Transcatheter aortic valve implantation improves left ventricular function and hemodynamics and reduces severe ventricular arrhythmias in patients with severe aortic stenosis

Abstract

Objective

To assess changes in LV function, hemodynamics, and ventricular arrhythmias (VAs) after transcatheter aortic valve implantation (TAVI) in severe aortic stenosis (AS) patients at 1-month and 1-year follow-up.

Methods

Eighty severe AS patients undergoing TAVI were analyzed after exclusions (prior pacemaker, post-TAVI complications, death, or missing data). Echocardiography (left ventricular ejection fraction [LVEF], left ventricular end-diastolic diameter [LVEDD], mean transaortic gradient), NT-proBNP levels, and 24-h Holter monitoring (modified Lown grading for VAs) were evaluated pre-TAVI, at 1 month, and 1 year post-TAVI.

Results

At 1 month, LVEF improved from 41.5 ± 7.8% to 48.0 ± 6.0% (P = 0.034), LVEDD decreased from 56.6 ± 11.5 mm to 54.0 ± 11.0 mm (P = 0.020), and mean gradient dropped from 54.8 ± 9.5 mmHg to 18.2 ± 4.5 mmHg (P < 0.001). NT-proBNP decreased from 3870 pg/mL (IQR: 780–26500) to 1015 pg/mL (IQR: 550–8500) (P < 0.01). Lown grade 3–4 VAs declined from 33.8% to 17.5% (P = 0.030). At 1 year, LVEF further improved to 51.5 ± 5.5% (P < 0.001), LVEDD to 52.5 ± 10.8 mm (P < 0.01), and mean gradient to 15.5 ± 4.0 mmHg (P < 0.001). NT-proBNP remained low (850 pg/mL, IQR: 450–15500; P < 0.001), and Lown 3–4 VAs decreased to 12.5% (P < 0.001). Ventricular tachycardia incidence reduced from 12.5% pre-TAVI to 5.0% at 1 year (P = 0.016).

Conclusion

TAVI significantly improves LV function, promotes reverse remodeling, and reduces severe VAs in severe AS patients, with sustained benefits at 1 year, highlighting its positive impact on cardiac structure, function, and arrhythmic burden.

Introduction

Aortic stenosis (AS) is the most common valvular heart disease in developed countries, primarily affecting the elderly population due to calcific degeneration of the aortic valve [1]. Severe AS imposes a significant pressure overload on the left ventricle (LV), leading to LV hypertrophy, diastolic dysfunction, and eventually systolic failure [2]. These hemodynamic derangements contribute significantly to symptoms and increase the risk of heart failure and mortality [3]. Patients with symptomatic severe AS have a dismal prognosis if left untreated, with mortality rates approaching 50% at 2 years [4]. Ventricular arrhythmias (VAs), ranging from premature ventricular contractions (PVCs) to non-sustained or sustained ventricular tachycardia (VT) and ventricular fibrillation (VF), are frequently observed in patients with severe AS [5, 6]. These arrhythmias are significant contributors to syncope, heart failure exacerbations, and sudden cardiac death (SCD), which is a major cause of mortality in this patient group [3]. The mechanisms underlying VAs in AS are multifactorial, including myocardial ischemia, LV hypertrophy, fibrosis, and electrolyte imbalances secondary to neurohormonal activation [6, 7].

For several decades, surgical aortic valve replacement (SAVR) has been the gold standard treatment for symptomatic severe AS, offering significant improvements in symptoms, LV function, and survival [4]. However, a substantial proportion of patients, particularly elderly individuals with multiple comorbidities, are considered high-risk or inoperable for SAVR [8]. Transcatheter aortic valve implantation (TAVI) has emerged as a less invasive and effective alternative for these patients, and its indications have progressively expanded to intermediate and even low-risk populations [4, 9]. TAVI has been shown to improve hemodynamics, alleviate symptoms, and enhance survival rates comparable to or, in some cohorts, superior to SAVR [9, 10].

