Biomedical subjects

F R Bech

Publications and source records attributed to F R Bech.

11 recordsLinked to original sources

PubMed2001

Levels of expression of Fcgamma receptor IIA (CD32) are decreased on peripheral blood monocytes in patients with severe atherosclerosis.

To obtain information in vivo concerning the role of Fcgamma receptors (FcgammaR) in atherosclerosis, we used quantitative flow cytometry to measure the levels of expression of FcgammaRI and FcgammaRIIA on peripheral monocytes in patients with severe atherosclerosis. Expression of several other markers was also measured. We found that differences in the levels of expression of FcgammaRI were not statistically significant when compared between patients and control subjects. For FcgammaRIIA, levels of expression were decreased in the patient group, a difference that was statistically significant. Levels of expression of CD14 and CD36 were also significantly decreased in the patient group. The decrease in expression of FcgammaRIIA was statistically significant when the effects of current cigarette smoking status or medication use, including statins, were taken into account. There was also a positive and statistically significant correlation between high-density lipoprotein-cholesterol and levels of expression of FcgammaRIIA for all subjects. In contrast, decreased levels of expression of CD14 and CD36 were strongly associated with current smoking status or statin use. In summary, levels of expression of FcgammaRIIA on peripheral blood monocytes were significantly decreased in patients with clinical atherosclerosis. Additional studies are warranted to determine if levels of expression of FcgammaRIIA have utility as a phenotypic marker for assessing relative risk of atherosclerotic disease.

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PubMed1997

Celiac artery compression syndromes.

Compression of the visceral arteries can produce true mesenteric ischemia, but the syndrome is rare. The syndrome is caused by unfavorable anatomic relationships at the aortic hiatus among the CA, the SMA, and overlying structures, particularly the diaphragmatic crura. These anatomic relationships, in contrast to the syndrome they sometimes produce, are relatively common, which makes the detection of CA compression only a prerequisite to the diagnosis of the clinical entity. The diagnosis of CA compression syndrome ultimately depends on the relentless elimination of other possible causes for abdominal pain and on the knowledge that this curious syndrome does indeed exist. If properly diagnosed, the CA compression syndrome can be corrected with a safe, relatively simple surgical procedure. Past treatment series reflect too little appreciation for the extensiveness of a true, chronic CA injury. Revascularization of the CA, in addition to release of compression, should therefore be performed with greater frequency in the future. The young patients who are successfully diagnosed and treated for this unusual syndrome are frequently entirely relieved of long-standing, debilitating pain, and, like other patients with chronic mesenteric ischemia, they typically enjoy dramatic improvement in the quality of their lives. Thus, with the prospect of these patients in mind, a clinician should accept the opinion that the syndrome "does not exist" only after careful consideration of the entire literature.

Abdominal Pain↗

PubMed1997

Thrombolysis of occluded infrainguinal vein grafts: predictors of outcome.

PURPOSE: The purpose of this study was to identify factors that influence graft patency and limb salvage rates after thrombolysis of occluded infrainguinal vein grafts. METHODS: The records of patients who underwent percutaneous catheter-directed thrombolysis of occluded infrainguinal vein bypass grafts at our institution between 1985 and 1995 were reviewed. Life table analysis was used to determine survival and patency differences. Univariate and multivariate analyses were used to identify the patient-specific factors that affected outcomes. RESULTS: Forty-four patients with 44 thrombosed infrainguinal vein grafts underwent thrombolysis with urokinase. The thrombolysis-related mortality rate was 2%, and nonfatal complications occurred in 16%. Thrombolysis was unable to restore graft patency in 25% of grafts (11 of 44). Of the remaining 33 successfully lysed grafts, 88% required adjunctive surgery or percutaneous transluminal angioplasty after thrombolysis. Overall, the primary graft patency rate was 25% at 1 year and 19% at 2 years after thrombolysis. Considering only successfully lysed grafts, the primary patency rate improved to 34% at 1 year and 25% at 2 years. Multivariate analysis revealed that the graft patency rate was substantially better in patients without diabetes and in vein grafts that had been in place for longer than 12 months (p < 0.01). The limb salvage rate was significantly improved by successful thrombolysis (63% at 2 years vs 31% if lysis failed; p < 0.01). The patient survival rate was high-89% 2 years after thrombolysis. CONCLUSIONS: Even with adjunctive therapy, vein graft thrombolysis is unlikely to yield durable patency overall. However, successful thrombolysis improves limb salvage rates and may be beneficial in patients without diabetes who have mature vein grafts but who do not have options for other autogenous revascularization procedures.

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PubMed1997

Cost-effectiveness of carotid endarterectomy in asymptomatic patients.

