Key result
Induced pulmonary regurgitation in infant pigs reduced right ventricular contractility at 6 months (11 vs 19 Mw.ml-1.s-1; P<0.001), though sustained ventricular arrhythmias were not inducible.
Why the study?
Although mechano-electrical coupling in TOF is well known, its time effect on the inducibility of arrhythmia remains ill-defined.
Absolute Event Rate: 11% vs 19%
p-value: p=<0.001
In a pig model of tetralogy of Fallot, haemodynamic right ventricular deterioration precedes the risk of inducible sustained ventricular arrhythmias.
Pulmonary regurgitation may impair RV contractility in developing hearts; leaves open arrhythmia risk and human translation.
OBJECTIVES: The long-term outcome of tetralogy of Fallot (TOF) is determined by progressive right ventricular (RV) dysfunction through pulmonary regurgitation (PR) and the risk of malignant arrhythmia. Although mechano-electrical coupling in TOF is well-known, its time effect on the inducibility of arrhythmia remains ill-defined. The goal of this study was to investigate the mechano-electrical properties at different times in animals with chronic PR. METHODS: PR was induced by a transannular patch with limited RV scarring in infant pigs. Haemodynamic assessment included biventricular pressure-volume loops after 3 (n = 8) and 6 months (n = 7) compared to controls (n = 5). The electrophysiological study included endocardial monophasic action potential registration, intraventricular conduction velocity and induction of ventricular arrhythmia by burst pacing. RESULTS: Progressive RV dilation was achieved at 6 months (RV end-diastolic volume 143 ± 13 ml/m2-RV end-systolic volume 96 ± 7 ml/m2; P < 0.001), in association with depressed RV contractility (preload recruitable stroke work-slope: 19 ± 1 and 11 ± 3 Mw.ml-1.s-1 for control and 6 m; P < 0.001) and left ventricular contractility (preload recruitable stroke work-slope: 60 ± 13 and 40 ± 11 Mw.ml-1.s-1 for control and 6 m; P = 0.005). Concomitant to QRS prolongation, monophasic action potential90-duration and dispersion at the RV and left ventricle were increased at 6 months. Intraventricular conduction was delayed only in the RV at 6 months (1.8 ± 0.2 and 2.4 ± 0.6 m/s for group 6M and the control group; P = 0.035). Sustained ventricular arrhythmias were not inducible. CONCLUSIONS: In animals yielding the sequelae of a contemporary operation for TOF, mechano-electrical alterations are progressive and affect predominantly the RV after midterm exposure of PR. Because ventricular arrhythmias were not inducible despite significant RV dilation, the data suggest that the haemodynamic RV deterioration effectively precedes the risk of inducing sustained arrhythmia after TOF repair and opens a window for renewed stratification of contemporary risk factors of ventricular arrhythmias in patients operated on with currently used pulmonary valve- and RV-related techniques.
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Bové et al. (2020) studied Tetralogy of Fallot (chronic pulmonary regurgitation) (n=20). Induced pulmonary regurgitation via transannular patch vs. Controls was evaluated on Right ventricular contractility (preload recruitable stroke work-slope) (p=<0.001). Induced pulmonary regurgitation in infant pigs reduced right ventricular contractility at 6 months (11 vs 19 Mw.ml-1.s-1; P<0.001), though sustained ventricular arrhythmias were not inducible.
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