Vascular Investigation and Therapy

: 2022  |  Volume : 5  |  Issue : 3  |  Page : 68--74

Arterial claudication

Pierre Abraham1, Simon Lecoq1, Jeanne Hersant2, Samir Henni2,  
1 Department of Vascular Medicine; Department of Sports Medicine, Hospital and University of Angers, Angers, France
2 Department of Vascular Medicine, Hospital and University of Angers, Angers, France

Correspondence Address:
Dr. Pierre Abraham
Department of Vascular Medicine; Department of Sports Medicine, Hospital and University of Angers, Angers


Arterial claudication is generally the revealing form of clinically symptomatic lower extremity artery disease. It is defined as a pain of limb muscles that occurs during exercise and is relieved within 10 min when exercise is lowered or stopped. Atherosclerosis is the first underlying cause of arterial intermittent claudication. As such, the occurrence of arterial claudication is a severe medical event sharing almost similar the long-term morbidity and mortality risk as other arterial events such as stroke or myocardial infarction. Comorbid (both vascular and nonvascular) affections must be actively searched. Surgery is generally indicated only when medical treatment and training have failed to improve symptoms. This paper shortly reviews the cause, presentation, diagnostic algorithm, and treatments of arterial claudication.

How to cite this article:
Abraham P, Lecoq S, Hersant J, Henni S. Arterial claudication.Vasc Invest Ther 2022;5:68-74

How to cite this URL:
Abraham P, Lecoq S, Hersant J, Henni S. Arterial claudication. Vasc Invest Ther [serial online] 2022 [cited 2023 Feb 2 ];5:68-74
Available from:

Full Text


Arterial intermittent claudication (AIC) is a specific form of intermittent claudication resulting from impaired inflow to the exercising lower limb muscles and one of the first causes of referral to vascular medicine physicians or surgeons. Etymologically, claudication refers to the alteration of walking pattern associated with the pain that occurs during exercise. In fact, pain in AIC does not result “stricto-sensus” to the mismatch of blood flow supply and blood flow requirement of exercising muscles, but rather from the mismatch between oxygen requirement and oxygen delivery by impaired blood flow due to lower extremity arterial disease (LEAD).[1] Most patients with AIC report discomfort or pain at the calf level but may also experience pain at the lower back, buttock, thigh, or foot depending on the localization of the arterial lesions. Typically, pain is absent at rest, occurs for an individual level of exercise level, and is relieved within 10 min when exercise is stopped. Nevertheless, exertional leg symptoms other than intermittent claudication are common in LEAD.[2] The level of exercise at which pain occurs depends on the severity of arterial lesions and on the presence or absence of comorbid conditions that may worsen the tolerance to exercise.[3] Thereby athletes may suffer AIC from minor lesions that shall remain asymptomatic during usual daily life activities as can be observed in endofibrosis.[4] Inversely, severe atherosclerotic lesions may remain asymptomatic in sedentary or very inactive subjects, or the presence of collateral circulation.[5] Last, lesions of similar severity shall result in more severe walking impairment in case of comorbid conditions (exercise-induced hypoxemia, anemia).[3]


The prevalence of LEAD and AIC depends on the diagnostic criteria used for the diagnosis[6],[7],[8] and is likely increasing in the worlds even in middle age subjects[9] In 19748, adults between 40 and 69 years of age, the age-adjusted prevalence of intermittent claudication was 1.1% for men and 1.2% for women and increased by age.[10] It is highly sensitive to the risk factors of the exposed population,[11] but increases with aging.[12],[13]

 Risk Factors

Atherosclerosis being the major cause of AIC, risk factors for AIC include smoking, obesity diabetes, or chronic immune-inflammatory arterial diseases.[14],[15] These are important to consider because some are modifiable with lifestyle changes and prevention. Diabetes mellitus, hypertension, and dyslipidemias are important risk factors too and their treatments reduce the risk an evolution of atherosclerosis and AIC. Last, the prevalence of AIC increases with age and shows a male dominance as does atherosclerosis. The pathophysiology of atherosclerosis has been largely described elsewhere and will not be recalled here. Numerous biological factors (among which: C-reactive protein, infection, homocysteinemia, lipoprotein (a), reduced adiponectin, and fibrinogen) have been studied and are associated with the presence, severity, or evolution of AIC but are not typically used in routine.[16],[17],[18],[19],[20],[21],[22],[23],[24],[25] Last, specific factors associated with nonatherosclerotic arterial lesions, such as radiations (postradic disease),[26] long-lasting high-level endurance training (endofibrosis),[27],[28] ABCC6 mutation (pseudoxanthoma elasticum),[29] may also be considered in unusual or specific clinical situations.

