Fig. 19.1
(a) The tricuspid valve is exposed after the posteroanterior commissure has been cut. (b) Surgical vision of the tricuspid valve from the atrial side. A anterior leaflet, S septal leaflet, P Posterior leaflet, MB moderator band, cut to expose the tricuspid valve, AP comm. anteroposterior commissure, PS comm. posteroseptal commissure, AS comm. anteroseptal commissure, post PM posterior papillary muscle, CS coronary sinus (From Calafiore et al. [2], with permission)
Fig. 19.2
Reconstructed tricuspid annular shape in healthy subjects when tricuspid annulaur area is the smallest. The part in red indicates the highest portion toward the atrium. A anterior, L lateral, P posterior, S septum (From Fukuda et al. [3], with permission)
The Right Ventricle
The shape of the RV is difficult to assess. It appears triangular when viewed laterally, whereas in cross-section, it appears crescent shaped (Fig. 19.3). Its shape is also dependent of the position and function of the interventricular septum. In the normal, the septum is concave toward the LV in both systole and diastole. The RV volume is larger than the LV volume. The RV has three walls: anterior, inferior, and septal, with the last wall in common with the LV. These walls are muscular in nature, apart from a small portion of the basal septum, which is fibrous. Three RV components are described: the inlet portion, the apical trabecular portion, and the outlet portion. The inlet portion, which extends from the atrioventricular junction to the insertions of the papillary muscles, contains the tricuspid valvular apparatus. The apical trabecular portion shows coarser trabeculations than does the LV, and the outlet corresponds to the outflow tract, where there are no trabeculations except at the transitional zone with the apical portion [5]. The apical trabecular portion is often considered as part of the inflow.
Fig. 19.3
The inflow is not well seen, as the free wall was opened. The septum, in its lowest portion, is part of the inflow and in the upper portion of the outflow, which ends at the level of the pulmonary valve (PV). Ant PM anterior papillary muscle (From Calafiore et al. [2], with permission)
Physiology
The RV contracts in a “peristaltic” pattern that proceeds from the sinus, with an average major radius of curvature of nearly 4 cm, to the conus, with a small radius of curvature of 0.8 cm [6]. The RV is composed of superficial and deep muscle layers. The fibers of the superficial layer are arranged more or less circumferentially in a direction that is parallel to the atrioventricular groove These fibers turn obliquely toward the cardiac apex and continue into the superficial myofibers of the LV [7, 8]. The deep muscle fibers of the RV are longitudinally aligned base to apex. In contrast to the RV, the LV contains obliquely oriented myofibers superficially, longitudinally oriented myofibers in the subendocardium, and predominantly circular fibers in between. This arrangement contributes to the more complex movement of the LV, which includes torsion, translation, rotation, and thickening [7, 8]. The continuity between the muscle fibers of the RV and LV contributes, along with the interventricular septum and pericardium, to ventricular interdependence [8]. The RV propels blood into the pulmonary circulation, a huge territory at low hydraulic impedance. As a consequence, the thickness of its free wall is lower than the LV. In the LV there is a third layer of fibers (circumferential constrictor fibers) which account of reduction of the ventricular diameter. The RV, lacking of this layer, has to rely more on the longitudinal shortening than the LV. Moreover the septum contains longitudinal fibers belonging to the RV. As both ventricles share also both superficial and deep fibers, it is evident that they are a unique, interdependent, entity and that the pathology of one side affects the other side. Being the RV normally connected in series with the LV, the stroke volume of both ventricles is similar. Because of the greater end-diastolic volume of the right ventricle, RV ejection fraction is lower than the left, 61 ± 7 vs 67 ± 5 %, being the lower ranges >40 and >50 % for LV ejection fraction [9].
Part of stroke volume of the RV goes directly from the early inflow to the outflow as a result of preserved kinetic energy This direct flow follows a smoothly curving route that did not extend into the apical region of the ventricle and represents a larger part of the end-diastolic blood volume compared to the LV direct flow. This suggests that diastolic flow patterns distinct to the normal RV create favorable conditions for ensuing systolic ejection of the direct flow component [10].
