ReviewCurrent treatment options in cardiovascular medicine2018
Ablation Approaches for Ventricular Fibrillation.
Review in Current treatment options in cardiovascular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- [History of catheter ablation].Herzschrittmachertherapie & Elektrophysiologie · 2019Review
- Handling of Ventricular Fibrillation in the Emergency Setting.Frontiers in pharmacology · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Invasive electrophysiology (EP) mapping and catheter ablation has increasingly become the standard of care for many cardiac arrhythmias like supraventricular tachycardias, atrial fibrillation, premature ventricular complexes (PVC), and monomorphic ventricular tachycardia. In this review, we discuss the recent progress made in the mapping and ablation of ventricular fibrillation (VF). Ventricular activation during VF is apparently disorganized, making mapping and interpretation difficult. Prolonged mapping during VF would require mechanical circulatory support as VF causes complete hemodynamic collapse. These limitations have been addressed by the realization that there is often a reliable trigger arrhythmia that initiates the clinical VF episodes, and an approach to map and ablate this trigger can be successful. Such triggers can be PVCs localizing to the Purkinje/fascicular system, and in other cases can be ectopy from outflow tracts or intracavitary structures like papillary muscles, false tendons or moderator band, or can be monomorphic VT or preexcited atrial fibrillation that degenerate into VF. More recently, approaches beyond trigger elimination directly targeting the VF substrate have been devised. This includes elimination of the arrhythmogenic substrate localizing to the epicardial right ventricular outflow tract in patients with Brugada syndrome, akin to elimination of the arrhythmogenic substrate harbored by regions within scar in ischemic and non-ischemic cardiomyopathies. Further, recent attempts have been made to try to identify and ablate rotors during VF that may be important in perpetuating the VF episode. Such exciting advances in "curing" VF are proving to be life saving for resuscitated survivors of arrhythmic death.
Indexed as
Identifiers
29508083What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.