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Background:
Systematic Review

Effects of Propofol in the Cardiac Conduction System in Electrophysiologic Study: Systematic Review and Meta-Analysis †

by
Paulo Warpechowski
1,*,
Rodrigo B. Warpechowski
2,
Barbara A. De Lima
2,
Emanuella F. A. Pinto
1,
Mariana L. S. Bastos
1,
Bruna Eibel
2,
Rubens D. Trindade
1 and
Tiago L. Leiria
2
1
CET SANE Sociedade de Anestesiologia, Porto Alegre 90430-160, Brazil
2
Programa de Pós-Graduação da Fundação Universitária de Cardiologia de Porto Alegre, Porto Alegre 90620-001, Brazil
*
Author to whom correspondence should be addressed.
†
This paper was presented as a poster at the Brazilian Congress of Anesthesiology held in Rio de Janeiro from 11th to 15th November 2022.
Anesth. Res. 2025, 2(3), 16; https://doi.org/10.3390/anesthres2030016
Submission received: 14 April 2025 / Revised: 18 May 2025 / Accepted: 21 May 2025 / Published: 2 July 2025
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Abstract

Introduction: Propofol is a widely used sedative drug in electrophysiological studies (EPS). However, literature has shown that this drug may interfere with the cardiac conduction system (CCS). Our objective is to evaluate whether propofol interferes with CCS and the inducibility of arrhythmias during EPS. Method: A systematic review and a meta-analysis were performed. The databases were PubMed, Embase, Web of Science, and Scopus. Rayyan software was used to select the studies. Three Mesh terms were used: Propofol, Cardiac arrhythmias, Electrophysiologic Study, and Cardiac. Cohort studies and randomized clinical trials were included. Results: Only one of the six studies showed four cases where it was impossible to induce arrhythmia. We found no significant difference between propofol and the control group in the analyzed variables: cycle length, atrial-His, His-ventricular, corrected sinus node recovery time, atrial effective refractory factor, and ventricular effective refractory period, with low heterogeneity (I2 = 0% to a maximum of I2 = 8%). A significant difference in favor of the control group was found in the analysis of the atrioventricular node effective refractory period (MD:18.67 {95% CI 4.86 to 32.47} p = 0.008, I2 = 44%). Discussion: The meta-analyzed data in this study showed that propofol possibly does not interfere with CCS, making it a safe drug for this type of procedure. Conclusions: However, extra care should be exercised with pediatric patients when the arrhythmia’s mechanism is automatic. More robust studies are still needed in this class.

1. Introduction

Electrophysiological Study (EPS) is a minimally invasive procedure and an efficient and effective resource in evaluating patients with cardiac arrhythmias and conduction disorders. This type of procedure can cause anxiety, pain, and discomfort, which are issues that can be observed in up to 50% of cases [1]. Thus, the ideal anesthetic strategy should provide patient comfort, maintain a protective airway and ventilation, minimize patient movements, and improve catheter stability. For this purpose, anesthetic as well as sedative medications are used [2].
Some of these drugs can affect electrophysiology and cardiac conduction, hindering or preventing the ability to induce the abnormal rhythm [2,3,4,5,6]. Although many of these effects of anesthetics on the cardiac conduction system (CCS) have already been well understood, some of them, caused by newer drugs, lack further detail, and their effects are not yet completely understood. This is the case of propofol, an intravenous anesthetic widely used in general anesthesia or as a sedative in diagnostic or therapeutic examination procedures. This is partly due to its favorable pharmacokinetic properties, among which we can mention the absence of cumulative effects, antiemetic effects, and ease of titration, providing rapid awakening without the residual sensation of sedation [6,7,8].
It is known that propofol can promote a reduction in blood pressure and peripheral vascular resistance; these changes, in general, are not followed by a compensatory increase in heart rate [7,8]. This lack of heart rate compensation, reports of bradyarrhythmia [5], suppression of tachyarrhythmias [4,9], and conversion of other rhythms to sinus rhythm during the use of propofol point to the possibility that this medication causes baroreceptor blockade or CCS depression [9,10,11]. These reported effects and studies in animals in which propofol was shown to suppress CCS, especially the AV node and/or His-Purkinje conduction [12,13,14], suggest that it may interfere with CCS [4,9] and therefore may not be indicated for EPS and ablation procedures [10].
Some studies have shown that propofol has no clinically significant effects on accessory pathways, the refractoriness of the normal AV conduction system, sinoatrial node activity, intra-atrial conduction, or reentry tachyarrhythmias. Therefore, its use is considered appropriate in procedures involving these pathologies. However, some authors have noted that this medication may interfere with automatic supraventricular tachycardias, particularly in pediatric populations suggesting that its use in such contexts should be approached with caution [15,16].
Due to these divergent conclusions, we found the need for additional studies to verify the possible interference of this medication in the inducibility of arrhythmias. Therefore, we propose to carry out a Systematic Review (SSR) and Meta-Analysis of contemporary literature on the possible effects of propofol on the inducibility of arrhythmias and the possibility of propofol interference in CCS.

2. Methods

2.1. Search Strategy, Inclusion, and Exclusion Criteria

An SSR with a meta-analysis of randomized clinical trials (RCT) was performed. This systematic review was described according to the Preferred Reporting Items for Systematic Review and Meta-Analysis Protocols (PRISMA-P) [17]. This study protocol is registered in the International Prospective Register of Systematic Reviews (PROSPERO) under number CRD42021279890.

2.2. Search Strategy

An electronic search was conducted using the following databases: PubMed, Embase, Scopus, and Web of Science. The initial search included studies from inception through February 2023, with no restrictions on language or patient age. The reference lists of selected articles were also screened to identify additional relevant studies. The search strategy was subject to modification if more relevant keywords were identified during the initial screening process. All searches will be updated prior to submission for review. The following Mesh Terms were used in Embase, Scopus, and Web of Science: Propofol, Arrhythmias, Cardiac, Electrophysiologic Studies, Cardiac. The search strategy used in PubMed is shown in Table 1.

2.3. Eligibility and Exclusion Criteria

2.3.1. Eligibility Criteria

  • Type of study: RCTs, observational, retrospective, and prospective cohort studies were included. Case reports, case series, and review articles were not included.
  • Type of participants: adults and children with or without heart disease who underwent EPS and were sedated with propofol. All the RCTs or clinical control trials comparing propofol with other anesthetic agents were included in the study. There was no age, gender, or type of heart disease restriction.
  • Type of intervention: EPS with or without radiofrequency ablation with propofol sedation.
  • Types of comparison group: patients who were sedated with propofol and patients who were sedated with other anesthetic agents such as fentanyl, midazolam, ketamine, and dexmedetomidine, among others.
  • Types of results:
    Primary outcomes: whether propofol interfered in the CCS and the inducibility of arrhythmias.
    Secondary outcomes: whether propofol interferes or not with cycle length (CL), atrial-His (AH), His-ventricular (HV), corrected sinus node recovery time (CSNRT), atrial effective refractory factor (AERP/FT), ventricular effective refractory period (VERP) and atrial ventricular node effective refractory period (AVNERP). And whether propofol is or is not an ideal anesthetic agent for sedation in EPS procedures compared to other anesthetics.

