Intermittent claudication. A comparison between subjective and measured claudication walking distance.
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INTRODUCTION: Intermittent arterial claudication is the master symptom in lower limbs arteriopathy. It is used as a reference in invasive or non-invasive arterial explorations. It allows to assess the evolutive degree of the disease and above all helps the therapeutic decision. The seat of claudication is traditionally acknowledged as being located immediately downstream of the significant arterial lesion. The purpose of our work was to verify such a notion and ascertain the relation between spontaneous and tread-mill induced claudication. PROTOCOL: 60 stage-2 arteritic patients were included in a prospective mode study. They were all taken in hospital for arteriographic check-up and vascular functional explorations: Doppler velocimetry, segment pressures, treadmill tests and pressure measurements after stress. The patients were classified according to age (table I), time of claudication record (table II) and lesions location (table III). All clinical and paraclinical data were recorded with a view to correlations interpretation. RESULTS AND DISCUSSION: The relation between spontaneous claudication and tread-mill induced claudication was studied with respect to lesion sites (table IV). Among 37 patients 46% of the claudications observed appeared at iliac stage in both cases (fig. 1). In 35 cases, femoral claudication was observed in 48% (fig. 2). As for distal claudication among 6 patients, 3 showed calf claudication in both cases, i had foot claudication and 2 showed discrepant claudication types. The relation between claudication and lesion site was not confirmed in all cases. Buttock claudication always appeared in relation with a lesion upstream or an internal iliac lesion.(ABSTRACT TRUNCATED AT 250 WORDS)
Conservative measures to improve claudication distance include advice on smoking, exercise, diet and weight reduction. Although the effects of smoking, exercise and diet are established, the effect of weight is less clear. The aim of this study was to investigate the effect of carrying extra weight on the maximum walking distance in stable claudicants. Twenty stable claudicants were exercised on a treadmill (3.5 km/h, 0 degrees slope) carrying 0, 2.5, 5, 7.5 and 10 kg weights in randomized sequence. Maximum claudication distance and ankle: brachial pressure indices were recorded. Patients were categorized into mild or severe claudicants depending on their ability to walk 200 m. A response index (RI) was calculated as the reduction in claudication distance per kilogram load; RI = [CD0-CD10]/10 m/kg, where CD0 and CD10 represent claudication distance with 0 and 10 kg weights, respectively. Claudication distance was significantly reduced in subjects carrying 5 kg or more (P less than 0.01). A linear relationship was demonstrated between the mean claudication distance and the load carried (r = 0.98, P less than 0.01) with a mean response index of 10.2 m/kg. The mean(s.e.m.) RI in mild claudicants (25.9(9.5) m/kg) was greater than the value observed in the severe claudicants (3.3(0.8) m/kg; P less than 0.01, Mann-Whitney U test). This study demonstrates that weight adversely affects claudication distance and suggests that weight reduction may deserve greater emphasis in the management of some patients with intermittent claudication.
Treadmill testing is used to estimate the severity of claudication, but routine use is not practical or cost-effective in all settings. Thus, the purposes of this study were: (1) to develop and cross-validate prediction equations for treadmill claudication pain distances in a heterogeneous cohort of peripheral arterial occlusive disease patients, and (2) to determine if the regression equations were more accurate in assessing claudication distances than self-reported distances of patients. Medical history, vital signs, resting ankle/brachial systolic pressure index (ABI), and claudication distances during a graded treadmill test were obtained on a validation group of 178 claudicants and on a cross-validation group of 94 claudicants. The independent predictors of claudication pain distances of the validation group were ABI, body mass index, gender, and current smoking status, with multiple correlation coefficients of R = 0.73 and R = 0.82 for the distances to onset and to maximal pain, respectively. These equations were successfully cross-validated on an independent group of claudicants, as the predicted distances to onset of claudication pain (167.2 +/- 102.6 m) and to maximal pain (354.6 +/- 154.3 m) were similar (p = 0.99) to measured distances (169.1 +/- 127.8 m and 356.6 +/- 181.0 m, respectively). However, the self-reported distances to onset (89.5 +/- 126.3) and to maximal claudication pain (189.2 +/- 284.3) were 1-2 blocks less than either the measured or predicted distances (p < 0.01). It is concluded that claudication pain distances during an incremental treadmill test can be more accurately estimated from a composite of variables obtained during medical screening than by relying on the self-report of patients. Consequently, in clinical settings where treadmill testing is impractical, the functional severity of claudication can be assessed without exercise testing.
