Diastolic Dysfunction in Congenital Heart Disease: A Pressure-Volume Loop Analysis of Borderline Left Heart
Authors' conclusion
The primary mechanism of diastolic dysfunction in bLV is increased passive ventricular stiffness, while no differences were detected in active relaxation. These findings suggest a limited role for lusitropic medications and therapeutic strategies that focus on mitigating ventricular stiffness (such as surgical endocardial fibroelastosis resection) may be more valuable.
Study context
- Population
- Children with borderline left heart (bLV), compared with patients with congenitally corrected transposition of the great arteries
- Participants
- 13 vs 14
- Comparison
- bLV versus congenitally corrected transposition of the great arteries (ccTGA)
- bLVn = 13
- ccTGAn = 14
- Outcome
- τ (isovolumetric relaxation time constant)
Methodological detailsinvasive pressure-volume (PV) loops, transient preload alteration
- Invasive PV loops
- Transient preload alteration
Main finding
As reported in the abstract
P = 0.11
Further findings
Iβ (indexed stiffness constant) · higher in bLV
P = 0.003
| Outcome | bLV | ccTGA | P value |
|---|---|---|---|
| dP/dt min /peak systolic pressure | −10.6 (range as printed −11.0–-9.4) s - 1 | −9.9 (range as printed −10.5–-8.7) s - 1 | P = 0.17 |
| β w (dimensionless stiffness constant)Higher in bLV | 4.08 (range as printed 1.6–7.52) | 1.21 (range as printed 0.95–1.77) | P = 0.002 |
End-diastolic PV relationship
- Shifted upward and to the left in bLV
Original publication
Diastolic Dysfunction in Congenital Heart Disease: A Pressure-Volume Loop Analysis of Borderline Left Heart. Circ Heart Fail. Published 28 October 2026. doi:10.
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