2.3.2. Exclusion Criteria

  • Animal studies, case reports, case series studies, protocols, letters, surveys, and review articles.
  • Sedation with anesthetics other than propofol.
  • Studies evaluating outcomes unrelated to cardiac conduction or EPS were excluded.

2.3.3. Selection of Studies

Two reviewers (RBW and BAL) independently evaluated the titles and abstracts of the retrieved articles. Abstracts that did not provide sufficient information regarding eligibility criteria were retained for full-text evaluation. The same two reviewers then independently assessed the full-text articles to determine their potential eligibility for inclusion in the study. Disagreements were resolved by consensus; if consensus could not be reached, a third reviewer (PW) evaluated the article.
The Rayyan 1.5.0 platform was used to assist in the study selection process. The PRISMA 2020 flowchart was followed for new systematic reviews that include searches of databases, registries, and other sources [17,18].

2.3.4. Data Extraction

A standardized data organization form was developed using Microsoft Excel 2019. All potentially relevant studies were retrieved as full manuscripts and thoroughly assessed for compliance with the inclusion criteria. Two reviewers independently performed the data extraction. In the event of disagreement, a third reviewer’s opinion was considered. The extracted data included year of publication, authors, geographic location of the first author, study design, eligibility criteria, sample size, gender and mean age of participants, type of arrhythmia, arrhythmia inducibility during EPS, and the occurrence of loss of pre-excitation.

2.4. Statistical Analysis and Data Synthesis

A descriptive analysis of the characteristics of observational studies and a meta-analysis were performed to summarize quantitative data from randomized controlled trials. Meta-analyses were conducted using Review Manager (RevMan) version 5.4 (Nordic Cochrane Centre, Cochrane Collaboration). RevMan was used to pool and analyze eligible studies when two or more studies reported outcomes of interest. Publication bias was assessed using a funnel plot, which evaluates the effect size of each study against its standard error.
A random-effects model was applied in the presence of clinically and statistically significant heterogeneity (p < 0.05, I2 > 50%). For dichotomous outcomes, pooled results were calculated as odds ratios (ORs) with 95% confidence intervals (CIs). For continuous outcomes, we calculated and meta-analyzed mean differences (MDs) or standardized mean differences (SMDs), along with their 95% CIs.
We assessed heterogeneity using Cochran’s Q test and the I2 statistic derived from the standard χ2 test. When I2 ≤ 40%, heterogeneity was considered acceptable, and a fixed-effects model was used for the pooled analysis. If I2 > 40%, heterogeneity was considered substantial, and its sources were explored. Sensitivity analysis and meta-regression were employed to identify potential sources of heterogeneity. Clinical and methodological heterogeneity between studies was also reassessed. If no adequate explanation for high heterogeneity was found, a random-effects model was used to account for it. Statistical significance was set at a p-value < 0.05.
Following the meta-analysis of all eligible outcomes, a summary of findings tables was generated using the Grading of Recommendations Assessment, Development, and Evaluation (GRADE) system to assess the quality of the evidence. The trim-and-fill method was applied to estimate the potential impact of publication bias on the interpretation of results.

2.5. Quality Assessment

We assessed the quality of the evidence following the steps proposed by the GRADE system to evaluate the overall quality of treatment effects and the strength of recommendations. This approach considers five domains: study limitations, consistency of results, imprecision, indirectness, and publication bias, to assess the quality of the body of evidence for each outcome. Case-control and cohort studies were assessed using the Newcastle-Ottawa Scale. The quality of cross-sectional studies was evaluated based on the Cochrane risk of bias assessment, and Review Manager version 5.4 was used in the analysis.
The following items were considered: blinding of outcome assessment, incomplete outcome data, and selective reporting. Additionally, measurement methods were required to be adequate and accurate, and the sample needed to be representative. Articles were not excluded based on quality alone; however, their potential influence on the meta-analysis was analyzed. Two reviewers (RBW and BAL) independently conducted the quality assessment. Disagreements were resolved by consensus, and if disagreement persisted, a third reviewer (PW) was consulted.

3. Results

A total of 1000 articles were retrieved from the database search. A flowchart following PRISMA guidelines is presented in Figure 1. Of the 1000 articles, 514 were duplicates, leaving 586 potentially relevant studies for analysis. After screening titles and abstracts, 433 studies were excluded, resulting in 53 articles selected for full-text review. Among these, 37 addressed the topic of interest but focused on different stages or outcomes unrelated to CCS or electrophysiological parameters. Additionally, 6 studies evaluated anesthetic agents other than propofol. One study obtained from personal data was also included.
In this way, we reached the result of our search, in which we included six cohort studies in the SSR [19,20,21,22,23,24] and five selected RCTs [15,25,26,27,28] for the meta-analysis. The flow diagram for the included studies can be found in Figure 1.
The database search included systematic screening and review (SSR) of studies published between 1994 and 2023. Most of the included articles were prospective cohort studies. In total, the studies involved 266 trained patients, of whom 152 were male (57%) and 114 were female (43%). Among them, 124 were pediatric patients (46%) and 142 were adults (54%). Additionally, 71 trained patients had underlying automatic arrhythmia pathologies (such as VT or SVT), followed by 68 with AVRT, 64 with WPW syndrome, 31 with AVNRT, 24 with atrial flutter, and 10 with no underlying arrhythmic condition.
The main characteristics of the six studies are shown in Table 2.

3.1. Primary Results

Among the total of 266 patients compiled from the six articles, one study (Lai et al. [20]) reported four cases (1.5%) in which arrhythmia could not be induced. All four were pediatric patients with ectopic atrial tachycardia. According to the authors, ablation could not be performed in these cases [20].
Another study (Paech et al. [23]) found that in six cases (2.25%), pre-excitation disappeared, indicating interference with the anterograde conduction of the accessory pathway during sedation with propofol. Therefore, in these cases, propofol appeared to interfere with the cardiac electrophysiological conduction (CEC) [23].
In one of the selected studies (Matsushima, 2021 [24]), propofol was found to suppress intrinsic HV conduction, indicating interference with the cardiac conduction system (CCS). However, it did not affect the sinus node recovery time (SNRT), sinoatrial conduction time (SACT), or the AH interval. Moreover, propofol did not prevent arrhythmia induction or its treatment through ablation [24].
We did not find AV conduction suppression by propofol in any study.
Furthermore, other studies did not demonstrate the drug’s effect on CCS [19,21,22]. These data are represented in Table 2.
For the question of the researched outcome regarding the interference of propofol in CCS, it was possible to carry out a meta-analysis of 7 outcomes among the allocated studies.
In this meta-analysis, no significant differences were detected between propofol and the control group in the following meta-analyzed outcomes: Cycle Length (CL), as shown in the Forest Plot Figure 2 and the Funnel Plot in Figure 3, Atrial-His (AH) as shown in the Forest Plot Figure 4 and the Funnel Plot in Figure 5, His-Ventricular (HV), as shown in the Forest Plot Figure 6 and the Funnel Plot in Figure 7, Node Recovery Time Corrected Sinus (CSNRT) as shown in the Forest Plot Figure 8 and the Funnel Plot in Figure 9, Atrial Effective Refractory Period/Fast Pathway (AERP/FP), as shown in the Forest Plot Figure 10 and the Funnel Plot in Figure 11 and Ventricular Effective Refractory Period (VERP), as shown in the Forest Plot Figure 12 and the Funnel Plot in Figure 13.
All these variables demonstrated low heterogeneity (I2 = 0%, I2 = 3%, I2 = 0%, I2 = 0%, I2 = 0%, and I2 = 8%, respectively), as demonstrated in the Funnel Plot Figures.
However, when a meta-analysis of the AV node effective refractory period (AVNERP) evaluated in 4 studies and involving 94 patients was performed, we found a significant difference in favor of the control group, determined specifically by one study (Erb et al.) [27] (MD:18.67 {95% CI 4.86 to 32.47} p = 0.008, I2 = 44%); although, according to the Higgins et al. this is classified as moderate heterogeneity, represented in Figure 14 and Figure 15, respectively.