 History and Physical Examination

Atherosclerotic, the major cause of AIC, generally results in a progressive narrowing of the arterial lumen, except in case of plaque rupture or thrombosis. In the early evolution of lesions, moderately active or sedentary subjects with LEAD mild-to-moderate lesions will remain asymptomatic for years before claudication occurs while walking, probably explaining why claudication mostly appears in patients in their sixties. A history of AIC will include analysis of the personal and familial history of risk factors and the presence of comorbid conditions. Symptoms and their localization are optimally described using standard questionnaires such as the Edinburg[30] or San-Diego[31] questionnaires and help define whether symptoms are of vascular type. Similarly, the evaluation of self-reported walking impairment with the WIQ or Walking Estimated-Limitation Calculated by History questionnaires[32],[33],[34],[35],[36] [Figure 1] and of quality of life[37],[38] can be standardized with self-completed tools that can participate in the evaluation the clinical severity and guide treatment options.[39]{Figure 1}

Last, detecting symptoms of cardiac or cerebral-associated arterial lesions are essential because atherosclerosis is a systemic disease.

Physical examination should include palpation of arterial pulses and auscultation searching for a bruit (including at the carotid level). Although essential, pulse palpation in AIC has a poor sensitivity at rest particularly if AIC appears only for moderate-to-high level of exercise or if the lesions are located on branches (internal iliac or profunda femoris arteries) and the presence of normal pulses should not be used to argue against the arterial origin of pain. Muscle palpation and osteoarticular passive mobilization at rest are strictly nonpainful. Facing proximal claudication, the presence of sensitive or motor deficits might guide to the presence of a lumbar spine stenosis. Classical signs associated with severe LEAD such as ulcers, pallor, decrease of limb temperature, or hair loss, are generally absent at rest when LEAD is only responsible for AIC.

 Primary Care Investigation

The technical requirements for measuring lower limb pressures (a sphygmomanometer and a hand-held pocket Doppler) are so simple, that measurement of the ankle to brachial index (ratio of ankle to the highest of the two arms systolic arterial pressure) should be systematically used by primary care physicians to argue for the presence of LEAD.[40] Attention must be paid to the conditions of the recording and specifically to respect a strict lying position otherwise ankle-brachial index (ABI) may be overestimated [Table 1] and [Figure 2].{Figure 2}{Table 1}

In case of severe claudication, a normal ABI (results between 0.90 and 1.30) makes an arterial origin of symptoms unlikely but in AIC occurring only during significant heavy-load exercise (as in claudication in athletes), ABI will generally be normal at rest. Limits to the use or interpretation of ABI must be kept in mind, such as cardiac arrhythmia, artery calcification (that are frequent in the presence of renal disease or diabetes),[41] inability to tolerate the strict lying position leading to overestimation of ankle values (heart and respiratory failure), or localizations of lesions on branches that are not in the measurement axis (internal iliac or profunda femoris arteries).

 Additional Nonradiological Investigations

When ABI is normal at rest, its measurement after exercise is essential.[42] ABI will decrease after exercise in proportion to the maximal workload performed. Then, in normal individuals, ABI will remain mostly unchanged after walking but will decrease significantly in athletes following heavy-load exercise. Thereby postexercise ABI will be considered useful after walking tests,[43] but values as low as 0.50–0.65 can be found normal after maximal heavy-load cycle exercise in athletes.[44],[45] Ultrasound imaging is the most powerful and largely used investigation for patients with AIC. It determines the presence and location of arterial lesions, can complete the investigation of cerebral and renal arteries in case of lower limb lesions, and detect the presence of arterial aneurysms. Other tests such as postexercise magnetic resonance imaging,[46],[47] near infrared spectroscopy,[48],[49],[50] exercise transcutaneous oximetry [Figure 3][51],[52] are of interest and are used in secondary care specialized units but are hardly accessible in routine practice. They can be of interest if claudication is a debatable of doubtful arterial origin. Blood tests searching for unknown risk factors (glycemic and fatty acid investigations), renal cardiac or cerebral complications (urea creatinine) must be part of the initial and follow-up investigations{Figure 3}

 Noninvasive Treatments

Patients with intermittent claudication must first be treated with medical interventions, including lifestyle changes to improve risk factors (sedentary, smoking, pharmacological control of risk factors (dyslipidemia and diabetes mellitus), and prevention of LEAD aggravation with a triad of antiplatelet/anticoagulant drugs, ACE inhibitors, and cholesterol-lowering agents (mostly statins).[53] Cilostazol was proved effective in improving walking capacity but is of no benefit on LEAD evolution.[54] In debilitating AIC, structured supervised walking programs improve walking capacity better than pharmacologic therapy alone and may even have better results on long-term prognosis than revascularization.[55],[56] In the absence of complications (aneurysms, ulcers, etc…), failure to improve symptoms of claudication or increase the walking capacity to a level that is acceptable for a physically active patient should be the sole reason leading to invasive investigations and revascularization.

