Erin M. Spinner

In Vitro Characterization of the Mechanisms Responsible for Functional Tricuspid Regurgitation

Background— Functional tricuspid regurgitation (TR) is increasingly recognized as a source of morbidity. Current repair strategies focus on annular remodeling because annular dilatation is common in patients with TR. Although papillary muscle (PM) displacement is recognized in functional mitral regurgitation, its role in TR is less well characterized. The objective of this in vitro study was to further clarify the mechanisms by which TR occurs as an effect of annular dilatation and PM displacement. Methods and Results— Porcine tricuspid valves (n=16) were studied in an in vitro right heart simulator. The valve dynamics were quantified with isolated annular dilatation starting with a normal annular size (6 cm2) and incrementally dilated up to 100%, isolated PM displacement, and a combination of the 2. All valves lost competence at 40% dilatation, resulting in a TR of 7.9±3.4 mL (P⩽0.05) compared with baseline and central residual leaflet length of 0.5±0.2 cm. Multidirectional displacement of the anterior and posterior/septal PMs and all PMs significantly (P⩽0.05) increased TR, with normal annular area. Malcoaptation was observed where the 3 leaflets joined with all significant levels of TR. The anterior leaflet had the greatest percent change in residual leaflet length, whereas PM displacement caused a reduction in residual leaflet length for the septal leaflet for all conditions. Conclusions— This study shows that although annular dilatation alone leads to TR, isolated PM displacement can also cause TR; annular remodeling strategies should be tailored in the setting of severe PM displacement.

Correlates of Tricuspid Regurgitation as Determined by 3D Echocardiography: Pulmonary Arterial Pressure, Ventricle Geometry, Annular Dilatation, and Papillary Muscle Displacement

Background— While it is understood that annular dilatation contributes to tricuspid regurgitation (TR), other factors are less clear. The geometry of the right ventricle (RV) and left ventricle (LV) may alter tricuspid annulus size and papillary muscle (PM) positions leading to TR. Methods and Results— Three-dimensional echocardiographic images were obtained at Emory University Hospital using a GE Vivid 7 ultrasound system. End-diastolic area was used to classify ventricle geometry: control (n=21), isolated RV dilatation (n=17), isolated LV dilatation (n=13), and both RV and LV dilatation (n=13). GE EchoPAC was used to measure annulus area and position of the PM tips. Patients with RV dilatation had significant (P⩽ 0.05) displacement of all PMs apically and the septal PM and posterior PM away from the center of the RV toward the LV. Patients with LV dilatation had significant (P⩽0.05) apical displacement of the anterior PM. Pulmonary arterial pressure (r=0.66), annulus area (r=0.51), apical displacement of the anterior PM (r=0.26), posterior PM (r=0.49), and septal PM (r=0.40), lateral displacement of the septal PM (r=0.37) and posterior PM (r=0.40), and tenting area and height (r=0.54, 0.49), were significantly (P⩽0.05) correlated to the grade of TR. Ventricle classification (r=0.46) and RV end-diastolic area (r=0.48) also were correlated with the grade of TR. A regression analysis found ventricle classification (P=0.001), pulmonary arterial pressure (P⩽0.001) annulus area (P=0.027), and apical displacement of the anterior PM (P=0.061) to be associated with the grade of TR. Conclusions— Alterations in ventricular geometry can lead to TR by altering both tricuspid annulus size and PM position. Understanding these geometric interactions with the aim of correcting pathological alterations of the tricuspid valve apparatus may lead to more robust repairs.

Altered right ventricular papillary muscle position and orientation in patients with a dilated left ventricle

