Exercise intolerance is a hallmark symptom in adults with repaired tetralogy of Fallot (TOF). This may be attributed to the disease-related impairment in RV systolic function, augmentation in right ventricular (RV) load, and their combined effect on altering left ventricular (LV) hemodynamics. To further elucidate these mechanisms, we examined oxygen uptake (VO2) by indirect-calorimetry and cardiac hemodynamics by echocardiography in 34 TOF (48 ± 14 yrs) and 29 healthy controls (41 ± 15 yrs), at rest and during exercise. At peak exercise, VO2 (VO2 peak) was 15% lower in TOF compared to controls (P < 0.001). This was partially attributed to a 15% lower heart rate (P < 0.001) in conjunction with a blunted exercise-induced change in LV stroke volume (SV) from rest (58% lower in TOF compared to controls, P = 0.015) to compensate for the chronotropic incompetence. Pulmonary-right ventricular (P-RV) coupling, a measure of RV systolic load indexed to RV systolic function, was 75% higher at peak exercise in TOF compared to controls (P < 0.001). Additionally, in TOF, P-RV coupling at peak exercise negatively correlated with VO2 peak (R = -0.65, P < 0.001), changes in LV end-diastolic volume (R = -0.50, P < 0.001), and changes in LV SV (R = -0.56, P < 0.001) from rest. These findings reveal the reliance of LV hemodynamics on the interplay between RV systolic load and function during exercise in TOF, and further illuminates the underlying cardiovascular mechanisms contributing to the impairment in aerobic capacity evident in this patient group.
Keywords: Tetralogy of Fallot; exercise; hemodynamics; right ventricle.
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