 Radiological Investigations and Revascularizations

We believe that lower limb angiography, computed tomography, or magnetic resonance angiography [Figure 4] should not be done until noninvasive treatments have failed to sufficiently improve AIC and a revascularization has been proposed. Imaging modalities depend on the patient status, the location of the lesions, the accessibility to the techniques, the advantage and limits of each approach, and overall, whether revascularization is proposed through and endovascular or surgical approach. The advantage and limits of each revascularization technique will not be discussed here and depend on the location, number, length, and severity of the stenosis.[57],[58],[59]{Figure 4}


AIC is a severe disease with a high risk of morbidity[60] and mortality[61],[62],[63],[64],[65],[66] underlying the importance of secondary medical prevention. Morbidity includes the evolution of LEAD, occurrence of arterial complication in other vascular territories (infraction, stroke), and complications of medical or surgical treatments (statin intolerance, graft infection, or angioplasty thrombosis). Education of the patients through a multidisciplinary approach is mandatory.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.


1Ledermann HP, Schulte AC, Heidecker HG, Aschwanden M, Jäger KA, Scheffler K, et al. Blood oxygenation level-dependent magnetic resonance imaging of the skeletal muscle in patients with peripheral arterial occlusive disease. Circulation 2006;113:2929-35.
2McDermott MM, Mehta S, Greenland P. Exertional leg symptoms other than intermittent claudication are common in peripheral arterial disease. Arch Intern Med 1999;159:387-92.
3Colas-Ribas C, Signolet I, Henni S, Feuillloy M, Gagnadoux F, Abraham P. High prevalence of known and unknown pulmonary diseases in patients with claudication during exercise oximetry: A retrospective analysis. Medicine (Baltimore) 2016;95:e4888.
4Chevalier JM, Enon B, Walder J, Barral X, Pillet J, Megret A, et al. Endofibrosis of the external iliac artery in bicycle racers: An unrecognized pathological state. Ann Vasc Surg 1986;1:297-303.
5De Vivo S, Palmer-Kazen U, Kalin B, Wahlberg E. Risk factors for poor collateral development in claudication. Vasc Endovascular Surg 2005;39:519-24.
6Hiatt WR, Hoag S, Hamman RF. Effect of diagnostic criteria on the prevalence of peripheral arterial disease. The San Luis Valley Diabetes Study. Circulation 1995;91:1472-9.
7Schorr EN, Treat-Jacobson D. Methods of symptom evaluation and their impact on peripheral artery disease (PAD) symptom prevalence: A review. Vasc Med 2013;18:95-111.
8Ramos R, Quesada M, Solanas P, Subirana I, Sala J, Vila J, et al. Prevalence of symptomatic and asymptomatic peripheral arterial disease and the value of the ankle-brachial index to stratify cardiovascular risk. Eur J Vasc Endovasc Surg 2009;38:305-11.
9Mehta A, Dhindsa DS, Hooda A, Nayak A, Massad CS, Rao B, et al. Premature atherosclerotic peripheral artery disease: An underrecognized and undertreated disorder with a rising global prevalence. Trends Cardiovasc Med 2021;31:351-8.
10Jensen SA, Vatten LJ, Romundstad PR, Myhre HO. The prevalence of intermittent claudication. Sex-related differences have been eliminated. Eur J Vasc Endovasc Surg 2003;25:209-12.
11Ingolfsson IO, Sigurdsson G, Sigvaldason H, Thorgeirsson G, Sigfusson N. A marked decline in the prevalence and incidence of intermittent claudication in Icelandic men 1968-1986: A strong relationship to smoking and serum cholesterol - The Reykjavik Study. J Clin Epidemiol 1994;47:1237-43.
12Postiglione A, Cicerano U, Gallotta G, Gnasso A, Lamenza F, Rubba P, et al. Prevalence of peripheral arterial disease and related risk factors in elderly institutionalized subjects. Gerontology 1992;38:330-7.
