Evidence mapPaperPMID 26527692Full record

ReviewCirculation2015

Molecular Mechanisms of Right Ventricular Failure.

Sushma Reddy, Daniel Bernstein

2 registry-linked trialsOpen access · bronzeAbstract readReview
In one paragraph

Review in Circulation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to 2 registered trials, which are not on this map. Cited by 98 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
98citing papers in PubMed, 1 pooled it
9.3field-weighted citation impact, top 2% of its field
1 · What the graph read from it

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.

2 · The registry

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.

NCT04130243 unknown statusnot on this mapstarted 2017, after this paper: background citation

Biomarkers in Congenital Heart Diseases and Pulmonary Arterial Hypertension

Typeobservational_patient_registrySponsorUniversity Medical Center GroningenRan2017 to 2024Enrolled380ConditionsCongenital Heart Disease, Pulmonary Arterial HypertensionArmsBlood test
NCT05117736 naterminatednot on this mapstarted 2022, after this paper: background citation

Prospective Comparison of ARNI Versus plAcebo in Patients With Congenital sYStemic Right Ventricle Heart Failure

TypeinterventionalSponsorMontreal Heart InstituteRan2022 to 2023Enrolled15ConditionsSystemic Right Ventricle, Heart FailureArmsSacubitril / Valsartan Oral Tablet, Placebo
3 · Its place in the literature

Who cites it

98 citing papers in PubMed, 1 synthesis or guideline pooled it, 165 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Review
  12. Molecular Mechanisms of Cardiac Adaptation After Device Deployment.Journal of cardiovascular development and disease · 2025
    Review
  13. Review
  14. Review
  15. Article
  16. Right ventricle remodelling: fromJournal of molecular and cellular cardiology plus · 2025
    Review
  17. Observational
  18. Review
  19. Review
  20. Mitochondrial Dysfunction in Congenital Heart Disease.Journal of cardiovascular development and disease · 2025
    Review

38 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Sushma ReddyFrom Department of Pediatrics (Cardiology) and the Stanford Cardiovascular Institute, Stanford University, Palo Alto, CA. sureddy@stanford.edu.
Daniel BernsteinFrom Department of Pediatrics (Cardiology) and the Stanford Cardiovascular Institute, Stanford University, Palo Alto, CA.
Cardiovascular Institute of the South · US

Funding

ROLE OF BETA-RECEPTOR SIGNALING IN CARDIOMYOPATHYR01HL061535 · STANFORD UNIVERSITY · 2000 to 2004
$1.7M
NHLBI NIH HHS HL061535NHLBI NIH HHS K08 HL127277NHLBI NIH HHS R01 HL061535
6 · The paper itself

Abstract

An abundance of data has provided insight into the mechanisms underlying the development of left ventricular (LV) hypertrophy and its progression to LV failure. In contrast, there is minimal data on the adaptation of the right ventricle (RV) to pressure and volume overload and the transition to RV failure. This is a critical clinical question, because the RV is uniquely at risk in many patients with repaired or palliated congenital heart disease and in those with pulmonary hypertension. Standard heart failure therapies have failed to improve function or survival in these patients, suggesting a divergence in the molecular mechanisms of RV versus LV failure. Although, on the cellular level, the remodeling responses of the RV and LV to pressure overload are largely similar, there are several key differences: the stressed RV is more susceptible to oxidative stress, has a reduced angiogenic response, and is more likely to activate cell death pathways than the stressed LV. Together, these differences could explain the more rapid progression of the RV to failure versus the LV. This review will highlight known molecular differences between the RV and LV responses to hemodynamic stress, the unique stressors on the RV associated with congenital heart disease, and the need to better understand these molecular mechanisms if we are to develop RV-specific heart failure therapeutics.

Indexed as

Gene Expression RegulationHemodynamicsAdaptation, PhysiologicalAnimalsCell HypoxiaDisease Models, AnimalHeart FailureHeart VentriclesHumansMicroRNAsMitochondria, HeartMyocardial IschemiaMyocardiumNeovascularization, PhysiologicOxidative StressReactive Oxygen SpeciesMicroRNAsReactive Oxygen Speciesangiogenesisheart defects, congenitalheart failurehypertrophyoxidative stress

Identifiers

PMID26527692
PMCPMC4635965
OpenAlexW1944669821

What Socratic holds

Textmetadata
LicenceTDM
Read underepoch 390

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 Socratic graph.