3.2. Risk of Bias Analysis

We assessed the risk of bias using the Cochrane Risk of Bias Tool (RoB 1.0), following the recommendations of the Cochrane Handbook for Systematic Reviews of Interventions, version 5.0, published in 2008 and updated in 2011. This tool evaluates seven domains, and based on the reviewers’ judgment, each study or outcome was classified as having a low, high, or unclear risk of bias. The risk of bias was predominantly low regarding selective outcome reporting, the use of control groups for placebo effects, and randomization for group allocation. However, the risk was classified as unclear for sequence generation, allocation concealment, blinding of participants, and blinding of outcome assessment. These classifications are summarized in Table 3.

3.3. Evidence Quality Assessment

The GRADE system was used to assess the quality of the evidence, which reflects the level of confidence in the available information. In the GRADE approach, the quality of evidence is evaluated for each outcome based on the body of evidence available [29,30].
The quality assessment (GRADE) for the five meta-analyzed outcomes (CL, AH, HV, CSNRT, and AERP/FP) demonstrated high certainty of the evidence and is summarized in Table 4.
For the AVNERP and VERP outcomes, the certainty of the evidence was rated as moderate. This classification was based on two studies that presented an unclear risk regarding the method of random sequence generation. Additionally, one of these studies showed a high risk related to random sequence generation. Allocation concealment was also rated as unclear in two studies, and one study classified as having a high risk due to the use of an unreliable method of allocation concealment [25,26,28].

4. Discussion

Radiofrequency catheter ablation of arrhythmogenic foci has proven to be an effective treatment, often safer than pharmacological therapy. Advances in technology and in the understanding of arrhythmic substrates now make it possible to ablate multiple and unstable tachyarrhythmias with acceptable safety and efficacy, even in patients with advanced cardiac disease [31,32].
However, in some patients undergoing electrophysiological study (EPS) aimed at treating arrhythmogenic foci through ablation, sedation with certain drugs may interfere with or even prevent proper diagnosis and treatment. In certain cases, the initiation of sedative infusion inhibits the induction of the arrhythmia, which cannot be reproduced either by programmed atrial or ventricular stimulation or even by the infusion of β-adrenergic agents such as isoproterenol [20,24]. When such sedatives are identified, they should be avoided or contraindicated during EPS and/or ablation procedures, as they may interfere with both the diagnosis and treatment of arrhythmias. Therefore, proper anesthesia management in patients undergoing EPS requires that pathological tachycardia remains inducible throughout the procedure.
Propofol has been associated with an arrhythmia-suppressive effect and, for this reason, has been replaced in some cases by other agents, such as GABAergic agonists like midazolam, based on the belief that these drugs cause less suppression of arrhythmia, particularly those classified as automatic. Consequently, propofol has occasionally been avoided during these procedures, which may prevent the use of its favorable properties for EPS and ablation.
Suspicions regarding the interference of this sedative with the cardiac electrical system began with observations of the absence of a compensatory increase in heart rate in response to vasodilation caused by propofol. These suspicions were later supported by publications attributing to this medication’s effects such as bradyarrhythmia and the reversion of tachyarrhythmias to sinus rhythm [33,34]. However, beyond the direct effect of propofol, it has been suggested that its interference with the cardiac conduction system (CCS) may be secondary to the modulation of the autonomic nervous system. This was supported by studies conducted by Erb et al., who proposed that propofol alters the balance between parasympathetic and sympathetic tone, as well as baroreflex regulatory responses. According to these authors, changes observed in the CCS could be attributed to reduced baroreflex inhibition and enhanced parasympathetic tone induced by propofol [35].
This bradycardic effect was demonstrated in animal experiments conducted in the absence of autonomic influence, strongly suggesting a direct effect of this sedative on the cardiac conduction system (CCS) [36]. One of the mechanisms that could explain the direct effects of propofol on the cardiac conduction system (CCS) was proposed by Kurokawa H and Murray PA (2002) [37]. In an animal experiment using isolated cardiac cells, they found that although propofol did not appear to exert a direct effect on L-type calcium channels (LTCC), it significantly attenuated the expected increase in cytosolic calcium induced by adrenergic stimulation [37]. Additionally, Pires et al. reported prolonged sinus node recovery time and depressed His-Purkinje conduction in pigs. In isolated animal hearts, propofol has also been shown to suppress atrioventricular (AV) nodal conduction and shorten the duration of the myocardial action potential [13].
Human studies evaluating the effects of propofol on the cardiac conduction system (CCS) suggest a tendency to believe that propofol exerts inhibitory effects when the underlying mechanism of the arrhythmia is enhanced automaticity (Lavoie J et al., 1995) [25]. In contrast, it appears to have minimal or no effect on arrhythmia mediated by reentry mechanisms, as described in studies by Sharpe MD et al., 1995, and Warpechowski P et al. [15,26].
Similarly, Miró et al. described two cases—one involving a 70-year-old man and the other a 58-year-old woman with atrial fibrillation—in which the arrhythmia was reversed following intravenous administration of 50 mg and 75 mg of propofol, respectively, as the patients were being prepared for electrical cardioversion. According to the authors, both patients had previously received 1 g of intravenous amiodarone over a 24-h period, which failed to reverse the arrhythmia. Amiodarone administration was discontinued approximately one hour before the initiation of sedation with propofol [4]. Propofol induces rapid hypnosis and provides effective anesthesia. Due to its short half-life, it is commonly used for brief invasive procedures, including cardioversion. Its administration may occasionally lead to mild hemodynamic effects, such as hypotension and bradycardia. Based on animal studies, the proposed mechanisms underlying its dromotropic and negative chronotropic effects include a reduction in atrial rate and nodal conduction velocity, depression of His-Purkinje system function, prolongation of the Wenckebach cycle duration, and an increase in the effective refractory period. As a result, some researchers have suggested that propofol possibly may offer antiarrhythmic protection in patients susceptible to supraventricular tachycardias. In line with this hypothesis, several other authors have reported that propofol was able to convert abnormal rhythms to sinus rhythm [3,6,9,38,39,40].
However, studies by Romano et al. did not demonstrate a depressant effect of propofol on the cardiac electrical system. None of the patients in their study exhibited bradyarrhythmias during anesthesia; on the contrary, the duration of the sinus cycle was significantly reduced compared to baseline values. Furthermore, the drug did not impair atrioventricular (AV) conduction [19].
Matsushima et al. [24], in their study involving pediatric patients—most of whom had Wolff-Parkinson-White (WPW) syndrome—found a significant prolongation of the HV interval. However, no significant changes were observed in the SNRT, SACT, or AH interval. In other words, propofol suppressed intrinsic HV conduction without affecting the other measured intervals. The authors concluded that this change was likely because of propofol on sympathetic activity [24].
Our systematic search and review (SSR) followed the recommendations of the Preferred Reporting Items for Systematic Review and Meta-Analysis Protocols (PRISMA-P). This process involved an extensive bibliographic and cross-sectional search of scientific publications retrieved electronically from PubMed, Embase, Scopus, and Web of Science, with no restrictions on start date, language, or patient age, up to February 2023. Given the breadth of this search, we believe that the available literature on this topic has been comprehensively explored. It is not an overstatement to suggest that the objective of this analysis brings a degree of novelty to the field. To the best of our knowledge, this is the first meta-analysis to specifically evaluate the effects of propofol on the cardiac conduction system (CCS). In this SSR, we identified a low incidence of arrhythmia non-inducibility (1.5%), reported in a single study (Lai LP, 1999) involving a group of pediatric patients with ectopic atrial tachycardia [20]. In these cases, it was also not possible to perform diagnostic evaluation or ablation. Additionally, we found a study (Paech, 2019) that observed, in a few cases, the disappearance of pre-excitation—indicating interference with the anterograde conduction of the accessory pathway during the administration of propofol sedation [23].
In another SSR study (Matsushima, 2021 [24]), propofol was found to suppress intrinsic HV conduction, while having no effect on SNRT or the AH interval. It also did not prevent the induction of arrhythmia or its treatment through ablation [24].
The meta-analysis of five randomized controlled trials (RCTs) showed no significant differences between propofol and the control group across the evaluated outcomes: CL, AH, HV, CSNRT, AERP/FP, and VERP. The analysis of these variables demonstrated low heterogeneity (I2 ranging from 0% to a maximum of 8%), indicating a consistent absence of drug interference in these parameters compared to the control. These findings are consistent with those of Sharpe MD et al. (1995), Warpechowski P et al., and Romano et al., whose RCTs similarly failed to demonstrate any significant effect of propofol on the cardiac conduction system (CCS) [15,19,26].
Only in the meta-analysis of the AVNERP interval, evaluated in four studies involving a total of 94 patients, was a significant difference found in favor of the control group. This result was primarily driven by one study (Erb et al.) (MD: 18.67 [95% CI: 4.86 to 32.47], p = 0.008, I2 = 44%). The study demonstrated evidence of slower intracardiac atrioventricular node conduction under the influence of propofol, as reflected by a longer AVNERP interval in the propofol group. This parameter serves as a nonspecific surrogate marker for atrioventricular nodal conduction velocity. According to the authors, this effect may be explained either by autonomic reflex mechanisms or by direct pharmacologic action of the drug. It is known, for instance, that propofol alters the balance between parasympathetic and sympathetic tone, as well as baroreflex regulatory responses [27]. According to the authors, the difference observed in this outcome could be explained by reduced baroreflex inhibition and increased parasympathetic tone induced by propofol. However, they concluded that, regardless of the mechanism, the observed influence on atrioventricular node function was not clinically significant. These conclusions are supported by studies conducted by Harris et al. (1994) [35], which found that propofol reduces sympathetic tone to a greater extent than parasympathetic tone, thereby allowing parasympathetic responses to predominate. This autonomic shift results in bradycardia due to enhanced parasympathetic activity [35].
This allows us to conclude that, although a statistically significant difference was found in the meta-analysis of one outcome (AVNERP), the authors considered this finding to be clinically insignificant. Moreover, our study demonstrated that, for all other intervals evaluated, there is no evidence that propofol interferes with the cardiac conduction system (CCS). The strength of this evidence is supported by the low heterogeneity observed across the analyses.
Furthermore, the GRADE assessment of the certainty of evidence—indicating high certainty for four outcomes and moderate certainty for two—supports the conclusion that, within the periods evaluated in these meta-analyzed RCTs, propofol does not interfere with the cardiac conduction system (CCS). Therefore, it can be considered a suitable anesthetic agent for use in procedures of this nature.

