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Eur J Cardiothorac Surg 2005;28:779
© 2005 Elsevier Science NL
Letter to the Editor |
a University Clinic, Experimental Heart Surgery, Domagkstrasse 11, 48149 Muenster, Germany
b University College, Institute of Child Health, Cardiac Unit, London, UK
Received 5 July 2005; accepted 9 August 2005.
* Corresponding author. Tel.: +49 251 8352541; fax: +49 251 8356257. (Email: redmann{at}uni-muenster.de).
Key Words: Myocardial band • Microsonometry • Myocardial fibres • Triebwerkzeug
In the current issue of the Journal, Corno argues that the ‘new concepts on cardiac anatomy and physiology...deserve for further and deeper investigations’ [1]. Should he not first examine existing anatomic investigations of the past 400 years showing that the heart is formed on the basis of a modified blood vessel, and not in the fashion of skeletal musculature, rather than obfuscate the issue with comments about the free-standing subpulmonary infundibulum, an important feature of anatomy that owes nothing to the presence or absence of a unique myocardial band [2]?
Castella and colleagues [3] describe microsonometric findings, which display a widely variable pattern of regional shortening in discrete areas of the ventricular walls. The authors continue to interpret the regional dephasing observed in onset and termination of shortening as being the result of delayed excitation and contraction. In reality, onset and termination of myocardial shortening are widely modulated by the amount and time-course of the action of structural afterload over the heart cycle. Delayed shortening primarily heralds the action of intrinsic resistances sustained by the inhomogeneous three-dimensional arrangement of the myocardial syncytium [4]. Onset of mechanical activation, in other words the onset of contraction, unfortunately, cannot be measured by methods designed to assess distances of shortening. If ‘the main objective of the study’, therefore, was to establish ‘the sequence of contraction within the myocardial mass’, then unfortunately the authors [3] have chosen the wrong method.
It is equally disturbing to find them using the neologism ‘nerve muscle anatomy’. Are the authors, in this regard, referring to the insulated network of musculature which is responsible for dissemination of the impulse of excitation within the ventricles, and generally called the ‘conduction system’? This, of course, is made up of specialised myocardial tissue, with any autonomic nerves present in the ventricles performing no more than a modulating function.
It is when commenting on the purported myocardial band, however, that they commit their most egregious error. They make reference to the ‘Treibwerk’, meaning Krehl's ‘Triebwerkzeug’ [5], which consists of the circular fibres which encircle the left ventricle. Krehl believed that these fibres were the driving force for ventricular ejection. But Krehl also took into consideration the function of inner and outer myocardial layers, which he considered to be continuous in the apex and anchored at the base. Krehl assumed that systolic circular constriction and thickening of the ‘Triebwerkzeug’ is partially reversed at end-systole, or during diastole when contraction in the circular fibres ceases, by a remaining amount of tension in the embracing layers of longitudinal fibres. This concept is entirely at odds with the hypothesis of the unique myocardial band proposed by Torrent-Guasp [2]. It is an anatomic fact that dissections produced by Torrent-Guasp systematically destroy the continuum of the bordering fibres when separating the purported basal and apical loops [2]. The authors, therefore, should refrain from seeking to support the spurious notion of the unique myocardial band by misquoting classical works, even if these solecisms might have been caused by difficulties in translating the original work [5] from the German language.
References
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