A new study concludes that almost one half of ventricular tachycardia (VT) episodes are associated with failure to enhance the sinus rate (SR), as researchers suggest the link indicates a possible vasovagal response to VT. Led by Margarida Pujol-Lopez, MD, from the University of Chicago Medicine and University of Arizona College of Medicine, the research team attributed these inappropriate SR responses to an indicator of autonomic tone and pathologic vagal reflex during a VT episode. “The inability to compensate vasomotor tone to maintain blood pressure may be explained by a Bezold-Jarisch mechanism with concomitant cardioinhibitory response,” the paper suggests. “Classically, sympathetic nerve activity increases during sustained VT and is mediated primarily by the arterial baroreflex response to hypotension. The appropriate increase in SR during VT has been described previously, reflecting changes in cardiac autonomic tone and the sympathetic parasympathetic interaction.” The researchers went on to suggest that inappropriate SR responses were more predictive of hemodynamic instability than VT rate and left ventricular ejection fraction (LVEF) and that vagolytic therapy may augment blood pressure during VT. Study’s main findings Results from the retrospective study, which appears in the Sept. 12 issue of the Journal of the American College of Cardiology, were gathered from 150 patients, where 261 VT episodes were analyzed (29% untolerated, 71% tolerated) with a median VT duration of 1.6 minutes. The research team found that 52% of VT episodes were associated with a sympathetic response, with 31% registering an unchanged SR, and 17% of VTs exhibiting a vagal response. A significantly higher prevalence of inappropriate SR responses was observed during untolerated VT (sustained VT requiring cardioversion within 150 seconds) compared with tolerated VT (84% vs 34%; P<0.001). Untolerated VT was significantly different between groups: 9% sympathetic, 82% vagal and 32% unchanged (P<0.001), noted the paper’s authors. Further findings revealed that administration of atropine improved hemodynamic tolerance to VT in 70% of patients who were initially intolerant, allowing mapping without immediate cardioversion. “In the present cohort, 17% of VT episodes exhibited slowing of SR and 31% of SR remained unchanged, reflecting in both cases an abnormal autonomic, response (failure of sympathetic activation or a vagal response),” the paper’s authors said. “However, slowing SR could be influenced by other factors such as perfusion of sinus node because of fast rate and hypotension within a VT episode, or concomitant sinus node dysfunction. Blunted SR may also itself be a biomarker for impaired autonomic tone and associated reduced vascular tone as well.” Study commentary and critique The investigation, which was also published Monday online, was the subject of an accompanying editorial in which the commenters said the authors had built upon the researchers’ body of work, advancing the mechanistic understanding of VT, and improving strategies for the mapping and ablation of VT. Andre d’Avila, MD, and Robert N. D’Angelo, MD, from the Beth Israel Deaconess Medical Center in Boston, added that improvement in 70% of patients using atropine was the “inhibition of the vasodepressor and cardioinhibitory responses by atropine, thereby augmenting blood pressure.” “Notably, use of atropine may reduce need for vasopressors during VT ablation and obviate the need for mechanical circulatory support (MCS) in patients at otherwise high risk of hemodynamic decompensation because of high PAINESD risk score,” the editorialists added. “Avoiding MCS limits risk of intraprocedural and postprocedural complications and resultant hospital length of stay.” The experts went on to discuss atropine as a valuable tool to improve hemodynamics during VT, which may allow better and safer catheter ablation. “Based on the results of this study, we should consider administering atropine prophylactically before induction of VT, balancing benefits with risks including urinary retention and sinus tachycardia that limits substrate mapping from a ventricular paced wavefront,” they said. “Effects of tachycardia could be ameliorated by inducing VT after substrate mapping from a sinus- or right ventricle (RV)-paced wavefront.” Study approach The retrospective analysis identified 150 patients undergoing scar-related VT ablation with vasovagal responses evaluated by analyzing sinus cycle length before VT induction and during VT. The mean age of the patients was 65±10 years, and 15% were women. SR responses were classified into three groups: increasing (≥5 beats/min, sympathetic), decreasing (≥5 beats/min, vagal), and unchanged, with the latter two categorized as inappropriate SR. In a prospective cohort (n=30) that exhibited a failure to increase SR, atropine was administered to improve hemodynamic tolerance to VT. Sources: Pujol-Lopez M, Du Fay de Lavallaz J, Rangan P, et al. Vasovagal Responses to Human Monomorphic Ventricular Tachycardia: Hemodynamic Implications From Sinus Rate Analysis. J Am Coll Cardiol. 2023;82:1096–1105. d’Avila A, D’Angelo RN. Vasovagal Responses to Human Monomorphic Ventricular Tachycardia: Atropine to the Rescue. J Am Coll Cardiol. 2023;82:1106–1107 Image Credit: tloventures – stock.adobe.com