The effect of 5 min treadmill exercise was investigated in claudicant patients and healthy controls; systemic neutrophil count, plasma thromboxane and von Willebrand's factor (a marker for endothelial injury) were measured. Median (interquartile range (i.q.r.)) resting neutrophil count was 5.6 (5.2-6.0) x 10(6) cells l-1 in claudicants and 2.8 (2.6-3.2) x 10(6) l-1 in controls (P < 0.05); this increased in those with claudication to 7.1 (6.2-7.7) x 10(6) l-1 immediately after exercise (P < 0.05). The resting plasma thromboxane level was 32.1 (25.0-60.0) pg ml-1 in claudicants and rose to 135.0 (104.0-141.3) pg ml-1 15 min after exercise, compared with a rise from 25.0 (22.0-33.5) to 55.5 (33.0-67.0) pg ml-1 in controls (P < 0.05). The resting serum von Willebrand's factor level was 127 (110-135) units dl-1 in claudicants compared with 60 (48-71) units dl-1 in controls; this difference persisted after exercise (P < 0.01). In patients with claudication, the level of von Willebrand's factor increased to 150 (140-156) units dl-1 60 min after exercise (P < 0.05). Free radical scavenging capacity was also investigated by measuring the plasma antioxidant activity of glutathione peroxidase and its essential non-metal cofactor selenium. Scavenging capacity was lower in claudicant patients whose median (i.q.r.) glutathione peroxidase activity (change in absorbance per min per ml plasma) was 2.84 (2.39-3.61) versus 3.24 (3.06-3.79) in controls (P < 0.05). Similarly, plasma concentrations of selenium were lower in claudicants at a median (i.q.r.) of 75.0 (58.0-81.0) micrograms l-1 compared with 88.0 (75.0-92.5) micrograms l-1 in controls (P < 0.05). Exercise in claudicant patients leads to neutrophilia and thromboxane production with subsequent endothelial injury. The antioxidant activity of glutathione peroxidase is reduced in patients with claudication and may allow the unopposed action of free radicals to damage endothelium.
BACKGROUND: recent research has shown that episodes of claudication may be associated with a systemic inflammatory response that causes injury to the vascular endothelium. As claudicants are often directed to undertake regular walking exercises there has been a concern that this may accelerate endothelial injury. AIMS: the aim of our study was to assess the baseline markers of ischaemia-reperfusion injury (IRI) in claudicants and controls after acute treadmill exercise and to then examine the effect of a 3 month supervised exercise-training programme, on these markers, in the claudicant group. METHODS: forty-six claudicants and 22 age-matched controls undertook acute treadmill exercise. Neutrophil activation, degranulation, free radical damage and antioxidants were measured (by flow cytometry, ELISA, and chemiluminescence) at rest and at 5, 30 and 60 min post-exercise. Claudicants were then recruited into an intensive 3 month supervised exercise programme (SEP) after which the same parameters of IRI were reassessed at different time points, at 3 and 6 months. RESULTS: resting markers of IRI were similar in both groups. Exercise had no effect on the control group. Immediately after exercise, claudicants developed significant neutrophil activation and degranulation with free radical damage. This effect decreased sequentially after 3 months of exercise training. CONCLUSION: this study for the first time demonstrates that the exercise training of claudicants is beneficial, not only in terms of improving their walking distance, but also by decreasing the injurious effects of IRI that occur during claudication. Exercise training should be an essential part of the medical management of the majority of claudicants.