PURPOSE: The purpose of this study was to determine the cost-effectiveness of carotid endarterectomy for treating asymptomatic patients with > or = 60% internal carotid stenosis, based on outcomes reported in the Asymptomatic Carotid Atherosclerosis Study (ACAS). METHODS: A cost-effectiveness analysis was performed using a Markov decision model in which the probabilities for base-case analysis (average age, 67 years; 66% male; perioperative stroke plus death rate, 2.3%; ipsilateral stroke rate during medical management, 2.3% per year) were based on ACAS. The model assumed that patients who had TIAs or minor strokes during medical management crossed over to surgical treatment, and used the NASCET data to model the outcome of these now-symptomatic patients. Average cost of surgery ($8500), major stroke ($34,000 plus $18,000 per year), and other costs were based on local cost determinations plus a review of the published literature. Cost-effectiveness was calculated as the incremental cost of surgery per quality-adjusted life year (QALY) saved when compared with medical treatment, discounting at 5% per year. Sensitivity analysis was performed to determine the impact of key variables on cost-effectiveness. RESULTS: In the base-case analysis, surgical treatment improved quality-adjusted life expectancy from 7.87 to 8.12 QALYs, at an incremental lifetime cost of $2041. This yielded an incremental cost-effectiveness ratio of $8,000 per QALY saved by surgical compared with medical treatment. The high cost of care after major stroke during medical management largely offset the initial cost of endarterectomy in the surgical group. Furthermore, 26% of medically managed patients eventually underwent endarterectomy because of symptom development, which also decreased the cost differential. Sensitivity analysis demonstrated that the relative cost of surgical treatment increased substantially with increasing age, increasing perioperative stroke rate, and decreasing stroke rate during medical management. CONCLUSION: For the typical asymptomatic patient in ACAS with > or = 60% carotid stenosis, our results indicate that carotid endarterectomy is cost-effective when compared with other commonly accepted health care practices. Surgery does not appear cost-effective in very elderly patients, in settings where the operative stroke risk is high, or in patients with very low stroke risk without surgery.

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PubMed1996

Endothelial cells modulate smooth muscle cell morphology by inhibition of transforming growth factor-beta 1 activation.

BACKGROUND: We have previously demonstrated in a coculture model that endothelial cells (ECs) exert regulatory control over smooth muscle cell (SMC) morphology. This study was performed to test the hypothesis that ECs inhibit transforming growth factor-beta 2 (TGF-beta 1) activation through the release of plasminogen activator inhibitor (PAI-1). METHODS: Bovine SMCs were cultured on a thin, semipermeable membrane, either alone or opposite ECs in coculture (SMC/EC). Conditioned media and cell lysates at 1, 5, and 21 days were assayed for TGF-beta 1 and PAI-1 by enzyme-linked immunoabsorbent assay. Cell proliferation rates, protein, and DNA content were measured and compared with SMC morphology. RESULTS: Activation of TGF-beta 1 was significantly decreased (1.2% versus 18.9% active TGF-beta 1 p < 0.05) and PAI-1 was increased (659 pg/ml versus 343 pg/ml p < 0.05) in SMC/EC medium on day 1, compared with the medium of SMC alone. Significantly higher levels of PAI-1 were measured in cell lysates of cocultured ECs (128 pg/micrograms DNA) than in cocultured SMCs (5.8 pg/micrograms DNA, p < 0.05). SMC/EC coculture prevented the SMC hill-and-valley growth morphology seen in SMCs cultured alone. CONCLUSIONS: In a model designed to study SMC/EC interactions, it was seen that ECs can alter growth characteristics of SMCs by producing PAI-1, which interferes with the plasminogen pathway of TGF-beta 1 activation. This suggests that reduced EC PAI-1 production could play a role in alteration of SMC phenotype in vivo.

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PubMed1996

Carotid duplex criteria for a 60% or greater angiographic stenosis: variation according to equipment.

