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Letters to the Editor |
Department of Biosurgery and Surgical Technology, Imperial College London, St Mary's Hospital, London W2 1NY, United Kingdom
Received 21 April 2008; accepted 22 April 2008.
* Corresponding author. Tel.: +44 207 886 1310; fax: +44 207 886 1810. (Email: tathan5253{at}aol.com).
Key Words: Takotsubo syndrome • Chordal preservation • Mitral valve
We would like to thank Professor Ghosh et al. [1] for their response to our systematic review [2]. It is well known that in our routine cardiac surgical practice transient low-cardiac output (LCO) state following mitral valve replacement (MVR) can occur. It has often been considered a complication of cardiopulmonary bypass and related to; intolerance to cardioplegic asystolic hypoxic arrest, reperfusion injury, inadequate myocardial protection, or a cardiopulmonary bypass associated systemic inflammatory response. Transient LCO state following mitral valve replacement can also occur for several other reasons: firstly due to an embolic phenomenon, for example, air emboli after inadequate de-airing; clot or particulate atheromatic emboli. Secondly, it can be due to metabolic causes such as hypoxia, hypercarbia, or electrolyte abnormalities. Thirdly, it can be related to conduction abnormalities and arrhythmias. Fourthly, it can be due to concomitant mechanical and technical failures, such as abnormal prosthetic valve function. Finally, transient low-cardiac output states can occur because of graft-flow related factors when simultaneous coronary artery bypass grafting is performed [3].
We agree with Professor Ghosh et al. that the association between Takotsubo syndrome and physiological or psychological stress [4] makes it an important differential alongside these recognized causes of low-cardiac output state following cardiac surgery. Particularly after mitral valve replacement, as the pathognomonic pattern of left-ventricular wall motion abnormality that occurs in Takotsubo syndrome resulting in left-ventricular apical dilation may resemble sphericalization due to loss of mitral annuloventricular continuity [1]. Comparatively high estimates of the incidence of Takotsubo syndrome in patients presenting with acute coronary syndromes [4] suggest that Takotsubo syndrome is more common than previously thought, and may further implicate Takotsubo syndrome in the transient low-cardiac output syndrome that can occur after mitral valve replacement. The importance of Takotsubo syndrome after cardiac surgery needs to be better understood, and clearly further research is needed to quantify the incidence and risk factors for this syndrome. The important case study in which Takotsubo syndrome is described for the first time after cardiac surgery by Professor Ghosh's group [5] was not included in our review of the literature [2] as it has only recently been published and was not available at the time of our literature search.
It is important to note however, that the incidence of low-cardiac output syndrome is markedly higher following mitral valve replacement when the mitral subvalvular apparatus are not preserved. Furthermore this effect, unlike Takotsubo syndrome, is often not reversible. This suggests that whilst Takotsubo syndrome may be an important differential when low-cardiac output occurs following mitral valve replacement, the predominant cause when the mitral subvalvular apparatus are not preserved is probably the disruption of annuloventricular continuity and ventricular geometry, resulting in permanent myocardial and valvular dysfunction [2].
References
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