Isolated pulmonary regurgitation causes decreased right ventricular longitudinal function and compensatory increased septal pumping in a porcine model

Abstract

Aim: Longitudinal ventricular contraction is a parameter of cardiac performance with predictive power. Right ventricular (RV) longitudinal function is impaired in patients with free pulmonary regurgitation (PR) following corrective surgery for Tetralogy of Fallot (TOF). It remains unclear whether this is a consequence of the surgical repair, or whether it is inherent to PR. The aim of this study was to assess the relationship between longitudinal, lateral and septal pumping in a porcine model of isolated PR.

Methods: Piglets were divided into a control (n = 8) group and a treatment (n = 12) group, which received a stent in the pulmonary valve orifice, inducing PR. After 2-3 months, animals were subjected to cardiac magnetic resonance imaging. A subset of animals (n = 6) then underwent percutaneous pulmonary valve replacement (PPVR) with follow-up 1 month later. Longitudinal, lateral and septal contributions to stroke volume (SV) were quantified by measuring volumetric displacements from end-diastole to end-systole in the cardiac short axis and long axis.

Results: PR resulted in a lower longitudinal contribution to RV stroke volume, compared to controls (60.0 ± 2.6% vs. 73.6 ± 3.8%; P = 0.012). Furthermore, a compensatory increase in septal contribution to RVSV was observed (11.0 ± 1.6% vs. -3.1 ± 1.5%; P < 0.0001). The left ventricle (LV) showed counter-regulation with an increased longitudinal LVSV. Changes in RV longitudinal function were reversed by PPVR.

Conclusion: These findings suggest that PR contributes to decreased RV longitudinal function in the absence of scarring from cardiac surgery. Measurement of longitudinal RVSV may aid risk stratification and timing for interventional correction of PR in TOF patients.

Keywords: Cardiac magnetic resonance; Tetralogy of Fallot; mitral annular plane systolic excursion (MAPSE); tricuspid annular plane systolic excursion; ventricular function.

Figure 1

Ventricular volumes indexed as fractions of total heart volume (THV). Pulmonary regurgitation (PR; grey columns) results in a significant decrease in both left ventricular end‐diastolic (EDV) and end‐systolic volumes (ESV) expressed as fractions of THV, while the right ventricle increases its EDV and ESV as a result of volume overload. Percutaneous pulmonary valve replacement (PPVR; blue columns) restores ventricular volumes in the right ventricle. In the left ventricle, ESV remains unchanged, while EDV increases, albeit not to control levels (white columns). Columns (EDV and ESV) are not additive; hence, the difference between both columns represents the respective stroke volume normalized to THV. †P < 0.01; ‡P < 0.001, ns: non‐significant.

Figure 2

Individual contributions to ventricular stroke volume (SV). Pulmonary regurgitation (PR; grey columns) results in an increase in left ventricular longitudinal and lateral stroke volume compared to control animals (white columns). A marked negative septal contribution to left ventricular stroke volume can be observed in piglets with PR. In the right ventricle, PR causes reductions in both longitudinal and lateral pumping, while the septum significantly contributes to right ventricular stroke volume. Changes are mostly reversible 1 month after percutaneous pulmonary valve replacement (PPVR; blue columns). *P < 0.05; †P < 0.01; ‡P < 0.001, ns: non‐significant.

Figure 3

Before–after comparison of longitudinal pumping after percutaneous pulmonary valve replacement (PPVR). Individual pigs with pulmonary regurgitation (PR) who underwent PPVR showed a significant recovery of right ventricular longitudinal pumping 1 month after restoration of valve function (b). Changes in left ventricular longitudinal pumping were not significant (a). *P < 0.05; ns: non‐significant.

Figure 4

Correlation between corrected RV EF and longitudinal contribution to LVSV. Corrected RV EF is defined as the net pulmonary forward flow/RVEDV, that is RVSV minus pulmonary regurgitant volume and tricuspid regurgitant volume (if present); R ²=0.623; P = 0.002.

Figure 5

Correlations between mean PCWP and longitudinal contribution to RVSV (a) and PR (b). a: PCWP correlates with the degree of longitudinal contribution to RVSV in animals with PR (R ²=0.940; P < 0.001). b: PCWP does not correlate with the degree of PR (R ²=0.020; P = 0.738).

Figure 6

Long‐axis view of the heart. Panels (a) and (b) show the heart of a control animal in end‐diastole (a) and end‐systole (b) respectively. Dashed line represents the AVP in end‐diastole. Dotted line represents the AVP in end‐systole. Panels c and d depict the heart of an animal suffering from PR (3 months) at corresponding imaging time points. Note the increased RV volume and the decreased RV AVP movement with a compensatory increase in LV AVP movement.