Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 4 complete abstracts (1,005 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
A potentially lethal cardiac arrhythmia that is characterized by uncoordinated extremely rapid firing of electrical impulses (400-600/min) in heart ventricles. Such asynchronous ventricular quivering or fibrillation prevents any effective cardiac output and results in unconsciousness (syncope). It is one of the major electrocardiographic patterns seen with cardiac arrest.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Fibrillations, Ventricular; Fibrillation, Ventricular; Ventricular Fibrillations.
Where it fits in the MeSH classification
- Broader topics
- Arrhythmias, Cardiac
Related concepts
- Heart Ventricles
- Syncope
- Cardiac Arrest
Research landscape
PubMed indexes 18,420 records tagged with the MeSH heading “Ventricular Fibrillation” (counts retrieved 2026-10-29). 1,376 of them (7.5%) were published from 2020 onward, and the busiest period so far is through 1999 with 9,777 records.
Reviews account for 1,716 records (9.3%) and meta-analyses for 72. Randomized controlled trials number 464 (2.5%) as a share of all records on the topic.
Show the data
| Period | Records |
|---|---|
| through 1999 | 9,777 |
| 2000-2009 | 3,720 |
| 2010-2019 | 3,547 |
| 2020 onward | 1,376 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 1,716 | 9.3% |
| Meta-analyses | 72 | 0.4% |
| Randomized controlled trials | 464 | 2.5% |
Method: PubMed query "Ventricular Fibrillation"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-29.
Reading the evidence in cardiovascular medicine
Cardiovascular medicine has an unusually large body of randomized trials, so the type of outcome matters: hard clinical events such as death, heart attack and stroke carry more weight than changes in blood pressure, cholesterol or imaging markers that only predict risk. Observational studies can show associations but are confounded by age, lifestyle and other illness. Check whether a result is about prevention or treatment, the baseline risk of participants, and the absolute rather than only the relative size of any benefit.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
Ventricular fibrillation mechanism and global fibrillatory organization are determined by gap junction coupling and fibrosis pattern [1]
Abstract reading summary — source excerpts
- Opening excerpt
- AimsConflicting data exist supporting differing mechanisms for sustaining ventricular fibrillation (VF), ranging from disorganized multiple-wavelet activation to organized rotational activities (RAs).
- Closing excerpt
- There is a continuous spectrum of organization in VF, ranging between globally organized fibrillation sustained by stable RAs and disorganized, possibly multiple-wavelet driven fibrillation with no RAs.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (190 words)
AimsConflicting data exist supporting differing mechanisms for sustaining ventricular fibrillation (VF), ranging from disorganized multiple-wavelet activation to organized rotational activities (RAs). Abnormal gap junction (GJ) coupling and fibrosis are important in initiation and maintenance of VF. We investigated whether differing ventricular fibrosis patterns and the degree of GJ coupling affected the underlying VF mechanism.Methods and resultsOptical mapping of 65 Langendorff-perfused rat hearts was performed to study VF mechanisms in control hearts with acute GJ modulation, and separately in three differing chronic ventricular fibrosis models; compact fibrosis (CF), diffuse fibrosis (DiF), and patchy fibrosis (PF). VF dynamics were quantified with phase mapping and frequency dominance index (FDI) analysis, a power ratio of the highest amplitude dominant frequency in the cardiac frequency spectrum. Enhanced GJ coupling with rotigaptide (n = 10) progressively organized fibrillation in a concentration-dependent manner; increasing FDI (0 nM: 0.53 ± 0.04, 80 nM: 0.78 ± 0.03, P ConclusionThe degree of GJ coupling and pattern of fibrosis influences the mechanism sustaining VF. There is a continuous spectrum of organization in VF, ranging between globally organized fibrillation sustained by stable RAs and disorganized, possibly multiple-wavelet driven fibrillation with no RAs.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 32402067 · DOI · PMC7983010
Safety and efficacy of a lattice-tip catheter for ventricular arrhythmia ablation: the AFFERA Ventricular Arrhythmia Ablation Registry (AVAAR) [2]
Abstract reading summary — source excerpts
- Opening excerpt
- AimsThe feasibility and safety of the lattice-tip catheter for ventricular arrhythmia (VA) ablation in humans remain largely unknown.
