Clin Res Cardiol (2022). https://doi.org/10.1007/s00392-022-02002-5
Echocardiographic Characterization of Cardiac Remodeling after TAVI
N. Licari1, K. Lenk1, J. Kandels1, D. Jurisch1, U. Laufs1, A. Hagendorff1, S. Stöbe1
1Klinik und Poliklinik für Kardiologie, Universitätsklinikum Leipzig, Leipzig;
Purpose: This retrospective study aimed to characterize left ventricular (LV) remodelling in patients with aortic stenosis (AS) after transcatheter aortic valve implantation (TAVI).

Methods and Results:  98 patients (79 ± 7 years; 60% male) after TAVI implantation due to severe AS were included. All patients underwent TAVI procedure from April 2016 to June 2020. Transthoracic echocardiography (TTE) was performed shortly before and at follow-ups 3 and 12 months after TAVI. Patients were divided into 4 subgroups defined by pre-interventional flow conditions and pressure gradients according to the proposal of Lancellotti et al. (2018):
1. (1)    low flow/low gradient-AS (LFLG, n=29),
2. (2)    normal flow/low gradient-AS (NFLG, n=33),
3. (3)    low flow/high gradient-AS with (LFHG, n=12) and
4. (4)    normal flow/high gradient-AS (NFHG, n=24).

EOA, mean pressure gradient (PGmean), interventricular septal wall thickness (IVST) and relative wall thickness (RWT) were significantly lower 3 months after TAVI and remained significantly different after 12 months. LV global longitudinal strain (LV GLS) and left atrial (LA) strain significantly improved 3 months after TAVI, although improvements of LA strain did not persist after 12 months. Regarding all echocardiographic parameters there were no further significant differences between 3 and 12 months after TAVI. LV ejection fraction (LVEF) showed normal values in all subgroups and did not differ significantly between the baseline group and the follow up groups (Table 1).

Criteria for patient-prosthesis-mismatch (PPM) (e.g., indexed EOA ≤ 0.85cm2/m2; maximum transprosthetic flow velocity (Vmax) ≥ 3.0m/s and PGmean ≥ 20mmHg) were not fulfilled. However, in some subgroups TAVI patients with Vmax > 3m/s were observed (LFLG-AS: 0% (n=0/29), NFLG-AS: 0% (n=0/33), LFHG-AS: 8.3% (n=1/12), NFHG-AS: 8.3% (n=2/24)).

Variables

Baseline

(N=98)

3 months after TAVI (N=98)

12 months after TAVI (N=55)

p-value

EOA (cm2/m2)

0.41 ± 0.09*†

1.0 ± 0.29

1.0 ± 0.28

< 0.001

PGmean (mmHg)

38.4 ± 12.5*†

10.4 ± 12.5

9.2 ± 4.4

< 0.001

LVEDV (ml)

124.6 ± 36.0

120.7 ± 33.6

124.4 ± 36.5

0.702

LVEF (%)

60.0 ± 8.7

60.7 ± 9.3

58.9 ± 8.7

0.490

LVMi (g/m2)

155.8 ± 42.6

148.5 ± 35.4

148.1 ± 39.9

0.343

LV GLS (%)

-12.3 ± 3.4*†

-13.9 ± 3.9

-13.7 ± 3.9

0.007

IVST (mm)

13.3 ± 2.3*†

12.4 ± 2.1

12.5 ± 2.1

0.010

RWT

0.56 ± 0.1*†

0.52 ± 0.1

0.53 ± 0.1

0.017

LAEDV (ml)

73.1 ± 24.8

68.3 ± 30.4

71.6 ± 32.6

0.498

LA strain (%)

18.0 ± 10.2*

20.9 ± 10.7

20.6 ± 12.6

0.144
















Table 1. Echocardiographic parameters before, 3 and 12 months after TAVI. 

*p < 0.05 Baseline vs. 3 months after TAVI; †p < 0.05 Baseline vs. 12 months after TAVI.

 

Conclusions: TAVI seems to have a significant impact on cardiac remodeling, which can be documented by a decrease of RWT indicating reverse LV remodelling. Further, the improvement of LV GLS indicates a potential recovery of  longitudinal deformation of the left ventricle.
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