Listening to the Right Ventricle: Invasive Hemodynamics to Refine Risk Before Ventricular Tachycardia Ablation

1.

Urgent ventricular tachycardia (VT) ablation in patients with structural heart disease is inherently high‐risk, yet in carefully selected cases it can prove life‐altering. These patients may be hemodynamically unstable at presentation and often in VT storm. The importance of robust peri‐procedural support, contingency planning, and bail‐out strategies cannot be overstated [1]. Against this backdrop, identifying which patients are most vulnerable to decompensation and adverse outcomes continues to present a clinical challenge. While structured scoring tools can help guide pre‐, intra‐, and post‐procedural decision‐making [2, 3, 4], outcome heterogeneity persists even within high‐risk score cohorts. This suggests that currently available clinical scores have not fully captured the spectrum of hemodynamic vulnerability in this population.

In this issue of the Journal of Cardiovascular Electrophysiology, Calcagno and colleagues aim to address this gap with a retrospective analysis of the prognostic value of invasive right ventricular (RV) functional assessment in 102 patients undergoing urgent inpatient VT ablation in a high‐volume referral center [5]. This was a selected subset of patients who had information from right heart catheterization (RHC), which was performed per standard clinical practice within the preceding 12 months, often unrelated to their VT or the ablation procedure. The central finding is that an elevated right atrial pressure to pulmonary capillary wedge pressure ratio (RAP:PCWP > 0.6) was independently associated with acute kidney injury (AKI) after ablation (OR 10.4, 95% CI 2.4‐14.1; p = 0.002) and with intraprocedural hemodynamic instability (OR 6.1, 95% CI 1.5‐16.3; p = 0.050). The pulmonary artery pulsatility index (PAPi) failed to demonstrate a significant association with any of the pre‐specified outcomes.

The physiologic rationale for these findings is intuitive. During VT, diastole is curtailed, LV preload is reduced, and forward flow is impaired. In a patient with preserved biventricular reserve, compensatory increases in venous return and RV contractility can partially mitigate this hemodynamic perturbation. In a patient with disproportionate right‐sided dysfunction, this compensatory mechanism is limited. The RAP:PCWP ratio highlights the mismatch between RV and LV filling dynamics, with a ratio exceeding 0.6, suggesting venous congestion and impaired preload reserve [6]. PAPi reflects the pulsatile RV stroke work, a surrogate of acute RV contractile reserve [7]. In the presence of elevated pulmonary artery pressures or significant left‐sided filling pressure elevation (both common in this cohort), the pulsatile component of the RV is distorted and may explain why it was not associated with adverse outcomes in the study. The study also makes an important negative finding that LVEF below 25% was not independently associated with adverse outcomes. This is not a new observation, but it reinforces the notion that systolic function alone is an inadequate surrogate for the hemodynamic reserve in this patient population [4].

Several methodological considerations deserve acknowledgment. The inclusion of RHC data obtained up to 12 months prior to ablation is a meaningful limitation in a condition where the hemodynamic state can evolve rapidly, though, somewhat reassuringly, the median RHC‐to‐ablation interval was 11 days. The authors attempt to address this potential limitation by performing a sensitivity analysis restricted to patients with RHC within 3 months of ablation, in which directional consistency was preserved, though statistical significance was lost. Further, there was heterogeneity in the clinical setting of RHC as roughly half were performed via indwelling Swan‐Ganz catheter in the ICU and half via elective cath lab measurement. Positive‐pressure ventilation, vasopressor support, and loading conditions at the time of RHC can alter derived indices. The cohort's inclusion of nine LVAD patients warrants consideration. These patients exist in a fundamentally different hemodynamic context with LV filling pressures largely offset by continuous‐flow support, and they cannot be generalized to the broader structural heart disease population.

A subtler but important caveat is that clinicians with access to pre‐procedural RHC data may have modified their approach accordingly, thus limiting VT induction or escalating hemodynamic support in high‐risk patients, which could either attenuate or obscure the true associations reported here. The study cannot fully determine whether RAP:PCWP predicts outcomes independent of the clinical decisions it may have already influenced.

In the context of these limitations, the study addresses a critical question: whether invasive hemodynamic characterization of RV function can refine risk stratification in patients undergoing urgent VT ablation. This is important as echocardiographic RV assessment is frequently unreliable. The study's observation that four of five patients with RV dysfunction who decompensated did so following VT induction underscores the hemodynamic stress of VT in this cohort. The study raises an actionable hypothesis: an operator who identifies an elevated RAP:PCWP pre‐procedurally may elect for a more substrate‐based ablation strategy and minimize VT induction. Additional considerations in response to unfavorable RHC hemodynamic data may include pre‐emptive use of inotropic or mechanical circulatory support, avoidance of excessive vasodepressor anesthetic agents, and even postponement of the procedure in select cases. These findings should also be considered in the context of existing clinical risk scores such as PAINESD, which integrate variables such as chronic obstructive pulmonary disease, age, anesthesia, LV dysfunction, electrical storm, and diabetes to stratify procedural risk prior to VT ablation. Whether RAP:PCWP adds value beyond PAINESD is an unanswered question [2]. An RHC may provide complementary information where PAINESD captures the clinical phenotype and an RHC the hemodynamic reserve.

The investigators should be congratulated for shining a light on the importance of hemodynamic, functional assessment in the urgent VT ablation setting, where hemodynamic vulnerability is high. Additional key questions remain: how to best select which patients should undergo RHC? When should RHC be performed? Does RHC‐directed optimization actually translate to better outcomes? These questions may be best addressed with a prospective study with standardized RHC acquisition, pre‐specified hemodynamic optimization, and adequately powered endpoints including AKI, hemodynamic decompensation, and 30‐day mortality. Such a study would ideally incorporate continuous intraoperative hemodynamic monitoring to correlate baseline RV function with the trajectory of hemodynamic change during VT induction(s). Until that evidence emerges, the RAP:PCWP ratio can serve as a corroborating hemodynamic signal informing the level of reserve that the patient has prior to ablation. The right ventricle has been speaking to us throughout; we are only now starting to listen.

Conflicts of Interest

The authors declare no conflicts of interest.

Data Availability Statement

Data sharing is not applicable to this article, as no data sets were generated or analyzed during the current study.