5. Conclusions

In the present study, we found a low incidence of non-inducibility of arrhythmias during propofol sedation in EPS procedures. This non-inducibility occurred specifically in patients whose arrhythmia was driven by automaticity mechanisms. Therefore, propofol may potentially suppress ectopic atrial tachycardia in pediatric patients.
The studies included in this meta-analysis showed consistent findings with low heterogeneity. The evidence supports, with a high level of certainty, that propofol does not interfere with the cardiac conduction system (CCS), confirming its efficacy and safety for use in such procedures.
The results of this study provide further evidence for the effectiveness and safety of propofol in EPS and fluoroscopy-guided ablation procedures. These findings may help reduce fluoroscopy exposure, procedure duration, and associated healthcare costs.
In conclusion, propofol can be safely used in EPS and ablation procedures, benefiting from its excellent pharmacological profile. However, caution should be exercised in pediatric patients with arrhythmia of automatic origin. Further high-quality studies are warranted in this specific population.

Key Messages

To date, no meta-analysis on this subject has been published in the literature. This is the first article to compile all available data regarding propofol and its interaction with the cardiac conduction system (CCS) during electrophysiological studies (EPS). We believe that the findings of this study will assist electrophysiologists in selecting appropriate anesthetic strategies and achieving better outcomes for their patients.
The quality of the evidence was assessed using the Grading of Recommendations Assessment, Development, and Evaluation (GRADE) approach.
This systematic review was conducted in accordance with the Preferred Reporting Items for Systematic Review and Meta-Analysis Protocols (PRISMA-P). It adheres to the full PRISMA checklist and includes a complete PRISMA flow diagram (Appendix A).
Our results may be limited by the number of studies available for analysis and the heterogeneity in study quality, which could impact the generalizability of the findings.
Furthermore, this paper may not fully address the variability in propofol’s effects across different patient populations (e.g., by age or underlying cardiac conditions), which may also limit the applicability of the conclusions drawn.

Author Contributions

P.W. and R.B.W. contributed substantially to the conception and design of the manuscript. B.A.D.L., E.F.A.P. and M.L.S.B. contributed to the acquisition, analysis, and interpretation of the data. All authors participated in drafting the manuscript; T.L.L., R.D.T. and B.E. revised it critically. All authors have read and agreed to the published version of the manuscript.

Funding

This research received no external funding.

Conflicts of Interest

The authors certify no conflicts of interest with any financial organization regarding the material discussed in the manuscript.

