|
|
||||||||
J Thorac Cardiovasc Surg 2000;120:830-831
© 2000 The American Association for Thoracic Surgery
Letters to the Editor |
Missouri Baptist Heart Center
3015 N Ballas Rd St Louis, MO 63131
To the Editor:
We read with interest the commentary regarding the recently published series of articles on the role of S-100ß protein and neuron-specific enolase as biochemical markers of brain injury in cardiac surgery.
1 In their commentary, Hammond and Stump state that these markers are detectable in the cerebrospinal fluid after brain injury and that their levels are increased after acute stroke. Although the levels are increased in these settings, these proteins are also present in the cerebrospinal fluid of neurologically normal individuals, and their concentration in spinal fluid increases at a rate of approximately 1% per year between the ages of 1 and 65 years.
2 This age-related increase occurs in normal cerebral tissue as well, and higher levels have also been reported in patients with Down syndrome and Alzheimer disease. (The ß subunit of S-100 is mapped in the q22 region of chromosome 21, which is duplicated in Down syndrome; thus higher levels are expressed.)
3
A positive correlation between S-100ß serum levels and increasing age in patients undergoing coronary artery bypass grafting with or without cardiopulmonary bypass was shown in the recent study by Westaby and associates,
4 and it has been inferred in other studies. Thus, in any analysis of S-100ß as a marker of cerebral injury after cardiac surgical procedures, with or without cardiopulmonary bypass, patients should be carefully matched for age and for diseases that are associated with elevated S-100ß blood levels.
We share the skepticism of Hammon and Stump concerning the role of these proteins as markers of neurologic injury after cardiac surgery.
We find it intriguing that the S-100ß serum levels reported after uneventful cardiac and aortic surgical procedures reached peak levels (2.5-6 µg/L) on completion of cardiopulmonary bypass, especially if circulatory arrest was used, and then disappeared within 6 to 12 hours.
5 In patients with large acute ischemic strokes who have not undergone cardiac surgery, the maximum serum levels of S-100ß are lower (0.6-1.8 µg/L) and peak later after the event, approximately 3 days after the infarction.
6 These observations suggest that leakage of S-100ß from the cerebrospinal fluid into the capillaries, due to an alteration of the blood-brain barrier in patients undergoing surgical procedures, may be responsible for the higher levels observed after cardiopulmonary bypass.
Origin from extracerebral sources may also be responsible for the elevated S-100ß levels in patients undergoing cardiac surgery. The S-100 family of proteins consists of heterodimers and homodimers of the
and ß subunits (
,
ß, and ßß), and the ß subunit (encoding messenger RNA) is present in bladder, skin, adipose tissue, aorta, and myocardium.
7 The first evidence that myocardium could be a site for anomalous expression of S-100ß was the observation that S-100ß protein was detectable in the hearts of human beings with chronic respiratory disease who were treated with systemic bronchodilators and inotropic adrenergic agonists.
8
Furthermore, subsequent investigations have demonstrated, by immunohistochemical staining techniques, the induction of S-100ß by cyclic adenosine monophosphate in patients with hypertension, and after acute myocardial infarction, as part of the response of cardiomyocytes to trophic stimuli. Cyclic adenosine monophosphate levels can also be increased by endogenous catecholamine release in congestive heart failure, by phosphodiesterase inhibiting drugs, and by ventricular remodeling.
9 Thus, it is of interest that higher S-100ß serum levels were found by Taggart and associates
10 in "intracardiac" (valve replacement) operations than in "extracardiac" (coronary artery bypass grafting) procedures (0.76 vs 0.3 µg/L, respectively).
We believe that alternative hypotheses and other mechanisms should be considered as possible explanations of the elevated S-100ß serum levels observed after cardiac surgical operations.
[Response declined]
12/8/109549
doi:10.1067/mtc.2000.109549
References
1-adrenergic induction of the hypertrophic phenotype in cardiac myocytes. J Biol Chem 1997;272:31915-21.
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| ANN THORAC SURG | ASIAN CARDIOVASC THORAC ANN | EUR J CARDIOTHORAC SURG |
| J THORAC CARDIOVASC SURG | ICVTS | ALL CTSNet JOURNALS |