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Ann Thorac Surg 2005;79:871
© 2005 The Society of Thoracic Surgeons

INVITED COMMENTARY

Department of Surgery, Ulleval University Hospital, Oslo, 0407 Norway

(E-mail: i.j.vaage{at}medisin.uio.no).

Heat shock proteins (HSP) are characterized as molecular chaperones; they are phylogenetically very old and have important functions in the preservation and protection of cells and organs towards stress and injury [1]. Heat shock proteins protect against ischemia-reperfusion injury of the heart and improve postcardioplegic function [2].

A search on Pubmed for "heart surgery" and "heat shock proteins" resulted in 82 articles, the majority of which are very relevant to clinical surgery. This demonstrates that HSP are already well involved in the research areas of cardiac surgeons. However, there is no situation in which the presence or increased expression of HSP have become a part of prevention or therapy to prevent organ dysfunction and clinical complications.

The present article has three important conclusions: (1) There is an association between high intracellular levels of inducible HSP70 and atrial fibrillation after coronary artery bypass grafting. (2) There is no association between atrial fibrillation and serum levels of HSP70. (3) There is no correlation between intracellular atrial HSP70 and HSP70 in serum.

This article is an interesting investigation, but it is partly a repetition of the work of Rammos and colleagues [3]. Although the latter included a few valve patients, there are no fundamental differences except that the present work uses more advanced techniques and includes measurements of HSP in serum. The comparison between tissue and soluble HSP is interesting and the investigators suggest that intracellular and serum HSP may have completely different functions.

The present work creates more questions than it gives answers and may be a powerful stimulus for further research. We need more information concerning different stimuli that may possibly cause increased HSP70 in the nonfibrillating group. Why do some patients have a higher level of intracellular HSP from the beginning? Is there anything in the patient characteristics that has not come forward, or do some patients genetically have a higher level of intracellular HSP70 that makes them more resistant to stress and trauma? There is relatively scarce information about patient characteristics, but all patients were elective cases. How is this defined without unstable angina? Unstable angina may be a cause of increased HSP [4]. There is not any information on whether some patients were exposed to other stimuli or drugs that may increase the expression of HSP in hearts, such as steroid medication [5]. Another question is: May the reduction of atrial fibrillation be directly related to the high levels of HSP70, or are the high levels of HSP70 and reduced atrial fibrillation parallel phenomena and not causally related? The authors have no data or answers to these questions, but there is an abundance of questions for further investigations.

The patients who had atrial fibrillation had a more complicated postoperative course; they stayed longer on ventilator and had a longer stay in the intensive care unit. Was this protracted course due to atrial fibrillation and arrhythmias or was it due to some other reason like infection, heart failure, etc? There was more use of inotropic support in the fibrillating group. Was this secondary to the arrhythmias or was there reduced myocardial function even when the patients had sinus rhythm? Is it so that patients with low tissue levels of HSP are more likely to have complications develop after major surgery? Thus, a technique that is easy applicable to increase tissue levels of HSP in patients may be a major breakthrough in the efforts to reduce postoperative morbidity; it would be a "whole body preconditioning."

	References

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1. Latchman DS. Heat shock proteins and cardiac protection Cardiovasc Res 2001;51:637-646.[Abstract/Free Full Text]
2. Amrani M, Corbett J, Allen NJ, et al. Induction of heat-shock enhances myocardial and endothelial functional recovery after prolonged cardioplegic arrest Ann Thorac Surg 1994;57:157-160.[Abstract]
3. Rammos K, Koullias GJ, Hassan MO, et al. Low preoperative HSP70 atrial myocardial levels correlate significantly with high incidence of postoperative atrial fibrillation after cardiac surgery Cardiovasc Surg 2002;10:228-233.[Medline]
4. Valen G, Hansson G, Dumitrescu A, Vaage J. Unstable angina activates myocardial heat shock protein 72, endothelial nitric oxide synthetase, and transcription factors NFB and AP-1 Cardiovasc Res 2000;47:49-56.[Abstract/Free Full Text]
5. Valen G, Kawakami T, Tähepöld P, Dumitrescu A, Löwbeer C, Vaage J. Glucocorticoid pretreatment protects cardiac function and induces cardiac heat shock protein 72 Amer J Physiol 2000;279:H836-H843.

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): Jarle Vaage Permission Requests Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Vaage, J. Search for Related Content PubMed Articles by Vaage, J. Related Collections Electrophysiology - arrhythmias Related Article