eISSN: 1896-9151
ISSN: 1734-1922
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4/2005
vol. 1
 
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abstract:

INVITED COMMENTARY to:
A reappraisal of concepts in heart failure: Central role of cardiac power reserve, Simon G. Williams, Diane Barker, David F. Goldspink, Lip-Bun Tan, Arch Med Sci 2005; 1, 2: 65-74

Jochen D. Schipke
,
Frank-Chris Schoebel
,
Emmeran Gams

Arch Med Sci 2005; 1, 4: 195-197
Online publish date: 2005/12/22
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Submitted: 9 December 2005
Accepted: 9 December 2005


Corresponding author:
Prof. Dr. Jochen D Schipke
Research Group Experimental Surgery
Department of Surgery
University Hospital Duesseldorf Moorenstrasse 5
D-40225 Duesseldorf, Germany
Phone: +49 211 81199 49
Fax: +49 211 811 69 96
E-mail:
schipke@med.uni-duesseldorf.de


Heart failure (HF) is frequent, essential and hard to define. A reappraisal of this pathophysiologic condition is, therefore, reasonable. The review paper of Williams and colleagues addresses the difficulty to define HF. In its first part, four presumably misleading concepts are presented.
Cardiac imaging and presentation of the left ventricular ejection fraction (EF) in order to describe cardiac function is widely employed. It is agreed that its usefulness to assess HF is limited. On the one hand, acute EF values or changes in EF might solely reflect conditions of the total peripheral resistance. On the other hand, an EF of 30% does not necessarily describe HF, as long as the patient's quality of life is maintained. The authors of the review article are wrong, as they claim that EF is misleading because it is measuring cardiac structure and not cardiac function: the more appropriate term “geometry” cannot simply be translated into function.
The second conceptional “flaw” pertains to myocardial contractility, a term that seems to be misperceived by the authors. Contractility was not primarily used to differentiate between normal and failing hearts. Sonnenblick [1, 2] and Siegel [3] presented the concept of contractility to better describe cardiac contraction and its properties independent of loading conditions and heart rate. It is also inaccurate to argue that “a major objective of therapy… became to… increase myocardial contractility”. Contractile or systolic force would have been more accurate, as it is known that the accelerated development of force, i.e. an increase in contractility, is associated with “oxygen wasting” which is highly undesirable in the already compromised heart [4, 5]. Along the same line, levosimendan, as a Ca2+ – sensitizing agent, has purposely been developed to produce contractile force more economically [6, 7].
The definition of heart failure is discussed as the third misleading concept. It...


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