13Fowkes FG, Housley E, Cawood EH, Macintyre CC, Ruckley CV, Prescott RJ. Edinburgh Artery Study: Prevalence of asymptomatic and symptomatic peripheral arterial disease in the general population. Int J Epidemiol 1991;20:384-92.
14Agüero F, González-Zobl G, Baena-Díez JM, Dégano IR, Garcia-Gil M, Alzamora MT, et al. Prevalence of lower extremity peripheral arterial disease in individuals with chronic immune mediated inflammatory disorders. Atherosclerosis 2015;242:1-7.
15Okello S, Millard A, Owori R, Asiimwe SB, Siedner MJ, Rwebembera J, et al. Prevalence of lower extremity peripheral artery disease among adult diabetes patients in southwestern Uganda. BMC Cardiovasc Disord 2014;14:75.
16Gardner AW, Montgomery PS, Wang M, Shen B, Zhang S, Pomilla WA. Association between meeting physical activity time-intensity guidelines with ambulation, quality of life, and inflammation in claudication. J Cardiopulm Rehabil Prev 2022;[In press]. [doi: 10.1097/HCR.0000000000000686].
17Gardner AW, Montgomery PS, Wang M, Shen B, Casanegra AI, Silva-Palacios F, et al. Diet is associated with ankle-brachial index, inflammation, and ambulation in patients with intermittent claudication. J Vasc Surg 2020;72:1375-84.
18Altes P, Perez P, Esteban C, Sánchez Muñoz-Torrero JF, Aguilar E, García-Díaz AM, et al. Raised fibrinogen levels and outcome in outpatients with peripheral artery disease. Angiology 2018;69:507-12.
19Banerjee AK, Pearson J, Gilliland EL, Goss D, Lewis JD, Stirling Y, et al. A six year prospective study of fibrinogen and other risk factors associated with mortality in stable claudicants. Thromb Haemost 1992;68:261-3.
20Komai H, Shibata R, Juri M, Matsushita K, Ouchi N, Murohara T. Plasma adiponectin as a predictive factor of survival after a bypass operation for peripheral arterial disease. J Vasc Surg 2009;50:95-9.
21Fukase T, Dohi T, Kato Y, Chikata Y, Takahashi N, Endo H, et al. Long-term impact of high-sensitivity C-reactive protein in patients with intermittent claudication due to peripheral artery disease following endovascular treatment. Heart Vessels 2021;36:1670-8.
22Shahin Y, Hatfield J, Chetter I. C-reactive protein and the Framingham coronary risk score in patients newly diagnosed with intermittent claudication: A prospective study. Vasc Endovascular Surg 2012;46:242-5.
23Jud P, Hafner F, Verheyen N, Gary T, Meinitzer A, Brodmann M, et al. Age-dependent effects of homocysteine and dimethylarginines on cardiovascular mortality in claudicant patients with lower extremity arterial disease. Heart Vessels 2018;33:1453-62.
24Riba R, Nicolaou A, Troxler M, Homer-Vaniasinkam S, Naseem KM. Altered platelet reactivity in peripheral vascular disease complicated with elevated plasma homocysteine levels. Atherosclerosis 2004;175:69-75.
25Masson W, Lobo M, Barbagelata L, Molinero G, Bluro I, Nogueira JP. Elevated lipoprotein (a) levels and risk of peripheral artery disease outcomes: A systematic review. Vasc Med 2022:1358863X221091320.
26Fredericson M, Waite BL. An unusual cause of ischemic claudication: A case report. Arch Phys Med Rehabil 2003;84:766-7.
27Feugier P, Chevalier JM. Endofibrosis of the iliac arteries: An underestimated problem. Acta Chir Belg 2004;104:635-40.
28INSITE Collaborators (INternational Study group for Identification and Treatment of Endofibrosis). Diagnosis and management of iliac artery endofibrosis: Results of a delphi consensus study. Eur J Vasc Endovasc Surg 2016;52:90-8.
29Lefthériotis G, Omarjee L, Le Saux O, Henrion D, Abraham P, Prunier F, et al. The vascular phenotype in Pseudoxanthoma elasticum and related disorders: Contribution of a genetic disease to the understanding of vascular calcification. Front Genet 2013;4:4.
30Leng GC, Fowkes FG. The Edinburgh Claudication Questionnaire: An improved version of the WHO/Rose Questionnaire for use in epidemiological surveys. J Clin Epidemiol 1992;45:1101-9.
