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Share This Paper. Figures from this paper. In D , reduced interventricular relaxation dyssynchrony induced by LV hypotrophy attenuated septal motion, as observed in B after onset of AR. Figure is reproduced from Palau-Caballero et al. Modelling has shown that this motion is caused by asynchronous ventricular relaxation.
This motion can be abolished through either reduced RV tissue load due to afterload reduction or hypertrophic remodelling, or an increase in LV myocardial load causing prolonged LV contraction Figure 3. This can have two clinical consequences: i septal motion is a marker for RV decompensation in PAH that does not require strain measurements and ii reduction of septal motion could imply either improvement in RV condition or deterioration of LV condition and should be interpreted cautiously.
Model simulations have shown that pre-excitation of the RV free wall to resynchronize relaxation relieves the RV of extremely high myofibre work while increasing LV free wall and septal myofibre work. Whilst the CircAdapt model used in the studies above allows qualitative assessment of the causes of abnormal findings of imaging in PAH, its simplified structure and highly phenomenological contraction model make quantitative comparisons to patient data challenging.
A recent study has proposed that imaging-derived anatomical computer models can be used to extract functional parameters representing myocardial condition in PAH patients Figure 4. The myocardium was modelled using a transversely isotropic and hyperelastic model of passive behaviour and biophysically detailed representations of electrophysiology and sarcomere contraction. A rule-based fibre orientation was used for tissue anisotropy.
Personalized finite element modelling of pulmonary arterial hypertension. A Segmentation and meshing of a biventricular model from CMR. Fibre orientation was assigned using a rule-based method. Windkessel models were used as boundary conditions for the LV and RV.
C Simulated regional distribution of peak myofibre stress within the ventricles. Figure is modified from Xi et al. Furthermore, simulations with increased RV preload or afterload exhibited a flattening of the septum in line with earlier imaging studies.
Strain patterns in the model showed qualitative differences with clinical recordings, with a greater strain amplitude in the RV and a much more rapid LV contraction in the model as compared with the subjects. Both the RV and LV in the PAH model were considerably stiffer and more contractile than that in the normal subject, suggesting that tissue properties can be extracted from imaging with the use of a computer model and that LV tissue has also remodelled in the PAH heart.
However, it is unclear whether the fitted changes in LV stiffness are due to changes in LV tissue properties or due to mechanical interactions with the late-contracting RV as described in the previous section. Electrophysiological abnormalities are believed to precede structural alterations, leading to three clinical ARVC stages: subclinical, electrical, and structural. Recent imaging studies have shown that individuals with ARVC-causing mutations frequently exhibit abnormal RV deformation whose severity is associated with arrhythmic events.
Mast et al. Type II was most prevalent in the electrical staged subjects, and the severely abnormal Type III was most prevalent in the structurally staged subjects. Imaging and modelling to explain mechanical abnormalities in ARVC clinical stages. Left Type I, normal deformation as seen in healthy controls and approximately half of the subclinical mutation carriers.
Figure is reproduced from Mast et al. Computer simulations of RV deformation were used to determine the substrates underlying these abnormal deformation patterns. Reduced regional contractility and mildly increased stiffness sufficed to reproduce a Type II pattern, and the Type III pattern arose through further increases in regional passive stiffness of the tissue, although systolic stretch in the simulations was considerably higher than that seen in the patient data Figure 5.
Electrical delay alone could not reproduce either the Type II or the Type III pattern, suggesting that delayed onset of shortening does not necessarily represent delayed activation, as originally proposed. Consequently, abnormal deformation reflects the severity of ARVC and can appear before overt structural abnormalities such as RV dilation, or electrophysiological diagnosis criteria on the ECG.
Subclinically staged individuals with a Type II pattern are therefore likely to be showing the earliest signs of ARVC, which could help to improve sensitivity of ARVC diagnosis, and the appearance of mechanical abnormalities prior to detectable electrophysiological abnormalities challenges current thinking on ARVC progression.
The interaction between dyssynchronous contraction, RV function, and CRT response has received relatively little attention in the literature, and the relation between RV function and CRT response is controversial. Previous experimental work has shown that dyssynchronous electrical activation redistributes the myofibre work performed within the LV, with earlier activated regions performing relatively less external work, and late-activated regions performing relatively more external work.
The LV myocardium then contracts against the early-activated and weak RV, forcing the LV free wall to increase its contribution to RV pump work while also stretching the early-activated septum. Pacing redistributes work from the LV lateral wall to the RV and septum. Red asterisks indicate pacing sites. C Colour maps indicate myofibre work per ventricular wall segment. D Bar charts indicate the proportion of ventricular pump work that is performed by the LV red and RV blue myocardium. Figure is modified from Lumens et al. Experimental studies in paced canine hearts suggested that this motion arose from a transient increase in RV pressure over LV pressure consistent with passive models of septal position.
Consequently, lack of septal beaking may imply RV dysfunction or presence of RV activation delays coexisting with LV activation delays. Consequently, CRT redistributes work away from the LV free wall and towards both the septum and the RV free wall, as demonstrated by computer modelling. However, patient measurements and canine experiments demonstrated that LV free wall pacing could produce similar acute benefit to biventricular pacing, despite a lack of fusion that was confirmed by electrocardiographic imaging Figure 6 A. Through direct mechanical interaction, the RV could compensate for lost external work within the LV, boosting overall cardiac pump function.
These computer modelling results suggest that LV-only pacing should be avoided in patients with RV dysfunction, which merits experimental and clinical investigation.
How LV only pacing interacts with RV dysfunction remains unclear, and is of clinical interest as device manufacturers start to implement fusion pacing. Recent advances in cardiac imaging have led to the first applications of personalized computer models of CHD in the clinic. Computer simulations have demonstrated that the choice of palliation for hypoplastic left heart syndrome HLHS can have significant effects on ventricular load. These simulations were performed by coupling a 3D finite volume computational fluid dynamics model of the modified Blalock—Taussig shunt, RV—pulmonary artery shunt, and the hybrid procedure used for the first stage of palliation in HLHS with a network model of the heart and circulation.
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