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Biomedical subjects

G Stansby

Publications and source records attributed to G Stansby.

At least 19 recordsLinked to original sources

Homocysteine lowering interventions for peripheral arterial disease and bypass grafts.

BACKGROUND: Elevated plasma levels of the amino acid homocysteine (hyperhomocysteinaemia) are associated with hardening or blocking of the arteries (atherosclerosis) In addition, there is a poorer prognosis, both in the progression of the disease and outcome after therapy. Treatment to lower homocysteine levels has been shown to be both effective and cheap in healthy volunteers. However, the impact of reducing homocysteine levels on the progression of atherosclerosis and patency of vessels after treatment for atherosclerosis is still unknown and forms the basis for this review. OBJECTIVES: To assess the effects of plasma homocysteine-lowering therapy on the clinical progression of disease in patients with peripheral arterial disease (PAD) and hyperhomocysteinaemia, including, as a subset, those who have undergone surgical or radiological intervention. SEARCH STRATEGY: The reviewers (MH,GS) searched the Cochrane Peripheral Vascular Diseases Group trials register, the Cochrane Controlled trials register (2002, Issue 1), MEDLINE, EMBASE and reference lists of relevant articles. SELECTION CRITERIA: Randomised trials of the treatment of hyperhomocysteinaemia in patients with peripheral arterial disease, before and after surgical or radiological intervention versus no treatment for hyperhomocysteinaemia. DATA COLLECTION AND ANALYSIS: Two reviewers (MH,GS) independently assessed trial quality and extracted data. Information on adverse events was collected from the trials. MAIN RESULTS: There are currently no randomised trials available for analysis. REVIEWER'S CONCLUSIONS: Well constructed trials assessing the impact of the treatment of hyperhomocysteinaemia in patients with peripheral arterial disease are urgently required.

Arteriosclerosis↗

Intravascular brachytherapy for peripheral vascular disease.

BACKGROUND: International treatment of atherosclerotic narrowed and blocked arteries involves either bypassing the blockage using a graft, widening it from the inside with a balloon, a procedure known as percutaneous transluminal angioplasty (PTA), or providing a strut to hold the vessel open, known as a stent. All of these treatments are however limited by the high numbers that fail within a year. Intravascular brachytherapy (IVBT) is the application of radiation directly to the site of vessel narrowing. It is known to inhibit the processes that lead to restenosis (narrowing) of vessels and grafts after treatment. OBJECTIVES: The objective of this review was to assess the efficacy and complications of intravascular brachytherapy on maintaining patency after angioplasty or stent insertion in native vessels or bypass grafts of the iliac or infrainguinal arteries. SEARCH STRATEGY: The reviewers searched the Cochrane Peripheral Vascular Diseases Group Trials Register (last searched 5 July 2002), the Cochrane Controlled Trials Register (last searched Issue 2, 2002), MEDLINE, EMBASE and reference lists of relevant articles. SELECTION CRITERIA: Randomised trials of the use of brachytherapy as an adjunct to the treatment of patients with peripheral arterial diseases (PAD) or stenosed bypass grafts of the iliac or infrainguinal arteries arteries versus the procedure without brachytherapy. DATA COLLECTION AND ANALYSIS: Two reviewers independently assessed trial quality and extracted data. Adverse events information was collected from the trials. MAIN RESULTS: One trial was identified which met the inclusion criteria, involving 117 patients, mean age 71 years (43-89). The trial compared PTA versus PTA and IVBT in patients with long-segment de novo or restenotic lesions or occlusions of any length in the femoropopliteal artery. Results were provided at six month follow up in 107 patients (54 PTA alone, 53 PTA+IVBT). The results favoured adjuvant IVBT in preventing restenosis/occlusion with an odds ratio (OR) of 0.35 (95% CI 0.24 to 0.53). Analysis of subgroups showed a significant benefit of IVBT in non-diabetics, OR 0.22 (95% CI 0.07 to 0.69), in those undergoing IVBT in restenotic lesions, OR 0.32 (95% CI 0.10 to 1.01), occlusive lesions, OR 0.19 (95% CI 0.06 to 0.62) and lesions in which the PTA length was greater than 10cm, OR 0.24 (95% CI 0.09 to 0.62). REVIEWER'S CONCLUSIONS: Results from the only trial available would suggest that IVBT is effective at improving the patency of femoropopliteal arteries undergoing PTA in the short-term, particularly in non-diabetics with long occlusions (>10cm).

