Impact on clinical outcome of ventricular arrhythmias in patients undergoing transcatheter aortic valve implantation (TAVI)

Abstract

Abstract Background Transcatheter aortic valve implantation (TAVI) in the treatment of severe aortic stenosis has considerably grown in the latest years. There are limited data, however, about predictors of long-term prognosis in this population. Particularly, whether ventricular arrhythmic burden is associated with clinical outcome has poorly been investigated. Purpose The aim of our study was to investigate the association between ventricular arrhythmias and adverse clinical outcomes in patients undergoing TAVI. Methods We performed a 24-hour 3-channel ECG Holter monitoring (HM) in 267 consecutive patients who underwent TAVI for severe aortic stenosis at our Centre within 30 days from a successful procedure (average 10.2 days, range 2-30). For each patient we obtained the number of premature ventricular complexes (PVCs) and the presence of non-sustained ventricular tachycardia (NSVT, >3 PVCs with a rate >100 bpm). Frequent PVCs were defined as the presence of at least 30 PVCs per hour. We also collected clinical and echocardiographic findings for each patient. Assessment of clinical events at follow-up was performed by clinical visits or telephone interviews of patients or relatives (in case of fatal events). The primary endpoint of the study was the occurrence of cardiovascular events (CVE), a composite of cardiovascular death and resuscitation from cardiac arrest. All-cause-mortality was assessed as secondary endpoint. Survival Cox regression was applied to assess the univariate and multivariate association of clinical, echocardiographic and HM variables with endpoints. Results Clinical outcome could be obtained for 228 patients (85%), for an average follow-up of 3.5 years (range 1.0-8.6). Among these patients, frequent PVCs (≥30/hour) and episodes of NSVT at HM were found in 47 (20.6%) and 52 (22.4%) patients, respectively. CVE occurred in 26 patients (11.4%) and 63 patients died (27.6%). Frequent PVCs at HM were detected in 12 patients with (46.2%) and 35 patients without (17.3%) CVE (HR 2.29; 95% CI 1.03-5.09; p=0.04). One or more episodes of NSVT were detected in 9 patients with (34.6%) and 43 patients without (21.3%) CVE (HR 2.29; 95% CI 1.03-5.09; p=0.04), although it was not predictive of all-cause mortality (HR 1.18; 95% CI 0.48-2.77; p=0.52). Both the presence of PVCs>30/hour (HR 1.19; 95% CI 0.69-2.08; p=0.53) and NSVT (HR 0.93; 95% CI 0.52-1.65; p=0.22) were not significantly associated with all-cause mortality. Moreover, no clinical (age, gender, cardiovascular risk factors) and echocardiographic (aortic valve area, trans-aortic mean gradient, left ventricle mass and ejection fraction) variable showed significant association with both the primary and secondary outcome in our patients. Conclusions In our study the detection of frequent PVCs at HM after TAVI was a major predictor of CVE (cardiovascular death/cardiac arrest), suggesting that a 24-hour HM after TAVI can be helpful for risk stratification of these patients.