To the editor: I read with interest Dr Cramariuc and colleagues excellent article published in Heart.1 The study showed the presence of abnormal
longitudinal left ventricular strain in patients with aortic stenosis and concentric left ventricular hypertrophy. Similar observations of reduced (less
negative) peak longitudinal strain have been made in hypertensive-hypertrophic
heart disease,2 heart failure with a normal
ejection fraction (HFNEF),3, 4
and other causes of pathological left ventricular hypertrophy5, 6, 7
Further, abnormalities of midwall
circumferential shortening have been shown in hypertensive-hypertrophic left
ventricular disease2 and in HFNEF.8 Wang also showed a trend to reduced
circumferential strain from -20% to -15% in HFNEF.3 The effect of myocardial disease on
circumferential strain appears to be slightly less marked than that on
longitudinal strain.3 In addition, there is significantly reduced radial
strain in HFNEF despite the apparent normal radial ‘function’ and ejection
fraction.3, 4
An increase in end-diastolic wall thickness may explain the combination
of reduced myocardial shortening and yet a normal ejection fraction. This can be understood by considering a cube
of myocardium 9 x 9 x 9 mm as a non-compressible elastomer. If circumferential and longitudinal strain
are both normal (-20%) then radial strain (i.e. relative wall thickening) is +56%
and absolute wall thickening is 5.1 mm (see Table). When there is left ventricular hypertrophy
with an end-diastolic wall thickness of 13 mm and circumferential and
longitudinal strain are reduced (-15%), radial strain is also significantly reduced
(38%) but absolute wall thickening remains almost identical at 5.0 mm (see
Table). Therefore, it is important to
differentiate between absolute and relative radial thickening.
Three dimensional modelling demonstrates that ejection
fraction is principally determined by both myocardial shortening (strain) and
end-diastolic wall thickness independently of loading conditions.9 The normal absolute wall thickening in
presence of reduced strain results in the normal ejection fraction.9, 10 End-diastolic wall thickness and strain are the
determinants of absolute wall thickening; absolute wall thickening is the main
determinant of left ventricular ejection fraction in a curvilinear manner.10
An individual’s resting metabolic requirements demand a
reasonably normal stroke volume (SV) in stable heart failure regardless of
ejection fraction.10 Ejection fraction is merely the ratio of gross
SV and end-diastolic volume (where, gross SV = net SV + valvular regurgitant
volume). If the numerator is relatively fixed
the denominator must change; accordingly the relationship between ejection
fraction and end-diastolic volume is reciprocal even in heart failure.11 Three-dimensional modelling suggests thatthe
end-diastolic volume may be physiologically regulated by the need to have an
appropriate net stroke volume to satisfy the physiological needs of peripheral tissues
in health (e.g. growth, pregnancy) and in heart disease.10
An increase in end-diastolic wall thickness with normal
shortening must lead to an increased absolute thickening; in order for the
absolute wall thickening to remain normal, myocardial shortening must be
reduced. Myocardial strain has to be
reduced proportionally to the degree of concentric hypertrophy otherwise the
ejection fraction and stroke volume will be inappropriately increased.
Hypertrophic left ventricular disease occurs in numerous
conditions including hypertension, aortic stenosis,
hypertrophic cardiomyopathy, HFNEF, Fabry disease and amyloid. Each condition can be explained by the
combination of abnormal myocardial shortening and increased end-diastolic wall
thickness determining the absolute myocardial thickening and ejection
fraction. The end-diastolic volume being
adjusted to normalise net stroke volume for the given ejection fraction.10
These proposals explain the geometric findings in
hypertrophic heart disease regardless of the cause. A normal ejection fraction does not equate to
normal deformation or even normal systolic function. The term ‘global systolic function’ is
meaningless, misleading and should be abandoned.
Table |
Normal peak strain -20% |
Abnormal peak strain -15% |
Abnormal strain -10% |
End-diastolic thickness (mm) |
9 |
13 |
17 |
21 |
9 |
13 |
17 |
21 |
9 |
13 |
17 |
21 |
End-systolic thickness (mm) |
14 |
20 |
27 |
33 |
13 |
19 |
25 |
31 |
13 |
18 |
24 |
29 |
Radial strain (%) |
56 |
56 |
56 |
56 |
38 |
38 |
38 |
38 |
23 |
23 |
23 |
23 |
Absolute wall thickening
(mm) |
5.1 |
7.3 |
9.6 |
11.8 |
3.5 |
5.0 |
6.5 |
8.1 |
2.1 |
3.1 |
4.0 |
4.9 |
DH MacIver
Taunton
& Somerset Hospital, Taunton, UK.
