Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “INTERMITTENT CLAUDICATION”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 469 records · Page 26Linked to original sources
PubMed1981

Natural history of angina pectoris, possible previous myocardial infarction and intermittent claudication during the eighth decade. A longitudinal epidemiologic study.

A ten-year longitudinal cardiovascular survey of an unselected population of 70- and 80-year-old men and women was carried out as part of the Glostrup Population Studies in Denmark. With small reservations, the population at entry was representative of the Danish people of that age group, and representative in terms of mortality during the following decade. The prevalences of three major cardiovascular symptoms are given together with their courses, incidences and relationship to some common cardiovascular risk factors. At 70, the prevalence of angina pectoris was 10% in men and 5% in women, the corresponding values for possible previous myocardial infarction being 5% and 3%, and for intermittent claudication 9% and 3%, with statistically significant differences between the sexes for any of the three symptoms. At 80, the prevalences of all three symptoms in women had risen to equal that of men, which had not changed. Total ten-year mortality was significantly increased among men who had confirmed angina pectoris or possible previous myocardial infarction at 70 and among women who had confirmed intermittent claudication. Ten-year mortality from all cardiovascular diseases, and also from acute myocardial infarction alone, showed exactly the same pattern. In those examined at both 70 and 80, the ten-year incidences of the three symptoms were 3-11%. Few participants who had confirmed a symptom at 70 denied it at 80.

Aged↗
PubMed1977

Histochemical changes in striated muscle in patients with intermittent claudication.

Biopsy specimens from the gastrocnemius or rectus femoris muscle of 20 patients with intermittent claudication were studied using fresh frozen cryostat sections and histochemical reactions for adenosine triphosphatase, nicotinamide adenine nucleotide dehydrogenase reductase and phosphorylase and modified Gomori trichrome staining. Neuropathic changes, such as fibertype grouping and small group atrophy, were present to some extent in all of the biopsy specimens. Myogenic muscle changes such as necrosis and phagocytosis were seen in approximately one third and various forms of myofibrillar disorganization in approximately two thirds of the specimens. The amount and size of the type I aerobic fibers increased with the increasing severity of the ischemic disease.

Aged↗
PubMed1999

Cilostazol pharmacokinetics after single and multiple oral doses in healthy males and patients with intermittent claudication resulting from peripheral arterial disease.

OBJECTIVE: To study the pharmacokinetics of cilostazol following single oral administration of 50 to 200 mg in healthy young males, and after repeated oral administration of 100 mg every 12 hours to patients with peripheral arterial disease (PAD). DESIGN: The healthy male single dose study was a single-centre, randomised sequence, open-label, incomplete block, 3-period, 4-treatment, crossover design. The patient study was a single-centre, multiple dose, open-label study. STUDY PARTICIPANTS: 20 healthy nonsmoking male volunteers were enrolled and successfully completed the single dose study. 26 patients (21 males, 5 females) with intermittent claudication resulting from PAD were enrolled and completed the single/multiple dose study. MAIN OUTCOME MEASURES: Noncompartmental pharmacokinetic parameters, the area under the plasma concentration-time curve from zero to the time of last measurable plasma concentration, and maximum plasma concentration. RESULTS: Peak plasma concentrations of cilostazol occurred about 3 hours after drug administration and then declined biexponentially with concentrations detectable (> 20 micrograms/L) in the plasma for at least 36 hours postdose. The apparent elimination half-life of cilostazol (approximately 11 hours) was similar after a single dose or after multiple doses, with steady state being reached within 4 days. Cilostazol accumulated 1.7-fold following multiple dose administration. The apparent volume of distribution (Vz/F; 2.76 L/kg) suggested extensive distribution of cilostazol in the tissues. The oral clearance of cilostazol (CL/F; 0.18 L/h/kg) was much lower than liver blood flow, indicating a low extraction ratio drug, and hence low probability of a significant first-pass effect. None of the administered doses were recovered in the urine as unchanged cilostazol, suggesting that metabolism, rather than urinary excretion, is the major elimination route. Following single oral doses of 50 to 200 mg, the plasma concentrations of cilostazol and its metabolites increased less than proportionally to the dose. The pharmacokinetics of cilostazol in normal healthy volunteers are predictive of those in patients with PAD. Single oral doses of 50 to 200 mg cilostazol as well as 100 mg cilostazol every 12 hours were well tolerated. CONCLUSION: The plasma concentration of cilostazol and its metabolites increased less than proportionally with increasing doses. The relatively low plasma clearance and high volume of distribution of cilostazol suggest a low first-pass effect and extensive distribution. The pharmacokinetics of cilostazol in normal volunteers is predictive of that in patients with PAD. Cilostazol was well tolerated in healthy volunteers and patients with intermittent claudication resulting from PAD.