Angioplasty↗

Homocysteine in myointimal hyperplasia.

INTRODUCTION: homocysteine, a sulphur-containing non-essential amino acid, appears to play a role in the pathophysiology of atherosclerosis. However, its role in myointimal hyperplasia, the cause of almost 30% of failures of interventional therapeutic procedures, is much less clear. METHODS: a review of the published scientific data concerning the role of homocysteine in myointimal hyperplasia was performed using MEDLINE and other on-line databases. Evidence was sought from cell culture experiments, animal models and clinical studies. RESULTS: several clinical studies have recently been published linking plasma homocysteine levels to restenosis in coronary and peripheral arterial disease. However, several contradictory studies also exist making the role of homocysteine unclear. There are currently no published randomised trials. Cell culture and animal model experiments have elucidated several potential mechanisms by which may stimulate myointimal hyperplasia. Possible mechanisms include endothelial cell activation with the enhanced release of inflammatory cytokines and growth factors and a direct effect on vascular smooth muscle cell migration and proliferation. CONCLUSIONS: further studies are required before the true role of homocysteine in the pathogenesis of myointimal hyperplasia can be clearly evaluated. If evidence does confirm a role, the ease with which homocysteine levels can be normalised makes it an attractive alternative therapeutic target for intervention.

Animals↗

Prevention of experimental myointimal hyperplasia by immunomodulation.

INTRODUCTION: we have tested the hypothesis that treatment with a mycobacterial preparation that modulates the antibody response, would diminish restenosis in a rat angioplasty model. MATERIALS/METHODS: male Sprague-Dawley rats were used. All immunisations were given subcutaneously. Group A (control) received normal saline on days 0, 21, and 42. Group B received SRL172 on days 0, 21, and 42. Group C received SRL172 on days 0, 21, and 42, and hsp65/Incomplete Freund's on days 21 and 42. Group D received hsp65/Freund's on days 21 and 42. Right common carotid arteries were balloon-injured on day 63 using a standard technique known to produce MIH and animals were sacrificed on day 77. For each carotid 6 microm cross sections were cut from paraffin blocks. Cross-sectional areas were measured by computerised planimetry. RESULTS: balloon injury resulted in MIH in all animals. Data represents mean+/-SEM for the percentage of area enclosed within the internal elastic lamina occupied by MIH (% MIH); which for groups A, B, C, and D was 85+/-11, 24+/-3, 27+/-7, and 17+/-3 respectively. All the treatment groups had significantly less MIH when compared to the control group but no statistically significant difference was found between any of the treatment groups. CONCLUSIONS: this is the first report that immunomodulation with mycobacterial material suitable for use in man, can reduce MIH. Since such modulation has low risk, this raises the prospect of an important new therapeutic modality to combat restenosis.

Adjuvants, Immunologic↗

Bypass or angioplasty for severe limb ischaemia? A Delphi Consensus Study.

OBJECTIVES: To examine the level of agreement among vascular surgeons and interventional radiologists regarding their preference for the surgical or endovascular management of severe limb ischaemia. DESIGN: Delphi consensus study using 596 different hypothetical patient scenarios. PARTICIPANTS: Delphi consensus group for the Bypass versus Angioplasty in Severe Ischaemia of the Leg (BASIL) trial. METHODS: Twenty consultant vascular surgeons and 17 interventional radiologists completed both rounds of the study. The scenarios detailed the anatomical extent of disease, whether the patients had rest pain only or had tissue loss, and whether or not a suitable vein for bypass was available. Panellists were asked to score their treatment preference for either surgery or angioplasty on an eight-point scale. Outliers (top 10% and bottom 10% responses) were removed. If the remaining 80% of responses fell within a 3-point range, this was defined as "agreement". If they did not, this was considered "disagreement". RESULTS: There was substantial disagreement in 484 (81%) of scenarios in round 1 and 401 (67%) in round 2. This disagreement was greater among surgeon than radiologists in both round 1 (83 vs 65%) and round 2 (69 vs 42%). Surgeons also demonstrated less convergence between rounds. CONCLUSIONS: There is substantial disagreement between and among surgeons and radiologists with regard to the appropriateness of surgery or angioplasty for severe limb ischaemia. This lack of consensus stems from the absence of an evidence base and means that the same patient may receive entirely different treatment depending on which hospital and consultant they attend. Not only may this unexplained variation be clinically unsatisfactory, it has major implications for the planning and use of health service resources.

