Download Progress in Developing a Noninvasive Load-Independent

JACC Vol. 31, No. 4
March 15, 1998:869 –70
Editorial Comment
Progress in Developing a
Noninvasive Load-Independent
Marker of Ventricular
Contractility*
HENRY SHIN, MD,
NELSON B. SCHILLER, MD, FACC
San Francisco, California
The Frank-Starling model of myocardial work (1,2), which
relates pressure to volume changes throughout the cardiac
cycle, and the subsequent work of Sarnoff and Berglund on the
preload dependence of the stroke work index set the experimental stage for evaluating intrinsic myocardial performance.
Unfortunately, these relations were nonlinear and required
extensive invasive manipulation, which prevented their application to the clinical field.
In 1991, Kass and Beyer (3) revisited the pressure–volume
relation and found that when stroke work was divided by the
square of the end-diastolic volume (EDV2), stroke work
remained independent of preload and afterload changes. They
called this index “preload-adjusted maximal power” and suggested applying this index as a clinical marker of myocardial
performance now that technologic advances in echocardiography allowed accurate estimates of volume changes through the
cardiac cycle. Kass and Beyer (3) explained the preload
independence of the index as follows: Mean power is the
product of mean pressure and flow; pressure is the product of
flow and resistance; and, therefore, power is the product of
resistance and flow squared. Power divided by volume squared
is then proportional to resistance divided by seconds squared.
Mean arterial resistance is minimally altered with steady state
changes of circulating volume. Thus, at constant heart rate and
contractility, preload-adjusted maximal power reflects contractility (3).
In response to this suggestion, Mandarino et al. (4), in this
issue of the Journal, report the results of their derivation of
preload-adjusted maximal power using automatic border detection (ABD) from canine echocardiographic images to measure cross-sectional area changes (dA/dt) through the cardiac
cycle. The product of dA/dt and instantaneous central arterial
pressure yields a stroke work analog that is adjusted for
*Editorials published in Journal of the American College of Cardiology reflect
the views of the authors and do not necessarily represent the views of JACC or
the American College of Cardiology.
From the Echocardiography Laboratory, University of California San Francisco, San Francisco, California.
Address for correspondence: Dr. Nelson B. Schiller, Echocardiography
Laboratory, University of California San Francisco, 505 Parnassus Avenue,
Room 342A, San Francisco, California 94143-0214.
©1998 by the American College of Cardiology
Published by Elsevier Science Inc.
869
loading conditions by the term EDV3/2 based on the substitution of dA/dt for dV/dt (Kass and Beyer [3] used EDV2 instead
of EDV3/2 as a correction term because they used dV/dt). The
resulting preload-adjusted maximal power index was found to
be independent of preload changes experimentally achieved
through vena caval occlusions and independent of afterload
changes through aortic occlusion.
Potential limitations of preload-adjusted maximal power as
a clinical index of myocardial performance. First, as noted by
Mandarino et al. (4), the contribution of the autonomic
nervous system is ignored in this canine model. This effect may
be important in humans subject to continuous inotropic and
chronotropic modulation by the autonomic nervous system.
Second, the studies of Kass and Beyer (3) and Mandarino et
al. (4) were performed in normal dog hearts. Underestimation
of true myocardial stroke work may occur in patients with
severely dilated cardiomyopathies, where the denominator
term is EDV2 or EDV3/2.
Third, a noninvasive surrogate of central arterial pressure is
highly preferable to an invasive measurement for clinical
application. Although studies (5) have been performed to
correlate pressures in the carotid or femoral arteries using
ultrasound transducers, the procedure is too burdensome to
make it practical.
Fourth, most pharmacologic interventions, including dobutamine, will affect not only contractility but other variables as
well, such as afterload. These interrelated hemodynamic effects must be carefully considered before drawing the conclusion that preload-adjusted maximal power is a loadindependent measure of end-systolic elastance.
Future steps in the development of preload-adjusted maximal power as an index of myocardial performance. A successful index must be easy to use and to understand. The
variables necessary to calculate preload-adjusted maximal
power include central arterial pressure, instantaneous EDV
and ESV. The index is unlikely to gain wide acceptance unless
a noninvasive surrogate of central arterial pressure is used.