Administration, Oral↗
PubMed1985

Placebo-controlled, double-blind, two-centre trial of ketanserin in intermittent claudication.

The effects of ketanserin, a serotonin antagonist, were studied in 37 patients with intermittent claudication in a double-blind placebo-controlled, trial done in London and Leuven. 40 mg ketanserin taken orally three times a day for 4 months was associated with a clear-cut inhibition of serotonin-induced platelet aggregation but no changes were observed in pain-free and maximum walking distance on a treadmill, in ankle/arm Doppler systolic blood pressure ratio, or in reactive hyperaemia after 3 min of ischaemia. In contrast, the placebo group had increases in both pain-free and maximum walking distance (p less than 0.05).

Adult↗
PubMed2001

[Cystic adventitial degeneration. An important differential diagnosis in intermittent claudication].

The cystic adventitial degeneration is a rare disease, but an important differential diagnosis in patients with intermittent claudication. The amount of fluid in the cysts may vary and cause an intermittent compression of the artery. This explains the frequently intermittent symptomatology, leading to a critical ischemia if there is a complete obstruction of the artery. The histologic findings indicate that adventitial cysts are true ganglions. The intramural, uni- or multilocular cysts contain a gelatinous, muciform fluid. The diagnosis of a cystic adventitial degeneration should be considered in cases of isolated stenosis or occlusion of the popliteal artery. Realtime ultrasound helps to establish the diagnosis. The standard treatment has been surgical and has consisted a resectional and non-resectional technique. The ultrasound-directed percutaneous aspiration as a less invasive technique seems to be an effective treatment for this condition. The course, diagnostic and therapy of four patients is demonstrated.

Adult↗
PubMed2001

Assessment and management of intermittent claudication: importance of secondary prevention.

Atherosclerotic peripheral arterial disease (PAD) is a common disorder with a steep age-related incidence that affects 5-10% of the over 55-year age group. Because of the association with atherosclerotic disease elsewhere, particularly coronary heart disease (CHD), the ankle-brachial pressure index (ABPI) correlates inversely with survival. Clinical management centres around detection, assessment, symptom relief and prevention of secondary cardiovascular complications. Non-invasive ultrasound and colour duplex techniques have revolutionised the detection of PAD, and the long-term surveillance of disease progression, while antiplatelet therapy coupled with risk factor modification (lipids, blood pressure and glycaemic control and smoking cessation) are aimed at reducing direct or indirect vascular complications, e.g. amputation or CHD death. The natural history of intermittent claudication, although troublesome and disabling, often runs a stable, fairly benign course, so the majority of patients (73%) are treated medically. Selecting patients for surgical revascularisation (angioplasty, bypass or endarterectomy) is guided principally by the severity of clinical symptoms, but discrete, proximal, short-segmental lesions are the most amenable to surgical intervention. In general, surgery is indicated to relieve disabling symptoms when medical therapy had failed; for treatment of symptoms of limb-threatening ischaemia, including rest pain, ischaemic ulceration and gangrene; and to remove or bypass sources of thrombo-embolism. Thus, medical therapies for symptom relief and secondary prevention of complications form the mainstay of treatment for three-quarters of patients with uncomplicated intermittent claudication.

Angioplasty, Balloon↗
PubMedDate not supplied

High prevalence of coronary heart disease in patients with intermittent claudication. A preliminary report.

