Changes in overall ventricular myocardial architecture in the setting of a porcine animal model of right ventricular dilation

Abstract

BackgroundChronic pulmonary regurgitation often leads to myocardial dysfunction and heart failure. It is not fully known why secondary hypertrophy cannot fully protect against the increase in wall stress brought about by the increased end-diastolic volume in ventricular dilation. It has been assumed that mural architecture is not deranged in this situation, but we hypothesised that there might be a change in the pattern of orientation of the aggregations of cardiomyocytes, which would contribute to contractile impairment.MethodsWe created pulmonary valvular regurgitation by open chest, surgical suturing of its leaflets in seven piglets, performing sham operations in seven control animals. Using cardiovascular magnetic resonance imaging after 12 weeks of recovery, we demonstrated significantly increased right ventricular volumes in the test group. After sacrifice, diffusion tensor imaging of their hearts permitted measurement of the orientation of the cardiomyocytes.ResultsThe helical angles in the right ventricle approached a more circumferential orientation in the setting of right ventricular RV dilation (p = 0.007), with an increased proportion of surface-parallel cardiomyocytes. In contrast, this proportion decreased in the left ventricle. Also in the left ventricle a higher proportion of E3 angles with a value around zero was found, and conversely a lower proportion of angles was found with a numerical higher value. In the dilated right ventricle the proportion of E3 angles around −90° is increased, while the proportion around 90° is decreased.ConclusionContrary to traditional views, there is a change in the orientation of both the left ventricular and right ventricular cardiomyocytes subsequent to right ventricular dilation. This will change their direction of contraction and hinder the achievement of normalisation of cardiomyocytic strain, affecting overall contractility. We suggest that the aetiology of the cardiac failure induced by right vetricular dilation may be partly explained by morphological changes in the myocardium itself.

Anatomically correct assessment of the orientation of the cardiomyocytes using diffusion tensor imaging

“…As the secondary eigenvector follows the surface of the aggregates the tertiary eigenvector is then by definition the normal vector of the aggregate plane. This can be used to assess the orientation of the aggregates themselves …”

“…Although all approaches were mathematically correct, the results were often substantially different. This is because some studies calculated the orientation of the aggregates using the secondary eigenvector while others used the tertiary eigenvector . The majority of studies, furthermore, project the vector prior to angle quantification, while others do not .…”

“…With only a few exceptions, this methodology has now become the most common strategy for assessment of helical angles. The alternative is to omit projection, and assess the helical angle as the angle between the primary eigenvector and the local horizontal plane (Plane C, in Figure J) …”

“…Such tools have now been provided with modern techniques for three-dimensional imaging. [8][9][10][11] Of these, diffusion tensor imaging is by far the most prevalent, and best-validated, method for assessing the myocardial microanatomy. [12][13][14][15] Only when a comprehensive understanding of myocardial structure is established, we can begin to understand myocardial function.…”

Myoarchitectural disarray of hypertrophic cardiomyopathy begins pre‐birth

“…It has been hypothesised that such mural antagonism serves to stabilise ventricular shape and size, to sustain late systolic dilation, to confine the amplitude of ventricular mural thickening, and to facilitate and enhance the spiralling intracavity flow (Lunkenheimer et al 2018). Finally, some authors have also described the existence of myocardial 'sheets' or 'sheetlets,' thus proposing a third angle to describe the orientation of myocytes (McGill et al 2013;Agger et al 2017;Nielles-Vallespin et al 2017;Stoeck et al 2018). Although myocytes aggregate to form bunches, we did not find any visual evidence in our HREM images to support myocardial sheets and therefore we have not calculated the 'sheet'/'sheetlet' angle.…”