The well-documented benefits of TAVI include immediate relief of aortic valve obstruction, leading to improvements in LV hemodynamics and promoting reverse LV remodeling [11, 12]. Studies have consistently demonstrated improvements in left ventricular ejection fraction (LVEF), reductions in LV mass and end-diastolic diameter (LVEDD), and decreases in biomarkers such as N-terminal pro-B-type natriuretic peptide (NT-proBNP) post-TAVI. Despite these benefits, the impact of TAVI on the burden of VAs is less clearly defined, with existing studies reporting varied outcomes. Some studies suggest a reduction in VA frequency and complexity post-TAVI, potentially mediated by the relief of pressure overload, regression of LV hypertrophy, and improvement in myocardial perfusion [11, 13]. For instance, Tempio et al. [14] reported a significant decrease in severe VAs at 1 month and 1 year post-TAVI. However, other reports indicate that new-onset VAs or even conduction disturbances requiring pacemaker implantation can occur following TAVI, possibly related to procedural trauma or inflammation [15]. Data from Chinese cohorts, where TAVI is a rapidly evolving field, remain relatively scarce concerning changes in both cardiac function, hemodynamics, and VA profiles post-procedure, especially with longer-term follow-up.

Given the prognostic importance of LV function, favorable remodeling, and VAs in patients with AS and the increasing utilization of TAVI, a better understanding of how TAVI influences these comprehensive cardiac parameters over time is crucial for risk stratification and management. Therefore, this study aimed to retrospectively evaluate echocardiographic parameters (LVEF, LVEDD, mean transaortic pressure gradient), NT-proBNP levels, and the incidence and severity of VAs before TAVI and at one month and one year after TAVI in patients with symptomatic severe AS, and to identify potential factors associated with changes in VA burden at one month.

Methods

Study population and design

This was a single-center, retrospective observational study. We continuously collected data from patients with symptomatic severe AS who underwent TAVI at The Second Hospital of Hebei Medical University between January 1, 2022, and May 31, 2024. All patients received self-expanding aortic valve prostheses, including Venus A (Venus Medtech, Hangzhou, China) [16] or VitaFlow (MicroPort, Shanghai, China) [17]. Inclusion criteria were: [1] elderly patients (defined as age ≥ 70 years) with degenerative calcific severe AS; [2] clinical symptoms attributable to AS (Stage D) or reduced cardiac function (defined as LVEF < 50%); [3] contraindication or high risk for SAVR; [4] anatomical suitability for TAVI according to established guidelines [9]; [5] life expectancy >1 year. Exclusion criteria were: [1] permanent pacemaker implantation (PPM) for other reasons before TAVI; [2] new PPM due to bradyarrhythmias post-TAVI; [3] all-cause mortality within 30 days post-TAVI; [4] missing baseline (pre-TAVI) or 1-month or 1-year follow-up data for primary endpoints (including 24-hour Holter monitoring, critical echocardiographic parameters, or NT-proBNP); [5] loss to follow-up. Exclusion of patients requiring new PPM was to avoid the confounding effects of ventricular pacing on the analysis of spontaneous VAs and on the assessment of LV reverse remodeling. Patients with early mortality were excluded to allow for a focused analysis of cardiac remodeling and arrhythmic changes over the complete follow-up period in survivors. We acknowledge that these exclusions may introduce a selection bias, which is noted as a study limitation. The study was approved by the Ethics Committee of The Second Hospital of Hebei Medical University, and all patients or their legal guardians provided written informed consent.

Patient inclusion

From January 1, 2022 to May 31, 2024, a total of 97 patients with symptomatic severe AS undergoing TAVI at The Second Hospital of Hebei Medical University were prospectively screened for eligibility. Of these, 17 patients were excluded for the following reasons: history of PPM before TAVI (n = 1), new PPM due to post-TAVI complications (n = 8), death within 30 days post-procedure (n = 3), absence of critical baseline or 1-month or 1-year follow-up data for primary endpoints (n = 4), and loss to follow-up (n = 1). Consequently, the final analysis included 80 patients who had complete echocardiographic, NT-proBNP, and Holter data at baseline, 1 month, and 1 year (Fig. 1).