Appendix A

Table A1. Recomendações do Preferred Reporting Items for Systematic Review and Meta-Analysis Protocols (PRISMA-P).
Table A1. Recomendações do Preferred Reporting Items for Systematic Review and Meta-Analysis Protocols (PRISMA-P).
Section and TopicItem #Checklist ItemLocation Where Item is Reported
Title
Title1Identify the report as a systematic review.01
Abstract
Abstract2See the PRISMA 2020 for Abstract’s checklist.01
Introduction
Rationale3Describe the rationale for the review in the context of existing knowledge.01, 02
Objectives4Provide an explicit statement of the objective(s) or question(s) the review addresses.03
Methods
Eligibility criteria5Specify the inclusion and exclusion criteria for the review and how studies were grouped for the syntheses.03
Information sources6Specify all databases, registers, websites, organizations, reference lists, and other sources searched or consulted to identify studies. Specify the date when each source was last searched or consulted.03
Search strategy7Present the full search strategies for all databases, registers, and websites, including any filters and limits used.02, 03
Selection process8Specify the methods used to decide whether a study met the inclusion criteria of the review, including how many reviewers screened each record and each report retrieved, whether they worked independently, and if applicable, details of automation tools used in the process.03
Data collection process9Specify the methods used to collect data from reports, including how many reviewers collected data from each report, whether they worked independently, any processes for obtaining or confirming data from study investigators, and if applicable, details of automation tools used in the process.03, 04
Data items10aList and define all outcomes for which data were sought. Specify whether all results that were compatible with each outcome domain in each study were sought (e.g., for all measures, time points, analyses), and if not, the methods used to decide which results to collect.04
10bList and define all other variables for which data were sought (e.g., participant and intervention characteristics, funding sources). Describe any assumptions made about any missing or unclear information.04
Study risk of bias assessment11Specify the methods used to assess the risk of bias in the included studies, including details of the tool(s) used, how many reviewers assessed each study, whether they worked independently, and if applicable, details of automation tools used in the process.04
Effect measures12Specify for each outcome the effect measure(s) (e.g., risk ratio, mean difference) used in the synthesis or presentation of results.04
Synthesis methods13aDescribe the processes used to decide which studies were eligible for each synthesis (e.g., tabulating the study intervention characteristics and comparing against the planned groups for each synthesis (item #5)).04
13bDescribe any methods required to prepare the data for presentation or synthesis, such as handling of missing summary statistics, or data conversions.04
13cDescribe any methods used to tabulate or visually display results of individual studies and syntheses.04
13dDescribe any methods used to synthesize results and provide a rationale for the choice(s). If meta-analysis was performed, describe the model(s), method(s) to identify the presence and extent of statistical heterogeneity, and software package(s) used.04
13eDescribe any methods used to explore possible causes of heterogeneity among study results (e.g., subgroup analysis, meta-regression).04
13fDescribe any sensitivity analyses conducted to assess robustness of the synthesized results.04
Reporting bias assessment14Describe any methods used to assess risk of bias due to missing results in a synthesis (arising from reporting biases).04
Certainty assessment15Describe any methods used to assess certainty (or confidence) in the body of evidence for an outcome.04
Results
Study selection16aDescribe the results of the search and selection process, from the number of records identified in the search to the number of studies included in the review, ideally using a flow diagram.05
16bCite studies that might appear to meet the inclusion criteria, but which were excluded, and explain why they were excluded.05
Study characteristics17Cite each included study and present its characteristics.05, 06
Risk of bias in studies18Present assessments of risk of bias for each included study.11
Results of individual studies19For all outcomes, present, for each study: (a) summary statistics for each group (where appropriate) and (b) an effect estimate and its precision (e.g., confidence/credible interval), ideally using structured tables or plots.06, 07, 08, 09
Results of syntheses20aFor each synthesis, briefly summarize the characteristics and risk of bias among contributing studies.07, 08
20bPresent results of all statistical syntheses conducted. If meta-analysis was conducted, present for each the summary estimate and its precision (e.g., confidence/credible interval) and measures of statistical heterogeneity. If comparing groups, describe the direction of the effect.09, 10
20cPresent results of all investigations of possible causes of heterogeneity among study results.09, 10, 11
20dPresent results of all sensitivity analyses conducted to assess the robustness of the synthesized results.09, 10
Reporting biases21Present assessments of risk of bias due to missing results (arising from reporting biases) for each synthesis assessed.11
Certainty of evidence22Present assessments of certainty (or confidence) in the body of evidence for each outcome assessed.11, 12
Discussion
Discussion23aProvide a general interpretation of the results in the context of other evidence.12
23bDiscuss any limitations of the evidence included in the review.12, 13
23cDiscuss any limitations of the review processes used.13, 14
23dDiscuss implications of the results for practice, policy, and future research.14, 15
Other Information
Registration and protocol24aProvide registration information for the review, including register name and registration number, or state that the review was not registered.02
24bIndicate where the review protocol can be accessed, or state that a protocol was not prepared.02, 15
24cDescribe and explain any amendments to information provided at registration or in the protocol.02
Support25Describe sources of financial or non-financial support for the review, and the role of the funders or sponsors in the review.15
Competing interests26Declare any competing interests of review authors.15
Availability of data, code, and other materials27Report which of the following are publicly available and where they can be found: template data collection forms; data extracted from included studies; data used for all analyses; analytic code; and any other materials used in the review.4, 5, 15