Twenty-five men aged 53-70 years, with stable intermittent claudication and similar symptoms and walking distance, were investigated with myocardial scintigraphy, duplex ultrasonography of carotid arteries and femoral angiography. Each patient was scored according to the degree of stenosis in the popliteal trifurcation and the aortoiliac and carotid arteries. Eighteen of the 25 men had coronary heart disease, which was clinically evident in nine cases and scintigraphically demonstrated in 17/24. Ischemia or infarction without clinical manifestation was located in the atrio-ventricular septal region in all nine cases. Eight of the 25 patients were shown to have carotid lesions. Significant correlation was found between lesions in the trifurcation and in the carotid arteries, but not between aortoiliac and carotid lesions. Trifurcational disease was a somewhat weaker marker for coronary heart disease. The high prevalence of coronary heart disease is noteworthy, especially the septal pathology, and further studies on the clinical significance of the findings appear to be urgently required.

Aged↗
PubMed2005

Insertion loads of the X STOP interspinous process distraction system designed to treat neurogenic intermittent claudication.

An interspinous process implant has been developed to treat patients suffering from neurogenic intermittent claudication secondary to lumbar spinal stenosis. As most patients who suffer from spinal stenosis are over the age of 50 and may have weaker bones, it is imperative to know how bone mineral density (BMD) correlates with lateral spinous process strength. The study was undertaken to characterize the lateral failure loads of the spinous process, correlate the failure loads to BMD, and compare the failure loads to the loads required to insert an interspinous process implant. Spinous process lateral failure loads were assessed, correlated to BMD, and compared to the loads required to insert an interspinous process implant. Mean spinous process failure loads were significantly greater than the lateral insertion load of the interspinous process implant. There was a significant relationship between the BMD and spinous process failure load. The technique used to insert the interspinous implant poses little risk to spinous process failure. There is ample margin of safety between the insertion loads and spinous process failure loads. The significant relationship between BMD and spinous process failure load suggests that patients with lower BMD must be approached with more caution during the implant insertion procedure.

Biomechanical Phenomena↗
PubMed1999

Walking training for intermittent claudication in diabetes.

OBJECTIVE: Walking training (WT) is an established treatment for patients with intermittent claudication (IC). Abnormalities specific to diabetes, such as a relative preponderance of distal lesions and the contribution of microcirculatory disease, might well influence the results of WT. We compared changes in walking distance during WT in diabetic patients with those in nondiabetic control subjects. RESEARCH DESIGN AND METHODS: In consecutive patients with limiting IC and proven peripheral vascular disease, 33 patients with diabetes were compared with 136 control subjects during a half-year supervised WT program. Walking parameters were determined every 2 months, while vascular parameters were obtained at the start and end of the program. RESULTS: Of the 33 diabetic patients, 25 (76%) completed the program, as did 87 of the 136 (64%) control subjects. Thereafter, the symptom-free walking distance and the maximum walking distance (MWD) were significantly increased in diabetic patients from 142 +/- 30 to 339 +/- 57 m and from 266 +/- 39 to 603 +/- 52 m, respectively, and in control subjects from 126 +/- 8 to 400 +/- 39 m and from 292 +/- 18 to 628 +/- 36 m, respectively. The relative gain in MWD was 88% greater in those with diabetes. The vascular parameters were comparable for both groups before and after WT. CONCLUSIONS: WT is an effective treatment for IC, with a greater relative gain in diabetic patients.

Blood Pressure↗
PubMed1985

[Evaluation of intermittent claudication using a treadmill with measurement of systolic pressure at the ankle following exercise].

Intermittent claudication (IC) and maximum walking distance (MWD) were studied in 173 patients and compared to post-stress Doppler claudicant ankle pressure (PSCAP) and to ankle index (PSCAI) recorded 2 minutes after exercise. Self-evaluation of MWD by the patient was inaccurate in 60% of cases. The treadmill testing (at 12% of rate and 2 miles/hour) exhibited a clinically overt IC in 93 cases with MWD of 166 m +/- 76, a PSCAP of 24 mm Hg +/- 24 and a PSCAI of 0.17 +/- 0.17. A clinically questionable IC occurred in 50 cases with significantly higher values (p less than 0.001) for MWD (278 m +/- 75) PSCAP (52 mm Hg +/- 24) and PSCAI (0.34 +/- 0.16). In 30 cases without IC after 400 m on treadmill, the PSCAP (81 mm HG +/- 26) and the PSCAI (0.57 +/- 0.18) were significantly (p less than 0.001) higher than in IC groups and related to milder iliofemoral stenosis. Overall reproducibility of MWD (mean = 190 m +/- 90) with 2 or 3 repeated measures in 75 cases, was 10.8% +/- 8.6 with large individual variations. Overall reproducibility of PSCAP after standardized treadmill testing in 42 cases was 6.5 +/- 5.3 (range of CV = 0 to 16%). A variation of PSCAP of more than 15 mm Hg is considered significant at level 0.01. It is concluded that overt IC with foot pallor and PSACP at 40 mm Hg or less reflects actual and reproducible MWD (especially below 300 m).(ABSTRACT TRUNCATED AT 250 WORDS)