31Criqui MH, Denenberg JO, Bird CE, Fronek A, Klauber MR, Langer RD. The correlation between symptoms and non-invasive test results in patients referred for peripheral arterial disease testing. Vasc Med 1996;1:65-71.
32Abraham P, Godet R, Harbonnier M, Laneelle D, Leftheriotis G, Ouedraogo N. External validation of the “walking estimated limitation calculated by history” (WELCH) questionnaire in patients with claudication. Eur J Vasc Endovasc Surg 2014;47:319-25.
33Rezvani F, Härter M, Dirmaier J. Measuring walking impairment in patients with intermittent claudication: Psychometric properties of the Walking Estimated-Limitation Calculated by History (WELCH) questionnaire. PeerJ 2021;9:e12039.
34Lozano FS, March JR, González-Porras JR, Carrasco E, Lobos JM, Areitio-Aurtena A. Validation of the Walking Impairment Questionnaire for Spanish patients. Vasa 2013;42:350-6.
35Mahe G, Ouedraogo N, Vasseur M, Faligant C, Saidi K, Leftheriotis G, et al. Limitations of self-reported estimates of functional capacity using the Walking Impairment Questionnaire. Eur J Vasc Endovasc Surg 2011;41:104-9.
36Collins E, O'Connell S, Jelinek C, Miskevics S, Budiman-Mak E. Evaluation of psychometric properties of Walking Impairment Questionnaire in overweight patients with osteoarthritis of knee. J Rehabil Res Dev 2008;45:559-66.
37Izquierdo-Porrera AM, Gardner AW, Bradham DD, Montgomery PS, Sorkin JD, Powell CC, et al. Relationship between objective measures of peripheral arterial disease severity to self-reported quality of life in older adults with intermittent claudication. J Vasc Surg 2005;41:625-30.
38Hedeager Momsen AM, Bach Jensen M, Norager CB, Roerbæk Madsen M, Vestersgaard-Andersen T, Lindholt JS. Quality of life and functional status after revascularization or conservative treatment in patients with intermittent claudication. Vasc Endovascular Surg 2011;45:122-9.
39Collins TC, Petersen NJ, Suarez-Almazor M. Peripheral arterial disease symptom subtype and walking impairment. Vasc Med 2005;10:177-83.
40Crawford F, Welch K, Andras A, Chappell FM. Ankle brachial index for the diagnosis of lower limb peripheral arterial disease. Cochrane Database Syst Rev 2016;9:CD010680.
41Suominen V, Rantanen T, Venermo M, Saarinen J, Salenius J. Prevalence and risk factors of PAD among patients with elevated ABI. Eur J Vasc Endovasc Surg 2008;35:709-14.
42Stein R, Hriljac I, Halperin JL, Gustavson SM, Teodorescu V, Olin JW. Limitation of the resting ankle-brachial index in symptomatic patients with peripheral arterial disease. Vasc Med 2006;11:29-33.
43van Langen H, van Gurp J, Rubbens L. Interobserver variability of ankle-brachial index measurements at rest and post exercise in patients with intermittent claudication. Vasc Med 2009;14:221-6.
44Abraham P, Desvaux B, Saumet JL. Ankle-brachial index after maximum exercise in treadmill and cycle ergometers in athletes. Clin Physiol 1998;18:321-6.
45Godet R, Bruneau A, Vielle B, Vincent F, Le Tourneau T, Carre F, et al. Post-exercise ankle blood pressure and ankle to brachial index after heavy load bicycle exercise. Scand J Med Sci Sports 2018;28:2144-52.
46Zhang JL, Layec G, Hanrahan C, Conlin CC, Hart C, Hu N, et al. Exercise-induced calf muscle hyperemia: Quantitative mapping with low-dose dynamic contrast enhanced magnetic resonance imaging. Am J Physiol Heart Circ Physiol 2019;316:H201-11.
47Jiji RS, Pollak AW, Epstein FH, Antkowiak PF, Meyer CH, Weltman AL, et al. Reproducibility of rest and exercise stress contrast-enhanced calf perfusion magnetic resonance imaging in peripheral arterial disease. J Cardiovasc Magn Reson 2013;15:14.
48Komiyama T, Onozuka A, Miyata T, Shigematsu H. Oxygen saturation measurement of calf muscle during exercise in intermittent claudication. Eur J Vasc Endovasc Surg 2002;23:388-92.
49Seifalian AM, Atwal A, White S, Mikhailidis DP, Baker D, Hamilton G. A role for near infrared spectroscopy in the assessment of intermittent claudication. Int Angiol 2001;20:301-6.
