Women, pregnancy, and varicose veins.
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Aged↗
Biomedical subjects
G Stansby
Publications and source records attributed to G Stansby.
Effect of posture on popliteal artery hemodynamics.
HYPOTHESIS: Marked peripheral vasodilation and rubor characterize critically ischemic limbs on dependency. We believe that intermittent claudication is also associated with peripheral hemodynamic changes on postural alteration, which differ distinctly from normal. Evaluation of such differences and understanding of the underlying physiological derangements may be essential in the development of treatments for intermittent claudication. We comparatively assess the effect of posture on lower limb arterial hemodynamics in normal subjects and in patients with intermittent claudication (or Fontaine II) due to peripheral vascular disease, determined in the popliteal artery. DESIGN: A cohort study. SETTING: A university-associated tertiary care hospital. PATIENTS: Thirty-seven legs of 29 normal subjects (group A) and 50 legs of 36 patients with intermittent claudication (ankle-brachial index range, 0.39-0.76; median, 0.57) (group B). INTERVENTIONS: Popliteal artery volume flow (vFl), mean velocity, and luminal diameter were measured on (1) recumbency, (2) sitting, and (3) return to recumbency in groups A and B using color duplex imaging. MAIN OUTCOME MEASURES: The pulsatility index, peak systolic velocity, and end diastolic velocity (EDV) were measured on (1) recumbency, (2) sitting, and (3) return to recumbency. RESULTS: Popliteal artery vFl in normal subjects decreased from 110 +/- 43 mL/min on recumbency to 57 +/- 27 mL/min on sitting (P<.001) and returned to 111 +/- 46 mL/ min on resumption of recumbency (P<.001). Similarly, in patients with intermittent claudication, vFl decreased from 113 +/- 52 mL/min on recumbency to 76 +/- 41 mL/min on sitting (P<.001) and increased on resumption of recumbency to 114 +/- 53 mL/min (P<.001). There was no difference (P = .97) in the vFl between the study groups on recumbency, but sitting vFl in normal subjects was significantly lower than in patients with intermittent claudication (P = .04). The mean velocity, peak systolic velocity, and EDV displayed a similar pattern of change as vFl. The pulsatility index in both groups increased significantly on sitting (P<.001) and decreased on return to recumbency (P<.001). All data are given as mean +/- SD. CONCLUSIONS: Lower limb arterial vFl, mean velocity, peak systolic velocity, and EDV decrease significantly (P<.001) when posture is altered from recumbency to sitting, in normal subjects and in patients with intermittent claudication. A decrease in the EDV and an increase in the pulsatility index on sitting indicate enhancement of arterial resistance to flow secondary to peripheral vasoconstriction. Quantitative differences between the groups in vFl (P<.04), EDV (P<.01), and pulsatility index (P<.001) on dependency indicate that the orthostatic vasoactive response in patients with intermittent claudication is significantly subdued, reflecting a marked derangement in venoarteriolar response.
Adult↗
Inhibition of diabetic bladder smooth muscle cell proliferation by endothelin receptor antagonists.
Urinary bladder hypertrophy and hyperplasia are well recognised in diabetic cystopathy. The urinary bladder is known to synthesise endothelin-1 (ET-1), a potent vasoconstrictor peptide with mitogenic properties. Using diabetic New Zealand White (NZW) rabbits, we investigated the potential role of ET receptor subtypes (ETA and ET(B)) on the proliferation of bladder smooth muscle cells (SMC). Diabetes mellitus was induced in adult male NZW rabbits. After 6 months, control (n = 6) and diabetic (n = 6) bladders were removed and SMC from the dome and bladder neck were grown using standard explant methodology. At passage two, the cells were made quiescent and then further incubated in foetal calf serum (FCS), control age-matched rabbit serum (CRS) or diabetic rabbit serum (DRS) in the presence or absence of ET(A)-antagonist (BQ123) or ET(B)-antagonist (BQ788). SMC proliferation was then measured with 5-bromo-2'deoxy-uracil 24 h later and by cell counting (using a haemocytometer) at 48 h. Neither BQ123 nor BQ788 influenced detrusor or bladder neck SMC proliferation in FCS or CRS. However, in the presence of DRS, BQ123 and BQ788 significantly inhibited diabetic detrusor and bladder neck SMC proliferation at 30 and 100 nmol/l (P < 0.03 and P < 0.01, respectively). Cell counts were also significantly reduced from the diabetic detrusor and bladder neck (P < 0.01 and P < 0.03 with BQ123 and BQ788, respectively). These results suggest that ET may play a pathophysiological role in the bladder SMC hyperplasia associated with diabetes mellitus.