Ankle↗
PubMed2005

Natural history of stenosis in the iliac arteries in patients with intermittent claudication undergoing clinical treatment.

PURPOSE: Inspite of the long experience with the treatment of intermittent claudication, little is known about the natural history of stenotic lesions in the iliac segment. With the advent of endovascular treatment, this knowledge has become important. METHODS: Fifty-two stenosis, diagnosed using arteriography, in 38 claudicant patients were analyzed. After a minimum time interval of 6 months, a magnetic resonance angiography was performed to determine whether there was arterial occlusion. The primary factors that could influence the progression of a stenosis were analyzed, such as risk factors (smoking, hypertension, diabetes, sex, and age), compliance with clinical treatment, initial degree of stenosis, site of the stenosis, and length of follow-up. RESULTS: The average length of follow-up was 39 months. From the 52 lesions analyzed, 13 (25%) evolved to occlusion. When occlusion occurred, there was clinical deterioration in 63.2% of cases. This association was statistically significant (P = .002). There was no statistically significant association of the progression of the lesion with the degree or site of stenosis, compliance with treatment, or length of follow-up. Patients who evolved to occlusion were younger (P = .02). The logistic regression model showed that the determinant factors for clinical deterioration were arterial occlusion and noncompliance with clinical treatment. CONCLUSIONS: The progression of a stenosis to occlusion, which occurred in 25% of the cases, caused clinical deterioration. Clinical treatment was important, but it did not forestall the arterial occlusion. Prevention of occlusion could be achieved by early endovascular intervention or with the development of drugs that might stabilize the atherosclerotic plaque.

Adult↗
PubMed2004

The role of cilostazol in the treatment of intermittent claudication.

This paper represents a review, by experts, of current opinion and information on intermittent claudication (IC) and the role that cilostazol plays in its treatment. IC is a common and debilitating condition that has a significant adverse impact on health-related quality of life (HR-QoL). It is currently under-recognised as a powerful marker of increased cardiovascular (CV) risk. The clinical priority is secondary prevention -- sometimes referred to as best medical therapy aimed at reducing CV risk. However, the priority for most patients (often overlooked by clinicians) is symptom relief: an increase in walking distance leading to an improvement in HR-QoL. The symptoms of IC may be improved by exercise, pharmacotherapy, and when these are unsuitable or unsuccessful, endovascular or surgical intervention. Cilostazol is indicated for the improvement of maximal and pain-free walking distance in patients with IC who do not have rest pain or tissue necrosis. In clinical trials, cilostazol improved symptoms both objectively and subjectively, and also improved HR-QoL. Cilostazol is usually well tolerated, with adverse events being generally mild to moderate in intensity, and transient or resolved after symptomatic treatment (e.g. non-prescription analgesics). Such events only infrequently require permanent drug withdrawal. There are no interactions with other drugs commonly prescribed in patients with IC, such as statins and anti-platelet agents. Cilostazol also has a range of potentially beneficial effects that may in the future be proven to decrease CV risk and modify the underlying process of atherosclerosis. Cilostazol represents the best evidence-based pharmacological therapy available for the symptoms of IC and should be the first-line treatment for symptom improvement in appropriate patients. Based on the available treatment strategies, the paper presents a suggested algorithm for the management of IC highlighting the role of cilostazol.

Algorithms↗
PubMed1988

Excretion of thromboxane A2 and prostacyclin metabolites during treadmill exercise in patients with intermittent claudication.