References

  1. Lau, W.; Kovoor, P.; Ross, D.L. Cardiac electrophysiologic effects of midazolam combined with fentanyl. Am. J. Cardiol. 1993, 72, 177–182. [Google Scholar] [CrossRef] [PubMed]
  2. Vladinov, G.; Fermin, L.; Longini, R.; Ramos, Y.; Maratea, E. Choosing the anesthetic and sedative drugs for supraventricular tachycardia ablations: A focused review. Pacing Clin. Electrophysiol. 2018, 41, 1555–1563. [Google Scholar] [CrossRef] [PubMed]
  3. Terashima, S.; Muroya, T.; Ikegawa, H.; Kajino, K.; Sakuramoto, K.; Yui, R.; Kishimoto, M.; Takahashi, H.; Nakajima, M.; Nakamura, F.; et al. Propofol suppresses ventricular arrhythmias: A case report of acute caffeine intoxication. Acute Med. Surg. 2020, 7, 514. [Google Scholar] [CrossRef] [PubMed]
  4. Miró, O.; de la Red, G.; Fontanals, J. Cessation of paroxysmal atrial fibrillation during acute intravenous propofol administration. Anesthesiol. 2000, 92, 910. [Google Scholar] [CrossRef]
  5. Thomson, S.J.; Yate, P.M. Bradycardia after propofol infusion. Anaesthesia 1987, 42, 430. [Google Scholar] [CrossRef]
  6. Shannon, K.; Saltzman, D.; Li, I.; Mokszycki, R.; Galletta, G. Ventricular tachycardia converts to sinus rhythm after propofol administration. Am. J. Emerg. Med. 2021, 48, 377.e1–377.e3. [Google Scholar] [CrossRef]
  7. Hug, C.C.; McLeskey, C.H.; Nahrwold, M.L.; Roizen, M.F.; Stanley, T.H.; Thisted, R.A.; Walawander, C.A.; White, P.F.; Apfelbaum, J.L.; Grasela, T.H. Hemodynamic effects of propofol: Data from over 25,000 patients. Anesth. Analg. 1993, 77, 21–29. [Google Scholar]
  8. Vuyk, J.; Engbers, F.H.M.; Lemmens, H.J.M.; Burm, A.G.L.; Vletter, A.A.; Gladines, M.P.R.R.; Bovill, J.G. Pharmacodynamics of propofol in female patients. Anesthesiology 1992, 77, 3–9. [Google Scholar] [CrossRef]
  9. Kannan, S.; Sherwood, N. Termination of supraventricular tachycardia by propofol. Br. J. Anaesth. 2002, 88, 874–875. [Google Scholar] [CrossRef]
  10. Tramèr, M.R.; Moore, R.A.; McQuay, H.J. Propofol and bradycardia: Causation, frequency and severity. Br. J. Anaesth. 1997, 78, 642–651. [Google Scholar] [CrossRef]
  11. Wu, M.-H.; Lin, J.-L.; Lai, L.-P.; Young, M.-L.; Lu, C.-W.; Chang, Y.-C.; Wang, J.-K.; Lue, H.-C. Radiofrequency catheter ablation of tachycardia in children with and without congenital heart disease: Indications and limitations. Int. J. Cardiol. 2000, 72, 221–227. [Google Scholar] [CrossRef] [PubMed]
  12. Alphin, R.S.; Martens, J.R.; Dennis, D.M. Frequency-dependent effects of propofol on atrioventricular nodal conduction in guinea pig isolated heart. Mechanism and potential antidysrhythmic properties. Anesthesiology 1995, 83, 382–394. [Google Scholar] [CrossRef] [PubMed]
  13. Pires, L.A.; Huang, S.K.; Wagshal, A.B.; Kulkarni, R.S. Electrophysiological effects of propofol on the normal cardiac conduction system. Cardiology 1996, 87, 319–324. [Google Scholar] [CrossRef] [PubMed]
  14. Wu, M.H.; Su, M.J.; Sun, S.S. Age-related propofol effects on electrophysiological properties of isolated hearts. Anesth. Analg. 1997, 84, 964–971. [Google Scholar] [CrossRef]
  15. Warpechowski, P.; Lima, G.G.; Medeiros, C.M.; Santos, A.T.L.; Kruse, M.; Migloransa, M.H.; Kalil, R.A. Randomized study of propofol effect on electrophysiological properties of the atrioventricular node in patients with nodal reentrant tachycardia. Pacing Clin. Electrophysiol. 2006, 29, 1375–1382. [Google Scholar] [CrossRef]
  16. Warpechowski, P.; dos Santos, A.T.L.; Pereira, P.J.I.; de Lima, G.G. Effects of propofol on the cardiac conduction system. Rev. Bras. Anestesiol. 2010, 60, 438–444. [Google Scholar] [CrossRef]
  17. Page, M.J.; McKenzie, J.E.; Bossuyt, P.M.; Boutron, I.; Hoffmann, T.C.; Mulrow, C.D.; Shamseer, L.; Tetzlaff, J.M.; Akl, E.A.; Brennan, S.E.; et al. The PRISMA 2020 statement: An updated guideline for reporting systematic reviews. Syst. Rev. 2021, 10, 89. [Google Scholar] [CrossRef]
  18. Ouzzani, M.; Hammady, H.; Fedorowicz, Z.; Elmagarmid, A. Rayyan—A web and mobile app for systematic reviews. Syst. Rev. 2016, 5, 210. [Google Scholar] [CrossRef]
  19. Romano, R.; Ciccaglioni, A.; Fattorini, F.; Quaglione, R.; Favaro, R.; Arcioni, R.; Conti, G.; Gasparetto, A. Effects of propofol on the human heart electrical system: A transesophageal pacing electrophysiologic study. Acta Anaesthesiol. Scand. 1994, 38, 30–32. [Google Scholar] [CrossRef]
  20. Lai, L.; Lin, J.; Wu, M.; Wang, M.; Huang, C.; Yeh, H.; Tseng, Y.; Lien, W.; Huang, S.K.S. Usefulness of Intravenous Propofol Anesthesia for Radiofrequency Catheter Ablation in Patients with Tachyarrhythmias: Infeasibility for Pediatric Patients with Ectopic Atrial Tachycardia. Pacing Clin. Electrophysiol. 1999, 22, 1358–1364. [Google Scholar] [CrossRef]
  21. Pérez, E.R.; Bartolomé, F.B.; Carretero, P.S.; Fernández, C.S.; Mateos, E.J.; Tarlovsky, L.G. Efectos electrofisiológicos del sevoflurano versus propofol en niños con síndrome de Wolff-Parkinson-White. Rev. Española Anestesiol. Reanim. 2008, 55, 26–31. [Google Scholar] [CrossRef] [PubMed]
  22. Wutzler, A.; Huemer, M.; Boldt, L.-H.; Parwani, A.S.; Attanasio, P.; Tscholl, V.; Haverkamp, W. Effects of deep sedation on cardiac electrophysiology in patients undergoing radiofrequency ablation of supraventricular tachycardia: Impact of propofol and ketamine. EP Eur. 2013, 15, 1019–1024. [Google Scholar] [CrossRef] [PubMed]
  23. Paech, C.; Wagner, F.; Strehlow, V.; Gebauer, R.A. Drug-Induced Loss of Preexcitation in Pediatric Patients with WPW Pattern During Electrophysiologic Study. Pediatr. Cardiol. 2019, 40, 194–197. [Google Scholar] [CrossRef]
  24. Matsushima, M.; Kimura, S.; Kitaura, A.; Hamasaki, S.; Iwamoto, T.; Mino, T.; Masui, K.; Nakao, S. Propofol suppresses the His-ventricular conduction in paediatric patients. J. Clin. Pharm. Ther. 2021, 46, 433–439. [Google Scholar] [CrossRef]
  25. Lavoie, J.; Walsh, E.P.; Burrows, F.A.; Laussen, P.; Lulu, J.A.; Hansen, D.D. Effects of propofol or isoflurane anesthesia on cardiac conduction in children undergoing radiofrequency catheter ablation for tachydysrhythmias. Anesthesiology 1995, 82, 884–887. [Google Scholar] [CrossRef]
  26. Sharpe, M.D.; Dobkowski, W.B.; Murkin, J.M.; Klein, G.; Yee, R. Propofol has no direct effect on sinoatrial node function or on normal atrioventricular and accessory pathway conduction in Wolff-Parkinson-White syndrome during alfentanil/midazolam anesthesia. Anesthesiology 1995, 82, 888–895. [Google Scholar] [CrossRef]
  27. Erb, T.O.; Kanter, R.J.; Hall, J.M.; Gan, T.J.; Kern, F.H.; Schulman, S.R. Comparison of Electrophysiologic Effects of Propofol and Isoflurane-based Anesthetics in Children Undergoing Radiofrequency Catheter Ablation for Supraventricular Tachycardia. Anesthesiology 2002, 96, 1386–1394. [Google Scholar] [CrossRef]
  28. Fazelifar, A.; Eskandari, A.; Hashemi, M.; Alavi, M.; Totounchi, M.; Forghanian, A.; Zeighami, M.; Emkanjoo, Z.; Haghjoo, M. Deep sedation in patients undergoing atrioventricular nodal reentry tachycardia ablation. Res. Cardiovasc. Med. 2013, 2, 176. [Google Scholar] [CrossRef]
  29. Schünemann, H.J.; Oxman, A.D.; Brozek, J.; Glasziou, P.; Jaeschke, R.; Vist, G.E.; Williams, J.W., Jr.; Kunz, R.; Craig, J.; Montori, V.M.; et al. GRADE: Grading quality of evidence and strength of recommendations for diagnostic tests and strategies. BMJ 2008, 336, 1106–1110. [Google Scholar] [CrossRef]
  30. Granholm, A.; Alhazzani, W.; Møller, M.H. Use of the GRADE approach in systematic reviews and guidelines. Br. J. Anaesth. 2019, 123, 554–559. [Google Scholar] [CrossRef]
  31. Zipes, D.P. Guidelines for clinical intracardiac electrophysiological and catheter ablation procedures. A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on Clinical Intracardiac Electrophysiologic and Catheter Ablation Procedures), developed in collaboration with the North American Society of Pacing and Electrophysiology. J. Am. Coll. Cardiol. 1995, 26, 555–573. [Google Scholar] [PubMed]
  32. Aliot, E.M.; Stevenson, W.G.; Almendral-Garrote, J.M.; Bogun, F.; Calkins, C.H.; Delacretaz, E.; Della Bella, P.; Hindricks, G.; Jaïs, P.; Josephson, M.E.; et al. EHRA/HRS Expert Consensus on Catheter Ablation of Ventricular Arrhythmias: Developed in a partnership with the European Heart Rhythm Association (EHRA), a Registered Branch of the European Society of Cardiology (ESC), and the Heart Rhythm Society (HRS); in collaboration with the American College of Cardiology (ACC) and the American Heart Association (AHA). Europace: European pacing, arrhythmias, and cardiac electrophysiology: Journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology. EP Eur. 2009, 11, 771–817. [Google Scholar]
  33. Magaldi, M.; Fontanals, J.; Pérez, J. Sinusal reversion of atrial flutter after intravenous propofol administration. Med. Intensiv. 2014, 38, 127–128. [Google Scholar] [CrossRef] [PubMed]
  34. Hong, J.; Xu, M.; Kong, A.; Liu, Q.; Chen, R.; Dai, Q.; Wang, L.; Sun, B. Propofol terminates ventricular fibrillation storm caused by pulmonary embolism. Chin. Med. J. 2014, 127, 3840. [Google Scholar] [CrossRef]
