Author + information
- Eftihia Sbarouni, MD, FESC⁎ (, )
- Panagiota Georgiadou, MD,
- George N. Theodorakis, MD, FESC and
- Dimitrios Th. Kremastinos, MD, FESC
- ↵⁎Onassis Cardiac Surgery Center, 2nd Department of Cardiology, 356 Syngrou Avenue, 176 74 Athens, Greece
We appreciate the interest of Dr. Kalay and colleagues in our study assessing ischemia-modified albumin (IMA) levels in exercise stress testing (1). We address their comments:
1. All our patients had angiographically documented coronary artery disease, the exercise stress test (EST) being part of their regular follow-up, and the criteria we used for positivity were rather strict—2-mm horizontal or downsloping ST depression. In addition, our findings do not differ from Van der Zee et al. (2), who also observed a significant decrease of IMA plasma levels at peak exercise and subsequent return to baseline, without any difference between positive and negative exercise tests. In that study, single-photon emission computed tomography (SPECT) imaging, a more sensitive and specific method compared to treadmill testing, was used. Therefore, in that respect, we believe inaccuracies in the EST results (false positive or negative) cannot be substantiated.
2. Regarding the timing of IMA sampling, percutaneous coronary intervention (PCI) studies have shown a significant increase in IMA plasma levels immediately following balloon deflation and a return to baseline within 6 to 12 h (3,4), so we would think that peak exercise is the appropriate time point to assess whether IMA increases in exercise-induced ischemia.
3. Although we cannot exclude occult peripheral atherosclerosis in our patients, none of the study participants had clinically significant peripheral vascular disease, by history, physical examination or clinical presentation. Additionally, in no patient was the EST limited by skeletal muscle ischemia, rendering the mechanism of peripheral lactic acidosis as a cause of decreased exercise IMA levels extremely unlikely. Furthermore, a very recent report observed that the rise in IMA plasma levels after PCI parallels that of transmyocardial lactate, immediately after obstructive balloon inflation (5).
In the letter by Drs. Roy and Kaski regarding our study (1) they state that IMA decrease at exercise may relate to either albumin or lactate increase. Albumin plasma levels have been assessed during exercise (2) and have been nicely shown to correlate inversely with IMA changes, in patients with and without ischemia. Therefore, we believe that the IMA changes we observed are associated with hemoconcentration. It is well known that reactive oxygen species production during myocardial ischemia (PCI or acute coronary syndrome) may indeed induce changes in the amino terminus of albumin. In addition, we agree that further research regarding specific mechanisms is necessary.
In conclusion, our study demonstrated that IMA changes significantly during EST in patients with coronary disease but with no difference between positive and negative tests; these results, we believe, imply that IMA changes may not relate to myocardial ischemia.
- American College of Cardiology Foundation
- Sbarouni E.,
- Georgiadou P.,
- Theodorakis G.N.,
- Kremastinos D.T.
- Van der Zee P.M.,
- Verberne H.J.,
- Straalen J.P.,
- et al.
- Bar-Or D.,
- Winkler J.V.,
- VanBenthysen K.,
- et al.
- Sinha M.K.,
- Vasquez J.M.,
- Calvino R.,
- Gaze D.C.,
- Collinson P.O.,
- Kaski J.C.