Thorac Cardiovasc Surg 2020; 68(S 02): S79-S101
DOI: 10.1055/s-0040-1705565
Short Presentations
Monday, March 2nd, 2020
Intensive Care Medicine
Georg Thieme Verlag KG Stuttgart · New York

Increased Aortic Pulse Wave Velocity Has Impact on Clinical Course of the Fontan Circulation

M. Walser
1   München, Germany
,
M. Dietl
1   München, Germany
,
M. Hermann
1   München, Germany
,
F. Langhammer
1   München, Germany
,
G. Mandilaras
1   München, Germany
,
A. Lehner
1   München, Germany
,
S. Ulrich
1   München, Germany
,
R. Dalla-Pozza
1   München, Germany
,
N. Haas
1   München, Germany
,
A. Jakob
1   München, Germany
› Author Affiliations
Further Information

Publication History

Publication Date:
13 February 2020 (online)

 

    Objectives: Pulse wave velocity (PWV) increases with aortic stiffness which, in turn, affects cardiac function. The influence of univentricular heart-physiology, such as in Fontan’s circulation on aortic stiffness, is unknown. Purpose of this study was to investigate PWV, invasively measured during heart catheter in patients with Fontan’s circulation, compared with “normal heart” physiology. Furthermore the association of PWV with other Fontan’s hemodynamic parameters with a possible clinical implementation was studied.

    Methods: Seventeen Fontan’s patients with a breakdown of: hypoplastic left heart syndrome (n = 11), tricuspid atresia (n = 3), double inlet left ventricle (n = 2), unbalanced AVSD (n = 1), and double-outlet left ventricle with uncommitted VSD (n = 1) compared with 17 age- and sex-matched normal heart physiology controls (heart-transplant patients) were enrolled to this study. Mean age was 17.2 ± 9.1 (Fontan’s group) versus 16.4 ± 5.2 years (control group) with 7 males in each group. The PWVs were assessed for the ascending aorta and the aortic arch. Pressure puls waves were simultaneously documented from the catheter in the aortic position and arteria femoralis sheath. Via arterial pulse wave time delay between both puls waves and the distance between the PWV could be calculated. Additionally, central arterial pressure (cBP), venous pressure (ZVD), pulmonary artery pressure (PAP), and cardiac index (CI) were assessed.

    Result: Fontan’s patients had a significantly higher PWV in both measurement positions (AO asc.: 5.3 ± 1.5 vs. 4.8 ± 0.6 m/s; AO desc. 5.1 ± 1.5 vs. 4.6 ± 0.6 m/s; p < 0,05). The other hemodynamic parameters were not significantly different between both groups. Within the Fontan group, PWV differed not significantly between individual cardiac pathologies but there was a significant correlation between PWV and cBP (Pearson’s coefficient &≥ 0,4; p < 0,05). Furthermore, PWV had a moderate but not significant positive correlation with ZVD and PAP and negative correlation with the CI.

    Conclusion: PWV as a surrogate marker for arterial stiffness is increased in the Fontan patients. A tendency toward higher PWV in elevated the Fontan pressures may help to early predict changes in Fontan’s circulation. Therefore, monitoring arterial stiffness, also with ambulatory PWV measurement tools, may help to early predict a failing Fontan’s physiology. However, this is only an explorative study and further investigation in this field is needed.


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