  35. Harris, A.P.; Fleisher, L.A. Changes in Heart Rate Variability Under Propofol Anesthesia: A Possible Explanation for Propofol-Induced Bradycardia. Anesth. Analg. 1994, 79, 373–377. [Google Scholar]
  36. Napolitano, C.A.; Raatikainen, M.J.; Martens, J.R.; Dennis, D.M. Effects of intravenous anesthetics on atrial wavelength and atrioventricular nodal conduction in guinea pig heart. Potential antidysrhythmic properties and clinical implications. Anesthesiology 1996, 85, 393–402. [Google Scholar] [CrossRef]
  37. Kurokawa, H.; Murray, P.A.; Damron, D.S. Propofol attenuates beta-adrenoreceptor-mediated signal transduction via a protein kinase C-dependent pathway in cardiomyocytes. Anesthesiology 2002, 96, 688–698. [Google Scholar] [CrossRef]
  38. Burjorjee, J.E.; Milne, B. Propofol for electrical storm; a case report of cardioversion and suppression of ventricular tachycardia by propofol. Can. J. Anaesth. 2002, 49, 973–977. [Google Scholar] [CrossRef]
  39. Hermann, R.; Vettermann, J. Change of Ectopic Supraventricular Tachycardia to Sinus Rhythm During Administration of Propofol. Anesth. Analg. 1992, 75, 1030–1032. [Google Scholar] [CrossRef]
  40. Mulpuru, S.K.; Patel, D.V.; Wilbur, S.L.; Vasavada, B.C.; Furqan, T. Electrical storm and termination with propofol therapy: A case report. Int. J. Cardiol. 2008, 128, 6–8. [Google Scholar] [CrossRef]
Anesthres 02 00016 g001
Figure 1. PRISMA flow diagram for the studies selection process.
Figure 1. PRISMA flow diagram for the studies selection process.
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Figure 2. Forest Plot of propofol versus control for the Cycle length (CL) period.
Figure 2. Forest Plot of propofol versus control for the Cycle length (CL) period.
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Figure 3. Funnel Plot for the CL variable.
Figure 3. Funnel Plot for the CL variable.
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Figure 4. Forest Plot of propofol versus control for the Atrial-His (AH) period.
Figure 4. Forest Plot of propofol versus control for the Atrial-His (AH) period.
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Figure 5. Funnel Plot for the AH variable.
Figure 5. Funnel Plot for the AH variable.
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Figure 6. Forest Plot of propofol versus control for the HV period.
Figure 6. Forest Plot of propofol versus control for the HV period.
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Figure 7. Funnel Plot for the HV variable.
Figure 7. Funnel Plot for the HV variable.
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Figure 8. Forest Plot of propofol versus control for the CSNRT period.
Figure 8. Forest Plot of propofol versus control for the CSNRT period.
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Figure 9. Funnel Plot for the CSNRT variable.
Figure 9. Funnel Plot for the CSNRT variable.
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Figure 10. Forest Plot of propofol versus control for the AERP/FP period.
Figure 10. Forest Plot of propofol versus control for the AERP/FP period.
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Figure 11. Funnel Plot for the AERP/FP.
Figure 11. Funnel Plot for the AERP/FP.
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Figure 12. Forest Plot of propofol versus control for the VERP period.
Figure 12. Forest Plot of propofol versus control for the VERP period.
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Figure 13. Funnel Plot for the VERP variable.
Figure 13. Funnel Plot for the VERP variable.
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Figure 14. Forest Plot of propofol versus control for the AVNERP period.
Figure 14. Forest Plot of propofol versus control for the AVNERP period.
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Figure 15. Funnel Plot for the AVNERP variable.
Figure 15. Funnel Plot for the AVNERP variable.
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Table 1. Search strategy used in PubMed.
Table 1. Search strategy used in PubMed.
ConectorSearch Terms
“Propofol” [Mesh] OR “2,6-Diisopropylphenol” [TITLE/ABSTRACT] OR “2,6 Diisopropylphenol” [TITLE/ABSTRACT] OR “2,6-Bis(1-methylethyl)phenol” [TITLE/ABSTRACT] OR “Disoprofol” [TITLE/ABSTRACT] OR “Diprivan” [TITLE/ABSTRACT] OR “Disoprivan” [TITLE/ABSTRACT] OR “Fresofol” [TITLE/ABSTRACT] OR “Ivofol” [TITLE/ABSTRACT] OR “Propofol Fresenius” [TITLE/ABSTRACT] OR “Propofol MCT” [TITLE/ABSTRACT] OR “Propofol-Lipuro” [TITLE/ABSTRACT] OR “Recofol” [TITLE/ABSTRACT] OR “Aquafol” [TITLE/ABSTRACT] OR “Propofol Abbott” [TITLE/ABSTRACT]
AND“Arrhythmias, Cardiac” [Mesh] OR “Arrhythmia, Cardiac” [TITLE/ABSTRACT] OR “Cardiac Dysrhythmia” [TITLE/ABSTRACT] OR “Dysrhythmia, Cardiac” [TITLE/ABSTRACT] OR “Cardiac Arrhythmia” [TITLE/ABSTRACT] OR “Cardiac Arrhythmias” [TITLE/ABSTRACT] OR “Arrhythmia” [TITLE/ABSTRACT] OR “Arrythmia” [TITLE/ABSTRACT]
AND“Cardiac Electrophysiology” [Mesh] OR “Electrophysiology, Cardiac” [TITLE/ABSTRACT] OR “Electrophysiologic Techniques, Cardiac” [Mesh] OR “Cardiac Electrophysiologic Technique” [TITLE/ABSTRACT] OR “Electrophysiological Techniques, Intracardiac” [TITLE/ABSTRACT] OR “Transesophageal Electrophysiologic Study” [TITLE/ABSTRACT] OR “Atrial Electrograms” [TITLE/ABSTRACT] OR “Electrophysiologic Study, Cardiac” [TITLE/ABSTRACT] OR “His Bundle Electrogram” [TITLE/ABSTRACT] OR “Catheter Ablation” [Mesh] OR “Ablation, Catheter” [TITLE/ABSTRACT] OR “Catheter Ablation, Radiofrequency” [TITLE/ABSTRACT] OR “Radiofrequency Catheter Ablation” [TITLE/ABSTRACT] OR “Ablation, Radiofrequency Catheter” [TITLE/ABSTRACT]
Table 2. Baseline characteristics of patients from the included studies.
Table 2. Baseline characteristics of patients from the included studies.
Author and
Year		Study DesignSample SizeGender Male/FemMean AgeType of ArrhythmiaLoss of Pre-ExcitationArrhythmia InductionNo Induction of ArrhythmiaPrevented AblationSupressed AV Conduction
Romano R,
1994 [19]		Prospective cohort108/246 ± 19No base pathologyNo10NoNoNo
Lai LP, 1999 [20]Prospective cohort15078/72Adults (n = 86)
44 ± 16
Ped (n = 64)
11 ± 3.3		24 flutter
31 NRT
68 AVRT
12 EVT
17 EAT		No14844 out of 7 Ped with EATNo
Pérez, 2008 [21]Prospective cohort1511/49.3 ± 3.6WPWNo15NoNoNo
Wutzler, 2013 [22]Prospective cohort3115/1652 ± 16WPWNo31NoNoNo
Paech, 2019 [23]Prospective
cohort		3724/1313 ± 4WPW637NoNoNo
Matsushima,
2021 [24]		Prospective
cohort		2316/76 ± 1.512 WPW
8 SVT
3 TVE		No23NoNoNo
Ped: pediatric; NRT: nodal reentrante tachycardia; AVRT: atrioventricular reciprocity tachycardia; EAT: ectopic atrial tachycardia EVT: ectopic ventricular tachycardia; WPW: Wolff-Parkinson-White; SVT: supraventricular tachycardia.
Table 3. Risk of bias for allocated studies.
Table 3. Risk of bias for allocated studies.
StudiesControl Group for Placebo EffectRandomized Group AllocationRandom Sequence Generation (Selection Bias)Allocation Concealment (Selection Bias)Selective Reporting (Reporting Bias)
Lavoie, 1995 [25]Anesthres 02 00016 i001Anesthres 02 00016 i002Anesthres 02 00016 i003Anesthres 02 00016 i002Anesthres 02 00016 i002
Sharpe, 1995 [26]Anesthres 02 00016 i001Anesthres 02 00016 i001Anesthres 02 00016 i003Anesthres 02 00016 i002Anesthres 02 00016 i002
Erb, 2002 [27] Anesthres 02 00016 i001Anesthres 02 00016 i001Anesthres 02 00016 i001Anesthres 02 00016 i002Anesthres 02 00016 i002
Warpechowski, 2006 [15] Anesthres 02 00016 i001Anesthres 02 00016 i001Anesthres 02 00016 i001Anesthres 02 00016 i002Anesthres 02 00016 i002
Fazelifar, 2013 [28] Anesthres 02 00016 i001Anesthres 02 00016 i002Anesthres 02 00016 i003Anesthres 02 00016 i002Anesthres 02 00016 i002
Legend: Anesthres 02 00016 i001 Low risk of bias, Anesthres 02 00016 i002 Uncertain risk of bias, Anesthres 02 00016 i003 High risk of bias.
Table 4. Summary of studied effects of propofol on variables measured during EPS on outcomes of interest across included studies and quality evidence from the GRADE.
Table 4. Summary of studied effects of propofol on variables measured during EPS on outcomes of interest across included studies and quality evidence from the GRADE.
OutcomeNumber of StudiesNumber of ParticipantsStatistical MethodEffect Sizep-ValueHeterogeneity (I2)Certainty of Evidence (Grade)
CL4200MD, Random19.21 (16.59, 55)0.550⨁⨁⨁⨁
AH5209MD, Random1.68 (2.26, 6.51)0.390⨁⨁⨁⨁
HV5195MD, Random−0.39, 1.380.890⨁⨁⨁⨁
CSNRT366MD, Random21 (7.53, 52.31)0.460⨁⨁⨁⨁
AERP/FP5211MD, Random9.15 (3.64, 21.94)0.520⨁⨁⨁⨁
AVNERP4180MD, Random18.67 (−4.86, 32.47)0.150⨁⨁⨁◯
VERP268MD, Random9.79 (2.16, 17.86)0.130⨁⨁⨁◯
CL: cycle length; AH: atrial-His; HV: his-ventricular; CSNRT: corrected sinus node recovery time; AERP/FP: atrial effective refractory period/fast pathway; AVNERP: AV node refractory period; VERP: ventricular effective refractory period; MD: mean difference. Legend: ⨁⨁⨁⨁ High evidence, ⨁⨁⨁◯ Moderate evidence.
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Warpechowski, P.; Warpechowski, R.B.; De Lima, B.A.; Pinto, E.F.A.; Bastos, M.L.S.; Eibel, B.; Trindade, R.D.; Leiria, T.L. Effects of Propofol in the Cardiac Conduction System in Electrophysiologic Study: Systematic Review and Meta-Analysis. Anesth. Res. 2025, 2, 16. https://doi.org/10.3390/anesthres2030016