Correspondence to: Dr DH MacIver
Conflict of interest: None.
1 Cramariuc
D, Gerdts E, Davidsen ES, et al. Myocardial deformation in aortic valve stenosis
- relation to left ventricular geometry. Heart
2009:hrt.2009.172569.
2 Shimizu
G, Hirota Y, Kita Y, et al. Left ventricular midwall mechanics in systemic
arterial hypertension. Myocardial function is depressed in pressure-overload
hypertrophy. Circulation 1991;83:1676-84.
3 Wang
J, Khoury DS, Yue Y, et al. Preserved left ventricular twist and
circumferential deformation, but depressed longitudinal and radial deformation
in patients with diastolic heart failure. Eur
Heart J 2008;29:1283-9.
4 Tan
YT, Wenzelburger F, Lee E, et al. The pathophysiology of heart failure with
normal ejection fraction: exercise echocardiography reveals complex
abnormalities of both systolic and diastolic ventricular function involving
torsion, untwist, and longitudinal motion. J
Am Coll Cardiol 2009;54:36.
5 Nagueh
SF, Bachinski LL, Meyer D, et al. Tissue Doppler imaging consistently detects
myocardial abnormalities in patients with hypertrophic cardiomyopathy and
provides a novel means for an early diagnosis before and independently of
hypertrophy. Circulation 2001;104:128-30.
6 Weidemann
F, Breunig F, Beer M, et al. Improvement of cardiac function during enzyme
replacement therapy in patients with Fabry disease. A prospective strain rate
imaging study. Circulation 2003;108:1299-301.
7 Koyama
J, Ray-Sequin PA, Falk RH. Longitudinal myocardial function assessed by tissue
velocity, strain, and strain rate tissue Doppler echocardiography in patients
with AL (primary) cardiac amyloidosis. Circulation
2003;107:2446-52.
8 Vinch
C, Aurigemma G, Simon H, et al. Analysis of left ventricular systolic function
using midwall mechanics in patients > 60 years of age with hypertensive
heart disease and heart failure. Am J
Cardiol 2005;96:1299-303.
9 MacIver
DH, Townsend M. A novel mechanism of heart failure with normal ejection
fraction. Heart 2008;94:446-9.
10 MacIver
DH. Is remodeling the dominant compensatory mechanism in both chronic heart
failure with preserved and reduced left ventricular ejection fraction? Basic Res Cardiol 2009:Online first DOI:
10.1007/s00395-009-0063-x.
11 MacIver
DH. Surgical ventricular reconstruction: an oversimplified hypothesis? N Engl J Med 2009;361:529-32.
To the editor: I read with interest Dr Cramariuc and colleagues excellent article published in Heart.1 The study showed the presence of abnormal longitudinal left ventricular strain in patients with aortic stenosis and concentric left ventricular hypertrophy. Similar observations of reduced (less negative) peak longitudinal strain have been made in hypertensive-hypertrophic heart disease,2 heart failure with a normal ejection fraction (HFNEF),3, 4 and other causes of pathological left ventricular hypertrophy5, 6, 7
Further, abnormalities of midwall circumferential shortening have been shown in hypertensive-hypertrophic left ventricular disease2 and in HFNEF.8 Wang also showed a trend to reduced circumferential strain from -20% to -15% in HFNEF.3 The effect of myocardial disease on circumferential strain appears to be slightly less marked than that on longitudinal strain.3 In addition, there is significantly reduced radial strain in HFNEF despite the apparent normal radial ‘function’ and ejection fraction.3, 4
An increase in end-diastolic wall thickness may explain the combination of reduced myocardial shortening and yet a normal ejection fraction. This can be understood by considering a cube of myocardium 9 x 9 x 9 mm as a non-compressible elastomer. If circumferential and longitudinal strain are both normal (-20%) then radial strain (i.e. relative wall thickening) is +56% and absolute wall thickening is 5.1 mm (see Table). When there is left ventricular hypertrophy with an end-diastolic wall thickness of 13 mm and circumferential and longitudinal strain are reduced (-15%), radial strain is also significantly reduced (38%) but absolute wall thickening remains almost identical at 5.0 mm (see Table). Therefore, it is important to differentiate between absolute and relative radial thickening.
