Mechanical
In the past heart valve dysfunction was assumed as a degenerative and
passive deposition of calcium crystals. However, it has been established
that biological prosthetic valve dysfunction is a very dynamic and
progressive process, including noncalcific deterioration with important
mechanical and environmental contributions.
As part of the fabrication model of bioprosthesis, the structure is
fixed in a static geometry. The collagenous network is locked into a
single configuration of one phase of the cardiac cycle, inhibiting the
normal extracellular matrix readjustments of the valve during the
cardiac cycle (39, 40). The collagen crimps and corrugations are
preloaded in a defined configuration similar to that of a closed valve
(55). Thereby, functional and normal cardiac cycle stresses have to be
absorbed by the noncompliant and fixed collagen fibers (55). Having a
fixed configuration will produce damage in pericardial valves during
closure (in porcine valves mostly during opening but also during
closing), inducing repetitive accumulation of mechanical stress with
increased tissue fatigue (39, 40). Leaflets should display anisotropic
proprieties, especially regarding strain in the circumferential and
radial directions. It has been established that non-physiological strain
leads to pathologic processes by deregulation of inflammation and
remodeling, leading to calcification (18).
The pressure used during fixation is also important for the mechanical
changes induced in the tissues, as it determines the stress-strain
relation of the tissue strips (58). Low pressures have better mechanical
proprieties and most of the bioprosthesis used nowadays, such as Edwards
Lifesciences® Magna Perimount and LivaNova® Perceval Plus, are
manufactured with low pressure fixation (59). However, studies have
shown that as low as 2-4 mmHg are sufficient to induce significant
changes in collagen compliance (55), so zero-pressure methods have been
studied. Although in theory zero-pressure would offer a new approach to
reduce biological prosthetic dysfunction, the technique has not achieved
clinically significant results (60).
Although Glut-related dysfunction is more associated with calcification,
it also induces mechanical alterations to the valve tissue. It has been
shown that glut alters the stress-strain curves of strips of bovine and
porcine valve tissues (58). During the fixation process there is also a
considerable loss and incomplete stabilization of the GAGs (61), which
are responsible for the viscoelasticity and accommodation of the cuspal
layers. GAGs have an essential role in absorbing compressive loads,
modulating shear stress and avoiding tissue buckling, and they may be
important in mechanical abnormalities that lead to valve dysfunction.
The chemical and mechanical changes are possible synergetic, since
changes in tissue configuration can induce stress and fatigue
(especially in flexion lines of the cusps) that can expose and disrupt
collagen, initiating the calcification process. On the other hand,
calcifications can also induce structural changes and stiffness that
will eventually lead to more mechanical changes and damage.