Animals↗
Warfarin induced skin necrosis.
BACKGROUND: Warfarin induced skin necrosis is a rare complication with a prevalence of 0.01-0.1 per cent. It was first described in 1943. METHODS: A literature review was undertaken using Medline; all relevant papers on this rare compli-cation of warfarin therapy were used. RESULTS: There are several adverse skin manifestations associated with the use of oral anticoagulants, ranging from ecchymoses and purpura, haemorrhagic necrosis, maculopapular vesicular urticarial eruptions to purple toes. This article concentrates mainly on warfarin induced skin necrosis. The syndrome typically occurs during the first few days of warfarin therapy, often in association with the administration of a large initial loading dose of the drug. Although the precise nature of the disease is still unknown, advances in knowledge about protein C, protein S and antithrombin III anticoagulant pathways have led to a better understanding of the mechanisms involved in pathogenesis. Differential diagnosis between warfarin induced skin necrosis and necrotizing fasciitis, venous gangrene and other causes of skin necrosis may be difficult; the disease may also be confused with other dermatological entities. CONCLUSION: Warfarin induced skin necrosis, while rare, is an important complication. All surgeons should be aware of its existence.
Anticoagulants↗
Effect of intermittent pneumatic foot compression on popliteal artery haemodynamics.
PURPOSE: the aim was to investigate the effect of intermittent pneumatic foot compression (IPC(foot)) on popliteal artery haemodynamics in normal individuals and in patients with intermittent claudication due to peripheral vascular disease (PVD) (Fontaine stage II). MATERIAL AND METHODS: popliteal artery volume flow [vFl], pulsatility index [PI], mean velocity [mV], peak systolic [PSV] and end diastolic velocity [EDV], in 25 limbs of 20 normal subjects and 40 limbs of 32 stable claudicants were obtained in the sitting position before, during and within 30 seconds after the application of IPC(foot)(applied pressure: 120 mmHg; inflation time: 3 seconds; deflation time: 17 seconds) using colour-flow duplex imaging (CFDI). The reproducibility of flow velocity estimations using CFDI in the horizontal [hor] (recovery) and sitting [sit] positions was evaluated in 20 limbs of normal controls and 20 limbs of claudicants. RESULTS: popliteal artery vFl, mV, PSV and PI measurements were performed with a coefficient of variation (CV) of less than 14.6% among claudicants and of less than 13.3% in normal subjects. EDV is the least reproducible parameter with an overall CV range of 10.2-21.5% in normal controls and 9.1-18.6% in arteriopaths. On application of IPC(foot)popliteal artery vFl increased by 111% in the control group (p<0.001) and by 51% in the claudicants (p<0.001). Within 30 seconds of the cessation of pump action flow decreased significantly in both groups (p<0.001), but maintained a significantly higher level than that at baseline (p<0. 001, in both groups). The mV, PSV and EDV showed a similar pattern of significant changes. Both in normals and claudicants, the PI decreased with IPC(foot)(p<0.001) and increased post-compression; however, it was significantly lower than baseline (p<0.005) within 30 seconds of impulse delivery. CONCLUSIONS: current CFDI technology enables a reproducible estimation of popliteal artery flow velocities. IPC(foot)can significantly augment arterial calf inflow on an acute basis both in normals and claudicants. The increase of EDV and decrease of PI indicate that attenuation of peripheral resistance to flow is the main mechanism underlying the popliteal artery vFl enhancement on application of IPC(foot). Prospective trials on the long-term effect of IPC(foot)in the management of patients with PVD are indicated from the results of this study.
Adult↗
The significance of the cerebral collateral capacity in patients with carotid atheroma.