Three dimensional modelling demonstrates that ejection fraction is principally determined by both myocardial shortening (strain) and end-diastolic wall thickness independently of loading conditions.9 The normal absolute wall thickening in presence of reduced strain results in the normal ejection fraction.9, 10 End-diastolic wall thickness and strain are the determinants of absolute wall thickening; absolute wall thickening is the main determinant of left ventricular ejection fraction in a curvilinear manner.10
An individual’s resting metabolic requirements demand a reasonably normal stroke volume (SV) in stable heart failure regardless of ejection fraction.10 Ejection fraction is merely the ratio of gross SV and end-diastolic volume (where, gross SV = net SV + valvular regurgitant volume). If the numerator is relatively fixed the denominator must change; accordingly the relationship between ejection fraction and end-diastolic volume is reciprocal even in heart failure.11 Three-dimensional modelling suggests thatthe end-diastolic volume may be physiologically regulated by the need to have an appropriate net stroke volume to satisfy the physiological needs of peripheral tissues in health (e.g. growth, pregnancy) and in heart disease.10
An increase in end-diastolic wall thickness with normal shortening must lead to an increased absolute thickening; in order for the absolute wall thickening to remain normal, myocardial shortening must be reduced. Myocardial strain has to be reduced proportionally to the degree of concentric hypertrophy otherwise the ejection fraction and stroke volume will be inappropriately increased.
Hypertrophic left ventricular disease occurs in numerous conditions including hypertension, aortic stenosis, hypertrophic cardiomyopathy, HFNEF, Fabry disease and amyloid. Each condition can be explained by the combination of abnormal myocardial shortening and increased end-diastolic wall thickness determining the absolute myocardial thickening and ejection fraction. The end-diastolic volume being adjusted to normalise net stroke volume for the given ejection fraction.10
These proposals explain the geometric findings in hypertrophic heart disease regardless of the cause. A normal ejection fraction does not equate to normal deformation or even normal systolic function. The term ‘global systolic function’ is meaningless, misleading and should be abandoned.
Table
Normal peak strain
-20%
Abnormal peak strain
-15%
Abnormal strain
-10%
End-diastolic thickness (mm)
9
13
17
21
9
13
17
21
9
13
17
21
End-systolic thickness (mm)
14
20
27
33
13
19
25
31
13
18
24
29
Radial strain (%)
56
56
56
56
38
38
38
38
23
23
23
23
Absolute wall thickening (mm)
5.1
7.3
9.6
11.8
3.5
5.0
6.5
8.1
2.1
3.1
4.0
4.9
DH MacIver
Taunton & Somerset Hospital, Taunton, UK.
Correspondence to: Dr DH MacIver
Conflict of interest: None.
1 Cramariuc D, Gerdts E, Davidsen ES, et al. Myocardial deformation in aortic valve stenosis - relation to left ventricular geometry. Heart 2009:hrt.2009.172569.
2 Shimizu G, Hirota Y, Kita Y, et al. Left ventricular midwall mechanics in systemic arterial hypertension. Myocardial function is depressed in pressure-overload hypertrophy. Circulation 1991;83:1676-84.
3 Wang J, Khoury DS, Yue Y, et al. Preserved left ventricular twist and circumferential deformation, but depressed longitudinal and radial deformation in patients with diastolic heart failure. Eur Heart J 2008;29:1283-9.
4 Tan YT, Wenzelburger F, Lee E, et al. The pathophysiology of heart failure with normal ejection fraction: exercise echocardiography reveals complex abnormalities of both systolic and diastolic ventricular function involving torsion, untwist, and longitudinal motion. J Am Coll Cardiol 2009;54:36.
5 Nagueh SF, Bachinski LL, Meyer D, et al. Tissue Doppler imaging consistently detects myocardial abnormalities in patients with hypertrophic cardiomyopathy and provides a novel means for an early diagnosis before and independently of hypertrophy. Circulation 2001;104:128-30.
6 Weidemann F, Breunig F, Beer M, et al. Improvement of cardiac function during enzyme replacement therapy in patients with Fabry disease. A prospective strain rate imaging study. Circulation 2003;108:1299-301.
7 Koyama J, Ray-Sequin PA, Falk RH. Longitudinal myocardial function assessed by tissue velocity, strain, and strain rate tissue Doppler echocardiography in patients with AL (primary) cardiac amyloidosis. Circulation 2003;107:2446-52.
8 Vinch C, Aurigemma G, Simon H, et al. Analysis of left ventricular systolic function using midwall mechanics in patients > 60 years of age with hypertensive heart disease and heart failure. Am J Cardiol 2005;96:1299-303.
9 MacIver DH, Townsend M. A novel mechanism of heart failure with normal ejection fraction. Heart 2008;94:446-9.
10 MacIver DH. Is remodeling the dominant compensatory mechanism in both chronic heart failure with preserved and reduced left ventricular ejection fraction? Basic Res Cardiol 2009:Online first DOI: 10.1007/s00395-009-0063-x.
11 MacIver DH. Surgical ventricular reconstruction: an oversimplified hypothesis? N Engl J Med 2009;361:529-32.