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Eur J Cardiothorac Surg 2000;18:625-626
© 2000 Elsevier Science NL
Letter to the Editor |
a 2nd Medical Department, Krankenanstalt Rudolfstiftung, Vienna, Austria
b 2nd Neurological Department, Neurological Hospital Rosenhügel, Vienna, Austria
Received 5 July 2000; accepted 22 August 2000.
Corresponding author. Steingasse 31/18, A-1030 Wien, Austria. Tel./fax: +43-1-713-9870
e-mail: claudia.stoellberger{at}pips.co.at
Key Words: Left atrial appendage
Elimination of the left atrial appendage (LAA) might be an attractive alternative to anticoagulation since over 90% of thrombi occur within the LAA. However, before discussing about the most suitable technique for elimination of the LAA, evidence has to be provided for its role as an useless or even most lethal and disabling attachment as stated by Johnson WD et al. [1].
The physiologic role of the LAA has been studied by several investigations. One of them showed that sheep with crushed LAA did not increase their water intake after volume depletion, whereas control sheep with intact LAA did. Stretch receptors of the LAA may play a role in mediating thirst [2]. In dogs it was shown that the LAA has a higher distensibility than the left atrial body and that left atrial compliance is decreased after removal of the LAA. The LAA modulates the relation between pressure and volume in the left atrium and becomes important in states of left atrial pressure and volume overload [3]. In isolated working hearts of guinea pigs the LAA influences cardiac pump function. As compared to hearts with ligated LAA, cardiac output of hearts with intact LAA was almost twice as high. This difference was attributed to the preserved ability of the LAA to contract and subsequent better filling of the left ventricle [4].
In humans LAA size was larger in patients with left ventricular hypertrophy than in patients without hypertrophy. LAA size was larger in patients with myocardial scars than in patients without scars. LAA with thrombi were larger than LAA without thrombi. LAA were larger in patients with atrial fibrillation than in patients with sinus rhythm [5]. LAA enlargement may be a consequence to increased filling pressure. The LAA is a place for release of the atrial natriuretic factor (ANF), a peptide hormone which has natriuretic, diuretic and vasodilatory properties. In normal hearts, ANF concentration is 40-fold higher in the LAA than in the rest of the atrial free wall and in the ventricles. In failing hearts, ANF concentrations in the LAA still increase 5- to 10-fold, especially the concentrations of the prohomones ß- and
-ANF. Thus the LAA plays an important role in the neurohumoral response to cardiac pathologies. There is only one small follow-up study addressing the hemodynamic and neurohumoral consequences of bilateral atrial appendectomy in post-surgical patients. An attenuated ANF secretion in the early postoperative phase and after two years was found [6].
Elimination of the LAA may impede thirst in hypovolemia, deteriorate hemodynamic responses to volume or pressure overload, decrease cardiac output and promote heart failure. Instead of preventing strokes, the consequences of LAA elimination may thus create new risk factors for stroke. In general, elimination of the LAA might induce more harm than benefit to patients with atrial fibrillation. As long as the role of the LAA is not fully understood it should not be eliminated.
References
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