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Peri-procedural management and TAVI technique

All TAVI procedures were performed under general anesthesia. Pre-procedural planning involved detailed imaging assessment of access routes, including femoral and alternative approaches such as transcarotid (Fig. 2A and D). The transfemoral approach was the primary access route; patients unsuitable for transfemoral access underwent TAVI via the transcarotid approach. Intra-procedural imaging guided valve deployment (Fig. 2B and C). A temporary pacemaker was inserted via the jugular vein during the procedure, with rapid ventricular pacing (180 beats/min) employed during balloon valvuloplasty (if performed) and valve deployment. The temporary pacemaker was typically maintained for 24 h post-procedure. Valve sizing was based on the “Hangzhou experience“ [18]. Optimal valve implantation depth was targeted at 4–6 mm below the aortic annulus. After complete valve deployment, an aortogram was performed, and transesophageal echocardiography was used to assess valve function and identify any complications such as paravalvular leak.

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Echocardiographic and biomarker assessment

Comprehensive transthoracic echocardiography was performed by experienced sonographers according to American Society of Echocardiography guidelines at baseline (pre-TAVI), 1 month post-TAVI, and 1 year post-TAVI. Key parameters included LVEF (calculated using the biplane Simpson’s method), LVEDD, and mean transaortic pressure gradient. Aortic valve velocity was measured using continuous-wave Doppler from multiple acoustic windows (apical, right parasternal, and suprasternal), with the highest velocity used for analysis. Additional parameters included LV mass index (LVMI), relative wall thickness (RWT), stroke volume index (SVI), and the ratio of early mitral inflow velocity to mitral annular early diastolic velocity (E/e’). N-terminal pro-B-type natriuretic peptide (NT-proBNP) levels were also measured at these time points. Representative echocardiographic images demonstrating LV remodeling and hemodynamic improvement post-TAVI are shown in Fig. 3. The changes in these parameters over time are summarized in Table 1.

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Ventricular arrhythmia assessment

Twenty-four-hour Holter monitoring was performed before TAVI and at 1 month and 1 year post-TAVI to evaluate the occurrence of VAs. VAs were classified according to the modified Lown grading system [19]: Grade 0: No premature ventricular contractions (PVCs). Grade 1: Occasional, isolated PVCs (all hourly intervals with < 30 PVCs/hour). Grade 2: Frequent, isolated PVCs (any hourly interval with ≥ 30 PVCs/hour). Grade 3: Multiform PVCs. Grade 4a: Couplets (paired PVCs). Grade 4b: Ventricular tachycardia (VT), defined as ≥ 3 consecutive PVCs at a rate >100 beats/min. Severe VAs were defined as modified Lown grade 3 or 4 (4a and 4b).

Data collection

Baseline demographic data, clinical characteristics, baseline echocardiographic parameters, NT-proBNP levels, and procedural details were collected (Table 2). The Society of Thoracic Surgeons (STS) Predicted Risk of Mortality score was calculated. Atherosclerotic cardiovascular disease (ASCVD) was defined as a history of acute coronary syndrome, myocardial infarction, stable angina, coronary revascularization, stroke or transient ischemic attack of atherosclerotic origin, or peripheral artery disease or revascularization [20]. Baseline 12-lead electrocardiograms were analyzed for QRS duration and corrected QT (QTc) interval. Quality of life was assessed using the Kansas City Cardiomyopathy Questionnaire (KCCQ) summary score [21]. Follow-up echocardiographic parameters, NT-proBNP levels, and Holter data were collected at 1-month and 1-year follow-up.

