Key result
Pediatric heart transplantation significantly reduced median pulmonary artery pressure from 26 mmHg to 19.5 mmHg at last follow-up (p<0.05), with delayed normalization in CHD patients.
Why the study?
Pulmonary hypertension may limit the outcome of pediatric heart transplantation, prompting evaluation of pulmonary hemodynamics in children undergoing transplantation.
How does pediatric heart transplantation affect pulmonary hemodynamics in children with cardiomyopathy versus congenital heart disease?
Cross-Sectional (n=23)
No
How does pediatric heart transplantation affect pulmonary hemodynamics in children with cardiomyopathy versus congenital heart disease?
p-value: p=<.05
Pediatric heart transplantation effectively normalizes pulmonary hemodynamics, though the time course of improvement is delayed in patients with congenital heart disease compared to those with cardiomyopathy.
Pulmonary hemodynamics warrant prospective study in pediatric heart transplant candidates; leaves open prognostic value for outcomes.
Background Pulmonary hypertension (PH) may limit the outcome of pediatric heart transplantation (pHTx). We evaluated pulmonary hemodynamics in children undergoing pHTx. Methods Cross‐sectional, single‐center, observational study analyzing pulmonary hemodynamics in children undergoing pHTx. Results Twenty‐three children (female 15) underwent pHTx at median (IQR) age of 3.9 (.9–8.2) years with a time interval between first clinical signs and pHTx of 1.1 (.4–3.2) years. Indications for pHTx included cardiomyopathy (CMP) (n = 17, 74%), congenital heart disease (CHD) (n = 5, 22%), and intracardiac tumor (n = 1, 4%). Before pHTx, pulmonary hemodynamics included elevated pulmonary artery pressure (PAP) 26 (18.5–30) mmHg, pulmonary capillary wedge pressure (PCWP) 19 (14–21) mmHg, left ventricular enddiastolic pressure (LVEDP) 17 (13–22) mmHg. Transpulmonary pressure gradient (TPG) was 6.5 (3.5–10) mmHg and pulmonary vascular resistance (Rp) 2.65 WU*m2 (1.87–3.19). After pHTx, at immediate evaluation 2 weeks after pHTx PAP decreased to 20.5 (17–24) mmHg, PCWP 14.5 (10.5–18) mmHg (p < .05), LVEDP 16 (12.5–18) mmHg, TPG 6.5 (4–12) mmHg, Rp 1.49 (1.08–2.74) WU*m2 resp.at last invasive follow up 4.0 (1.4–6) years after pHTx, to PAP 19.5 (17–21) mmHg (p < .05), PCWP 13 (10.5–14.5) mmHg (p < .05), LVEDP 13 (10.5–14) mmHg, TPG 7 (5–9.5) mmHg, Rp 1.58 (1.38–2.19) WU*m2 (p < .05). In CHD patients PAP increased (p < .05) after pHTx at immediate evaluation and decreased until last follow‐up (p < .05), while in CMP patients there was a continuous decline of mean PAP values immediately after HTx (p < .05). Conclusions While PH before pHTx is frequent, after pHTx the normalization of PH starts immediately in CMP patients but is delayed in CHD patients.
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Biedermann et al. (2023) conducted a cross-sectional in Pulmonary hypertension in pediatric heart transplantation (n=23). Pediatric heart transplantation vs. Before transplantation (baseline) was evaluated on Pulmonary hemodynamics (including pulmonary artery pressure) (p=<.05). Pediatric heart transplantation significantly reduced median pulmonary artery pressure from 26 mmHg to 19.5 mmHg at last follow-up (p<0.05), with delayed normalization in CHD patients.
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