Angioplasty, Balloon↗

Intravascular brachytherapy: a systematic review of its role in reducing restenosis after endovascular treatment in peripheral arterial disease.

INTRODUCTION: Intravascular brachytherapy (IVBT) utilises the percutaneous insertion of a radioactive source to inhibit myointimal hyperplasia in arteries treated by balloon angioplasty or stenting. A systematic review was performed of trials of IVBT in patients with Peripheral Arterial Disease (PAD). METHODS: Search strategy - the reviewers searched Medline, Embase, the Cochrane Peripheral Vascular Diseases Group trials register, DARE, CCT and NHS EED for clinical studies and trials of adjuvant IVBT in PAD. Two reviewers assessed trial quality independently. RESULTS: Fourteen clinical trials were identified by the search, representing five clinical studies (all allocated D for not randomised) and one randomised controlled trial (allocated A). The randomised trial showed a benefit for IVBT compared with placebo (OR 0.35, 95% CI 0.24-0.53). In the non-randomised studies, 12 month cumulative patency rates ranged from 60-87%. There were few technical complications. In the only report involving IVBT and routine concurrent stent insertion acute thrombosis occurred in 7 (21%) of patients. CONCLUSION: Early reports have confirmed the safety and technical feasibility of IVBT. However, follow-up is too short at present to assess the durability and long-term complications of this new therapeutic option.

Angioplasty, Balloon↗

Platelet activation during carotid endarterectomy and the antiplatelet effect of Dextran 40.

OBJECTIVE: To determine changes in platelet activation during carotid endarterectomy (CEA) and the antiplatelet effect of Dextran 40. METHODS: Prospective study in 40 patients undergoing CEA. Platelet activity was measured by whole blood flow cytometry and platelet aggregometry during CEA. The expression of P-selectin and the PAC-1 antigen were used as markers of platelet activation and aggregation. Patients received aspirin (75-300 mg) preoperatively and 5,000 units unfractionated heparin during surgery. High intensity transient signals (HITS) in the ipsilateral middle cerebral artery were monitored using transcranial Doppler (TCD) perioperatively. RESULTS: P-selectin expression increased after carotid clamping (P < 0.01) and clamp release (P < 0.05). There was higher expression of PAC-1 after carotid clamping (p < 0.05). Spontaneous and ADP-induced platelet aggregation increased after carotid clamping (P< 0.01) and release (P < 0.01). TCD monitoring showed an increased HITS count from preoperative levels, after clamp release (P < 0.01) and during recovery (P < 0.01). After the operation, patients with more than 50 HITS per 30 min were started on an infusion of dextran 40 (n = 6). P-selectin expression decreased 24 h after dextran 40 (P < 0.01). CONCLUSION: Significant platelet activation and aggregation occurs during CEA despite the current use of antiplatelet treatment. Dextran 40 had an antiplatelet effect after CEA providing further evidence that it may contribute to reducing thromboembolic complications.

Aged↗

Systematic review of antiplatelet therapy for the prevention of myocardial infarction, stroke or vascular death in patients with peripheral vascular disease.

BACKGROUND: Antiplatelet agents may prevent vascular events and death in patients with peripheral vascular disease (PVD). METHODS: A systematic review of 39 randomized controlled trials of antiplatelet therapy in patients with PVD was performed. RESULTS: For patients with PVD the number suffering a non-fatal myocardial infarction, non-fatal stroke or vascular death in the antiplatelet group was 6.5 per cent compared with 8.1 per cent in the placebo group (odds ratio 0.78 (95 per cent confidence interval (c.i.) 0.63--0.96); P = 0.02), favouring antiplatelet treatment. For infrainguinal bypass surgery (ten trials) and balloon angioplasty (two) the differences were still in favour of antiplatelet therapy, but they did not reach statistical significance. In five trials of aspirin against another antiplatelet agent, 8.4 per cent in the aspirin group suffered a vascular event compared with 6.6 per cent in the second antiplatelet group (odds ratio 0.76 (95 per cent c.i. 0.64--0.91); P < 0.01), favouring ticlopidine/clopidogrel/aspirin + dipyridamole against aspirin alone. CONCLUSION: Antiplatelet therapy reduces serious vascular events and vascular death in patients with PVD. For infrainguinal arterial surgery or balloon angioplasty the benefit remains unproven, but the number of trials to date is small. There is also evidence to support the use of antiplatelet drugs other than aspirin for the prevention of vascular events in those with PVD.

Catheterization↗

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.

Aged↗

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↗