The pressure-volume relationship of the RV was defined in 1988 by Redington et al. [11] as a triangular or trapezoidal shape, with ill defined periods of isovolumic contraction, and particularly isovolumic relaxation (Fig. 19.4) [12]. Thus, unlike the square wave pump of the LV, the RV is an energetically efficient pump (with a myocardial energy cost of approximately one-fifth that of the left), almost entirely dependent by the low pulmonary hydraulic impedance. In fact, when the LV is beneath the pulmonary artery, as in corrected transposition of great arteries, its pressure-volume characteristics are identical to those of the normal RV [13]. The RV pressure-volume pattern, being related to low flow impedance, is a dynamic phenomenon. In fact a slowly progressive rise in pulmonary arterial impedance causes a progressive change towards an “LV” pattern of pressure–volume loop [14].
Fig. 19.4
Echocardiographic images of the right ventricle. (a) 4 chambers. RV shape is triangular. (b, c) Short axis. The RV is crescent shaped. Prox proximal, Dist distal (From Calafiore et al. [2], with permission)
Several mechanisms contribute to RV ejection, the most important being the bellows-like inward movement of the free wall. Other important mechanisms include the contraction of the longitudinal fibers, shortening of the long axis, drawing the tricuspid annulus toward the apex, and the traction on the free RV wall at its points of attachment to the LV as a result of LV contraction [15]. In contrast to the LV, twisting and rotational movements do not contribute significantly to RV contraction [16]. The lungs represent the afterload of the RV and influence RV hemodynamics even breathe by breathe. With each inspiration, the small (2–5 cm H2O) change in intrapleural pressure leads to a significant increase in venous return and RV preload. This causes a variation of the RV stroke volume during the respiratory cycle. The ventricles share not only the visceral cavity (pericardium) but also myofibers, particularly in their superficial layers, and the interventricular septum, which contributes to ejection of both cavities. The relationship between ventricular septum and RV function in normal hearts was studied by Dibble et al. [17] using cardiac MRI. They found that interventricular septal function was linked to RV systolic function independent of other left ventricular regions. This finding further confirmed the importance of septal function on the RV, suggesting that changes in septal function could cause RV dysfunction. Most of the effects of the LV contraction on the RV are mediated by the interventricular septum. During systole, the septum twists and shortens causing reduction in ventricular volume and forceful ejection of blood out of both ventricular cavities. In the case of the RV, in the absence of septal twisting due to septal damage, ventricular ejection is produced by circumferential constriction caused by contraction of the basal wall that contains predominantly transverse fibers. Such constriction may not allow delivery of enough contractile force to ensure adequate cardiac output when pulmonary vascular resistance is increased. Septal dysfunction may be at the basis of RV dysfunction that can develop perioperatively together with new septal akinesia or hypokinesia. The RV is not capable to sustain long-term pressure overload. Eventually, cardiac contractile force decreases, due to functional, structural or numerical (apoptosis) changes in cardiomyocytes and the RV dilates, due to the increased wall tension that increases myocardial oxygen demand and simultaneously decreases RV perfusion. When afterload increases, the mechanisms that drive the transition from hypertrophy to dilatation and finally to right heart failure have not been well defined.
When pulmonary pressure rises, the systolic blood flow to the RV decreases, leading finally to RV ischemia [18]. The RV coronary circulation becomes more like that of the LV: a greater oxygen extraction at rest and a higher dependence on an increase in coronary flow to meet an increase in myocardial oxygen demand. An increased wall tension increases oxygen consumption and decreases oxygen supply by compression of the coronary circulation. During the development of cardiac hypertrophy, a mismatch between the number of capillaries and the size of cardiomyocytes can lead to myocardial hypoxia, contractile dysfunction, and apoptosis [19, 20].
Cardiomyocyte apoptosis, rare in the normal human heart, can become frequent in heart failure (1 cell out of 400 [21, 22]). Even very low rates of apoptosis (one-fifth of that seen in human heart failure) have been shown to cause lethal dilated cardiomyopathy in a mouse model [23]. The influence on RV contractility will depend on the balance between cell death and formation of new cells due to cardiac stem cells contained into the cardiac muscle [24]. This mechanism very likely is efficient during the first phase of pressure overload, but becomes exhausted over time.
Interaction Between Right Ventricle and Functional Tricuspid Regurgitation
A vicious circle may occur between RV remodeling (dysfunction or dilatation) and functionaltricuspid regurgitation (FTR): one might beget the other one and vice versa. Functional tricuspid regurgitation occurs because of annular dilatation and RV enlargement, which can influence, with different mechanisms, leaflets coaptation. On the other hand, the presence of functional tricuspid regurgitation causes a volume overload of the right ventricle, that can cause right ventricle dilatation and dysfunction.
