Key result
Patients with repaired tetralogy of Fallot exhibited significantly lower exercise capacity, reduced pulmonary blood flow, and impaired biventricular function compared to healthy controls.
Why the study?
Reduced exercise capacity in corrected tetralogy of Fallot cannot be explained by pulmonary valve pathology and RV dysfunction alone, prompting exploration using CPET and real-time CMR exercise testing.
Does real-time cardiovascular magnetic resonance exercise testing reveal the mechanisms of impaired exercise capacity in patients with corrected tetralogy of Fallot compared to healthy controls?
Case-Control (n=68)
Does real-time cardiovascular magnetic resonance exercise testing reveal the mechanisms of impaired exercise capacity in patients with corrected tetralogy of Fallot compared to healthy controls?
Impaired exercise capacity in corrected tetralogy of Fallot is associated with both right and left ventricular dysfunction, suggesting CMR-ET-derived LV function could help stratify patients for pulmonary valve replacement.
Answers are grounded in this paper and cite their sources.
LV contractile reserve during exercise may contribute to cTOF intolerance; extends RV-centric models but remains hypothesis-generating for PVR stratification.
Background: Correction of tetralogy of Fallot (cTOF) often results in pulmonary valve pathology and right ventricular (RV) dysfunction. Reduced exercise capacity in cTOF patients cannot be explained by these findings alone. We aimed to explore why cTOF patients exhibit impaired exercise capacity with the aid of a comprehensive cardiopulmonary exercise testing (CPET) and real-time cardiovascular magnetic resonance exercise testing (CMR-ET) protocol. Methods: Thirty three cTOF patients and 35 matched healthy controls underwent CPET and CMR-ET in a prospective case-control study. Real-time steady-state free precession cine and phase-contrast sequences were obtained during incremental supine in-scanner cycling at 50, 70, and 90 W. RV and left ventricle (LV) volumes and pulmonary blood flow (Qp) were calculated. Differences of CPET and CMR-ET between cTOF versus controls and correlations between CPET and CMR-ET parameters in cTOF were evaluated statistically for all CMR exercise levels using Mann-Whitney U and Spearman rank-order correlation tests. Results: CPET capacity was significantly lower in cTOF than in controls. cTOF patients exhibited not only significantly reduced Qp and RV function but also lower LV function on CMR-ET. Higher CPET values in cTOF correlated with higher Qp (Qp 90 W versus carbon dioxide ventilatory equivalent %: R =−0.519, P <0.05), higher LV–end-diastolic volume indexed to body surface area (LV–end-diastolic volume indexed to body surface area at 50 W versus oxygen uptake in % at maximum exercise on CPET R =0.452, P <0.05), and change in LV ejection fraction (EF; LV-EF at 90 W versus Watt %: r =−0.463, P <0.05). No correlation was found with regard to RV-EF. Significant RV-LV interaction was observed during CMR-ET (RV-EF versus LV-EF at 50 W and 70 W: r =0.66, P <0.02 and r =0.52, P <0.05, respectively). Conclusions: Impaired exercise capacity in cTOF resulted from a reduction in not only RV, but also LV function. cTOF with good exercise capacity on CPET demonstrated higher LV reserve and pulmonary blood flow during incremental CMR-ET. Apart from RV parameters, CMR-ET–derived LV function could be a valuable tool to stratify cTOF patients for pulmonary valve replacement.
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Steinmetz et al. (2021) conducted a case-control in Repaired Tetralogy of Fallot (n=68). Repaired Tetralogy of Fallot vs. Matched healthy controls was evaluated on Cardiopulmonary exercise capacity and biventricular function on CMR-ET. Patients with repaired tetralogy of Fallot exhibited significantly lower exercise capacity, reduced pulmonary blood flow, and impaired biventricular function compared to healthy controls.
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