Thorac Cardiovasc Surg 2024; 72(S 02): S69-S96
DOI: 10.1055/s-0044-1780723
Sunday, 18 February
Katheterinterventionen im Kindesalter

Real-Time Biventricular Pressure–Volume Loops during Percutaneous Pulmonary Valve Implantation in Patients with RVOT Dysfunction

H. Latus
1   Centre for Congenital Heart Disease, Stuttgart, Deutschland
2   German Heart Centre Munich, Munich, Deutschland
,
V. Schindler
1   Centre for Congenital Heart Disease, Stuttgart, Deutschland
,
J. Cleuziou
2   German Heart Centre Munich, Munich, Deutschland
,
M. Khalil
3   University Hospital Giessen, Giessen, Deutschland
,
C. Jux
3   University Hospital Giessen, Giessen, Deutschland
,
C. Meierhofer
2   German Heart Centre Munich, Munich, Deutschland
,
D. Tanase
2   German Heart Centre Munich, Munich, Deutschland
,
A. Eicken
4   German Heart Centre Munich, München, Deutschland
,
P. Ewert
2   German Heart Centre Munich, Munich, Deutschland
,
S. Georgiev
2   German Heart Centre Munich, Munich, Deutschland
› Author Affiliations
 

    Background: In patients with RVOT stenosis and/or pulmonary regurgitation, percutaneous pulmonary valve implantation (PPVI) aims to preserve right (RV) and left (LV) ventricular integrity and function. Our study thought to assess acute changes in biventricular intrinsic myocardial function occurring with PPVI.

    Methods: Twenty patients with RVOT dysfunction (age 23.0 ± 10.9 years, 9 females, mean peak echocardiographic RVOT gradient 64 ± 25 mm Hg) underwent PPVI with biventricular assessment of pressure–volume loops using conductance catheter technique during the same catheterization. Load-independent parameters of systolic (Ees) and diastolic (Eed) function as well as pulmonary/systemic arterial elastance (Ea) and V–A coupling (Ea/Ees) were assessed before and directly after PPVI. Cardiac magnetic resonance (CMR) for quantification of biventricular volumes, function and pulmonary regurgitation (PR) was also performed.

    Results: After PPVI, both RV Ees (p = 0.036) and pulmonary Ea (p = 0.0002) decreased significantly while right V–A coupling (p = 0.76) remained impaired. LV Ees (p = 0.68) and left V–A coupling (p = 0.98) were not affected by PPVI although systemic Ea increased significantly (p = 0.03). Both RV (p = 0.37) and LV (p = 0.20) Eed showed no significant change with PPVI. Patients with relevant PR (≥25%, n = 10) had lower RV Ees (p = 0.03) before and higher LV Eed (p = 0.01) after PPVI as compared with patients with minor PR (<25%, n = 10) whereas V-A coupling was similar between the two groups.

    Conclusion: Acute unloading of the RV by PPVI is accompanied by an instantaneous decline in RV contractility with persistent abnormal V-A coupling. The LV adequately adapts to an increase in pre- and afterload with unchanged LV intrinsic function and V–A coupling. The relevance of these response patterns on long-term biventricular remodeling require further investigation.


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    No conflict of interest has been declared by the author(s).

    Publication History

    Article published online:
    13 February 2024

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