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Statistical analysis

Statistical analysis was performed using SPSS version 27.0 (IBM Corp., Armonk, NY, USA). Categorical variables are presented as counts and percentages (%), and differences between groups were assessed using the chi-square test or Fisher’s exact test as appropriate. Continuous variables with a normal distribution are presented as mean ± standard deviation (SD), and differences between groups were assessed using the independent samples t-test. Non-normally distributed continuous variables are presented as median (interquartile range, IQR: 25th percentile, 75th percentile), and differences were assessed using the Mann-Whitney U test. For paired comparisons of echocardiographic parameters, NT-proBNP levels (baseline vs. 1 month, baseline vs. 1 year, and 1 month vs. 1 year), and VA data (pre- vs. post-TAVI at 1 month and 1 year), the paired t-test or Wilcoxon signed-rank test was used for continuous variables, and McNemar’s test for categorical variables. Changes between 1-month and 1-year follow-up were also assessed using appropriate paired tests. A two-sided P-value < 0.05 was considered statistically significant. To identify independent predictors of VA improvement at 1 month, a multivariable logistic regression analysis was performed. Variables with P < 0.20 in univariate analysis and those considered clinically important were included in the model. Survival analysis was performed to assess the prognostic impact of baseline VAs. All-cause mortality during the 1-year follow-up was the primary endpoint. Survival curves were generated using the Kaplan-Meier method, and differences were compared using the log-rank test.

Results

Baseline characteristics

A total of 80 patients who met the inclusion criteria were included in the final analysis. The mean age of the patients was 76.3 ± 7.7 years, and 62.5% (n = 50) were male. The mean STS score was 4.65 ± 2.24%. Atrial fibrillation was present in 13.8% (n = 11) of patients pre-TAVI. Transthoracic echocardiography revealed an enlarged LVEDD of 56.6 ± 11.5 mm, a reduced LVEF of 41.5 ± 7.8%, and a mean transaortic pressure gradient of 54.8 ± 9.5 mmHg. The cohort presented with significant LV hypertrophy (mean LVMI 135.8 ± 28.4 g/m²) and concentric remodeling (mean RWT 0.48 ± 0.09), alongside evidence of diastolic dysfunction (mean E/e’ 16.5 ± 5.3) and reduced stroke volume index (34.1 ± 8.2 mL/m²). The median NT-proBNP level was significantly elevated at 3870 pg/mL (IQR: 780, 26500 pg/mL). Baseline 12-lead electrocardiogram analysis showed a mean QRS duration of 112.5 ± 15.8 ms and a mean QTc interval of 455.2 ± 25.1 ms. There were no statistically significant differences in these parameters between patients with and without VA improvement at 1 month, nor were there significant changes in these intervals post-TAVI (data not shown). Beta-blockers were used by 27.5% (n = 22) of patients. All patients received self-expanding aortic valves, with a mean implantation depth of 5.1 ± 1.5 mm and mean prosthesis oversizing of 18.5 ± 5.6%. Baseline characteristics are detailed in Table 2.

Changes in echocardiographic parameters and NT-proBNP Post-TAVI

Significant improvements in key echocardiographic parameters and NT-proBNP levels were observed at 1-month and 1-year follow-up post-TAVI, as detailed in Table 1. At 1-month follow-up, LVEF significantly improved from baseline (48.0 ± 6.0% vs. 41.5 ± 7.8%, P = 0.034). LVEDD decreased from 56.6 ± 11.5 mm to 54.0 ± 11.0 mm (P = 0.020). The mean transaortic pressure gradient significantly decreased from 54.8 ± 9.5 mmHg to 18.2 ± 4.5 mmHg (P < 0.001). NT-proBNP levels significantly decreased from a median of 3870 pg/mL to 1015 pg/mL (P < 0.01). At 1-year follow-up, further improvements were observed. LVEDD significantly decreased to 52.5 ± 10.8 mm compared to baseline (P < 0.01). LVEF further improved to 51.5 ± 5.5% (P < 0.001 vs. baseline). The mean transaortic pressure gradient was further reduced to 15.5 ± 4.0 mmHg (P < 0.001 vs. baseline). NT-proBNP levels remained significantly lower than baseline at 1 year (median 850 pg/mL, P < 0.001 vs. baseline). Significant reverse remodeling was evidenced by a progressive reduction in LVMI and RWT, alongside improved diastolic function (E/e’) and SVI at both follow-up points (all P < 0.05 vs. baseline, Table 1). Patient-reported quality of life significantly improved, with the mean KCCQ score rising from 45.2 ± 12.5 at baseline to 75.4 ± 14.8 at 1 year (P < 0.001) (Supplementary Table S1).

