Evidence map›Paper›PMID 34826024›Full record

ReviewHeart failure reviews2022

Right ventricular failure: a comorbidity or a clinical emergency?

Pamelika Das, Rajarajan A Thandavarayan, Kenichi Watanabe, Ravichandiran Velayutham, Somasundaram Arumugam

Abstract readReview
PubMed Publisher
In one paragraph

Review in Heart failure reviews, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.7field-weighted citation impact, top 27% 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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
  2. Systemic delivery of biotherapeutic RNA to the myocardium transiently modulates cardiac contractility in vivo.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
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

5 authors at 3 institutions in 3 countries.

Pamelika DasDepartment of Pharmacology and Toxicology, National Institute of Pharmaceutical Education and Research (NIPER)-Kolkata, Chunilal Bhawan, 168 Maniktala Main Road, Kolkata, 700054, West Bengal, India.
Rajarajan A ThandavarayanDepartment of Cardiology, Houston Methodist Hospital, Houston, TX, 77030, USA.
Kenichi WatanabeDepartment of Laboratory Medicine and Clinical Epidemiology for Prevention of Noncommunicable Diseases, Niigata University Graduate School of Medical and Dental Sciences, 1-757 Asahimachi-dori, Chuo-ku, NiigataNiigata, 951-8510, Japan.
Ravichandiran VelayuthamNational Institute of Pharmaceutical Education and Research (NIPER)-Kolkata, Chunilal Bhawan, 168 Maniktala Main Road, Kolkata, 700054, West Bengal, India. director@niperkolkata.edu.in.
Somasundaram ArumugamDepartment of Pharmacology and Toxicology, National Institute of Pharmaceutical Education and Research (NIPER)-Kolkata, Chunilal Bhawan, 168 Maniktala Main Road, Kolkata, 700054, West Bengal, India. somasundaram.niperk@nic.in.ORCID 0000-0002-2096-2552
National Institute of Pharmaceutical Education and Research · INMethodist Hospital · USNiigata University Medical and Dental Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

There has been ample data providing a convincing perception about the underlying mechanism pertaining to left ventricle (LV) hypertrophy progressing towards LV failure. In comparison, data available on the feedback of right ventricle (RV) due to volume or pressure overload is minimal. Advanced imaging techniques have aided the study of physiology, anatomy, and diseased state of RV. However, the treatment scenario of right ventricular failure (RVF) demands more attention. It is a critical clinical risk in patients with carcinoid syndrome, pulmonary hypertension, atrial septal defect, and several other concomitant diseases. Although the remodeling responses of both ventricles on an increase of end-diastolic pressure are mostly identical, the stressed RV becomes more prone to oxidative stress activating the apoptotic mechanism with diminished angiogenesis. This instigates the advancement of RV towards failure in contrast to LV. Empirical heart failure (HF) therapies have been ineffective in improving the mortality rate and cardiac function in patients, which prompted a difference between the underlying pathophysiology of RVF and LV failure. Treatment strategies should be devised, taking into consideration the anatomical and physiological characteristics of RV. This review would emphasize on the pathophysiology of the RVF and the differences between two ventricles in molecular response to stress. A proper insight into the underlying pathophysiology is required to develop optimized therapeutic management in RV-specific HF.

Indexed as

Heart FailureHypertension, PulmonaryVentricular Dysfunction, RightComorbidityDiastoleHeart VentriclesHumansVentricular Function, RightCor pulmonalePathophysiologyRight ventricular failureTreatment

Identifiers

PMID34826024
OpenAlexW3214968446

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.