235 Ventricular arrhythmias and cardiac autonomic function in patients with severe aortic valve stenosis before and after transcatheter aortic valve implantation
Authors: Telesca Alessandro , Gnan Eleonora , De Vita Antonio , Tremamunno Saverio , Felici Tamara , Ravenna Salvatore Emanuele , Filippo Crea , Lanza Gaetano Antonio 
Published: December 2021

Aims

Transcatheter aortic valve implantation (TAVI) has become a first-line treatment for most patients with severe aortic stenosis (AS) at intermediate/high surgical risk, resulting in significant improvement of clinical outcome. However, whether ventricular arrhythmias (VAs) or cardiac autonomic dysfunction influence outcome and whether TAVI has any effects on VAs and cardiac autonomic function is unknown. Thus, this study was aimed to investigate: I1) whether VAs and autonomic dysfunction [as assessed by heart rate variability (HRV)] are associated with clinical outcome and (2) the effects of TAVI on VAs and HRV, in patients with severe AS.

Methods and results

We studied 71 consecutive patients with severe aortic stenosis, admitted to our department of Cardiovascular Medicine to undergo TAVI. Patients with previous cardiac surgery, percutaneous coronary revascularization, acute coronary syndrome, and other significant heart valve disease or relevant comorbidities were excluded. The day before TAVI all patients underwent transthoracic Doppler echocardiography (TTDE), including global longitudinal strain (GLS) assessment, and 24-h ECG Holter monitoring (HM), to assess VA burden and HRV. A clinical follow-up was performed at 6 months from discharge. Furthermore, TTDE and 24-h HM were performed at follow-up in 38 (54.5%) and 29 (40.8%) patients, respectively. The primary endpoint was the occurrence of major clinical events (MACE), that include death, hospitalization for cardiac causes, pacemaker implantation, myocardial infarction, or stroke. Of 71 patients (48 female, mean age 80.5 ± 6.5 years) enrolled in the study, a 6-month clinical follow-up could be performed in 54 (76%). MACE occurred in 21 patients (38.9%), 8 of whom (14.8%) had hospitalization for heart failure, 13 (24%) required pacemaker implantation, and 3 had stroke (5.6%). Compared to baseline, at follow-up the mean aortic valve gradient (50.6 ± 11.4 vs. 8.38 ± 3.23 mmHg, P &lt; 0.001), left ventricle (LV) mass index (131.4 ± 38.9 vs. 112.9 ± 28.3 g, P = 0.007), pulmonary artery systolic pressure (37.3 ± 5.8 vs. 30.2 ± 9.8 mmHg; P &lt; 0.001), and the ratio of Doppler transmitral early filling velocity to tissue-Doppler early diastolic mitral annular velocity (E/e′) (16 ± 5.3 vs. 13.2 ± 4.7 P &lt; 0.001) were significantly reduced. In contrast no changes were observed in VAs. The number of premature ventricular complexes (PVCs) at HM was indeed 1062 ± 3833 vs. 1206 ± 3322 at follow-up and baseline, respectively (P = 0.11). Furthermore, PVCs &gt;10 per hour were detected in a higher number of patients at 6-month follow-up, compared to baseline (23.8% vs. 45.2%; P = 0.022). No significant differences were detected in most time-domain and frequency-domain HRV parameters. Unexpectedly, SDNNi (62.8 ± 19.1 vs. 41.9 ± 16.5; P = 0.008), RMSSD (54.6 ± 36.6 vs. 30.1 ± 17.9; P = 0.024) and VLF (56.4 ± 49.6 vs. 29 ± 12.7; P = 0.028) were found to be significantly higher at follow-up compared to baseline.

Conclusions

Our data show that, in patients with severe AS, TAVI does not seem to have significant effects on VA burden, despite echocardiographic and clinical improvement. Similarly, our data failed to show significant improvement of sympatho-vagal balance at follow-up compared to baseline in these patients.