAP kinase activation. MAP kinase activity was measured in cytosolic extracts of aortic VSM by quantifying myelin basic protein phosphorylation. Three peaks of activity were resolved chromatographically and identified as MAP kinase isoforms (MW 42, 44, and 46 kDa) by immunoblotting with antipeptide antibodies specific for MAP kinase. MAP kinase activity in quiescent growth-arrested cells (157 +/- 19 pmole 32P/min/mg) was markedly stimulated within 15 min by known mitogens (10% serum, 731 +/- 40 pmole 32P/min/mg; 40 ng/ml PDGF, 670 +/- 105 pmole 32P/min/mg; P < 0.01) and partially sustained for at least 90 min (serum, 606 +/- 34 pmole 32P/min/mg; PDGF, 323 +/- 59 pmole 32P/min/mg P < 0.05). Angiotensin II (AII, 0.1 microM) and a pharmacological PKC activator, phorbol 12,13-dibutyrate (PDB, 0.1 microM), are reported to be nonmitogenic hypertrophic stimuli in these cells. These stimuli transiently increased MAP kinase activity with a peak at 5 min (AII, 328 +/- 15 pmole 32P/min/mg; PDB, 592 +/- 41 pmole 32P/min/mg; P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Dobutamine stress echocardiography for cardiac risk assessment before aortic surgery.

PURPOSE: This study evaluates dobutamine stress echocardiography (DSE) for perioperative cardiac risk assessment with elective aortic surgery. METHODS: Dobutamine stress echocardiography was used to evaluate 81 patients before infrarenal aortic surgery. Patients were placed into three groups. Group I (n = 31) had normal DSEs. Group II (n = 25) had resting wall motion abnormalities without dobutamine-induced changes of ischemia. Group III (n = 25) had evidence of dobutamine-induced ischemia. Patient analysis revealed that of 46 patients with clinical indicators of coronary artery disease (CAD), only 23 had DSEs with inducible ischemia. Two of 35 patients without clinical indicators of CAD had DSEs with inducible ischemia. RESULTS: The 56 patients in group I and II underwent aortic reconstruction without cardiac complications or death. Of the 25 patients in group III, surgery was deferred in five (two patients with claudication and three with aneurysms < or = 5 cm), and four underwent coronary artery bypass grafting. Outcome after coronary artery bypass grafting included one death from stroke, one aneurysm rupture, and two uncomplicated aortic reconstructions. The remaining 16 patients in group III underwent aortic surgery, with three postoperative myocardial infarctions (MI) and no deaths. CONCLUSIONS: Using DSE for preoperative assessment of cardiac risk allowed us to operate on 74 of 81 patients being considered for elective aortic reconstruction, with no operative deaths and a 4.1% rate of perioperative MI. Dobutamine stress echocardiography has the ability to identify patients with asymptomatic stress-induced ischemic myocardium and its increased risk for perioperative MI (p < 0.001). Equally important, for patients with clinical indicators of CAD but without DSE-inducible ischemia, no further cardiac evaluation is necessary.

An algorithm for the surgical management of chronic abdominal aortic occlusion and occluded aortofemoral grafts.

An algorithm for the surgical management of chronic abdominal aortic occlusion is presented based upon experience of treating 60 consecutive patients. Of 33 patients with juxtarenal aortic occlusion, 17 underwent aortofemoral bypass (AFB), 10 descending thoracic aortofemoral (DTAF), 5 axillofemoral (AxF) bypass, and 1 ascending thoracic aortofemoral bypass. Of 11 patients with mid or distal aortic occlusion, 8 underwent AFB, 2 DTAF and 1 AxF. Of 16 patients with aortic graft occlusion, 1 underwent AFB, 10 DTAF and 5 AxF. Acceptable risk patients were selected for AFB (26). DTAF (22) was frequently preferred for patients with occluded aortic grafts or other hazardous intraabdominal pathology. AxF (11) was used for patients with severe cardiopulmonary risk, limited life expectancy from malignancy, or when emergency procedures were required for salvage of severely ischemic limbs in debilitated patients with chronic aortic occlusion. In the AFB, DTAF and AxF groups the perioperative mortality was 8%, 5% and 36% respectively, the late mortality was 15%, 36% and 45%, and the 5-year primary cumulative graft patency was 92%, 89% and 15%.