We read with interest the recent article on survival by stroke volume
index (SVI) in patients with low-gradient (LG) normal ejection fraction
(EF) severe aortic stenosis (AS), which demonstrated lower SVI is
incrementally associated with mortality [1].
The authors discuss a putative mechanism of low stroke volume
secondary to concentric remodeling which results in reduced LV cavity
size. This, is turn, impedes LV diastolic filling, culminating in
diminished systolic function despite EF. The authors quote evidence of
systolic impairment, e.g. reduced longitudinal strain, in similar cohorts
with preserved EF [2]. In the current study, the subgroup with lowest SVI,
and therefore presumed most severe systolic impairment despite EF >50%,
demonstrated the thickest relative wall measurements. We believe this
observation helps to explain the apparent paradox between significant
myocardial dysfunction and preservation of EF in this cohort and in the
wider 'heart failure with preserved ejection fraction' context. Recent
mathematical modeling of LV contraction has shown that both myocardial
shortening and end-diastolic wall thickness are determinants of EF [3].
Essentially, absolute LV wall thickening, as defined by the absolute
difference between wall thickness at end-systole and end-diastole, may be
nearly normal in patients with concentric LV hypertophy (LVH) because
absolute systolic thickening will be augmented in response to increased
end-diastolic LV wall thickness. As a result, the endocardial displacement
and EF will also be normal, as the external LV volume remains fairly
static throughout the cardiac cycle [4] and the absolute wall thickening
may appear to compensate for any contractile strain abnormality.
The development of concentric LVH ventricle may be viewed as a
compensatory response that normalises contractile stress and total
contractile force. However, if contractile stress remains reduced, the
contractile force will be inadequate and result in a fall in stroke volume
despite the preserved EF. In order to understand the apparent discrepancy
in SV and EF, one must distinguish between contractile strain and stress
and the relationship between end-diastolic wall thickness and EF.
The authors elected to investigate SV indexed to body surface area.
However, it would be interesting to know whether correcting EF for the
presence of concentric LVH (EFc), as described in mathematical modeling
studies of the LV [3], would be a useful prognostic marker in this cohort
of patients. After all, EFc is potentially an even more relevant
allometric indexed value given the importance of end-diastolic wall
thickness in patients with concentric LVH and systolic impairment but
preserved EF.
References:
[1] Eleid MF, Sorajla P, Michelena HI, et al. Survival by stroke
volume index in patients with low-gradient normal EF severe aortic
stenosis. Heart. Published Online First: 12 September 2014. Doi:
10.1136/heartjnl-2014-306151
[2] Adda J, Mielot C, Giorgi R, et al. Low-flow, low-gradient severe
aortic stenosis despite normal ejection fraction is associated with severe
left ventricular dysfunction as assessed by speckle-tracking
echocardiography: a multicenter study. Circ Cardiovasc Imaging 2012; 5: 27
-35.
[3] Maciver DH. A new method for quantification of left ventricular
systolic function using a corrected ejection fraction. Eur J Echocardiogr
2011; 12: 228-34.
[4] Emilsson K, Brudin L, Wandt B. The mode of left ventricular
pumping: is there an outer contour change in addition to atrioventricular
plane displacement? Clin Physiol 2001; 21: 437-446.
Acknowledgements:
NIHR Bristol Biomedical Research Unit in Cardiovascular Medicine.
The views expressed are those of the authors and not necessarily
those of the National Health Service, National Institute for Health
Research, or Department of Health.
Conflict of Interest:
None declared
We read with interest the recent article on survival by stroke volume index (SVI) in patients with low-gradient (LG) normal ejection fraction (EF) severe aortic stenosis (AS), which demonstrated lower SVI is incrementally associated with mortality [1].
The authors discuss a putative mechanism of low stroke volume secondary to concentric remodeling which results in reduced LV cavity size. This, is turn, impedes LV diastolic filling, culminating in diminished systolic function despite EF. The authors quote evidence of systolic impairment, e.g. reduced longitudinal strain, in similar cohorts with preserved EF [2]. In the current study, the subgroup with lowest SVI, and therefore presumed most severe systolic impairment despite EF >50%, demonstrated the thickest relative wall measurements. We believe this observation helps to explain the apparent paradox between significant myocardial dysfunction and preservation of EF in this cohort and in the wider 'heart failure with preserved ejection fraction' context. Recent mathematical modeling of LV contraction has shown that both myocardial shortening and end-diastolic wall thickness are determinants of EF [3]. Essentially, absolute LV wall thickening, as defined by the absolute difference between wall thickness at end-systole and end-diastole, may be nearly normal in patients with concentric LV hypertophy (LVH) because absolute systolic thickening will be augmented in response to increased end-diastolic LV wall thickness. As a result, the endocardial displacement and EF will also be normal, as the external LV volume remains fairly static throughout the cardiac cycle [4] and the absolute wall thickening may appear to compensate for any contractile strain abnormality. The development of concentric LVH ventricle may be viewed as a compensatory response that normalises contractile stress and total contractile force. However, if contractile stress remains reduced, the contractile force will be inadequate and result in a fall in stroke volume despite the preserved EF. In order to understand the apparent discrepancy in SV and EF, one must distinguish between contractile strain and stress and the relationship between end-diastolic wall thickness and EF.
The authors elected to investigate SV indexed to body surface area. However, it would be interesting to know whether correcting EF for the presence of concentric LVH (EFc), as described in mathematical modeling studies of the LV [3], would be a useful prognostic marker in this cohort of patients. After all, EFc is potentially an even more relevant allometric indexed value given the importance of end-diastolic wall thickness in patients with concentric LVH and systolic impairment but preserved EF.
References:
[1] Eleid MF, Sorajla P, Michelena HI, et al. Survival by stroke volume index in patients with low-gradient normal EF severe aortic stenosis. Heart. Published Online First: 12 September 2014. Doi: 10.1136/heartjnl-2014-306151
[2] Adda J, Mielot C, Giorgi R, et al. Low-flow, low-gradient severe aortic stenosis despite normal ejection fraction is associated with severe left ventricular dysfunction as assessed by speckle-tracking echocardiography: a multicenter study. Circ Cardiovasc Imaging 2012; 5: 27 -35.
[3] Maciver DH. A new method for quantification of left ventricular systolic function using a corrected ejection fraction. Eur J Echocardiogr 2011; 12: 228-34.
[4] Emilsson K, Brudin L, Wandt B. The mode of left ventricular pumping: is there an outer contour change in addition to atrioventricular plane displacement? Clin Physiol 2001; 21: 437-446.
Acknowledgements:
NIHR Bristol Biomedical Research Unit in Cardiovascular Medicine.
The views expressed are those of the authors and not necessarily those of the National Health Service, National Institute for Health Research, or Department of Health.
Conflict of Interest:
None declared