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J Am Coll Cardiol, 2006; 48:2482-2484, doi:10.1016/j.jacc.2006.06.007
(Published online 21 November 2006). © 2006 by the American College of Cardiology Foundation |
2nd Department of Cardiology, Onassis Cardiac Surgery Center, Athens, Greece.
Manuscript received February 14, 2006; revised manuscript received July 5, 2006, accepted September 7, 2006.
* Reprint requests and correspondence: Dr. Eftihia Sbarouni, Onassis Cardiac Surgery Center, 2nd Department of Cardiology, 356 Syngrou Avenue, 17674 Athens, Greece (Email: elbee{at}ath.forthnet.gr).
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Abstract |
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BACKGROUND: Ischemia modified albumin is considered a marker of myocardial ischemia and increases after coronary angioplasty and in acute coronary syndromes.
METHODS: We studied 40 consecutive patients with established coronary artery disease who underwent EST. Venous samples, for IMA measurement, were collected before the stress test (baseline), at peak exercise, and 60 min after the completion of the exercise test.
RESULTS: There was significant difference in the IMA values at the 3 prespecified time points (p = 0.012), whereas there was no interaction between the IMA changes and the result of the stress test, whether positive or negative (p for the interaction term = 0.94). Baseline, peak EST, and post-EST IMA levels were similar in patients with positive and negative exercise tests (p = 0.61). The IMA significantly decreased at peak exercise compared with baseline values in positive (p < 0.0001) and in negative EST (p = 0.012). Moreover, IMA concentration increased 60 min after EST compared with peak-EST values in positive (p < 0.0001) and in negative tests (p = 0.003), returning to pre-EST levels in both groups.
CONCLUSIONS: The IMA plasma levels change significantly during exercise testing in patients with coronary artery disease, but there is no difference between positive and negative stress tests; this possibly implies that the observed changes do not reflect myocardial ischemia.
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Methods |
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All patients performed the treadmill exercise test with the Bruce protocol. Peripheral venous samples were collected before the stress test (baseline), at peak exercise, and 60 min after the completion of the exercise test via an indwelling catheter. The blood samples were frozen at –70°C and stored until assayed. Serum IMA was measured with the albumin cobalt binding test on an Integra 800 analyzer (Roche, Rotkreuz, Switzerland). According to the manufacturer, expected values determined in a population of 283 healthy individuals range from 52 to 116 U/ml with a 95th percentile at 85 U/ml. The total interassay imprecision (coefficient variation) was 2.7% to 5.7% at 56.3 to 125.9 U/ml for quality control material. The EST was considered as positive when the patient developed significant ST-segment T-wave changes (>2 mm ST-segment horizontal or downslopping depression).
Statistical analysis. Data are presented as median values, range, and 25th and 75th percentiles. Analysis of variance with repeated measures was used to test for differences in IMA levels between time points. Furthermore, the Wilcoxon test was applied for pairwise comparisons with Bonferroni correction to account for the inflation in type I error. SPSS statistical software (SPSS Inc., Chicago, Illinois) was used in all data analyses.
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Results |
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Discussion |
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Our results confirm those of a previous report (8) that had investigated IMA kinetics in 38 patients with chest pain and suspected coronary artery disease undergoing single-proton emission computed tomography imaging. In that study, IMA levels were also significantly lower at maximum exercise than baseline and returned to baseline values within 1 h after stress; this occurred in patients with and without ischemia. Furthermore, IMA levels were similar between the 2 groups at all time points of the protocol—before exercise; at maximum exercise; and 1, 2, 3, 4, 5, and 6 h after exercise. Interestingly, in the same study albumin plasma levels were also evaluated and found to increase at maximum exercise, in correlation with IMA decrease, in all patients with and without ischemia. Therefore, it seems that the hemoconcentration that occurs during physical exercise induces an increase in albumin plasma levels and subsequently a decrease in the nonbound portion of a fixed amount of cobalt. The IMA concentration has also been shown to decrease immediately post-race compared with pre-race in 19 healthy marathon runners (9). Ischemia-modified albumin has been evaluated in healthy subjects after hand-grip and found to decrease significantly at 1, 3, and 5 min after forearm ischemia and return to baseline thereafter. The same changes were reported for IMA/albumin ratio (10). Likewise, in patients with documented peripheral vascular disease undergoing claudication, limited treadmill test IMA decreased significantly compared with baseline and returned to baseline at 1 h after stress, although in this study albumin concentration did not change with exercise and no correlation was found between IMA and albumin levels at any time point (11). In addition, in the same study all patients were evaluated with dobutamine stress echocardiography, which was negative in all; IMA levels were unchanged at baseline, peak stress, and 1 h after stress, unlike our negative exercise tests where IMA changed significantly and similarly to our positive stress tests. Still, one should also take into account that myocardial ischemia during stress test—either physical or pharmacological—might not be as severe as the ischemia that occurs during PCI or in the acute coronary syndrome setting. Because in the latter 2 conditions IMA increases (1–7), it is intriguing that its levels decrease in EST-induced ischemia, as found in our and other studies. Although speculative, it seems that during EST-induced ischemia, 2 different mechanisms might influence IMA levels; active ischemia tends to increase IMA, but eventually the hemoconcentration mechanism predominates, resulting in decreased IMA concentration.
We conclude that IMA plasma levels change significantly during exercise testing in patients with coronary artery disease, but there is no difference between positive and negative stress test; this might imply that the observed changes do not reflect myocardial ischemia. The IMA measurement does not seem to improve the accuracy of EST.
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