Hemodynamical Consequences and Tolerance of Sustained Ventricular Tachycardia

Hubert Delasnerie, Caroline Biendel, Meyer Elbaz, Franck Mandel, Maxime Beneyto, Guillaume Domain, Quentin Voglimacci-Stephanopoli, Pierre Mondoly, Clement Delmas, Vanina Bongard, Anne   Rollin, Philippe Maury



Factors underlying clinical tolerance and hemodynamic consequences of monomorphic sustained ventricular tachycardia (VT) need to be clarified.


Intra-arterial pressures (IAP) during VT were collected in patients admitted for VT ablation and correlated to clinical, ECG and baseline echocardiographical parameters.


114 VTs from 58 patients were included (median 67 years old, 81% ischemic heart disease, median left ventricular ejection fraction 30%). 61 VTs were untolerated needing immediate termination (54%). VT tolerance was tightly linked to the evolution of IAPs. Faster VT rates (p<0.0001), presence of resynchronization therapy (p = 0.008), previous anterior myocardial infarction (p = 0.009) and more marginally larger baseline QRS duration (p = 0.1) were independently associated with VT tolerance. Only an inferior myocardial infarction was more often present in patients with only tolerated VTs vs patients with only untolerated VTs in multivariate analysis (OR 3.7, 95% CI 1.4–1000, p = 0.03). In patients with both well-tolerated and untolerated VTs, a higher VT rate was the only variable independently associated with untolerated VT (p = 0.02). Two different patterns of hemodynamic profiles during VT could be observed: a regular 1:1 relationship between electrical (QRS) and mechanical (IAP) events or some dissociation between both. VT with the second pattern were more often untolerated compared to the first pattern (78% vs 29%, p<0.0001).


Clinical tolerance of sustained monomorphic ventricular tachycardia (VT) is variable and hemodynamical consequences of VT need to be clarified. Although VT rate is involved in hemodynamical tolerance, other mechanisms were described for explaining hemodynamical behavior during VT, such as atrio-ventricular dissociation [1, 2] and the uncoordinated ventricular contraction because of the ectopic pattern of ventricular activation [3–5]. Blurred or compensatory neuro-hormonal response to baroreceptor activation [2, 6] have been demonstrated. Finally, myocardial ischemia might explain some additional decrease in systolic function [7].
Currently, there are no clear individualized predictable factors correlating to hemodynamical consequences and clinical tolerance during monomorphic VT. Predicting VT tolerance in a given patient would have some clinical interest, for example for optimizing ICD programmation, favoring anti-tachycardia pacing maneuvers or immediate ICD shocks according to the expected VT tolerance, or for predicting if sustained episodes will be tolerated during VT ablation. This would also be of interest when selecting patients who will best benefit of an ICD, since this may be postponed when well-tolerated VTs are expected.

In this study, we analyzed invasive arterial pressures and their evolution during VT and correlated these with clinical features, ECG and echocardiographic parameters.


We performed a retrospective study of 114 VTs recorded in 58 successive patients referred for VT ablation at the University Hospital of Toulouse in the second half of 2019. Patients were referred for VT ablation either for an elective procedure (n = 37) or for electrical storm (n = 21). Patients with incessant or refractory VTs were not included, because hemodynamical behavior in this critical setting is not representative of stable balanced conditions, and any analysis would be furthermore precluded by the lack of stable baseline control conditions because of ongoing/incessant VTs. Patients with left ventricular assist techniques were not included.

For each patient, cardiac history, underlying cardiomyopathy, cardio-vascular risks factors, coronary status, medical therapy, symptoms and ECG were retrospectively collected. The most recent data was used regarding echocardiography or coronary angiography (performed during the same hospitalization, except if recent data over the preceding weeks or months was available).


1. Population characteristics
Fifty-eight successive patients with sustained monomorphic VTs were retrospectively included, allowing the analysis of 114 fully analyzable VTs. Clinical, ECG and echocardiographic characteristics of the patient’s population are depicted in Table 1.
Eighty-one percent had coronary artery disease cardiomyopathy, followed by valvular disease (n = 7), dilated cardiomyopathy (n = 6), hypertrophic cardiomyopathy (HCM) and arrhythmogenic right ventricular cardiomyopathy (ARVC) (n = 2 each), myocarditis and congenital heart disease (n = 1 each). Seven patients (12%) had mixed forms of cardiomyopathy. No patient had idiopathic VT. Coronary status was adequately managed before ablation in all patients with coronary artery disease. The clinical VT was judged untolerated (syncope or cardiac arrest) in 21 patients (36%).


This study using invasive evaluation gives some elements of understanding clinical tolerance and hemodynamical behavior during monomorphic sustained VT.

Although hemodynamical patterns during VT have been already described [3, 8], there are no clear predictable clinical factors of VT tolerance to date. This lack of evidence can be explained by the paucity of hemodynamical evaluation during VT. The few previous studies dedicated to this topic [6, 9–11] included a limited number of patients and concluded to an exaggerated decreased cardiac output during VT, especially in patients with impaired LV function, and sometimes to impaired baroreflex sensitivity to the initial drop of blood pressure. This work is the first one to gather abundant data in the context of VT ablation procedures, where IAPs are commonly and continuously monitored.


This study helps to explain the large variability in clinical tolerance during VT, which is clearly related to intra-arterial pressures. VT tolerance was independently linked to VT rate, presence of resynchronization therapy, location of previous myocardial infarction, presence of concordant VT and QRS duration during VT.

Citation: Delasnerie H, Biendel C, Elbaz M, Mandel F, Beneyto M, Domain G, et al. (2023) Hemodynamical consequences and tolerance of sustained ventricular tachycardia. PLoS ONE 18(5): e0285802.

Editor: Daniel M. Johnson, The Open University, UNITED KINGDOM

Received: December 28, 2022; Accepted: May 1, 2023; Published: May 17, 2023

Copyright: © 2023 Delasnerie et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Data Availability: All relevant data are within the manuscript and its Supporting Information files.
Funding: The authors received no specific funding for this work.

Competing interests: The authors have declared that no competing interests exist.

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