How does the heart pump? From sarcomere to ejection volume Piet Claus Cardiovascular Imaging and Dynamics Department of Cardiovascular Diseases University Leuven, Leuven, Belgium Course on deformation imaging EUROECHO 2011 Budapest, Dec. 07, 2011
Pump function? What is pump function? The ability of the heart to provide sufficient oxygenated blood to the organs (including itself) in all conditions. 1. Maintain cardiac output at rest and increase at stress The heart is a volume pump 2. Two circulations with different pressure levels reflected into differential properties of the LV and RV. - morphological, functional,... 3. Adaptation by changing (acute and chronic) boundary conditions (geometry, size, resistance) impact on functional parameters Output/Deformation versus Force development
LV pressure (mmhg) Longitudinal strain Function: at what level? Pump performance Global Function Myocardial function Regional Function Intrinsic function Fiber/Sarcomere Function 160 ESPVR PRSW 140 120 100 80 60 PVA 40 20 EDPVR 0-20 50 60 70 80 90 100110120 LV volume (ml) Stroke volume Cardiac output Ejection Fraction Pressure Resulting output 0 Strain Strain-rate Wall stress Fiber strain velocity of shortening Fiber stress isometric force Driving system
Papillary muscle experiments isometric isotonic in vivo auxotonic Strain Stress Varying load during the cycle Strain Stress Boron and Boulpaep, Medical Physiology Guccione et al. J. Biomech. 28(1) 1994
After-loaded contraction Velocity of fiber shortening v_max or v_0 is a measure of contractility (potential to shorten at zero load). v_max Normal homogeneous contracting left ventricle works at 80-90% of maximal load. Strain Rate
Force+Velocity+Length = contractility For any given constant total load, velocity of shortening is determined by instantaneous length only, irrespective of initial muscle length from where shortening started (preload) LT: resting length - tension relation Basic contractility Time independent part of relation (except near peak shortening) Independent of initial length Change in contractility True contractility changes shift the force-velocitylength surface and the unloaded velocity of shortening
From fibers to muscle Fiber architecture and function Laminar sheets Packed from base to apex Branching 4 cells thick Cleavage planes Tight coupling inside sheets Anisotropic mechanical properties Le Grice 2001 Implications for translation fiber function to myocardial deformation
Fiber shortening in the beating heart: transmurality Guccione et al 1997 Rodriguez et al 1992
Fiber mechanics in the beating heart: transmurality Ashikaga, JACC 2008 Transmural activation wave faster than onset of shortening (thetering) Implications for total work Ashikaga, JACC 2008 Active fiber stress Choi, AJP, 2011 Choi, AJP, 2011 Choi, AJP, 2011 Differences in pre-stretch!
Put all this in the wall of a heart We have to describe this in the complex 3D setting of the heart. But basic principles can be translated. Cardiac system Intrinsic system Radial Longitudinal Circumferential Fiber Fiber-Sheet Sheet-Normal Required for correct physiologic interpretation!!! (e.g. RR = wall thickening; CC/LL = circumferential/longitudinal shortening)
Deformation modes Longitudinal shortening Longitudinal lengthening Radial thickening Radial thinning Circumferential shortening + Endocardial inward motion for ejection Circumferential lengthening + Endocardial outward motion for filling + Shearing (twisting, ) optimize transmission of fiber force/deformation
Basic Quantities How to express deformation: strain L 0 e = L L 0 L 0 = -0.28 = -28% Length change normalised to original length L Independent of the size of the segment under investigation Strain ~ volume changes/ejection fraction
Basic quantities How fast does an object deform: strain rate De Dt -0.28 2 s -0.28 1 s = -0.14 s -1 = -0.28 s -1 Speed at which objects deform Strain and strain-rate are related by temporal derivation