50Cornelis N, Chatzinikolaou PN, Buys R, De Wilde C, Fourneau I, Claes J, et al. Near infrared spectroscopy to evaluate the effect of a hybrid exercise programme on peripheral muscle metabolism in patients with intermittent claudication: An exploratory PROSECO-IC sub study. J Sports Sci 2022;40:1031-41.
51Abraham P, Ramondou P, Hersant J, Sempore WY, Feuilloy M, Henni S. Investigation of arterial claudication with transcutaneous oxygen pressure at exercise: Interests and limits. Trends Cardiovasc Med 2021;31:218-23.
52Abraham P, Gu Y, Guo L, Kroeger K, Ouedraogo N, Wennberg P, et al. Clinical application of transcutaneous oxygen pressure measurements during exercise. Atherosclerosis 2018;276:117-23.
53Mohler ER 3rd, Hiatt WR, Creager MA. Cholesterol reduction with atorvastatin improves walking distance in patients with peripheral arterial disease. Circulation 2003;108:1481-6.
54Farkas K, Kolossváry E, Járai Z. Cilostazol improves the quality of life and lower-limb functional capacity also in diabetic patients Orv Hetil 2020;161:1637-45.
55Lane R, Harwood A, Watson L, Leng GC. Exercise for intermittent claudication. Cochrane Database Syst Rev 2017;12:CD000990.
56Cheetham DR, Burgess L, Ellis M, Williams A, Greenhalgh RM, Davies AH. Does supervised exercise offer adjuvant benefit over exercise advice alone for the treatment of intermittent claudication? A randomised trial. Eur J Vasc Endovasc Surg 2004;27:17-23.
57Jaff MR, White CJ, Hiatt WR, Fowkes GR, Dormandy J, Razavi M, et al. An update on methods for revascularization and expansion of the TASC lesion classification to include below-the-knee arteries: A supplement to the inter-society consensus for the management of peripheral arterial disease (TASC II): The TASC Steering Comittee(.). Ann Vasc Dis 2015;8:343-57.
58TASC Steering Committee; Jaff MR, White CJ, Hiatt WR, Fowkes GR, Dormandy J, et al. An update on methods for revascularization and expansion of the TASC lesion classification to include below-the-knee arteries: A supplement to the inter-society consensus for the management of peripheral arterial disease (TASC II). J Endovasc Ther 2015;22:663-77.
59Norgren L, Hiatt WR, Dormandy JA, Nehler MR, Harris KA, Fowkes FG, et al. Inter-society consensus for the management of peripheral arterial disease (TASC II). J Vasc Surg 2007;45 Suppl S: S5-67.
60Safley DM, Kennedy KF, Stansby G, Flather M, Cohen DJ, Spertus JA. Prevalence and predictors of persistent health status impairment in patients referred to a vascular clinic with intermittent claudication. Eur J Vasc Endovasc Surg 2011;42:355-62.
61Miller SM, Sumpio BJ, Miller MS, Erben Y, Cordova AC, Sumpio BE. Higher inpatient mortality for women after intervention for lifestyle limiting claudication. Ann Vasc Surg 2019;58:54-62.
62Erben Y, Mena-Hurtado CI, Miller SM, Jean RA, Sumpio BJ, Velasquez CA, et al. Increased mortality in octogenarians treated for lifestyle limiting claudication. Catheter Cardiovasc Interv 2018;91:1331-8.
63Gardner AW, Addison O, Katzel LI, Montgomery PS, Prior SJ, Serra MC, et al. Association between physical activity and mortality in patients with claudication. Med Sci Sports Exerc 2021;53:732-9.
64Inglis SC, Lewsey JD, Lowe GD, Jhund P, Gillies M, Stewart S, et al. Angina and intermittent claudication in 7403 participants of the 2003 Scottish Health Survey: Impact on general and mental health, quality of life and five-year mortality. Int J Cardiol 2013;167:2149-55.
65Kieback AG, Lorbeer R, Wallaschofski H, Ittermann T, Völzke H, Felix S, et al. Claudication, in contrast to angina pectoris, independently predicts mortality risk in the general population. Vasa 2012;41:105-13.
66Bowlin SJ, Medalie JH, Flocke SA, Zyzanski SJ, Yaari S, Goldbourt U. Intermittent claudication in 8343 men and 21-year specific mortality follow-up. Ann Epidemiol 1997;7:180-7.