Evidence map›Paper›PMID 26120322›Full record

ArticleCerebrovascular diseases extra

Plasma Catecholamine Profile of Subarachnoid Hemorrhage Patients with Neurogenic Cardiomyopathy.

Michael Moussouttas, Elizabeth Mearns, Arthur Walters, Matthew DeCaro

Open access · goldAbstract read
In one paragraph

Article in Cerebrovascular diseases extra. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
1.3field-weighted citation impact, top 18% 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

18 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Review
  5. Review
  6. Systemic Inflammation after Aneurysmal Subarachnoid Hemorrhage.International journal of molecular sciences · 2023
    Review
  7. Review
  8. Article
  9. Review
  10. Observational
  11. Takotsubo Syndrome: Translational Implications and Pathomechanisms.International journal of molecular sciences · 2022
    Review
  12. Review
  13. Article
  14. Review
  15. Systemic inflammation in hemorrhagic strokes - A novel neurological sign and therapeutic target?Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2019
    Review
  16. Hypertension After Severe Traumatic Brain Injury: Friend or Foe?Journal of neurosurgical anesthesiology · 2017
    Review
  17. Article
  18. 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

4 authors at 1 institution in 1 country.

Michael MoussouttasNeurocritical Care Division, Institute for Neurosciences, Capital Regional Medical Center, Trenton, N.J., USA.
Elizabeth MearnsPharmacy Department, Thomas Jefferson Medical Center, Philadelphia, Pa., USA.
Arthur WaltersDepartment of Neurology, Vanderbilt Medical Center, Nashville, Tenn., USA.
Matthew DeCaroDivision of Cardiology, Department of Medicine, Thomas Jefferson Medical Center, Philadelphia, Pa., USA.
Vanderbilt University Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeTo investigate the connection between sympathetic function and neurogenic cardiomyopathy (NC), and to determine whether NC is mediated primarily by circulating adrenal epinephrine (EPI) or neuronally transmitted norepinephrine (NE), following subarachnoid hemorrhage (SAH).

methodsThis is a prospective observational investigation of consecutive severe-grade SAH patients. All participants had transthoracic echocardiography and serological assays for catecholamine levels - dopamine (DA), NE and EPI - within 48 h of hemorrhage onset. Clinical and serological independent predictors of NC were determined using multivariate logistic regression analyses, and the accuracy of predictors was assessed by receiver operating characteristic (ROC) curves. Multivariate linear regression analyses were used to evaluate correlations among the catecholamines.

resultsThe investigation included a total of 94 subjects: the mean age was 55 years, 81% were female and 57% were Caucasian. NC was identified in approximately 10% (9/94) of cases. Univariate analyses revealed associations between NC and worse clinical severity (p = 0.019), plasma DA (p = 0.018) and NE levels (p = 0.024). Plasma NE correlated with DA levels (ρ = 0.206, p = 0.046) and EPI levels (ρ = 0.392, p < 0.001), but was predicted only by plasma EPI in bivariate [parameter estimate (PE) = 1.95, p < 0.001] and multivariate (PE = 1.89, p < 0.001) linear regression models. Multivariate logistic regression analyses consistently demonstrated the predictive value of clinical grade for NC (p < 0.05 for all analyses) except in models incorporating plasma NE, where NC was independently predicted by NE level (OR 1.25, 95% CI 1.01-1.55) over clinical grade (OR 4.19, 95% CI 0.874-20.1). ROC curves similarly revealed the greater accuracy of plasma NE [area under the curve (AUC) 0.727, 95% CI 0.56-0.90, p = 0.02] over clinical grade (AUC 0.704, 95% CI 0.55-0.86, p = 0.05) for identifying the presence or absence of NC.

conclusionsFollowing SAH, the development of NC is primarily related to elevated plasma NE levels. Findings implicate a predominantly neurogenic process mediated by neuronal NE (and not adrenal EPI), but cannot exclude synergy between the catecholamines.

Indexed as

CatecholaminesNeurogenic cardiomyopathyNorepinephrineStress cardiomyopathySubarachnoid hemorrhageSympathetic functionTakotsubo

Identifiers

PMID26120322
PMCPMC4478315
OpenAlexW2122276757

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.