This is a prospective study of adults (age ≥18 years) with repaired COA that underwent exercise echocardiography at Mayo Clinic Rochester between January 1, 2019, and June 30, 2024. Patients were recruited from the P rospective Observational R eg i stry of Outcomes in Adults with Congenital Heart Disease at M ayo Clinic (PRISM), which is part of the Mayo Adult Congenital Heart Disease (MACHD) Biobank database. The MACHD Biobank database is a prospective database of adults with congenital heart disease that underwent cardiovascular imaging, cardiopulmonary exercise test, invasive hemodynamic assessment, and biomarker assay from January 1, 2019. The Mayo Clinic Institutional Review Board approved the study, and all patients provided informed consent. From the MACHD Biobank database, we identified control subjects without structural heart disease (normal resting echocardiogram) that underwent exercise echocardiography using the same protocol. Patients in the COA group and control group were matched based on age and sex.

(1) Compare LA stiffness at rest, and cardiac reserve, pulmonary congestion, and aerobic capacity during exercise between the COA and control groups. (2) Identify the correlates of LA stiffness in the COA group. (3) Assess the relationship between LA stiffness, and cardiac reserve, pulmonary congestion, and aerobic capacity in the COA group.

All subjects underwent exercise echocardiography (cardiopulmonary exercise test with simultaneous echocardiogram), lung ultrasound, and treadmill cardiopulmonary exercise test.

Data were presented as mean ± standard deviation, median (interquartile range), and count (%). Between-group comparisons were performed using unpaired t-test, and Fisher’s exact test. Cardiac reserve (ie, exercise-induced change in cardiac function) was assessed using paired t-test. Pearson correlation was used to assess the relationship between continuous variables. Linear regression analysis was used to identify the correlates of LA stiffness index. The covariates used in the model were selected based on clinical relevance, and the final covariate selection was based on stepwise backwards selection with P <.1 required for a covariate to remain in the model. Similarly, linear regression analysis was used to assess the relationship between LA stiffness index and outcomes (cardiac reserve and aerobic capacity), while logistic regression analysis was used to assess the relationship between LA stiffness index and pulmonary congestion. These models were adjusted for age and sex, and biventricular function (RVFWS and LV global longitudinal strain) in stepwise fashion. Variance inflation factor was used to assess collinearity defined as variance inflation factor >10. All statistical analyses were performed with BlueSky Statistics software (version. 7.10; BlueSky Statistics LLC, Chicago, IL, USA), and JMP statistical software (version 17.1.0, JMP Statistical Discovery LLC, NC). P value <.05 was considered to be statistically significant for all analyses.

The study comprised of 46 adults with repaired COA, and 46 subjects in the control group. Table 1 shows a comparison of the baseline clinical and echocardiographic data of the COA group vs the control group.

The COA group had higher lower LA reservoir strain, and higher Doppler-derived arterial load indices (effective arterial elastance and total arterial compliance), and higher LV mass index, consistent with higher LV afterload and worse LV hypertrophy, respectively, in the COA group ( Table 2 ).

Although both groups had similar RV systolic function at rest (RVFWS −28% ± 5% vs −29% ± 4%, P =.41), the COA group had higher RV afterload (RVSP 31 ± 9 vs 26 ± 5 mmHg, P =.03), and in turn, worse RV-PA coupling (RVSP −0.96 ± 0.37 vs −1.15 ± 0.32 %/mmHg, P =.03), compared to the control group ( Table 2 ).

Both groups exercised to maximum effort, but the COA group achieved a lower peak workload (122 ± 24 vs 139 ± 22 W, P =.01), and lower peak VO ₂ during exercise echocardiogram (1,203 ± 368 vs 1,898 ± 575 ml/min, P <.001) compared to the control group ( Table 3 ). The COA group had lower cardiac reserve at peak exercise as evidenced by lower absolute increase in LARS (4.2 ± 1.95 vs 9.7 ± 3.1%, P <.001), lower absolute increase in CO (4.07 ± 2.11 vs 8.13 ± 2.93 l/min, P <.001), and greater decline in RV-PA coupling (absolute change in RVFWS/RVSP −0.33 ± −0.12 vs −0.21 ± 0.11 %/mmHg, P =.006), ( Table 3 ). Similarly, the COA group achieved lower predicted peak VO ₂ on treadmill exercise test (62 ± 8 vs 84% ± 10%, P =.006), and worse pulmonary congestion as evidenced by a higher proportion of patients with B-lines at peak exercise (39% [18/46] vs 7% [3/46], P <.001).