AIMS: to evaluate the prevalence of coronary artery disease (CAD) by means of modified stress electrocardiography in patients presenting with intermittent claudication. METHODS: three hundred consecutive patients (188 male) with intermittent claudication (post-exercise ankle brachial index <0.8), and 100 age and sex-matched controls, were assessed for CAD with resting and stress 12-lead-precordial ECG. A history of angina and previous myocardial infarction (MI) was recorded. EXCLUSION CRITERIA: recent (<1 month) MI; unstable angina; prior coronary intervention; arrhythmias; conduction abnormalities; uncontrolled hypertension; heart failure, digoxin therapy, and inability to perform tests. RESULTS: based on antecedent angina, MI and abnormal resting ECG, CAD prevalence was 47% in claudicants and 6% in controls; on 12-lead-precordial ECG stress testing, CAD prevalence was 46% (95% CI: 40.1-51.7%) in claudicants and 11% (95% CI: 4.8-17.2%) in controls (both p <0.0001). Only 67% of claudicants (n=141) with antecedent angina, MI or an abnormal resting ECG, met the criteria of CAD on stress testing; also 28% of claudicants without antecedent angina, MI and a normal resting ECG (n=159) had evidence of CAD. The odds ratio for CAD in claudicants was 6.9. Based on 12-lead-precordial ECG stress testing we detected the presence of: one-, two- and three-vessel disease in 14.7% (95% CI: 10.6-18.7%), 19% (95% CI: 14.5-23.5%) and in 12.3% (95% CI: 8.6-16%) of claudicants; and in 8, 3 and 0% of controls, respectively. CONCLUSIONS: forty six percent of patients with intermittent claudication had concomitant CAD, and 31% two- or three-vessel disease. In the presence of claudication the odds ratio for CAD is 6.9 (95% CI: 3.5-13.4) and for two- or three-vessel disease 14.8. Non-invasive modified stress electrocardiography by enabling identification of those with multi-vessel CAD and thus by providing cardiac risk stratification may help bridge the gap between clinical evaluation and invasive coronary imaging.
BACKGROUND: Most trials on the reliability of constant-load treadmill testing use one pair of treadmill settings (speed, grade) only. The question of whether the results can be applied to tests with different settings is left open. Also, claudication distances measured with differing settings are not comparable, rendering the comparison of the results from different trials difficult. This study evaluates the reliability of constant-load testing with various workloads and compares them with claudication distances achieved with walking at normal speed on level ground but also evaluates whether metabolic equivalent (MET) normalization can be used to translate the results of different treadmill tests into each other. METHODS: Fifteen patients with claudication underwent repeated treadmill testing with different treadmill settings, including speeds of 2.0, 3.2, and 4.0 km/h (1.25, 2.0, and 2.5 mph, respectively) and grades of 0% and 12%. The walking capacity was also tested on level ground with a speed chosen by the individual patient. Results of virtual treadmill tests with all possible combinations of the speeds and the grades used were predicted from real tests, with MET normalization. The relationship between real and predicted claudication distances was tested with regression modeling. RESULTS: Reliability coefficients (RCs) for the absolute claudication distance (ACD) were superior to RCs for the initial claudication distance. RCs for ACD ranged between 0.61 and 0.95, with increasing values found with increasing workloads. The best coefficients for the regression of measured on predicted claudication distances were achieved with a model on the basis of a power function (r = 0.963). The model was only appropriate for the prediction of group mean results from clinical trials but cannot be applied to single patient data. For proof of concept, the model was tested with six published studies in which the claudication distances of a patient sample were double treadmill tested with different workloads. The result of the second test was predicted from the first test, and estimated and measured claudication distances were compared. The mean difference (all trials) was 7.9%, whereas the maximum difference amounted to 16.5%. CONCLUSION: For an optimal treadmill test reliability, higher workloads should be used and ACD should be preferred over initial claudication distance. MET normalization provides the basis for the comparability of treadmill test results achieved with different test conditions.