OBJECTIVES: to identify the echodensity, stenosis of carotid plaques and cerebral collateral capacity that were associated with various ipsilateral presentations (retinal, cerebrovascular, asymptomatic). DESIGN: cross-sectional study. MATERIALS: forty-four patients, with 44 plaques associated with various presentations, were studied. METHODS: the duplex images of the plaques were analysed echomorphologically in a computer by means of Grey Scale Median (GSM) [hypoechoic (low GSM), hyperechoic (high GSM)]. The percentage (%) reduction of the mean velocity in the middle cerebral artery (PRMCA) on transcranial Doppler, during clamping in carotid endarterectomy, was evaluated to distinguish the competent cerebral collateral supply (low PRMCA) from the non-competent one (high PRMCA). RESULTS: the retinal symptoms were associated with plaques of low median GSM (0), severe median stenosis (90%) and low median PRMCA (0.31) as contrasted with the cerebrovascular symptoms (17, 84%, 0.47, respectively) and asymptomatic status (32, 83%, 0.4, respectively) [(p =0.038 (GSM), p =0.67 (stenosis), p=0.15 (PRMCA)]. The retinal and the cerebrovascular symptoms were distinct in terms of PRMCA (p=0.045). CONCLUSIONS: the retinal symptoms were produced by hypoechoic and possibly embologenic plaques, whereas the cerebrovascular ones possibly by the combination of carotid embolism and a non-competent cerebral collateral circulation. Asymptomatic status was associated with the absence of any relevant mechanism.
Adult↗
Myocardial injury in major aortic surgery.
PURPOSE: The purpose of this study was to examine the effects of major aortic surgery and its associated oxidative stress and injury on the myocardium. METHODS: Plasma from 27 patients who underwent thoracoabdominal aortic aneurysm (TAAA) repair and 17 patients who underwent infrarenal aortic aneurysm (AAA) repair was collected at incision, aortic crossclamping, and reperfusion and 1, 8, and 24 hours thereafter. Samples were assayed for the myocardial specific protein troponin-T, total antioxidant status, and lipid hydroperoxides. RESULTS: Ten patients experienced cardiac dysfunction in the first 24 hours after surgery (eight patients in the TAAA group and two patients in the AAA group). Immediately after reperfusion, total antioxidant status levels dropped in all patients with TAAA and with AAA; this was more marked in patients with TAAA, leading to a significant difference between the two groups at this time point and for up to 1 hour thereafter (P <.01). Patients with TAAA showed a sharp rise in lipid hydroperoxide levels immediately after reperfusion, and levels were significantly higher than in patients with AAA (P =.0007). In patients with AAA, no significant change in troponin-T was observed throughout the study period; whereas in patients with TAAA, levels were significantly elevated at 8 and 24 hours after reperfusion (P <.01). Troponin-T levels significantly correlated with total antioxidant status (r = -0.5) and lipid hydroperoxides (r = 0.78) but not with systolic blood pressure. CONCLUSION: Supracoeliac aortic crossclamping is associated with a significant release of the myocardial injury marker troponin-T. This seems to correlate with the severity of oxidative rather than hemodynamic stresses. Ameliorating oxidative injury during TAAA surgery may therefore have a cardioprotective effect.
APACHE↗
Improving walking ability and ankle brachial pressure indices in symptomatic peripheral vascular disease with intermittent pneumatic foot compression: a prospective controlled study with one-year follow-up.
