ReviewHerzschrittmachertherapie & Elektrophysiologie2019
[Cardiac arrhythmias in patients with chronic autoimmune diseases].
Review in Herzschrittmachertherapie & Elektrophysiologie, 2019. 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, 2 citations in OpenAlex.
- Autoimmune antibodies in arrhythmia: a narrative review of potential therapeutic targets to prevent overtreatment.Cardiovascular diagnosis and therapy · 2025Review
- Cardiac conduction disturbances in rheumatologic disease: a cross-sectional study.American journal of cardiovascular disease · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic inflammation due to autoimmune diseases is associated with a higher rate of supraventricular and ventricular arrhythmias leading to an increased risk for cardiovascular morbidity and mortality. Involvement of the cardiac conduction system is common in patients with chronic autoimmune diseases, although the penetrance of clinical signs and symptoms is variable and complete heart block with need for therapy is rare. The combination of the increased prevalence of structural cardiovascular disease and the direct impact of inflammatory mechanisms on cardiac electrophysiology seems to be responsible for the higher rate of tachyarrhythmias. In particular, fibroblast activation, gap junction impairment via changes in connexin composition and abnormalities in intracellular calcium-handling are mentioned. Electrocardiographic markers of an increased arrhythmogenic potential in patients with chronic autoimmune disorders may include prolonged P‑wave duration as well as abnormal QTc interval and reduced heart rate variability. Thus, minimizing the inflammatory burden through tight control of disease activity may help reduce the arrhythmic load.
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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.