ReviewCJC open2025
Consequences of Right Heart Disease for Cardiac Electrophysiology and Arrhythmias: Cellular and Structural Mechanisms.
Review in CJC open, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Conditions provoking the electrical and structural-functional remodelling of the myocardium can lead to the development of heart rhythm disorders, including atrial fibrillation (AF) and ventricular tachyarrhythmias that can cause sudden cardiac death. Right heart disease (RHD) causes progressive structural and functional remodelling of the right heart responsible for right ventricular and atrial dysfunction and arrhyhmias. Conditions contributing to the development of RHD include left heart disease, pulmonary arterial hypertension, congenital heart disease, right-sided myocardial infarction due to coronary artery occlusion, and amyloidosis. In adult patients with RHD associated with pulmonary arterial hypertension, the prevalence of AF is about 20%, and in adult patients with arrhythmogenic right ventricular cardiomyopathy, it is 14%. A study has suggested that compared to non patients without congenital heart disease, AF appears 30 years earlier in adult patients with congenital heart disease, with a 10-20-fold-higher incidence. This narrative review article aims to review knowledge about the pathophysiology of RHD associated with cardiac arrhythmia. Evidence is reported about the mechanisms underlying the initiation and maintenance of the arrhythmogenic substrate in RHD. We summarize the available experimental approaches to study RHD associated with cardiac arrhythmia, including
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