Evidence map›Paper›PMID 35246499›Full record

ArticleOpen heart2022

Prevalence and haemodynamic profiles of pulmonary hypertension in cardiac amyloidosis.

Jeremy Slivnick, Karolina M Zareba, Juliet Varghese, Vien Truong, Alexander L Wallner, Matthew S Tong, Christopher Hummel, Wojciech Mazur, Saurabh Rajpal

Open access · goldAbstract read
In one paragraph

Article in Open heart, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

9 citing papers in PubMed, 17 citations in OpenAlex.

  1. The pathophysiology of wild-type transthyretin amyloidosis: implications for exercise intolerance.American journal of physiology. Heart and circulatory physiology · 2026
    Review
  2. Review
  3. Article
  4. Article
  5. Review
  6. Observational
  7. Article
  8. Article
  9. 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

9 authors at 4 institutions in 1 country.

Jeremy SlivnickCardiovascular Medicine, University of Chicago Medicine, Chicago, Illinois, USA jslivnick@gmail.com.ORCID 0000-0002-2327-4544
Karolina M ZarebaCardiovascular Medicine, The Ohio State University Wexner Medical Center, Columbus, Ohio, USA.
Juliet VargheseCardiovascular Medicine, The Ohio State University Wexner Medical Center, Columbus, Ohio, USA.ORCID 0000-0003-2882-2893
Vien TruongCardiology, Christ Hospital, Cincinnati, Ohio, USA.
Alexander L WallnerCardiovascular Medicine, The Ohio State University Wexner Medical Center, Columbus, Ohio, USA.
Matthew S TongCardiovascular Medicine, The Ohio State University Wexner Medical Center, Columbus, Ohio, USA.
Christopher HummelCardiovascular Medicine, The Ohio State University Wexner Medical Center, Columbus, Ohio, USA.
Wojciech MazurCardiology, Christ Hospital, Cincinnati, Ohio, USA.
Saurabh RajpalInternal Medicine/Cardiology, Ohio State University Wexner Medical Center, Columbus, Ohio, USA.ORCID 0000-0003-0772-8478
The Ohio State University Wexner Medical Center · USChrist Hospital · USNationwide Children's Hospital · USUniversity of Chicago · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesWhile cardiac amyloidosis (CA) classically involves the left ventricle (LV), less is known about its impact on the right ventricle (RV) and pulmonary vasculature. We performed a retrospective analysis to identify the prevalence and types of pulmonary hypertension (PH) profiles in CA and to determine haemodynamic and cardiovascular magnetic resonance (CMR) predictors of major adverse cardiovascular events (MACE).

methodsPatients with CA who underwent CMR and right heart catheterisation (RHC) within 1 year between 2010 and 2019 were included. Patients were assigned the following haemodynamic profiles based on RHC: no PH, precapillary PH, isolated postcapillary PH (IPCPH), or combined precapillary and postcapillary PH (CPCPH). The relationship between PH profile and MACE (death, heart failure hospitalisation) was assessed using survival analysis. CMR and RV parameters were correlated with MACE using Cox-regression analysis.

resultsA total of 52 patients were included (age 69±9 years, 85% men). RHC was performed during biopsy in 44 (85%) and for clinical indications in 8 (15%) patients. Rates of no PH, precapillary PH, IPCPH and CPCPH were 5 (10%), 3 (6%), 29 (55%) and 15 (29%), respectively. Haemodynamic PH profile did not correlate with risk of death (p=0.98) or MACE (p=0.67). Transpulmonary gradient (TPG) (HR 0.88, CI 0.80 to 0.97), RV, (HR 0.95, CI 0.92 to 0.98) and LV ejection fraction (HR 0.95, CI 0.92 to 0.98) were significantly associated with MACE.

conclusionsPH is highly prevalent in CA, even at the time of diagnosis. While IPCPH was most common, CPCPH is not infrequent. TPG and RV ejection fraction (RVEF) are prognostic markers in this population.

Indexed as

AmyloidosisHypertension, PulmonaryAgedFemaleHemodynamicsHumansMaleMiddle AgedPrevalenceRetrospective Studiescardiomyopathy, restrictiveheart failure, diastolichypertension, pulmonary

Identifiers

PMID35246499
PMCPMC8900043
OpenAlexW4214900616

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.