Obstructive sleep apnoea and plasma homocysteine: reply
Division of Cardiovascular Diseases
Department of Internal Medicine
Mayo Clinic and Mayo Foundation
200 1st Street SW
Rochester
MN 55901
USA
Division of Cardiovascular Diseases
Department of Internal Medicine
Mayo Clinic and Mayo Foundation
200 1st Street SW
Rochester
MN 55901
USA
Mayo Clinic and Mayo Foundation
200 1st Street SW
Rochester
MN 55901
USA
Division of Cardiovascular Diseases
Department of Internal Medicine
Mayo Clinic and Mayo Foundation
200 1st Street SW
Rochester
MN 55901
USA
University of Iowa
Iowa City
IA
USA
Division of Cardiovascular Diseases
Department of Internal Medicine
Mayo Clinic and Mayo Foundation
200 1st Street SW
Rochester
MN 55901
USA
Tel: +1 507 255 1144
Fax: +1 507 255 7070
E-mail address: somers.virend{at}mayo.edu
We very much appreciate the interest and constructive comments of Lavie and Lavie regarding our recent article on measurements of plasma homocysteine in otherwise healthy individuals with obstructive sleep apnoea.1 We are also very grateful for the kind and encouraging comments made in the thoughtful review by Winnicki and Palatini,2 which focused on our article as well as on the initial work on plasma homocysteine by Lavie et al.3 We have carefully reviewed all three articles1–3 and it seems that both our article and the Winnicki and Palatini2 article provided an accurate assessment of the findings by Lavie et al.3 in the context of the subject matter.
In brief, our study confirmed their earlier novel and important finding that homocysteine was not elevated in OSA patients without any cardiovascular disease. This confirmation is relevant as their initial study excluded OSA by polysomnography in less than one-third of the control subjects and less than a quarter of those with ischaemic heart disease and presumed not to have OSA. As diurnal variation in homocysteine is known to occur, we measured plasma homocysteine not only in the morning but also at three different times during the day (before sleep, after sleep, and after being awake for several hours). Along with excluding patients with other cardiovascular diseases, we also excluded smokers and patients on medication; furthermore, our groups had similar BMI and age—all these factors may interact to change homocysteine levels.
Our a priori goal was to determine whether OSA in and of itself, and independent of other variables, was accompanied by increased homocysteine. Our data suggest that it is not. However, we do agree that patients presenting with both sleep apnoea and cardiovascular disease may well have increased homocysteine. Whether this is due to the cardiovascular abnormality or OSA alone or both remains unclear. Whether, to what degree, and through what mechanisms, OSA could possibly contribute to any elevated homocysteine in the presence of cardiac problems is still unknown and needs to be elucidated.
References
- Svatikova A, Wolk R, Magera MJ, Shamsuzzaman AS, Phillips BG, Somers VK. Plasma homocysteine in obstructive sleep apnoea. Eur Heart J 2004;25:1325–1329.
[Abstract/Free Full Text] - Winnicki M, Palatini P. Obstructive sleep apnoea and plasma homocysteine: an overview. Eur Heart J 2004;25:1281–1283.
[Free Full Text] - Lavie L, Perelman A, Lavie P. Plasma homocysteine levels in obstructive sleep apnea: association with cardiovascular morbidity. Chest 2001;120:900–908.
[Abstract/Free Full Text]
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