(Circulation. 2006;114:e372.)
© 2006 American Heart Association, Inc.
Correspondence |
Department of Cardiology, Leiden University Medical Center, Leiden, the Netherlands
Department of Medical Statistics, Leiden University Medical Center, Leiden, the Netherlands
We thank Knaapen et al for their interest in our work.1 We agree with them that our simple approach to calculating end-systolic elastance may be considered a limitation, and we value their suggestion that we apply single-beat algorithms to estimate end-systolic elastance from steady-state pressure-volume loops. Although load interventions by caval vein balloon occlusions are certainly feasible,2 we decided not to use this approach in our study to limit the length of our protocol, which included registration of pressure-volume loops at incremental pacing rates in patients with severe heart failure. Moreover, we and others3 have previously demonstrated that in addition to the slope of the end-systolic pressure-volume relation (end-systolic elastance), the position is also a sensitive indicator of changes in contractile state. Therefore, provided that end-systolic pressure is maintained, a reduced end-systolic volume also indicates an improvement in contractile state.
As correctly pointed out by Knaapen et al, we used the term "mechanical efficiency" to describe the energy transfer from pressure-volume area (PVA) to stroke work (SW). We carefully stated this definition and its calculation in our Methods section and the definition was repeated in the text and in the legend of our original Table 2. In his landmark review article, Dr Suga4 describes the various steps from myocardial oxygen consumption to, ultimately, production of external work. Unfortunately, however, there is no consistent terminology in the literature for the efficiencies of the intermediate energy conversion processes (ie, O2 to adenosine triphosphate, adenosine triphosphate to PVA, PVA to SW). Presumably, simply referring to these as, eg, SW/PVA efficiency, would be the best way to avoid confusion.
| Acknowledgments |
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Dr Tulner was supported by a grant from the Netherlands Heart Foundation (NHS-2002B133). Dr Bax received a research grant from Medtronic Inc.
Disclosures
None.
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2. Bleasdale RA, Turner MS, Mumford CE, Steendijk P, Paul V, Tyberg JV, Morris-Thurgood JA, Frenneaux MP. Left ventricular pacing minimizes diastolic ventricular interaction, allowing improved preload-dependent systolic performance. Circulation. 2004; 110: 23951400.
3. Steendijk P, Baan J Jr., Van der Velde ET, Baan J. Effects of critical coronary stenosis on global systolic left ventricular function quantified by pressure-volume relations during dobutamine stress in the canine heart. J Am Coll Cardiol. 1998; 32: 816826.
4. Suga H. Ventricular energetics. Physiol Rev. 1990; 70: 247277.
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