- Closing excerpt
- In the absence of large, randomized trials, exhaustive registry is of key importance to ensure safety and efficacy of new catheter technologies.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (263 words)
AimsThe feasibility and safety of the lattice-tip catheter for ventricular arrhythmia (VA) ablation in humans remain largely unknown. This study aimed to assess feasibility, safety profile as well as patient outcomes after VA ablation with a lattice-tip catheter in a multicentre European registry.Methods and resultsAll 18 European centres using the AFFERA system in September 2024 agreed to participate. Clinical, procedural, and follow-up data (minimum 3 months) were systematically collected and analysed. A total of 126 patients (18% female; mean age 59 ± 16 years) underwent VA ablation using the lattice-tip catheter during the inclusion period. Ablation indications included ventricular tachycardia (VT) in 99, premature ventricular complexes (PVCs) in 23, and ventricular fibrillation (VF) in 4 patients. Major and minor acute complications were observed in 7 (6%) and 18 (14%) procedures, respectively. They included thrombo-embolic event (n = 2), major bleeding (n = 2), ventricular fibrillation induction (n = 1), tamponade due to epicardial access (n = 1), and cardiogenic shock due to prolonged VT mapping (n = 1). Within the first month post-procedure, three patients died [from multi-organ failure (n = 2) and sepsis (n = 1)], two had worsening heart failure, one myocardial infarction, one sepsis, and one major gastro-intestinal bleeding. After a mean follow-up of 5.6 ± 3.7 months, absence of recurrence was 78% for PVC, 70% for VT, and 100% for VF.ConclusionIn this complex population with refractory VA, ablation using the lattice-tip catheter appears feasible and relatively safe. In the absence of large, randomized trials, exhaustive registry is of key importance to ensure safety and efficacy of new catheter technologies.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 40601816 · DOI · PMC12418093
Identification of loss-of-function RyR2 mutations associated with idiopathic ventricular fibrillation and sudden death [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Mutations in cardiac ryanodine receptor (RyR2) are linked to catecholaminergic polymorphic ventricular tachycardia (CPVT).
- Closing excerpt
- Thus, our data further support the link between RyR2 LOF and a new entity of cardiac arrhythmias distinct from CPVT.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (256 words)
Mutations in cardiac ryanodine receptor (RyR2) are linked to catecholaminergic polymorphic ventricular tachycardia (CPVT). Most CPVT RyR2 mutations characterized are gain-of-function (GOF), indicating enhanced RyR2 function as a major cause of CPVT. Loss-of-function (LOF) RyR2 mutations have also been identified and are linked to a distinct entity of cardiac arrhythmia termed RyR2 Ca2+ release deficiency syndrome (CRDS). Exercise stress testing (EST) is routinely used to diagnose CPVT, but it is ineffective for CRDS. There is currently no effective diagnostic tool for CRDS in humans. An alternative strategy to assess the risk for CRDS is to directly determine the functional impact of the associated RyR2 mutations. To this end, we have functionally screened 18 RyR2 mutations that are associated with idiopathic ventricular fibrillation (IVF) or sudden death. We found two additional RyR2 LOF mutations E4146K and G4935R. The E4146K mutation markedly suppressed caffeine activation of RyR2 and abolished store overload induced Ca2+ release (SOICR) in human embryonic kidney 293 (HEK293) cells. E4146K also severely reduced cytosolic Ca2+ activation and abolished luminal Ca2+ activation of single RyR2 channels. The G4935R mutation completely abolished caffeine activation of and [3H]ryanodine binding to RyR2. Co-expression studies showed that the G4935R mutation exerted dominant negative impact on the RyR2 wildtype (WT) channel. Interestingly, the RyR2-G4935R mutant carrier had a negative EST, and the E4146K carrier had a family history of sudden death during sleep, which are different from phenotypes of typical CPVT. Thus, our data further support the link between RyR2 LOF and a new entity of cardiac arrhythmias distinct from CPVT.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 33825858 · DOI · PMC8062958
Ventricular fibrillation dynamics reveal regional asymmetry in resilience to cardiac arrest and predict clinical outcome [4]
Abstract reading summary — source excerpts
- Opening excerpt
- AimsVentricular fibrillation (VF) is the leading cause of sudden cardiac death.