PURPOSE: Intermittent pneumatic foot compression (IPC(foot)) augments arterial leg inflow. It has been suggested that prolonged use of impulse leg compression at home might ameliorate claudication caused by peripheral vascular disease by improving collateral circulation. The purpose of this study was to determine the effect of IPC(foot) treatment on claudication distance and arterial hemodynamics in patients with intermittent claudication caused by peripheral vascular disease. METHODS: Thirty-seven patients with stable intermittent claudication were admitted to this prospective controlled study. Of these, 25 patients received IPC(foot) (>4 hr/d) for 4.5 months (group 1), and the other 12 patients acted as control patients (group 2). Both groups were advised to exercise unsupervised for a minimum of 1 hour daily and received aspirin (75 mg/d). Groups were matched for age, sex, risk factors, claudication distances, and ankle pressures at baseline. In each patient, initial claudication distance (ICD), absolute claudication distance (ACD), resting ankle brachial index (r-ABI), ankle brachial pressure index after exercise (p-eABI), and popliteal artery volume flow were measured at day 0, 2 weeks, and 1, 2, 3, and 4.5 months. On completion of the treatment period (4.5 months), both groups continued with aspirin (75 mg/d) and unsupervised exercise and were re-examined after 12 months. Data analysis is based on nonparametric statistics, the Wilcoxon signed ranks test, and the Mann-Whitney test for intragroup and intergroup comparisons, respectively. Results are expressed as median and interquartile ranges. RESULTS: Over the 4.5 months of active treatment, (1) median ICD in group 1 increased by 146% (P <.001), from 78 m (interquartile range, 65-102 m) at baseline to 191.5 m (interquartile range, 127-254 m); ICD did not significantly increase in group 2; (2) median ACD in group 1 improved by 106% (P <.001), from 124 m (interquartile range, 100-160 m) to 255 m (interquartile range, 149-398 m); no significant changes were documented in group 2; (3) median r-ABI in group 1 rose by 18% (P <.001), from 0.57 (interquartile range, 0.48-0.62) to 0.67 (interquartile range, 0.64-0.70); no improvement was noted in group 2; (4) median p-eABI in group 1 rose by 110% (P <.001), from 0.21 (interquartile range, 0.07-0.27) to 0.44 (interquartile range, 0. 36-0.52); no changes were noted in group 2; and (5) median popliteal artery volume flow in group 1 improved by 36% (P <.001), from 100 mL/min (interquartile range, 59-163 mL/min) to 136 mL/min (interquartile range, 99.5-173.4 mL/min); no significant changes were found in group 2. At 4.5 months, ICD, ACD, r-ABI, and p-eABI in group 1 were all significantly better than those in group 2 (P <.01). Twelve months' posttreatment, walking ability and ABIs in group 1 were not statistically different from those at 4.5 months and remained significantly better than those of control subjects. CONCLUSION: Intermittent pneumatic foot compression used at home for 4.5 months increases claudication distance by over 100%. Associated increases in r-ABI by 18%, p-eABI by 110%, and arterial calf inflow by 36% suggest an improved collateral circulation. Maximum benefit seems to be offered over the initial 3 months. Treatment benefits are maintained 1 year after treatment. A multicenter study is indicated to quantify actual benefits and to demonstrate cost effectiveness.
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The acute effects of intermittent pneumatic foot versus calf versus simultaneous foot and calf compression on popliteal artery hemodynamics: a comparative study.
INTRODUCTION: Intermittent pneumatic compression (IPC) is currently being investigated with respect to its effect on distal arterial volume flow in patients with peripheral vascular disease. Recently published data have shown a substantial acute enhancement in arterial calf inflow in response to IPC of the lower limb in both intermittent claudication and leg ischemia. PURPOSE: The aim of the study was to compare the immediate effects of intermittent pneumatic foot (IPC(foot)) versus calf (IPC(calf)) versus simultaneous foot and calf compression (IPC(foot+calf)) on popliteal artery hemodynamics in patients with intermittent claudication (Fontaine II) and in normal subjects, using duplex ultrasonography. For this purpose, 25 limbs of 20 healthy subjects (age range [mean], 51-74 [64] years) and 31 limbs of 25 claudicants (age range [mean], 56-81 [66.5] years; resting ankle-brachial indices, 0.38-0.75 [0.55]) were examined in the sitting position with and without IPC compression. RESULTS: Mean popliteal artery flow in healthy subjects increased by 98.8% on application of IPC(foot), 188% with IPC(calf), and 274% with IPC(foot+calf) (all P <.001). Mean flow in claudicants increased by 58% on application of IPC(foot), 132% with IPC(calf), and 174% with IPC(foot+calf) (all P <.001). The mean velocity, peak systolic velocity, and end diastolic velocity displayed a pattern of change similar to that for volume flow in both groups. Pulsatility index decreased in both groups on application of IPC; the lowest values were generated with IPC(foot+calf). CONCLUSION: Of the three compression modes investigated, IPC(foot+calf) was the most effective means of acutely augmenting arterial calf inflow in arteriopaths and normals. The significant increase in end diastolic velocity and decrease in pulsatility index indicate that peripheral vasodilatation is the central mechanism in this impulse-related flow augmentation. Prospective trials are indicated to determine the clinical potential of the long-term effects of IPC(foot+calf) in patients with symptomatic peripheral vascular disease.
