Structure of chordae tendineae in the left ventricle of the human heart

Abstract

The bicuspid (mitral) valve complex of the human heart consists of functional units which include the valve leaflets, chordae tendineae and the papillary muscles. The mechanical properties of these functional units depend to a large extent on the link between the muscle and the valve. This link is usually arranged in a branching network of avascular tendinous chordae composed of collagen and elastic fibres, which transmit contractions of the papillary muscle to the valve leaflets. In order to perform their function efficiently, the chordae have to possess a high degree of elasticity, as well as considerable strength and endurance. Human chordae tendineae originating from the left ventricles were obtained from 7 embalmed cadavers and 6 postmortem subjects of various ages. Samples washed in saline were fixed or postfixed in 9 % formol saline. Observations were made by illuminating the chordae along their axes. The reflected images originating from the superficial collagenous layers of the relaxed chordae showed a striped pattern 11 µm in width. Scanning electron and light microscopy of the chordae confirmed an undulating pattern of collagen fibrils arranged in bundles of planar waves in register and around the entire circumference of the chorda. The dimensions of the waves correlated with those of the striped reflected pattern. The observed undulating arrangement of the collagen fibrils appears to produce an inherent built-in elasticity which is likely to be of considerable advantage for a tissue which is under continuous repetitive stress. The chordae were covered by endocardium composed of a superficial layer of smooth squamous endothelial cells and an underlying dense layer of elastic fibres. It is suggested that the relaxed striped chordae, consisting of undulating collagen fibrils, straighten when the chordae become stretched by papillary muscle contraction, thereby mitigating the peak stress developed during muscle contraction. On relaxation the elastic tissue tends to return the collagen to its wavy configuration. It is also suggested that the regular wavy pattern of collagen seen in young individuals gradually changes with age by elongation of the wave pattern which eventually becomes randomised. In addition, with increasing age, substantial cushions of connective tissue appear below endocardium while the dense collagenous core has a reduced cross-sectional area which may lead to stretching and eventual rupture of the chordae.

Local Tenomodulin Absence, Angiogenesis, and Matrix Metalloproteinase Activation Are Associated With the Rupture of the Chordae Tendineae Cordis

“…This structure was consistent with that reported previously. 1 Tenomodulin was restricted to the elastin-rich mid layer ( Figure 2C) and was not detected in the other layers. The normal CTC showed no expression of chondromodulin-I ( Figure 2D) or VEGF-A ( Figure 2F), and there was no abnormal vessel formation.…”

“…1 This avascularity is abrogated in several valvular heart diseases (VHDs). [2][3][4] Chondromodulin-I, which is an antiangiogenic factor isolated from bovine cartilage, [5][6][7][8] is also expressed in the eye and is critically involved in the maintenance.…”

Mitral valve finite-element modelling from ultrasound data: a pilot study for a new approach to understand mitral function and clinical scenarios

“…The essential framework of the chordae tendineae is constituted by a central core of crimped collagen fibres covered by elastic fibres and both are enveloped by endothelium (Millington-Sanders et al 1998). This microstructure provides the mechanical response that is typical of collagenous tissues.…”

Periostin advances atherosclerotic and rheumatic cardiac valve degeneration by inducing angiogenesis and MMP production in humans and rodents

“…Although the onset of aortic valve stenosis has been reported in Smad6-deficient mice (14), in fibulin 4-deficient mice (15), and in humans with the NOTCH1 mutation (16), the abnormality has primarily been observed during cardiac valve development. As avascular tissues, the cardiac valve complex and cartilage share common structural properties (17,18). The cartilage and tendons are known to have unique angioinhibitory mechanisms (19), disruption of which results in angiogenesis and destruction of the joint, leading to arthritis (20).…”