ReviewCirculation research2026
Right Heart Diastology, Where Are We Now?
Review in Circulation research, 2026. 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
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Right heart diastolic dysfunction is increasingly recognized as an early and prognostically relevant process in patients with pulmonary vascular disease, heart failure, and congenital heart disease, among others. Despite this, right heart diastolic dysfunction remains poorly defined and inconsistently measured. This review reframes right heart diastology as a disorder of a unified diastolic unit, integrating right atrial function, right ventricular compliance, and pulmonary arterial load. We synthesize invasive physiology, imaging, and human myocardial data to show that abnormalities in relaxation and compliance commonly precede overt right heart systolic failure and are mediated by load-dependent coupling relationships rather than by isolated chamber dysfunction. Distinct pressure-volume relationships, strong afterload sensitivity, and distinct atrioventricular coupling interactions render left-ventricular paradigms inadequate to understand the right heart. At the molecular level, we examine chamber-specific determinants of right ventricular stiffness, including fibrosis, titin isoform switching, and neurohormonal signaling, grading the evidence across validated, supported, and inferred tiers. We critically appraise available invasive, echocardiographic, and cardiac magnetic resonance indices, highlighting where validation is robust and where extrapolation persists. Finally, we propose a tiered diagnostic data set and a grading framework centered on the right heart diastolic unit, intended to guide future mechanistic studies and prospective clinical validation.
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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.