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Clinical Chemistry 50: 1656-1660, 2004. First published July 20, 2004; 10.1373/clinchem.2004.031690
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(Clinical Chemistry. 2004;50:1656-1660.)
© 2004 American Association for Clinical Chemistry, Inc.


General Clinical Chemistry

Ischemia-Modified Albumin Concentrations in Patients with Peripheral Vascular Disease and Exercise-Induced Skeletal Muscle Ischemia

Debashis Roy1,1, Juan Quiles1,1, Rajan Sharma1, Manas Sinha1, Pablo Avanzas1, David Gaze2 and Juan Carlos Kaski1,a

Departments of1 Cardiological Sciences and 2 Chemical Pathology, St. George’s Hospital Medical School, London, UK.

aAddress correspondence to this author at: Cardiological Sciences, St. George’s Hospital Medical School, Cranmer Terrace, London SW17 0RE, UK. Fax 44-208-725-3328; e-mail jkaski{at}sghms.ac.uk.

Background: Ischemia-modified albumin (IMA) is a new marker of myocardial ischemia, there is concern that IMA concentrations may be affected by ischemia occurring in tissues other than the myocardium.

Methods: We assessed 23 consecutive patients (15 males; mean age, 67 years) with typical leg claudication and documented peripheral vascular disease (PVD). All patients underwent both treadmill-exercise stress testing to induce leg ischemia and dobutamine stress echocardiography 1 week apart for the assessment of myocardial ischemia. Blood samples for IMA measurements were obtained at baseline, immediately after peak exercise/stress, and 1 h after exercise/stress. Statistical analysis was performed with the ANOVA repeated-measures test.

Results: Compared with baseline, mean (SD) IMA was significantly lower after the induction of skeletal muscle ischemia and returned to baseline values at 1 h: baseline, 74.6 (15.6) kilounits/L; peak stress, 69.5 (14.0) kilounits/L (P <0.0001 vs baseline); 1 h after stress, 75.9 (15.7) kilounits/L (P <0.0001 vs peak stress; P = 0.3 vs baseline). Baseline, peak stress, and 1-h poststress IMA concentrations were inversely correlated with the ankle-brachial index after exercise (r = –0.4; P <0.05). None of the patients showed regional wall motion abnormalities during dobutamine stress echocardiography, and IMA concentrations remained unchanged from baseline. There were no differences in baseline [74.6 (15.6) vs 72.7 (11.5) kilounits/L; P = 0.6], peak stress, or poststress IMA concentrations when exercise testing and dobutamine stress echocardiography values were compared.

Conclusions: The relationship between disease severity (of a noncardiac origin) and baseline IMA values is an important and novel finding. IMA is significantly lower immediately after exercise-induced leg ischemia in patients with PVD and is related to disease severity. IMA concentrations can therefore be affected by the development of skeletal muscle ischemia, and this may have implications regarding the ability of IMA to detect myocardial ischemia in PVD patients.




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