Aged↗
The use of citrated whole blood in thromboelastography.
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Adult↗
Endotoxemia during supraceliac aortic crossclamping is associated with suppression of the monocyte CD14 mechanism: possible role of transforming growth factor-beta1.
PURPOSE: Monocyte CD14 and its soluble form (sCD14) mediate the proinflammatory response to endotoxemia. The aim of this study was to measure the changes to these factors after major aortic surgery and the possible inhibitory role of transforming growth factor-beta(1) (TGF-beta(1)) during these procedures. METHODS: Twenty-four patients with supraceliac aortic crossclamping during thoracoabdominal aortic aneurysm (TAAA) repair and 12 patients with infrarenal aortic crossclamping as part of infrarenal aneurysm repair (AAA) were studied. Blood was collected at incision, aortic clamping, and reperfusion and at 1, 8, and 24 hours after reperfusion. Samples were assayed for endotoxin, peripheral blood monocyte CD14 expression, sCD14, tumor necrosis factor-alpha, and TGF-beta(1). RESULTS: Although there was significant endotoxemia on reperfusion in both groups of patients, peak plasma endotoxin levels were significantly higher in patients with TAAA (P =.001). Monocyte CD14 and plasma sCD14 were significantly decreased in patients with TAAA at reperfusion and 1 hour after reperfusion (P <.01, both points). In patients with AAA, a significant upregulation of CD14 was observed at 24 hours after reperfusion (P <.01), but no significant changes in sCD14 were observed. TNF-alpha showed no significant changes during the study period in both groups. In patients with TAAA, TGF-beta(1) showed significant elevation at all time points (P <.01); whereas in patients with AAA, TGF-beta(1) showed no significant changes. CONCLUSION: Splanchnic ischemia reperfusion in patients who undergo supraceliac aortic clamping is associated with peripheral blood monocyte CD14 suppression and significant elevation of TGF-beta(1). TGF-beta(1) may play an important role in modulating the immune response to endotoxemia during major aortic aneurysm surgery.
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Nutritional hyperhomocysteinaemia.
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Diet↗
Improved management of infrainguinal bypass graft infection with methicillin-resistant Staphylococcus aureus.
BACKGROUND: There is considerable debate over the management of infected infrainguinal grafts. This report describes recent experience in this field and documents the change in clinical practice needed to deal with methicillin-resistant Staphylococcus aureus (MRSA). METHODS: All infected infrainguinal grafts between January 1991 and July 1997 were reviewed. In the light of the findings, clinical practice was modified considerably. A further 1 year was audited prospectively up to August 1998. RESULTS: Twenty-six patients were treated for 27 infrainguinal graft infections (25 prosthetic, two vein). Twenty were treated by complete graft excision as the initial therapy; graft preservation was attempted in six patients. Before 1995, the infecting organisms were predominantly Pseudomonas aeruginosa or methicillin-sensitive staphylococci. Subsequently all 14 patients treated up to 1997 had infection with MRSA. The overall amputation rate was 17 of 26; ten amputations were in patients with MRSA. Four patients died, all with MRSA sepsis. As a result of this experience a policy of complete isolation was adopted for all patients infected with MRSA. In the 12 months since this policy was introduced, 77 infrainguinal grafts (61 vein, 16 prosthetic) have been inserted. Two grafts (3 per cent) have become infected, necessitating graft excision and amputation. CONCLUSION: MRSA infection of an infrainguinal graft is a serious complication with high associated amputation and mortality rates. Isolation and barrier nursing appeared to contain the problem.