Effect of TAVI on VA incidence and severity

Compared to pre-TAVI findings, the proportion of patients with severe VAs (Lown grade 3–4) significantly decreased at 1 month post-TAVI (from 27 (33.8%) to 14 (17.5%), P = 0.030), while patients with no VAs (Lown grade 0) increased (from 5 (6.3%) to 14 (17.5%), P = 0.033) (Table 3; Fig. 2A). The incidence of VT decreased from 12.5% (10 cases) pre-TAVI to 7.5% (6 cases) post-TAVI at 1 month (P = 0.371). At 1-year follow-up, these beneficial effects were enhanced. Severe VAs further decreased to 10 cases (12.5%) (P < 0.001 vs. baseline), and the incidence of VT showed a significant reduction to 4 cases (5.0%) compared to pre-TAVI levels (P = 0.016) (Fig. 2B).

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A transition analysis at 1 month (Table 4) revealed that of the 27 patients with baseline Lown grade 3–4 VAs, 17 (63.0%) improved to grade 1–2. Concurrently, of the 48 patients with baseline grade 1–2 VAs, 35 (72.9%) remained in the same category, while 9 (18.8%) improved to grade 0. This confirms a significant net shift away from severe VAs towards less complex or no VAs.

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Predictors for VA improvement at 1 month Post-TAVI

To identify baseline predictors of VA improvement, patients were divided into two groups: Group 1 (VA improvement, n = 37) and Group 2 (VA worsening or no change, n = 43). In univariate analysis (Table 5), patients with higher baseline Lown grade VAs were significantly more likely to experience improvement (45.9% vs. 23.3%, P = 0.042). In the multivariable logistic regression analysis, including variables with P < 0.20 from univariate analysis, baseline Lown Grade > 2 VAs remained the only independent predictor of VA reduction at 1 month (Odds Ratio: 4.85; 95% CI: 1.52–15.45; P = 0.008) (Table 6).

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Prognostic impact of baseline ventricular arrhythmias

During the 1-year follow-up period, there were 7 deaths (8.8%) from all causes. To assess the prognostic significance of baseline VAs, a survival analysis was performed. Kaplan-Meier survival analysis demonstrated significantly lower 1-year survival rates in patients with severe VAs (Lown grade 3–4) at baseline compared to those with non-severe VAs (Lown grade 0–2) (81.5% vs. 96.2%; log-rank P = 0.041) (Fig. 3).

Discussion

This study demonstrates that in symptomatic patients with severe AS, TAVI leads to significant and sustained improvements in left ventricular systolic function, promotes favorable LV remodeling, normalizes transvalvular hemodynamics, and decreases myocardial wall stress. Concurrently, VAs are also significantly reduced following TAVI. The key finding is that TAVI leads to a significant reduction in the incidence of severe VAs (Lown grade 3–4) at 1-month follow-up, and these beneficial effects are sustained and even further improved at 1-year follow-up.

The relationship between AS and LV dysfunction and VAs is well-established [5,6,7, 22]. The chronic pressure overload in AS leads to LV hypertrophy, myocardial fibrosis, and subendocardial ischemia, impairing both systolic and diastolic function and creating an arrhythmogenic substrate [7, 23]. The presence of complex VAs in these patients is not a benign finding and has been linked to adverse outcomes, including sudden cardiac death, as demonstrated by Holter monitoring studies showing high rates of complex premature ventricular contractions (48%) and non-sustained ventricular tachycardia (9–29%) in severe AS patients, with reduced survival associated with these arrhythmias [24]. Our study observed a significant improvement in LVEF, a reduction in LVEDD, LVMI, and RWT, and a decrease in NT-proBNP levels post-TAVI. This hemodynamic and structural improvement is a direct consequence of relieving the valvular obstruction, which reduces LV wall stress and allows for reverse remodeling. This likely contributes to the observed reduction in severe VAs by favorably modifying the underlying arrhythmogenic substrate. The regression of LV hypertrophy and fibrosis are longer-term processes [25], and our 1-year data support the ongoing positive impact of TAVI on cardiac structure and function, which in turn influences arrhythmic potential.