PURPOSE: The role of infrainguinal arterial reconstructive surgery for claudication is controversial. We reviewed the results of femorotibial bypass procedures performed in a select group of patients with disabling claudication in an attempt to define a role for this aggressive approach. METHODS: Data were retrieved from the vascular registry, and hospital records were obtained for all patients undergoing femorotibial reconstruction for disabling claudication during the past 16 years at Brigham and Women's Hospital. Follow-up interviews were obtained to assess overall health, walking impairment, functional status, and patient satisfaction. RESULTS: During a 16-year period a total of 57 tibial reconstructions were performed in 53 patients for claudication (5% of all infrainguinal vein reconstructions). Autogenous vein conduit was used in all cases, most of which (70%) involved the greater saphenous vein in situ. Distal anastamoses were to the tibioperoneal trunk (12%), anterior tibial (18%), posterior tibial (47%), and peroneal (23%) arteries. Major complications occurred in 9%, and no perioperative deaths occurred. Overall 5-year survival was 54% +/- 15%, and no major amputations were performed. Cumulative primary and secondary graft patency at 5 years were 81% +/- 6% and 86% +/- 5%, respectively. Patency rates were significantly better than those achieved in a concurrent series of tibial bypasses for limb salvage and were equivalent to those achieved with femoropopliteal bypass for claudication. Interviewed patients reported improved walking distance, reduced claudication, and a high degree of overall satisfaction with their operation. CONCLUSION: Results obtained with femorotibial bypass performed for claudication were superior to those obtained for limb salvage and were equivalent to those obtained with femoropopliteal bypass for claudication. The results obtained in this highly selected cohort suggest that patients at low risk with significant functional impairment from claudication, available autogenous vein, and suitable tibial outflow to the ischemic muscular bed can be offered revascularization with the expectation of durable long-term results.
OBJECTIVES: This study aims to assess the impact of PTA on the quality of life (QoL) of claudicants and to analyse which patients and which arterial lesions derive the most benefit. DESIGN: A prospective observational study. MATERIALS: One hundred and seventeen claudicants undergoing PTA were studied; 35 patients had bilateral disease, whilst 82 had unilateral disease and underwent PTA to a solitary iliac lesion, solitary superficial femoral or a iliac lesion above a diseased superficial femoral artery in 24, 39 and 19 cases, respectively. METHODS: Patients completed the Short Form 36 (SF36) and EuroQol (EQ) QoL assessment instruments prior to and at 1, 3, 6, and 12 months following intervention. The SF36 produces a QoL profile, whilst the EQ produces two QoL indices. RESULTS: Claudication has a deleterious effect on QoL, especially in patients with multi-segment disease. PTA results in an immediate and lasting improvement in the QoL of claudicants. Unilateral claudicants undergoing PTA to a solitary iliac lesion demonstrate the most marked QoL benefits and 12 months post PTA report a QoL approaching that of an age-matched population. Patients with bilateral claudication undergoing unilateral PTA and unilateral claudicants undergoing PTA to a solitary SFA lesion demonstrate some QoL benefits, but at 12 months post PTA do not approach the QoL scores of an age-matched population. Unilateral claudicants undergoing iliac PTA above a diseased SFA demonstrate minimal QoL changes. CONCLUSIONS: These results should influence decision making in the management of claudication and it may be possible to prioritise PTA waiting lists to ensure patients with greatest potential benefit are treated with most urgency.
PURPOSE: The degree of ischemia during intermittent claudication is difficult to quantify. We evaluated calf muscle ischemia during exercise in patients with claudication with near infrared spectroscopy. METHODS: A Critikon Cerebral Redox Model 2001 (Johnson & Johnson Medical, Newport, Gwent, United Kingdom) was used to measure calf muscle deoxygenated hemoglobin (HHb), oxygenated hemoglobin (O(2)Hb), and total hemoglobin levels and oxygenation index (HbD; HbD = O(2)Hb - HHb) in 16 patients with claudication and in 14 control subjects before, during, and after walking on a treadmill for 1 minute (submaximal exercise). These measures were repeated after a second maximal exercise in patients with claudication and after 7 minutes walking in control subjects. Near-infrared spectroscopy readings during maximal exercise were then compared with a model of total ischemia induced with tourniquet in 16 young control subjects. RESULTS: Total hemoglobin level changed little during exercise in both patients with claudication and control subjects. HHb levels rose, and O(2)Hb level and HbD falls were more pronounced in patients with claudication than in control subjects after submaximal and maximal exercise. During maximal exercise, HbD fell markedly by a median (interquartile range) of 210.5 micromol/cm (108.2 to 337.0 micromol/cm) in patients with claudication compared with 66.0 micromol/cm (44.0 to 101.0 micromol/cm) in elderly control subjects and 41.0 micromol/cm (36.0 to 65.0 micromol/cm) in young control subjects (P <.001). This fall also was greater than the HbD fall induced with tourniquet ischemia at 90.8 micromol/cm (57.6 to 126.2 micromol/cm; P =.006). CONCLUSION: Hemoglobin desaturation in exercising calf muscle is profound in patients with claudication, considerably greater even than that induced with three minutes of tourniquet occlusion. Further studies are necessary to investigate the relationship between the inflammatory response and near-infrared spectroscopy during exercise in patients with claudication.