How do the curves look like S 30 20 s PSS 10 radial thickening e a 0 0 [s -1 ] 1 0-10 -1-20 AVO AVC MVO MVC longitudinal shortening Strain-rate Circumferential ~ longitudinal Strain
Myocardial pressure volume Passive body s load (t) = E x e (t) Active body (Myocardium) LOADING Wall stress (total force on a segment) - cavity pressure, - geometry (cavity radius of curvature, wall thickness) Laplace - neighbouring segment interaction segmental elasticity resulting deformation s load (t) - C(t) = E x e (t) Contractile active force - activation sequence - electro-mechanical coupling
Contractile segments in the heart Segment interaction Non working segment working segment s load Thetering in strain, because of different force development in adjacent segments + loading
Strain-rate and contractility? Systolic Strain (%) Peak syst SR (s -1 ) s load (t) + C(t) = E x e (t) As a first approximation ignore loading / keep elasticity constant. Velocity of fiber shortening Regional Strain Rate Correlates with dp/dt dp/dt max (mmhg/s) Regional Strain Correlates with Ejection Fraction Ejection Fraction (%) LV strain-rate = relatively load independent Weidemann et al., Am. J. Physiol. 2002
Strain-rate and contractility? Ferferieva V, AJP 2011 How strain and strain rate deformation parameters, measured by Doppler echocardiography, relate to the individual factors that determine cardiac performance Contractility Afterload Preload LVmass LAD ligation Aortic banding Dobutamine stress Changes in: Preload Afterload Contractility LVmass Multivariable statistical analysis
Multivariable analysis? Independent predictors = PRSW, Ea, EDP, LVMass Dependent = S/SR rad S rad primarily dependent on afterload (Ea) SR rad predominantly influenced by altered inotropic state and secondarily by LVMass Ferferieva V, AJP 2011
Longitudinal strain Longitudinal strain Longitudinal strain Longitudinal strain Interplay between geometry/load/deformation PRSW (9.3±1.8 to 8.9±2.0 mwatt.s/ml) HR (106±10 to 108 ±11 bpm) CO (3.8±0.5 l/min to 3.3±0.4 l/min) EDV (90±15 to 103 ± 20 ml) SV (36±11 to 31±8 ml) Baseline 0-10 -20 0-10 -20 septal lateral Acute aortic constriction 0-10 -20 0-10 -20 septal lateral SR (2.1± 0.4 to 1.6 ± 0.6 ) Lateral Septal Claus 2009
Claus 2009 Regional shape versus regional function Mid wall level Regional sphericity * Longitudinal strain * In acute afterload change in regional shape is reciprocal to changes in deformation. Regionally geometry can change to reduce decreases in function. Spherical dilated hearts have no reserve...
Interplay between geometry/load/deformation Heterogeneity in - transmural pre-stretch - myocardial work - active stress depends on shape Choi, AJP, 2011
Why: understand cardiac function Regional mechanical boundary conditions Perfusion Activation active force development within the fibres 1 cavity pressure development 2 FIBRE ORIENTATION Fibre rearrangements for optimal pressure built-up (shape change during IVC) 15% FIBRE SHORTENING TO 60% EJECTION FRACTION TISSUE CHARACTERISTICS e.g. ELASTICITY (collagen matrix, titin) SEGMENT INTERACTION GEOMETRY shape, wall thickness Volumes (preload) Systemic resistance AFTERLOAD 3 Ejection by wall deformation Abnormalities do not always affect how much (symptoms) but will affect how... remodeling Global mechanical boundary conditions
Conclusions 1. Fiber mechanics (deformation, force) is our ultimate measure of active myocardial function (contraction/active relaxation) 2. Fibers are embedded in the heart wall in an intricate fashion that allows for efficient ejection, but cause the 3D deformation to show major shearing. 3. Regional disease will cause segment interactions with regionally differential loading making the (mental) translation from segmental deformation measures to fiber function difficult. 4. Regional as well as global pathologies will introduce changes in segmental deformation patterns that are sensitive and could be specific. 5. Echocardiographic deformation imaging has the potential to resolve myocardial deformation, but beware of frame-rate (1D vs 2D vs 3D), through beam/plane motion and post-processing.