Furthermore, our survival analysis suggests that the baseline burden of severe VAs is associated with significantly worse 1-year survival. This finding elevates the clinical importance of the observed VA reduction post-TAVI, suggesting it may correlate not only with improved cardiac function but also with better long-term outcomes. By alleviating the hemodynamic stressors that contribute to arrhythmogenesis, TAVI may mitigate the long-term risk conferred by VAs in this high-risk population.

Beyond objective measures, these structural and functional improvements translated into a profound enhancement of patient-reported quality of life, as measured by the KCCQ score in our cohort (Supplementary Table S1). This underscores the significant symptomatic relief provided by TAVI. The importance of assessing QoL and the consistent finding that TAVI improves functional status and well-being are well-documented, as thoroughly reviewed by Metra et al. [26].

An important consideration in the post-TAVI electrical milieu is the high incidence of new conduction disturbances. In our cohort, 22.5% of patients developed a new LBBB, a common finding with self-expanding valves that is linked to implantation depth and prosthesis oversizing [27]. While the development of persistent LBBB is often associated with the need for future pacemakers and may impact LV function, the prognosis of temporary LBBB is more debated. For instance, a recent study by Leone et al. found that temporary LBBB after TAVI did not have a significant impact on 1-year mortality, highlighting the complex and varied nature of post-procedural conduction changes [28].

Our transition analysis (Table 4) clarifies that the stable number of patients with mild-to-moderate VAs post-TAVI is a net result of a significant downgrade from severe VAs, balanced by a smaller portion of patients developing new, non-severe VAs. The sustained reduction in VT observed at 1 year suggests that for many patients, the initial benefits are not transient. Our multivariate analysis identified baseline Lown grade > 2 VAs as the sole independent predictor for VA reduction. This suggests that patients with a higher burden of severe VAs at baseline are most likely to benefit from TAVI in terms of arrhythmia reduction.

This study has several limitations. First, its retrospective, single-center design limits the generalizability of our findings and may be subject to selection bias related to local referral patterns and operator experience. Unmeasured confounders could influence both the outcomes and the observed associations. Second, the exclusion of patients who required a new PPM or died within 30 days introduces a significant survivorship and selection bias. This per-protocol approach likely overestimates the true benefits of TAVI on VAs and cardiac remodeling in an unselected, all-comer population. The results should therefore be interpreted as the potential changes in a lower-risk cohort that survives the early post-procedural period without major conduction complications. Third, 24-hour Holter monitoring may not capture the true day-to-day variability of the VA burden; longer monitoring could provide more comprehensive data. Furthermore, we did not track longitudinal changes in medications such as beta-blockers or other antiarrhythmic drugs during the follow-up period, which could have influenced the observed VA trends. Fourth, the use of the modified Lown classification, while descriptive, is a historical scale that may not be as sensitive as modern quantitative metrics. A more detailed analysis using PVC burden (as a percentage of total heartbeats) and the duration and rate of NSVT episodes would provide a more robust assessment of the arrhythmic substrate.

Conclusion

Transcatheter aortic valve implantation is associated with a significant and sustained improvement in left ventricular systolic function, a reduction in left ventricular dimensions and hypertrophy, and normalization of transaortic hemodynamics in patients with severe aortic stenosis. Concurrently, TAVI significantly reduces the incidence and severity of VAs, particularly complex VAs. These benefits translate into improved quality of life and are maintained at 1-year follow-up. Patients with a higher burden of severe VAs at baseline are most likely to experience a reduction in VAs post-TAVI. These findings underscore the comprehensive efficacy of TAVI in reversing the adverse cardiac consequences of severe AS.

Data availability

The datasets analyzed during the current study are not publicly available due to personal privacy but are available from the corresponding author on reasonable request.

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