Mean peripheral arterial pressure is probably the best correlate of mean central arterial pressure. Although instantaneous
central arterial pressure cannot be obtained, mean peripheral
arterial pressure in the steady state may be an acceptable
substitute if supported by future studies. EDV and ESV may
be measured accurately by tedious volume manual planimetry
but may provide a more accurate component of preloadadjusted maximal power than ABD-derived area from a single
plane, especially in hearts with altered geometry. Because the
index is not intuitively physiologic (units are mW/cm4), a range
of normal and abnormal values must be established.
The index must be demonstrably superior to ejection fraction. Despite its shortcomings, ejection fraction is the preferred index of myocardial function because of its simplicity,
reproducibility and prognostic value. Only if an index such as
preload-adjusted maximal power turns out be robustly independent of preload and afterload factors can it improve on the
prognostic power and accuracy of ejection fraction.
0735-1097/98/$19.00
PII S0735-1097(98)00049-7
870
SHIN AND SCHILLER
EDITORIAL COMMENT
Abbreviations and Acronyms
ABD 5 automatic border detection
dA/dt 5 rate of change of left ventricular cross-sectional area
dV/dt 5 rate of change of left ventricular volume
EDV 5 end-diastolic volume
ESV 5 end-systolic volume
The evolutionary refinements in echocardiography may
now provide the tools for transferring benchwork pressure–
volume studies to the clinical arena.
References
1. Frank O. Zur Dynamik des Herzmuskels. Biology 1895;32:370.
2. Patterson SW, Starling EH. On mechanical factors which determine output
of ventricles. J Physiol (Lond) 1914;48:37.
3. Kass DA, Beyer R. Evaluation of contractile state by maximal ventricular
power divided by the square of end-diastolic volume. Circulation 1991;84:
1698 –708.
4. Mandarino WA, Pinsky MR, Gorcsan J. Assessment of left ventricular
contractile state by preload-adjusted maximal power using echocardiographic automated border detection. J Am Coll Cardiol 1998;31:861– 8.
JACC Vol. 31, No. 4
March 15, 1998:869 –70
5. Sharir T, et al. Validation of a method for noninvasive measurement of
central arterial pressure. Hypertension 1993;21:74 – 82.
6. Kass DA, Yamazaki T, Burkhoff D, Maughan WL, Sagawa K. Determination
of left ventricular end-systolic pressure-volume relationships by the conductance (volume) catheter technique. Circulation 1986;3:586 –95.
7. Kass DA, Beyar R, Lankford E, Heard M, Maughan WL, Sagawa K.
Influence of contractile state on curvilinearity of in situ end-systolic pressurevolume relations. Circulation 1989;79:167–78.
8. Glower DD, et al. Linearity of the Frank-Starling relationship in the intact
heart: the concept of preload recruitable stroke work. Circulation 1985;71:
994 –1009.
9. Gorcsan J, Romand J, Mandarino WA, Deneault LG, Pinsky MR. Assessment of left ventricular performance by on-line pressure-area relations using
echocardiographic automated border detection. J Am Coll Cardiol 1994;23:
242–52.
10. McKay RG, Aroesty JM, Heller GV, Royal HD, Warren SE, Grossman W.
Assessment of the end-systolic pressure-volume relationship in human
beings with the use of a time-varying elastance model. Circulation 1986;74:
97–104.
10. Sharir T, Feldman MD, Haber H, et al. Ventricular systolic assessment in
patients with dilated cardiomyopathy by preload-adjusted maximal power:
validation and noninvasive application. Circulation 1994;89:2045–53.
11. Little WC, Freeman GL, O’Rourke RA. Simultaneous determination of left
ventricular end-systolic pressure-volume and pressure-dimension relationships in closed-chest dogs. Circulation 1985;6:1301– 8.
12. Russell RO, Porter CM, Frimer M, Dodge HT. Left ventricular power in
man. Am Heart J 1971;81:799 – 808.
13. Snell RE, Luchsinger PC. Determination of the external work and power of
the left ventricle in intact man. Am Heart J 1965;69:529 –37.
14. Stein PD, Sabbah NH. Rate of change of ventricular power: an indicator of
ventricular performance during ejection. Am Heart J 1976;91:219 –27.