Platelet activation, with subsequent formation of thromboxane A2 (TxA2), is thought to play a role in the development of arterial occlusion. In patients with severe atherosclerosis of the lower limbs, characterized by leg ulcers and rest pain, the basal formation of TxA2 and prostacyclin (PGI2) is increased. Corresponding data in patients with more moderate atherosclerosis of the lower limbs have not been reported. Since the capacity to physical exercise is not blunted in such patients proper evaluation of their TxA2-PGI2 synthesis should comprise not only assessment of the basal formation, but also TxA2/PGI2 biosynthesis during conditions of elevated cardiovascular activity. To address this, we analysed these eicosanoids in patients with a history of intermittent claudication. Urinary dinor-metabolites of TxB2 and PGI2 (Tx-M and PGI-M, respectively) were estimated by gas chromatography/negative ion-chemical ionization mass spectrometry in samples collected prior to, during and immediately after 20 min of severe treadmill exertion. The basal excretion of Tx-M was 105 +/- 26 pg/mg creatinine. It was not changed during exercise, but increased to 176 +/- 48 pg/mg creatinine (P less than 0.05) during the recovery. The basal excretion of PGI-M was 142 +/- 25 pg/mg creatinine. The PGI-M response to exercise varied from no change at all to a 30-fold increase, without any obvious correlation to experienced leg pain, walking distance or other recorded variables. During the recovery period the outflow of PGI-M was significantly higher than at rest (482 +/- 145 pg/mg creatinine; P less than 0.01). We conclude that in patients with intermittent claudication due to atherosclerosis (1) platelet activation does not occur during the course of the exercise, and (2) vascular prostacyclin formation can be dissociated from of TxA2 synthesis. The observed increase in PGI-M in some of the patients is suggested to reflect tissue ischaemia induced by the lack of adequate hyperaemia during exercise.

6-Ketoprostaglandin F1 alpha↗
PubMed2003

Beneficial effects of exercise beyond the pain threshold in intermittent claudication.

BACKGROUND: The quality of life and autonomy may be severely hampered in patients with intermittent claudication, but the amputation rate is very low. Supervised exercise training is effective, but still very rarely employed. Many authors think that in these patients exercise over the pain threshold may be dangerous. The aim of this study was to assess whether supervised, 3-month duration, 3 times/week, beyond the pain threshold exercise training is safe and whether it improves both the performance and quality of life in patients with claudication. METHODS: Forty-three patients with claudication, confirmed at Doppler study and/or angiography, have been evaluated by means of graded treadmill testing, the ankle-brachial pressure index at rest and after walking and a Walking Impairment Questionnaire before and after 3 months of treadmill training beyond the claudication threshold. RESULTS: Patients showed an 86% increase in time to onset of claudication pain (p < 0.00001), a 50% increase in total walking time (p < 0.000001) and improved questionnaire scores of pain intensity (%, p < 0.005), distance covered (+87%, p < 0.005), speed (+42%, p < 0.05), and stair climbing (+25%, p = NS). The basal and post-exercise ankle-brachial pressure index was not modified by training. Analysis of all subgroups of patients (</> 65 years of age, with/without coronary artery disease and diabetes mellitus, pre-training time to onset of claudication pain </> 3 min, with angiographic/Doppler occlusion or stenosis) revealed a statistically significant increase in both time to onset of claudication pain and total walking time. CONCLUSIONS: Supervised physical training beyond the claudication threshold significantly improves the walking time and quality of life of patients with claudication.

Arterial Occlusive Diseases↗
PubMed1979

Intermittent claudication--epidemiology and natural history.

Epidemiological information on the prevalence, incidence and natural history of intermittent claudication and peripheral vascular disease is limited, partially by the limitation of techniques of their study. The available data from the literature are review and supplemented by results from an on-going survey the ankle blood pressure measurement with Doppler ultrasound.

Adult↗
PubMed1977

Skeletal muscle capillaries in intermittent claudication.

The ultrastructural dimensions and density of capillaries in 23 gastrocnemius or rectus femoris muscles in patients with intermittent claudication due to arteriosclerosis obliterans (ASO) were studied. Constant ultrastructural alterations that were not seen in the control patients were thickening, replication, and remnants of the capillary basement membrane (BM). Compared with the control patientes, the percentual area of the BM was significantly larger (P less than .01), the lumen was significantly smaller (P less than .01), and the ratio of capillaries to muscle fiber was significantly higher (P less than .01) in patients with ASO. These changes were probably due to ASO since they increased with growing severity of claudication.

Aged↗