Adult↗
Vascular surgical society of great britain and ireland: transcranial doppler ultrasonography as a predictor of haemodynamically significant carotid stenosis
BACKGROUND: Transcranial Doppler (TCD) ultrasonography can detect evidence of collateral flow across the anterior communicating artery and/or the posterior communicating artery, which occurs when there is significant alteration of 'inflow' to the brain. The aim of the study was to determine the blood flow velocity produced by a carotid stenosis which produces this haemodynamic effect on the cerebral circulation and evokes collateral circulation. METHODS: Forty-eight patients with varying degrees of carotid stenosis (10 per cent to occlusion) who underwent both carotid duplex and TCD examination were reviewed. An ATL HDI 3000 ultrasound system was used for the carotid and TCD studies. The carotid examination recorded peak-systolic velocity (PSV) and end-diastolic velocity (EDV) in the carotid systems bilaterally. TCD recorded Doppler spectra from the bilateral middle cerebral, anterior cerebral, posterior cerebral, intracranial vertebral and basilar arteries. Collateral flow was assessed in two ways: 'intracranial crossover' collateral and 'posterior to anterior' collateral. Each internal carotid artery (ICA), together with the ipsilateral hemisphere, was analysed for the presence or absence of collateral flow. Data were expressed as mean(s.e.m.). RESULTS: The PSV of the group with collateral circulation was 472(14) cm s-1 and that of the group without collateral flow was 164(3) cm s-1 (P < 0.0001, Mann-Whitney test). The respective EDVs were 158(13) and 58(7) cm s-1 (P < 0.0001). CONCLUSION: PSVs and EDVs in the ICA, in conjunction with collateral flow measured by TCD, are indicators of a haemodynamically significant carotid lesion, and provide more information than two-dimensional imaging studies. In the future, parameters set by combining carotid duplex and TCD investigations may represent the 'gold standard' for evaluation of cerebral blood flow.
Journal Article↗
Vascular surgical society of great britain and ireland: platelet function during carotid endarterectomy and the antiplatelet effect of dextran 40
BACKGROUND: Dextran 40 has been shown to reduce cerebral embolization following carotid endarterectomy (CEA). This study aimed to determine changes in platelet function during CEA and the antiplatelet effect of dextran 40. METHODS: Platelet function was measured by whole-blood flow cytometry in the peripheral arterial blood of patients during CEA and 24 h later. The binding index of P-selectin and PAC-1 expression were measured as markers of activation and aggregation. Patients were kept on aspirin 75-150 mg until the day of surgery and received an intravenous bolus of 5000 units unfractionated heparin before carotid artery clamping. High-intensity transient signals (HITS) in the ipsilateral middle cerebral artery were measured with transcranial Doppler (TCD) ultrasonography before, during and after operation. Results are presented as median (interquartile range) and statistical significance was determined using the Mann-Whitney U test. RESULTS: Thirty-eight patients undergoing CEA were studied. The P-selectin binding index rose significantly from incision (0.9 (0.2-2.7)) after carotid clamping (1.5 (0.6-3.6); P < 0.01), clamp release (1.7 (0. 3-3.0); P < 0.01), 1 h after operation (1.5 (0.3-2.6); P < 0.05) and 24 h after operation (1.3 (0.6-2.5); P < 0.05). PAC-1 binding index increased from incision (0.4 (0.1-0.8)) after carotid clamping (2.0 (0.4-4.2); P < 0.01) and clamp release (1.8 (0.3-2.9); P < 0.05). TCD monitoring showed an increase in preoperative HITS per 30 min (2 (0-3)) during dissection (8 (1-15); P < 0.05), after clamp release (16 (2-27); P < 0.01) and during recovery (10 (2-29); P < 0.01). After operation, patients with more than 50 HITS per 30 min were started on an infusion of dextran 40. Six patients had a dextran 40 infusion. The P-selectin binding index decreased from 1.6 (0.7-1.9) to 0.6 (0.3-1.5) 1 h after dextran (P < 0.05) and 0.1 (0.1-0.2) 24 h after dextran (P < 0.05). PAC-1 expression decreased from 0.4 (0.3-0. 5) to 0.1 (0.1-0.1) 24 h after dextran (P < 0.05). CONCLUSION: Significant platelet activation and aggregation occurs during CEA despite the use of antiplatelet treatment. A simultaneous increase in HITS was demonstrated with TCD. Dextran 40 was shown to have an antiplatelet effect after CEA; this is further evidence that it may have a role in reducing thromboembolic complications.
