Felicia Seemann1,2, Jonathan Berg1,3, Kristian Solem3, Robert Jablonowski1, Håkan Arheden1, Marcus Carlsson1, and Einar Heiberg1,2,4
1Clinical Physiology, Lund University, Lund, Sweden, 2Biomedical Engineering, Lund University, Lund, Sweden, 3Syntach AB, Lund, Sweden, 4Wallenberg Center for Molecular Medicine, Lund University, Lund, Sweden
Synopsis
The concept of global
left ventricular force-length loops is introduced as a method for quantifying
the contribution to stroke work resulting from longitudinal and radial pumping
mechanics, and validated in an animal model. The force-length loops can be derived
noninvasively using cardiovascular magnetic resonance and a brachial cuff
pressure. We found that longitudinal and radial pumping contributes equally to
stroke work in healthy controls and patients with dilated
ischemic cardiomyopathy, but that
the longitudinal pumping is more energy efficient in delivering stroke volume
compared to radial pumping.
Introduction
Left ventricular (LV) shortening can be described by the longitudinal
and radial pumping mechanisms. Longitudinal pumping refers to the atrioventricular
valve (AV) plane displacement in the apical-basal direction and has been shown
to be an independent predictor for major adverse cardiovascular events and
mortality1,2, with a contribution of ~60% to LV stroke volume (SV)3,4. The
remaining ~40% is accounted for by the radial pumping, which refers to the
squeezing inward motion of the epicardium3,4. The directional contribution to
stroke work (SW) has however not been investigated previously as it is calculated
from pressure-volume (PV) loops where longitudinal and radial function are not
reflected.
In this study we propose a novel method to calculate
SW from ventricular force-length (FL) loop representations of longitudinal and
radial pumping. We hypothesize that the sum of the area within these two FL
loops equals the PV loop-derived SW. The aim of this study was therefore to
develop and experimentally validate such method, and to further explore the directional
contributions to SW in healthy controls and patients with dilated ischemic
cardiomyopathy.Methods
A porcine experimental setup consisting of 13
cardiovascular magnetic resonance (CMR) examinations and invasive LV pressure
catheterizations was performed. Seven examinations were performed at baseline
and 6 at one week post induction of myocardial infarction. Additionally, 12 human
healthy controls (29±8 years, EF 59±5%, 8 male) and 14 patients with dilated
ischemic cardiomyopathy (69±8 years, EF 32±10%, 13 male) underwent CMR and a noninvasive
PV loop quantification based on the time-varying elastance model5.
Delineation of the LV endocardial and epicardial
borders was performed in short-axis cine images in all slices and phases, and
AV-plane displacement was quantified using feature-tracking in long-axis cine
images6. Invasive or noninvasive LV pressure over time was
synchronized to the LV volume curve measured in the CMR images.
Two FL loops were generated, one longitudinal and one
radial (Figure 1). Force (F) was
calculated as pressure (P) multiplied with the myocardial surface area (A) in
each respective direction, F=P·A. Length was defined as the AV-plane
displacement in the longitudinal loop, and as the average change in epicardial
radial displacement in the radial loop. Longitudinal and radial contributions
to SW were calculated as the area within each respective FL loop. The method
was validated by comparing the sum of longitudinal and radial SW with the PV
loop-derived SW.
Furthermore, the parameter work per ejected
volume (WEV) was calculated as a measure of ventricular energy efficiency in
delivering SV, and was defined as the ratio of SW and SV directional contributions
as
WEVlong=SWlong/SVlong and WEVradial=SWradial/SVradial, respectively. The directional contributions to
SV were calculated as previously proposed using AV-plane displacement the end-diastolic
basal epicardial cross-sectional area3,4.
Results
The proposed method was feasible in all subjects and
revealed an excellent agreement between FL and PV loop derived SW in the
experimental setup and human cohort (Figure 2). An example of two generated FL loops are shown in Figure 3. Longitudinal and radial
contribution to SW was approximately equal in swine at baseline (52% vs 48%), swine
post myocardial infarction (53% vs 47%), human controls (48% vs
52%), and patients (43% vs 57%), see Figure 4A-B.
WEV calculations revealed lower values for
longitudinal pumping compared radial in both controls and patients (Figure 4C-D),
meaning that longitudinal pumping require less work to eject blood.Discussion
This study found that longitudinal and radial pumping contribute equally
to SW in controls and patients with dilated ischemic cardiomyopathy. The maintained
equal contribution to SW in the patients is explained by an increased force due
to larger myocardial cross-sectional surface areas in the dilated LV, while length is reduced due
to decreased tissue displacements. With longitudinal and radial contributions
to SV being ~60% and ~40%, this finding might be surprising until also
considering WEV which found longitudinal pumping to be more energy
efficient in delivering SV compared to radial pumping.Conclusion
Longitudinal and radial contributions to SW can be
calculated from ventricular FL loops, and their sum agrees excellently with the
conventional PV loop-derived SW. Longitudinal and radial contribution to SW are
approximately equal in controls and dilated ischemic cardiomyopathy patients,
but longitudinal pumping is more energy efficient compared to
radial pumping.Acknowledgements
No acknowledgement found.References
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