AMA Style

Warpechowski P, Warpechowski RB, De Lima BA, Pinto EFA, Bastos MLS, Eibel B, Trindade RD, Leiria TL. Effects of Propofol in the Cardiac Conduction System in Electrophysiologic Study: Systematic Review and Meta-Analysis. Anesthesia Research. 2025; 2(3):16. https://doi.org/10.3390/anesthres2030016

Chicago/Turabian Style

Warpechowski, Paulo, Rodrigo B. Warpechowski, Barbara A. De Lima, Emanuella F. A. Pinto, Mariana L. S. Bastos, Bruna Eibel, Rubens D. Trindade, and Tiago L. Leiria. 2025. "Effects of Propofol in the Cardiac Conduction System in Electrophysiologic Study: Systematic Review and Meta-Analysis" Anesthesia Research 2, no. 3: 16. https://doi.org/10.3390/anesthres2030016

APA Style

Warpechowski, P., Warpechowski, R. B., De Lima, B. A., Pinto, E. F. A., Bastos, M. L. S., Eibel, B., Trindade, R. D., & Leiria, T. L. (2025). Effects of Propofol in the Cardiac Conduction System in Electrophysiologic Study: Systematic Review and Meta-Analysis. Anesthesia Research, 2(3), 16. https://doi.org/10.3390/anesthres2030016

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