STUDY DESIGN: Neurogenic intermittent claudication can be caused by spinal cord compression. In this study, 20 patients with spinal intermittent claudication due to degenerative spine diseases were evaluated. OBJECTIVES: This study clarified the clinical features and pathomechanism of spinal intermittent claudication due to degenerative spine diseases. SUMMARY OF BACKGROUND DATA: Spinal intermittent claudication may either be produced by intrinsic or extrinsic lesions. Little is known about spinal intermittent claudication due to extrinsic lesions such as spinal cord compression. Twenty patients with spinal intermittent claudication, caused by cervical or thoracic lesions, who were given surgical treatment except for one, were studied. Their main subjective symptoms were tightness, weakness, and numbness in the lower limbs and a strangulated sensation in the trunk to lower limbs. The objective findings were occurrence and/or aggravation of spinothalamic signs. METHODS: The gait loading test was performed on these 20 patients. Selective spinal angiography was performed on the patients with thoracic myelopathy and its therapeutic effects were evaluated. A radiographic assessment was made in all patients. RESULTS: The subjective symptoms and objective findings were reproduced by the gait loading test. Selective spinal angiography temporarily relieved or improved the spinal intermittent claudication due to the thoracic myelopathy. Spinal intermittent claudication disappeared immediately after surgical treatment. CONCLUSIONS: Circulatory impairment of the spinal cord seems to be closely related to the etiology of spinal intermittent claudication. Besides providing diagnostic information, selective spinal angiography may also have a temporary therapeutic effect.
Policosanol is a cholesterol-lowering drug with concomitant antiplatelet effects. This study was undertaken to investigate the long-term effects of policosanol administered to patients with moderately severe intermittent claudication. The study consisted of a 6-week single-blind, placebo-controlled run in phase, followed by a 2-year double-blind, randomized treatment step. Fifty-six patients who met study entry criteria were randomized to receive placebo or policosanol 10 mg twice daily. Walking distances on a treadmill (constant speed 3.2 km/h, slope 10 degrees, temperature 25 degrees C) were assessed before and after 6, 12, 18, and 24 months of treatment. Both groups were similar at randomization. After 6 months of therapy, policosanol significantly increased (p < 0.01) the initial claudication distance from 125.9 +/- 8.7 m to 201.1 +/- 24.8 m and the absolute claudication distance from 219.5 +/- 14.1 m to 380.7 +/- 50.2 m. Both variables remained unchanged in the placebo group (p < 0.01). These effects did not wear off but improved after long-term therapy, so that final values were 333.5 +/- 28.6 m (initial claudication distance) and 648.9 +/- 54.1 m (absolute claudication distance); both significantly greater (p < 0.0001) than those obtained in the placebo group, which showed values of 137.9 +/- 21.8 m (initial claudication distance) and 237.7 +/- 28.1 m (absolute claudication distance), respectively. At study completion, 21 policosanol and 5 placebo patients attained increases in claudication distance values > 50% (p < 0.001). Policosanol, but not placebo, significantly increased the ankle/arm pressure index. In addition, from month 6 up to study completion, the frequency of patients reporting improvement of lower limb symptoms was greater in the policosanol group than in the placebo group. The treatment was tolerated well. There were 16 withdrawals (12 placebo, 4 policosanol) from the study. Eight patients in the placebo group experienced a total of 10 serious adverse events, 8 of which were vascular events, compared with none in the policosanol group (p < 0.01). In addition, 3 patients in the policosanol group and 3 patients in the placebo group reported mild adverse events during the study. The present results demonstrate the long-term usefulness of policosanol therapy to treat patients with intermittent claudication.