Journal Article↗
Repair of ruptured thoracoabdominal aortic aneurysm is worthwhile in selected cases.
INTRODUCTION: The risks and benefits of operating on patients with ruptured thoracoabdominal aortic aneurysm (TAAA) have not been defined. The aim of the present study is to report this unit's experience with operations performed for ruptured TAAA over a 10-year period. METHODS: Interrogation of a prospectively gathered computerised database. PATIENTS: Between 1 January 1983 and 30 June 1996, 188 consecutive patients with TAAA were operated on, of whom 23 (12%) were operated for rupture. RESULTS: There were nine survivors (40%). Patients whose preoperative systolic blood pressure remained above 100 mmHg were significantly more likely to survive (4/8 vs. 13/15, p = 0.03 by Fisher's exact test). Survival was also related to Crawford type: type I (two of three survived); II (none of six); III (two of six); and IV (five of eight). All non-type II, non-shocked patients survived operation. Survivors spent a median of 28 (range 10-66) postoperative days in hospital, of which a median of 6 (range 2-24) days were spent in the intensive care unit. Survivor morbidity comprised prolonged ventilation (> 5 days) (n = 3); tracheostomy (n = 1); and temporary haemofiltration (n = 2). No survivor developed paraplegia or required permanent dialysis. CONCLUSIONS: Patients in shock with a Crawford type II aneurysm have such a poor prognosis that intervention has to be questioned except in the most favourable of circumstances. However, patients with types I, III and IV who are not shocked on presentation can be salvaged and, where possible, should be transferred to a unit where appropriate expertise and facilities are available.
Aged↗
Anti-heat-shock protein 70 kDa antibodies in vascular patients.
INTRODUCTION AND AIM OF STUDY: there is recent evidence that the immune system plays an essential role in the pathogenesis of atherosclerosis, with both cellular and humoral mechanisms being involved. Heat-shock proteins (HSPs) have been detected in atherosclerotic lesions, and antibodies to HSPs have also been found to be raised in patients with carotid stenoses. The aim of our study was to examine the level of anti-HSP70 antibodies in patients with other vascular diseases. MATERIALS AND METHODS: a questionnaire was designed for the subjects in the study, with documentation of clinical details and ankle-brachial pressure index. Patients with concomitant infection, malignancy, hepatorenal failure, or recent surgery were excluded. Enzyme-linked immunosorbent assay (ELISA) was used to identify anti-HSP70 antibodies in the sera in different dilutions. Graphs of optical density (OD) vs. negative log dilution were plotted, the gradient of which was taken to be the estimated optical density for each subject (proportional to antibody level). Our groups consisted of controls (n =21, mean age 59.0+/-19.2), lower limb claudicants ( n =19, mean age 60.0+/-12.6), patients with lower-limb critical ischaemia ( n =22, mean age 68.5+/-10.07), and patients with abdominal aortic aneurysms ( n =20, mean age 69.9+/-6.2). RESULTS: we found no correlation between age and the estimated OD in our subjects (Spearman's correlation coefficient ( r )=0.123, one-tailed p value was 0.135). Patients with intermittent claudication, critical lower limb ischaemia, and aneurysms had higher estimated OD, and therefore higher anti-HSP70 antibody levels, than controls (Mann-Whitney test p =0.0127, 0.0037, 0.0008, respectively). CONCLUSIONS: our data provide the first evidence of a correlation between anti-HSP70 antibodies and different types of vascular diseases, suggesting that HSP70 might be involved in the pathogenesis and propagation of atherosclerosis. Since the immune response to HSPs can be modulated, this opens up the possibility of new therapeutic approaches.
Adult↗
Endovascular repair of an iatrogenic left common carotid to innominate vein fistula.
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Angiography↗