PubMed · 5329020
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A M Harris. 1966. Endocardial pacing.. https://doi.org/10.1016/0002-8703(66)90638-7
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OBJECTIVE: We used the technique of peeling of myocardial aggregates, usually described as 'fibres', to determine the spatial arrangement of the myocytes in the left ventricular wall of a healthy autopsied human heart. METHODS: We digitised the left ventricular outer and inner boundaries, as well as the pathways in space, of almost 3000 aggregates harvested from the left ventricular myocardium. During the process of gradual peeling, we sought to identify the myocardial aggregates as uniformly as possible. Despite this, interpolation was necessary to complete the pattern so as to construct a unit vector field that represented the preferred direction of the myocardial aggregates throughout the entirety of the walls of the left ventricle of this individual human heart. RESULTS: Apart from the overall systematic arrangement of the aggregates necessary to achieve physiologic ventricular contraction, we documented substantial local heterogeneities in the orientation of the myocardial aggregates. In particular, a significant proportion of aggregates was found to intrude obliquely with respect to the ventricular boundaries, with markedly heterogeneous distribution. Moreover, the distribution of the helical angle of the aggregates relative to the ventricular base varied notably throughout the left ventricular free walls and the septum. Within the generally quite uniform and continuous structure of the ventricular mass, we were, however, unable to identify any organised tracts or functional subunits such as a 'helical ventricular band', nor did we find radial fibrous lamellas coursing across the ventricular wall. CONCLUSION: We suggest that the impact of local anatomical inhomogeneities, associated with gradients in regional contractile function on global ventricular dynamics, has been systematically underestimated in the past. Our analysis confirms furthermore the continuous nature of the myocardium associated with an overall gross organisation of the fibre direction field; however, there is no evidence of substructures compartmentalising the ventricles.
Radionuclide ventriculography findings in 24 subjects show that the ventricular blood pool motion goes from base to apex, a finding that contradicts the expectation that an apex to base relationship should exist, because excitation proceeds from apex to base. This discrepancy reflects a difference between motion caused by whole heart transmural action, and regional activity that does not require global movement. Confirmation of the radionuclide ventriculography findings was made from sonomicrometer crystals, echocardiography, and MRI that demonstrated early basal motion. During excitation, only the endocardial muscle is stimulated by the electrical impulse, but transmural motion that is needed for the endocardial motion that is detected by radionuclide ventriculography. Differences between the isometric and ejection phases are described, and there is discussion of how these findings relate to the myocardial band. The reality of twisting and downward motion of the heart observed during ejection only happens following transmural activation, a motion that exists far beyond the QRS electrical signal on the ECG.
Vascular endothelial growth factor (VEGF) is a specific growth factor for endothelium but plays also a role in the signaling involved in embryonic endocardial-to-mesenchymal transformation of the endocardial cushions. Furthermore, VEGF is the major vascular permeability factor in both fetal and postnatal life. Overexpression of VEGF during fetal life is associated with fetal hydrops and abnormal endocardial cushion development and therefore with congenital heart defects. Cases of prenatal cervical hygroma like in Turner syndrome show both hydrops and cardiac defects. We hypothesize that excess VEGF formed in the wall of the distended jugular sacs (cervical hygroma's) results in other abnormal features characteristic for Turner syndrome such as short stature and gonadal dysgenesis. This implicates that if excess VEGF could be limited prenatally, the phenotypical expression of Turner syndrome can possibly be reduced.