PURPOSE: The purpose of this study was to evaluate the carotid duplex criteria for a > or = 60% angiographic internal carotid artery (ICA) stenosis and the degree of variation among duplex scanners. METHODS: Carotid duplex criteria for a > or = 60% angiographic stenosis were evaluated in two ICAVL-accredited vascular laboratories with different brands of duplex scanners (Siemens-Quantum and Diasonics in Laboratory A, ATL and Diasonics in Laboratory B). Analysis was performed for 360 carotid bifurcations in 180 consecutive patients who had concurrent angiographic and duplex evaluation. Blinded angiogram evaluation was performed with precision electronic calipers on magnified views, with stenosis calculated by criteria of the Asymptomatic Carotid Atherosclerosis Study and the North American Symptomatic Carotid Endarterectomy Trial. Duplex data included internal carotid artery peak systolic velocity (ICA PSV), ICA end-diastolic velocity, and the ratio of ICA PSV to common carotid artery (CCA) PSV (ICA/CCA ratio). RESULTS: The most accurate determination of a > or = 60% ICA stenosis was obtained with ICA/CCA ratio and ICA PSV, but the optimal threshold differed for all four scanners. The optimal ICA/CCA ratio varied from 2.6 to 3.3, and the optimal ICA PSV varied from 190 to 240 cm/sec. All four scanners produced criteria that give a positive predictive value > 90% while maintaining accuracy at > or = 90%. Logarithmic transformation of duplex variables created a linear relationship between duplex values and angiographic stenosis, allowing statistical evaluation of scanner operating characteristics by linear regression analysis and analysis of covariance. This analysis revealed that the mathematic equation relating duplex values with angiographic percent stenosis was statistically different for one of the four scanners (p < 0.05). Scanner differences did not appear to be due to technologists, because the regression lines were nearly identical for the two Diasonics scanners despite use by different technologists. Ignoring the significant difference in operating characteristics for one of the four scanners would result in a mean error for predicting a 60% stenosis of 14% to 18% (equating a 46% or 78% stenosis with a 60% stenosis). CONCLUSIONS: We conclude that the correlation of duplex data with angiographic percent stenosis and the duplex criteria for a > or = 60% stenosis are machine-specific. Regression analysis can determine whether apparent differences are due to chance or significant differences in scanner characteristics. Future studies should include regression analysis according to equipment type.

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PubMed1991

The effect of ibuprofen on cardiac performance during abdominal aortic cross-clamping.

Decreased cardiac output and increased plasma thromboxane have been observed during aortic cross-clamping under general anesthesia. Amelioration of these changes has been reported by preoperative administration of cyclooxygenase inhibitors, but heterogeneity in patients' intravascular volume status has confounded analysis of the drugs' effects in previous studies. We studied hemodynamic conditions in 24 volume-loaded (pulmonary capillary wedge pressure greater than 10 mm Hg) patients undergoing abdominal aortic aneurysm repair under general plus epidural anesthesia, after preoperative double-blind administration of either ibuprofen 800 mg (n = 12) or placebo (n = 12). The hemodynamic response to aortic cross-clamping was similar in both groups. Pulse and mean arterial pressure remained unchanged; cardiac index decreased after aortic cross-clamping from 2.4 +/- 0.1 (mean +/- standard error of the mean [SEM]) to 2.1 +/- 0.1 1/min/m2 in the ibuprofen group and from 2.5 +/- 0.1 to 2.3 +/- 0.2 1/min/m2 in the placebo group (p less than 0.01 versus preclamp values in both groups, multivariate analysis of variance [MANOVA]), but improved after declamping. Both left and right ventricular stroke work indexes followed a similar pattern. Plasma 6-keto prostaglandin Fl alpha (6-k-PGF1 alpha) increased transiently from a baseline level of 304 +/- 44 to 2083 +/- 698 pg/ml plasma in mixed venous blood 30 minutes after incision in the placebo group (p less than 0.05), but no other significant change in plasma 6-keto prostaglandin Fl alpha or in thromboxane B2 occurred in either group at any other time.(ABSTRACT TRUNCATED AT 250 WORDS)

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PubMed1990

Hemodynamic effects of glucagon after acute mesenteric ischemia in rats.

We have previously shown that iv glucagon improved survival in rats from 33 to 83% when given after, but not during, superior mesenteric artery (SMA) occlusion. This study investigated potential hemodynamic mechanisms of this effect. In Part 1, cardiac output (CO) was measured in 12 male Sprague-Dawley rats with an electromagnetic flow-probe that had been placed around the ascending aorta 5 days previously. Under pentobarbital anesthesia, the SMA was occluded for 85 min. All rats received normal saline (NS, 15 ml/kg/hr) for 1 hr before and after SMA declamping. Control rats (n = 6) received only NS. Treated rats (n = 6) received NS plus glucagon (1.6 micrograms/kg/min iv) for 1 hr postocclusion. CO decreased 50% during the first hour after SMA declamping in control rats, but only 11% in glucagon-treated rats (P less than 0.02). Systemic vascular resistance (SVR) increased by 90% in control rats by 1 hr after declamp, but only 9% in glucagon rats (P less than 0.04). Systemic blood pressure and heart rate were not different in the two groups. In Part 2, relative distribution of visceral blood flow was measured with radiolabeled microspheres injected in the aortic root before clamping, before declamping, and 1 hr postdeclamping in 10 rats (5 glucagon, 5 control) using the above protocol. After SMA clamping, the proportion of visceral blood flow distributed to the intestine fell from 45 to 20% (P less than 0.05). During reperfusion, the proportion of intestinal flow exceeded baseline (P less than 0.05), but was not different in control (64%) and glucagon-treated rats (56%).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1990

Increased platelet deposition on polytetrafluoroethylene grafts after balloon catheter thrombectomy.

