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Article: Intermittent claudication - pathophysiological considerations

TitleIntermittent claudication - pathophysiological considerations
Authors
Issue Date1979
Citation
Acta Cardiologica, 1979, v. 34 n. 3, p. 125-132 How to Cite?
AbstractIntermittent claudication is a non-pathognomic symptom elicited by an imbalance between the metabolic demands of the exercising skeletal muscle and its blood supply. In normal conditions hyperemia to the working muscles will be impaired during the exercise by mechanical compression of the microvessels. The resulting anaerobic metabolism will cause further vasodilatation. Both phenomena (exercise and reactive hyperemia) contribute to a maximal increase in local blood flow as soon as the exercise is stopped. If the local circulation is impaired by occluding arterial disease (eventually complicated by aggravating factors) the tolerance to skeletal work is lowered and the circulatory reserves are entirely exhausted as demonstrated by the ischemic exercise-test. In the case of a major obstruction and poor collateralisation, a 'steal phenomenon' may occur. The pharmacotherapeutic possibilities to cope with in this situation are briefly discussed.
Persistent Identifierhttp://hdl.handle.net/10722/170595
ISSN
2015 Impact Factor: 0.6
2015 SCImago Journal Rankings: 0.303
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorVanhoutte, PMen_US
dc.contributor.authorDe Mey Chen_US
dc.contributor.authorWellens, Den_US
dc.date.accessioned2012-10-30T06:10:04Z-
dc.date.available2012-10-30T06:10:04Z-
dc.date.issued1979en_US
dc.identifier.citationActa Cardiologica, 1979, v. 34 n. 3, p. 125-132en_US
dc.identifier.issn0001-5385en_US
dc.identifier.urihttp://hdl.handle.net/10722/170595-
dc.description.abstractIntermittent claudication is a non-pathognomic symptom elicited by an imbalance between the metabolic demands of the exercising skeletal muscle and its blood supply. In normal conditions hyperemia to the working muscles will be impaired during the exercise by mechanical compression of the microvessels. The resulting anaerobic metabolism will cause further vasodilatation. Both phenomena (exercise and reactive hyperemia) contribute to a maximal increase in local blood flow as soon as the exercise is stopped. If the local circulation is impaired by occluding arterial disease (eventually complicated by aggravating factors) the tolerance to skeletal work is lowered and the circulatory reserves are entirely exhausted as demonstrated by the ischemic exercise-test. In the case of a major obstruction and poor collateralisation, a 'steal phenomenon' may occur. The pharmacotherapeutic possibilities to cope with in this situation are briefly discussed.en_US
dc.languageengen_US
dc.relation.ispartofActa Cardiologicaen_US
dc.subject.meshAdenosine Triphosphate - Metabolismen_US
dc.subject.meshCollateral Circulationen_US
dc.subject.meshHumansen_US
dc.subject.meshIntermittent Claudication - Metabolism - Physiopathologyen_US
dc.subject.meshMuscle Contractionen_US
dc.subject.meshMuscles - Blood Supply - Metabolismen_US
dc.subject.meshOxygen - Blooden_US
dc.subject.meshRegional Blood Flowen_US
dc.titleIntermittent claudication - pathophysiological considerationsen_US
dc.typeArticleen_US
dc.identifier.emailVanhoutte, PM:vanhoutt@hku.hken_US
dc.identifier.authorityVanhoutte, PM=rp00238en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.pmid315681-
dc.identifier.scopuseid_2-s2.0-0018755712en_US
dc.identifier.volume34en_US
dc.identifier.issue3en_US
dc.identifier.spage125en_US
dc.identifier.epage132en_US
dc.identifier.isiWOS:A1979HC73100003-
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US
dc.identifier.scopusauthoridDe Mey Ch=7006663615en_US
dc.identifier.scopusauthoridWellens, D=7003866572en_US

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