- Closing excerpt
- Among patients admitted after a VF-related cardiac arrest event, higher ARs prior to the first defibrillation shock are predictive of a favourable neurological outcome.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (296 words)
AimsVentricular fibrillation (VF) is the leading cause of sudden cardiac death. Nevertheless, the mechanisms underlying VF dynamics in structurally normal hearts and infarct-related substrates remain incompletely understood. We aimed to characterize the electrophysiological, structural and molecular properties that explain VF dynamics during early phases (seconds) and long-duration episodes (minutes) in experimental pig models. Additionally, we assessed the clinical impact of VF dynamics on neurological prognosis following resuscitated cardiac arrest.Methods and resultsA total of 72 pigs were included in the study. In vivo multipolar-catheter recordings revealed that early VF dynamics are independent of the infarct-related substrate. Healthy and infarcted animals consistently showed higher activation rates (AR) in the right ventricle (RV) than in the left ventricle (LV), and this gradient further increased during long-duration VF. Ex vivo panoramic optical mapping of long-duration VF episodes resembling cardiac arrest conditions confirmed in vivo findings and revealed earlier electrical depression in the LV. AR gradients during VF were primarily driven by an asymmetric response to the global ischaemia conditions intrinsically associated with VF, during which the RV exhibited greater resilience than the LV. Computational simulations, incorporating experimentally derived electrophysiological properties and region-specific metabolic parameters during ischaemia, demonstrated that the fibrillating RV preserves higher excitability than the LV, creating RV-to-LV AR gradients during VF. The translational relevance of these findings was evaluated in patients with VF events, in whom long-term (>2 min) ECG-derived AR patterns (N = 3) resembled those documented in pigs. Moreover, in 60 patients with out-of-hospital cardiac arrest, ECG-derived ARs prior to the first defibrillation shock for VF were associated with favourable neurological outcome.ConclusionVF dynamics are modulated by asymmetric myocardial tolerance to global ischaemia. Among patients admitted after a VF-related cardiac arrest event, higher ARs prior to the first defibrillation shock are predictive of a favourable neurological outcome.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42203211 · DOI · PMC13307562
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article ACC/AHA/ESC 2006 guidelines for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death: a report of the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Develop Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death) [5]
- Research article 2017 AHA/ACC/HRS Guideline for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society [6]
- Research article 2017 AHA/ACC/HRS Guideline for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death: Executive Summary: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society [7]
- Research article Rotors and the dynamics of cardiac fibrillation [8]
- Research article The Early Repolarization Pattern: A Consensus Paper [9]
- Research article The dynamics of cardiac fibrillation [10]
References
- Handa BS, Li X, Baxan N, Roney CH, Shchendrygina A, Mansfield CA, et al.. Ventricular fibrillation mechanism and global fibrillatory organization are determined by gap junction coupling and fibrosis pattern. . 2021. PMID 32402067 · DOI · PMC7983010
- Sacher F, Sarkozy A, Pürerfellner H, Steyer A, Lyne J, Coquard C, et al.. Safety and efficacy of a lattice-tip catheter for ventricular arrhythmia ablation: the AFFERA Ventricular Arrhythmia Ablation Registry (AVAAR). . 2025. PMID 40601816 · DOI · PMC12418093
- Zhong X, Guo W, Wei J, Tang Y, Liu Y, Zhang JZ, et al.. Identification of loss-of-function RyR2 mutations associated with idiopathic ventricular fibrillation and sudden death. . 2021. PMID 33825858 · DOI · PMC8062958
- Redondo-Rodríguez A, Quintanilla JG, Macías Á, Lee P, Calvo D, Couselo-Seijas M, et al.. Ventricular fibrillation dynamics reveal regional asymmetry in resilience to cardiac arrest and predict clinical outcome. . 2026. PMID 42203211 · DOI · PMC13307562
- European Heart Rhythm Association, Heart Rhythm Society, Zipes DP, Camm AJ, Borggrefe M, Buxton AE, et al.. ACC/AHA/ESC 2006 guidelines for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death: a report of the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Develop Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death). J Am Coll Cardiol. 2006. PMID 16949478 · DOI
- Al-Khatib SM, Stevenson WG, Ackerman MJ, Bryant WJ, Callans DJ, Curtis AB, et al.. 2017 AHA/ACC/HRS Guideline for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. Circulation. 2018. PMID 29084731 · DOI
- Al-Khatib SM, Stevenson WG, Ackerman MJ, Bryant WJ, Callans DJ, Curtis AB, et al.. 2017 AHA/ACC/HRS Guideline for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death: Executive Summary: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. Circulation. 2018. PMID 29084733 · DOI
- Pandit SV, Jalife J. Rotors and the dynamics of cardiac fibrillation. Circ Res. 2013. PMID 23449547 · DOI · PMC3650644
- Macfarlane PW, Antzelevitch C, Haissaguerre M, Huikuri HV, Potse M, Rosso R, et al.. The Early Repolarization Pattern: A Consensus Paper. J Am Coll Cardiol. 2015. PMID 26205599 · DOI
- Weiss JN, Qu Z, Chen PS, Lin SF, Karagueuzian HS, Hayashi H, et al.. The dynamics of cardiac fibrillation. Circulation. 2005. PMID 16116073 · DOI
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-29.
See how EvidenceLib is built. Spotted an error? Email support@evidencehelix.com.
Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.