Annular Enlargement
Annular enlargement happens at the level of the free wall, which include the part of the septal annulus on front of the coronary sinus. Annular dilatation is accompanied by changes in the planar shape. Ton-nu et al. [4] found that 3D shape attenuated in patients with significant TR (Fig. 19.5a, b) and that there was an inverse and continuous relationship between annular area and degree of planarity (Fig. 19.5c). In an experimental model Spinner et al. [25] found that isolated annular enlargement caused significant TR when reached 40 % increase. Further dilatation caused more significant regurgitation (Fig. 19.6a). The orifice was in the central region of the three leaflets, toward the septum (Fig. 19.6b). In this hypothetical setting the residual length to coapt was reduced for the anterior and the septal leaflet, almost normal for the posterior leaflet (Fig. 19.6c).
Fig. 19.5
Normal human left (LV) and right ventricular (RV) pressure–volume relationships. The RV loop is more trapezoidal, with poorly defined isovolumic periods (From Sheehan and Redington [12], with permission)
Fig. 19.6
Tricuspid valve annulus viewed from profile displaying anteroposterior view. (a) In the normal the 2 high points are located anteroposteriorly. (b) In functional tricuspid regurgitation there is no distinct high point. (c) Inverse and continuous relationship between tricuspid annular area (TV area) and degree of planarity (H-L distance). Ant anterior, Ao valve aortic valve, post posterior, RA right atrium (From Ton-nu et al. [4], with permission)
However, annular dilatation, by itself, even if can reduce the residual length to coapt of the leaflets, can be not enough to cause TR, at least significant. In an interesting study Sadeghi et al. [26], reported 27 patients with pulmonary thromboembolism who had severe pulmonary hypertension and severe TR. They underwent surgery without TV annuloplasty. In 19 patients (70 %) the pulmonary pressure dropped by a mean of 49 mmHg and TR was reduced to mild. In the remaining 30 % of patients, TR remained severe; pulmonary pressure reduced of 32 mmHg, less than in the other group. Interestingly, in both groups the annular size remained nearly unchanged (4 mm reduction between pre and postoperative echocardiograms) and similar (41 mm in the first group and 42 mm in the second one in the postoperative assessment). We can deduct that, even if the annulus remains dilated, this does not prevent TR reduction, but the mechanisms related to RV reverse remodeling, following PAP reduction of different degrees, are more important than the pure annular size.
Papillary Muscle Displacement
The position of PMs in the normal and in patients with dilated RV were explored by Spinner et al. [27] using MRI. It is notable that the sides of the triangle formed by the PMs were of similar length. The septal PM was the furthest from the centroid and the closest to the annular plane. The anterior PM was the most apical and furthest from the annular plane (Fig. 19.7). In patients with dilated RV the same relative position of the PMs was confirmed. But significant differences were detectable only with the septal PM, which was displaced in the posterior direction and toward the centroid (Fig. 19.8). RV dilatation then caused inward displacement toward the centroid of the 3 PMs, due to the displacement of the septal wall into the RV with the increased LV volume. Changes in the LV geometry are transferred to the RV though the interventricular septum [28], resulting in a configuration that may lead to TV leaflet prolapse [25]. When the septum is bowing toward the RV, mobility of septal leaflet is increased, thus changing the location of the coaptation line, resulting in a central malcoaptation in the center of the annulus because the septal leaflet is too short. This results in an insufficient residual length to coapt of the septal leaflet (Fig. 19.9). When RV is dilated and the septum is bowing toward the LV, a displacement of all PMs and annular enlargement occurs, which causes the highest grade of TR [25]. Septal displacement causes, in this scenario, increased tethering of septal leaflet and posterior leaflet. The same group [29], in a clinical setting, confirmed that alterations in ventricular geometry can lead to TR altering both annulus size and PMs position.
Fig. 19.7
(a) Tricuspid regurgitation fraction as an effect of annulus area times normal compared with control (1). (b) Residual leaflet length (RLL) as an effect of annulus area times normal, as shown for each individual leaflet: posterior (black), anterior (gray), and septal (light gray). (c) Mechanism of regurgitation as seen with 100 % dilatation. Anterior and posterior segments of annulus move away from center, creating a central hole toward the septum. With anterior leaflet extending to cover enlarged orifice and pulled away with dilatation, residual leaflet length is insufficient. *p < 0.05; APM anterior papillary muscle, SPM septal papillary muscle, PPM posterior papillary muscle (From Spinner et al. [25], with permission)
Fig. 19.8
Anatomic representation of the papillary muscles in the right ventricle (From Spinner et al. [27], with permission)
