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Review
. 2011 Sep-Oct;52(5):416-26.

Fluid dynamic aspects of ejection in hypertrophic cardiomyopathy

Ares Pasipoularides  1
Affiliations
Review

Fluid dynamic aspects of ejection in hypertrophic cardiomyopathy

Ares Pasipoularides. Hellenic J Cardiol. 2011 Sep-Oct.
No abstract available

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Figures

Figure 1
Figure 1
Pressure-flow relation with large early- and huge mid- and late-systolic pressure gradients in hypertrophic cardiomyopathy. From top downward: aortic velocity, and deep left ventricular (LV), LV outflow tract (LVOT), and aortic root (AO) micromanometric signals, by retrograde triple-tip pressure-plus-velocity left-heart catheter. The left atrial (LA) micromanometric signal was measured simultaneously by transseptal catheter. The vertical line identifies onset of SAM-septal contact, from a simultaneous M-mode mitral echocardiogram (not shown); most of the ejection is already completed by then, in this patient. The huge mid- and late-systolic gradient (hatched area) is maintained despite minuscule remaining forward or even negative aortic velocities. Inset: continuous lines designate the LV, LVOT, and AO signals, superposed on interrupted-line tracings from the other sites. AO – aortic; SAM – systolic anterior motion of the mitral valve. Reproduced with permission of PMPH-USA from Pasipoularides A. Heart’s vortex: intracardiac blood flow phenomena. Shelton, CT: People’s Medical Publishing House, 2010.
Figure 2
Figure 2
Geometry of model simulating late-systolic fluid dynamics in hypertrophic cardiomyopathy with “cavity obliteration.” The shrinking late-systolic left ventricular chamber is represented as a narrow tube with contracting walls. Local and especially convective (associated with wall collapse, which displaces sequentially increasing flow increments from apex to outlet) inertial as well as powerful viscous effects are salient. Note the wider subvalvular region.
Figure 3
Figure 3
Fluid dynamic computer simulation results; inset depicts geometry. As demonstrated in the top panel, the cross-sectionally averaged outlet velocity increases at an increasing rate with advancing cavity shrinkage, attaining nearly 2.5 m/s by the time the effective radius falls to 0.16 cm, only slightly more than half its starting value, shown in the lower panel.
Figure 4
Figure 4
The linear increase of the axial cross-sectionally averaged velocity along the chamber axis accruing from the uniform radial contraction pattern (cf. Figure 2). The constant slope reflects the constant dynamic convective acceleration along the cylinder axis. The radial contraction of the walls engenders forceful dynamic convective acceleration despite the uniform cross-section.
Figure 5
Figure 5
Late-systolic ejection flow-field kinematics in hypertrophic cardiomyopathy with cavity obliteration. The strong convective acceleration of the flow is reflected in converging streamlines toward the downstream outlet and in the concomitant elongation of the axial velocity-vector components. The zero axial components of the velocity vectors at the endocardial surface satisfy the “no-slip” condition. The opposite flow pattern is not applicable in the ensuing early filling because highly decelerated flows are unstable.
Figure 6
Figure 6
The effects of myocardial contraction-induced convective acceleration on the development of axial mid-to-late ejection velocity profiles. Blunt profiles corresponding to the computed fluid dynamic solution are plotted at successive normalized tubular chamber lengths (distance from apex/axis length). Note the progressive sharp increase in the slope of the velocity profile at the endocardial surface; this slope is proportional to the shear stress exerted by ejected blood locally at the endocardial surface. High shear stress may have important epigenetic influences in hypertrophic cardiomyopathy. The axially uniform parabolic Poiseuille profiles are plotted for comparison.
Figure 7
Figure 7
Enormous intraventricular gradient production without static or dynamic obstruction in the fluid dynamic model of “cavity obliteration.” Top panel: axial pressure gradient apportionment, highlighting gradient intensification nearer the outlet. Bottom panel: the pressure drop (ΔP) from the upstream closed end of the contracting cylinder to progressively increasing distances, from apex to outflow orifice, along its entire length (8 cm in this simulation) plotted against the corresponding local value of the cross-sectionally averaged velocity. Application of the “simplified Bernoulli formula” to the highest velocity (nearly 2.5 m/s) shown would predict ΔP≈25 mmHg—too low compared to the huge late gradients of hypertrophic cardiomyopathy and to the simulated gradient of almost 80 mmHg. This stems from neglecting the potent viscous (frictional) hydrodynamic shear forces in the simplified Bernoulli formula.
Figure 8
Figure 8
Stairstep graph plot demonstrating to best advantage the progressively explosive augmentation of the pressure gradient increments, which ensues in the face of minuscule ejected volume additions in late systole (cf. arrows, too).
See this image and copyright information in PMC

References

    1. Pasipoularides A. Heart’s vortex: intracardiac blood flow phenomena. Shelton, CT: People’s Medical Publishing House; 2010. p. 960. p.-See, in particular, Chapter 8. A gallery of multisensor catheter cardiodynamics, p. 408–41, and Chapter 16. A recapitulation with clinical and basic science perspectives, p. 851–888.
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