Table 3

Exercise data

	Rest		25 W		50 W		Peak
	COA	Control	COA	Control	COA	Control	COA	Control
O 2 consumption
VO 2 , ml/min	311 ± 62	307 ± 84	596 ± 110 *	658 ± 125 *	786 ± 131 *	893 ± 130 *	1203 ± 368	1898 ± 575 *
∆ VO 2 , ml/min	—	—	283 ± 84 * , †	353 ± 91 * , †	477 ± 87 * , †	589 ± 116 * , †	895 ± 205 * , †	1596 ± 411 * , †
HR, bpm	71 ± 12	72 ± 13	82 ± 15	84 ± 15	95 ± 12	103 ± 16	137 ± 21	145 ± 29
∆ HR, bpm	—	—	11 ± 4 †	12 ± 5 †	24 ± 8 * , †	33 ± 10 * , †	66 ± 17 †	73 ± 25 †
LA Function
LA reservoir strain	23.2 ± 4.7 *	36.6 ± 8.2 *	24.1 ± 5.2 *	41.7 ± 8.6 *	26.3 ± 4.9 *	43.9 ± 7.5 *	27.4 ± 4.7 *	45.6 ± 7.3 *
∆LA reservoir strain	—	—	0.9 ± 0.6 *	5.1 ± 1.9 * , †	3.1 ± 1.4 * , †	7.3 ± 3.4 * †	4.2 ± 1.9 * , †	9.7 ± 3.1 * , †
Cardiac output
CO, l/min	5.71 ± 1.43	5.84 ± 1.36	7.15 ± 2.11 *	8.56 ± 1.92 *	8.76 ± 2.21 *	11.31 ± 2.52 *	9.84 ± 2.82 *	14.02 ± 3.39 *
∆ CO, l/min	—	—	1.35 ± 1.06 * , †	2.68 ± 1.13 * , †	2.95 ± 1.53 * , †	5.45 ± 2.37 * , †	4.07 ± 2.11 * , †	8.13 ± 2.93 * , †
SV, ml	77 ± 21	83 ± 22	89 ± 29 *	102 ± 31 *	93 ± 22 *	106 ± 23 *	75 ± 18 *	94 ± 26 *
∆ SV, ml	—	—	12 ± 7 * , †	19 ± 13 * , †	16 ± 7 * , †	23 ± 10 * , †	−2 ± 4 *	11 ± 6 * , †
RV afterload
RVSP, mmHg	31 ± 9 *	26 ± 5 *	37 ± 14 *	29 ± 10 *	49 ± 17 *	34 ± 12 *	54 ± 19 *	41 ± 16 *
∆ RVSP, mmHg	—	—-	1 ± 2	3 ± 3	18 ± 6 * , †	8 ± 4 * , †	23 ± 10 * , †	15 ± 6 * , †
RV function
RVFWS	−28 ± 5	−29 ± 4	−29 ± 6 * , †	−32 ± 5 †	−29 ± 4 * , †	−34 ± 4 * , †	−28 ± 5 * , †	−37 ± 5 * , †
∆ RVFWS, %	—	—	1 ± 2 *	3 ± 2 * , †	1 ± 1 *	5 ± 2 * , †	0 ± 1 *	8 ± 3 * , †
RV-PA coupling
RVFWS/RVSP	−0.91 ± 22 *	−1.12 ± 0.29 *	−0.78 ± 0.19 *	−1.09 ± 0.26 *	−0.59 ± 0.16 *	−1.01 ± 0.23 *	−0.57 ± 0.18 *	−0.92 ± 0.36 *
∆ RVFWS	—	—	−0.12 ± 0.05	−0.01 ± 0.02	−0.32 ± 0.10 * , †	0.12 ± 0.05 *	−0.33 ± 0.12 * , †	−0.21 ± 0.11 * , †
LV afterload
SBP, mmHg	127 ± 14	121 ± 13	149 ± 18	132 ± 17	162 ± 29	145 ± 25	189 ± 34 *	165 ± 33 *
∆ SBP, mmHg	—	—	21 ± 8 * , †	11 ± 5 * , †	35 ± 22 * , †	24 ± 11 †	62 ± 29 * , †	44 ± 25 * , †
Ea, mmHg/ml	1.48 ± 0.26 *	1.31 ± 0.24 *	1.51 ± 0.27 *	1.18 ± 0.16 *	1.54 ± 0.32 *	1.28 ± 0.23 *	2.27 ± 0.83	1.61 ± 0.59
∆ Ea, mmHg/ml	—	—	0.02 ± 0.06 *	−0.15 ± 0.07 * , †	0.08 ± 0.05 *	−0.04 ± 0.04 *	0.78 ± 29 * , †	0.29 ± 0.16 * , †
TAC, ml/mmHg	1.51 ± 0.32 *	1.76 ± 0.38 *	1.16 ± 0.34	1.72 ± 0.45	1.05 ± 0.27	1.41 ± 0.42	0.64 ± 0.21	0.96 ± 0.35
∆ TAC, ml/mmHg	—	—	−0.36 ± 0.12 * , †	0.04 ± 0.03 * , †	−0.45 ± 0.17 * , †	−0.35 ± 0.15 * , †	−0.87 ± 0.31 * , †	−0.82 ± 0.32 * , †

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