Observational studyESC heart failure2025
Left ventricular diastolic dysfunction worsens prognosis in patients with heart failure due to dilated cardiomyopathy.
Observational study in ESC heart failure, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed.
- A new KLF13 loss-of-function mutation responsible for sporadic dilated cardiomyopathy.Molecular biology reports · 2025Article
- Discovery ofDiagnostics (Basel, Switzerland) · 2025Article
- Left ventricular diastolic dysfunction worsens prognosis in patients with heart failure due to dilated cardiomyopathy.ESC heart failure · 2025Observational
- Roles of Autophagy, Mitophagy, and Mitochondria in Left Ventricular Remodeling after Myocardial Infarction.Reviews in cardiovascular medicine · 2025Review
- The inflammatory and nutritional status in patients with dilated cardiomyopathy: Different impact for distinct phenogroups?International journal of cardiology. Heart & vasculature · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors.
Funding
Abstract
aimsThe prognostic significance of left ventricular (LV) diastolic dysfunction (LVDD) severity in patients with dilated cardiomyopathy (DCM) remains uncertain. This study aimed to evaluate the association of LVDD severity and elevated left atrial pressure (eLAP) with patient outcomes in stable, non-acutely decompensated patients with DCM.
methodsThis single-centre, retrospective, observational study involved 740 DCM patients (either inpatients or outpatients) managed at our tertiary cardiac centre between 2010 and 2021. Due to incomplete data, 96 patients were excluded. LVDD and eLAP were assessed using echocardiography according to the 2016 guidelines of the European Association of Cardiovascular Imaging (EACVI). The primary outcomes were all-cause mortality and heart failure (HF)-related mortality.
resultsThe final cohort comprised of 644 DCM patients [mean age: 52 ± 12 years, LV ejection fraction (LVEF): 26 ± 10%]. Over a median follow-up period of 41 (18.5-66.7) months, 105 (16.3%) patients died: 8 (5.3%) patients in the normal left atrial pressure (nLAP) group and 97 (19.6%) patients in the eLAP group. eLAP was identified as an independent prognostic factor for both all-cause mortality [hazard ratio (HR) 2.0; 95% confidence interval (CI) 1.1-3.7; P = 0.01] and HF-related mortality (HR 2.5; 95% CI 1.01-6.5; P = 0.04), even after adjusting for LVEF and atrial fibrillation (AF) presence. Additionally, HF-related mortality rates were significantly higher in patients with moderate to severe LVDD compared with those with mild LVDD [5 (3.3%) vs. 67 (13.6%), P < 0.05].
conclusionsThis study's findings highlight the importance of assessing the severity of LVDD in patients with DCM, which provides incremental prognostic information over LVEF.
Indexed as
Identifiers
What 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.