OBJECTIVE To investigate the impact of left ventricular dilatation on right ventricular papillary muscle displacement. METHODS Thirteen patients underwent high-resolution cardiac magnetic resonance imaging at Emory University Hospital: Seven patients with congestive heart failure and a dilated left ventricle composed the dilated left ventricular group, and 6 normal subjects were used as a control. A total of 120 cardiac magnetic resonance imaging slices were acquired in a short-axis view at end diastole for each subject. Cardiac magnetic resonance imaging slices were used to identify the papillary muscle tip position in 3-dimensional coordinates for the septal, posterior, and anterior papillary muscles. The centroid of the papillary muscle coordinates was used as the reference point for comparison between subjects. The relative orientation between the right ventricular papillary muscles was evaluated and compared between the dilated left ventricular group and normal subjects. RESULTS Dilatation of the left ventricle resulted in a significant (P = .05) displacement of the septal right ventricular papillary muscle toward the centroid: normal group, 0.0285 ± 0.036 mm/mm versus dilated left ventricular group, 0.1437 ± 0.026 mm/mm. More specifically, the septal papillary muscle significantly (P = .03) moved away from the septal wall (normal group: 0.61 ± 0.09 mm/mm, dilated left ventricular group: 0.379 ± 0.037 mm/mm). Specific locations of all 3 right ventricular papillary muscles were reported for normal subjects and patients with a dilated left ventricle. CONCLUSIONS Patients with a dilated left ventricle have significantly increased displacement of the septal right ventricular papillary muscle away from the septum when compared with normal controls. This demonstrates pathophysiologic contribution of the left ventricle to specific papillary muscle alterations within the right ventricle.

Peak Mechanical Loads Induced in the In Vitro Edge-to-Edge Repair of Posterior Leaflet Flail

BACKGROUND Percutaneous edge-to-edge mitral valve (MV) repair is a potential therapeutic option for patients presenting with mitral regurgitation, who may not be suitable for surgery. We characterized the edge-to-edge repair forces in a posterior leaflet flail MV model to identify potential modes of mechanical failure. METHODS Porcine MVs were evaluated in two different sizes (Physio II 32 and 40) in a left-side heart simulator under physiologic hemodynamic conditions. Edge-to-edge repair was simulated by suturing miniature force transducers near the free edge of the anterior and posterior leaflets, on the ventricular side, resulting in a double orifice MV. Posterior leaflet flail was created by selective chordal cutting. RESULTS Chordal cutting resulted in posterior leaflet flail and mitral regurgitation; all valves coapted normally before chordal cutting. Peak systolic control forces (size 32, 0.098 ± 0.058 N; size 40, 0.236 ± 0.149 N) were not significantly different from systolic flail forces (size 32, 0.136 ± 0.107 N; size 40, 0.220 ± 0.128 N) for either MV size. No correlation was observed between force magnitude and flail height or width. Peak systolic force was greater (p = 0.08) for the larger MVs (size 40 compared with size 32). Finally, peak diastolic force was significantly smaller (p = 0.04) than peak systolic force regardless of valve size. CONCLUSIONS For the first time, forces imparted on an edge-to-edge MV repair were quantified for a posterior leaflet flail model. Force magnitude was not significantly altered with flail compared with control; it was greatest during peak systole and increased with valve size.

Measurement of strut chordal forces of the tricuspid valve using miniature C ring transducers

Tricuspid valve (TV) leaflets, papillary muscles (PM), and tendinous chords must work together to ensure proper coaptation. Alterations in valvular mechanics, including chordal forces, may lead to improper coaptation resulting in tricuspid regurgitation. Little is known about TV mechanics as right-sided heart diseases have been overlooked. We sought to fill this gap by understanding the role of TV strut chords with the objective to understand how strut chordal force varies depending on papillary muscle (PM) origin and leaflet attachment in the normal state. Additionally we investigated how these forces are altered with abnormal geometry. Porcine TVs (n=18) were studied in a right-heart simulator capable of reproducing physiological and pathological conditions. Miniature force transducers were placed on strut chords to measure forces throughout the cardiac cycle. In the normal state, chordal force depended upon PM attachment in which chords branching from the septal PM (SPM) carried significantly less force compared to those branching from the anterior PM (APM) (p≤0.05). Annular dilatation resulted in significant increase in chordal force (p≤0.05) on all strut chords. Severe PM displacement led to increased chordal force in chords attaching the APM to the posterior leaflet as well as chords attaching the PPM to the septal leaflet. Elevated chordal force due to isolated annular dilatation was further increased only with addition of apical displacement of the APM. These results provide initial knowledge of TV chordal force mechanics and may be applied to future studies on TV repair techniques.

Alterations in Tricuspid Valve Mechanics as a Result of Annular Dilatation and Papillary Muscle Displacement: An In Vitro Study

Current information as to the mechanism which causes malcoaptation of the tricuspid leaflets and leads to regurgitation is lacking. This study investigated the effect isolated and combined annular dilatation and PM displacement on valve mechanics. 3D echocardiography was used to quantify the changes in valve mechanics in relation to changes in tricuspid regurgitation.Copyright