Prosthetic graft rethrombosis after thrombectomy may be potentiated by increased thrombogenicity of the restored flow surface. This experiment compared platelet deposition on polytetrafluoroethylene (PTFE) grafts after balloon catheter thrombectomy with deposition on new, nonthrombosed grafts. Three models of graft thrombosis were studied in eight dogs with 4 mm diameter by 7 cm PTFE graft segments: (1) in vitro model: grafts filled with blood, stored in 37 degrees C saline solution; (2) in vivo model: blood-filled grafts stored in subcutaneous tissue; and (3) in situ model: one end of grafts anastomosed to femoral or carotid artery as a blind tube. Duration of thrombosis (1, 2, and 3 weeks) was studied by initiating one graft of each type per week in each dog. After 3 weeks, nine thrombosed grafts per dog were harvested and graft thrombectomy was performed with a 3F balloon catheter. An ex vivo flow-controlled perfusion circuit was then created in each dog and platelet deposition was measured during the initial 20 minutes of graft perfusion after 111In platelet labeling. Thrombectomized grafts were compared with new, control grafts not previously exposed to blood, as well as with grafts exposed for 1 hour to blood or plasma. Compared with control grafts, platelet deposition was significantly increased on in vivo (3.7 times control; p less than 0.01), in situ (2.6 times control; p less than 0.05), and in vitro thrombosed grafts (2.0 times control; p less than 0.05). Age of thrombus was not a significant source of variation. Blood or plasma exposure alone did not significantly increase platelet deposition. These data suggest that antiplatelet therapy may be important at the time of PTFE graft thrombectomy.

Animals↗

PubMed1990

The effect of thromboxane receptor blockade versus thromboxane synthase inhibition on canine arterial graft patency.

This study compared the effects of a thromboxane synthase inhibitor, thromboxane receptor antagonist, and cyclooxygenase inhibitor in a canine arterial graft patency model. Fifty-six dogs were divided into a control (no treatment) and five treatment groups: thromboxane synthase inhibitor (U63557A; 15 mg/kg/tid); thromboxane receptor antagonist (SQ29548; 0.02 mg/kg/hr); high-dose aspirin (325 mg/day; low-dose aspirin (1 mg/kd/day; and aspirin plus dipyridamole (325 mg/day aspirin; 3 mg/kg/day dipyridamole). Drugs were orally administered except for thromboxane receptor antagonist, which was delivered intravenously by minosmotic pumps. After 24 hours of drug treatment, bilateral femoral artery prosthetic grafts (4 mm diameter x 7 cm; 1 polytetrafluoroethylene and 1 Dacron) were implanted. Patency was determined after 1 week. Dogs were classified before operation according to their epinephrine-enhanced arachidonate-stimulated platelet aggregation response. Polytetrafluoroethylene and Dacron graft patency rates were equivalent in all groups. Overall graft patency was significantly improved from 42% (control) to 94% by both high-dose aspirin and thromboxane receptor antagonist (p less than 0.001). Aspirin-dipyridamole also improved patency (83%; p less than 0.01 versus control), whereas thromboxane synthase inhibitor and low-dose aspirin were not effective. Baseline platelet aggregation was not predictive of patency. The drugs that promoted graft patency in this model either suppressed both thromboxane A2 and prostaglandin H2 formation (high-dose aspirin) or blocked their combined platelet receptor (thromboxane receptor antagonist). Thromboxane synthase inhibitor may be ineffective because prostaglandin H2 production is allowed. These data suggest that activation of the platelet thromboxane A2-prostaglandin H2 receptor is an essential event in early arterial graft thrombosis.

Animals↗

PubMed1990

The effect of glucose infusion on survival after acute mesenteric ischemia/reperfusion.

Perfusion of ischemic tissue with glucose has been shown to be deleterious to heart, spinal cord, and kidney. Observations that glucagon improves survival after acute mesenteric ischemia, however, suggest that hyperglycemia may not be deleterious during bowel ischemia. This experiment examined the effect of glucose infusion on survival in an established rat model of acute mesenteric ischemia. The superior (cranial) mesenteric artery (SMA) was occluded for 85 min in 36 anesthetized Sprague-Dawley rats. Animals were randomized to receive 5% glucose in normal saline (n = 15; 16.5 mL/kg.min iv), normal saline alone (n = 13; 16.4 mL/kg.min iv), or no intravenous fluid (n = 8). Ninety-minute intravenous infusions were initiated 10 min after SMA occlusion. Survival to 48 h was 47% in glucose-saline-treated rats, 31% in saline-only-treated rats, and 12.5% in control rats. These results demonstrate no deleterious effect of glucose infusion on mortality after acute mesenteric ischemia in this model.

Animals↗