Evidence map›Paper›PMID 31187936›Full record

ArticleJournal of clinical hypertension (Greenwich, Conn.)2019

Hypertension with primary aldosteronism is associated with increased carotid intima-media thickness and endothelial dysfunction.

Ahmet Demirkiran, Henk Everaars, Ali Elitok, Peter M van de Ven, Yvo M Smulders, Koen M Dreijerink, Refik Tanakol, Mustafa Ozcan

Open access · hybridAbstract read
In one paragraph

Article in Journal of clinical hypertension (Greenwich, Conn.), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
2.2field-weighted citation impact, top 12% 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

11 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Review
  5. Primary Aldosteronism: State-of-the-Art Review.American journal of hypertension · 2022
    Article
  6. Review
  7. Review
  8. Article
  9. Article
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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

8 authors at 3 institutions in 2 countries.

Ahmet DemirkiranDepartment of Cardiology, Istanbul Faculty of Medicine, Istanbul University, Istanbul, Turkey.ORCID 0000-0001-8104-3296
Henk EveraarsDepartment of Cardiology, Amsterdam University Medical Center - Vrije Universiteit Amsterdam, Amsterdam, the Netherlands.
Ali ElitokDepartment of Cardiology, Istanbul Faculty of Medicine, Istanbul University, Istanbul, Turkey.
Peter M van de VenDepartment of Epidemiology and Biostatistics, Amsterdam University Medical Center - Vrije Universiteit Amsterdam, Amsterdam, the Netherlands.
Yvo M SmuldersDivision of Vascular Medicine, Department of Internal Medicine, Amsterdam University Medical Center - Vrije Universiteit Amsterdam, Amsterdam, the Netherlands.
Koen M DreijerinkDivision of Endocrinology, Department of Internal Medicine, Amsterdam University Medical Center - Vrije Universiteit Amsterdam, Amsterdam, the Netherlands.
Refik TanakolDivision of Endocrinology, Department of Internal Medicine, Istanbul Faculty of Medicine, Istanbul University, Istanbul, Turkey.
Mustafa OzcanDepartment of Cardiology, Istanbul Faculty of Medicine, Istanbul University, Istanbul, Turkey.
Istanbul University · TRVrije Universiteit Amsterdam · NLAmsterdam University Medical Centers · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Patients with primary aldosteronism induced hypertension are more likely to experience cardiovascular events compared to patients with essential hypertension. Primary aldosteronism may therefore have distinct adverse effects on cardiovascular structure and function, independent of hypertension. However, current data on such effects of primary aldosteronism are conflicting. The aim of the present study was to investigate the influence of primary aldosteronism on vascular structure and endothelial function, using intima-media thickness as a vascular remodeling index and flow-mediated dilation as a functional parameter. In total, 70 participants were recruited from patients with resistant hypertension. Twenty-nine patients diagnosed with primary aldosteronism and 41 patients with essential hypertension were prospectively enrolled. Primary aldosteronism was due to aldosterone-producing adenoma in 10 cases and due to idiopathic adrenal hyperplasia in 19 cases. All patients underwent ultrasound of the common carotid intima-media thickness and flow-mediated dilation of the brachial artery. Primary aldosteronism patients had significantly lower flow-mediated dilation (3.3 [2.4-7.4] % vs 14.7 [10.3-19.9] %, P < 0.01) and significantly higher carotid intima-media thickness (0.9 [0.7-1.0] mm vs 0.8 [0.6-0.9] mm, P = 0.02) compared to patients with essential hypertension. These differences remained significant after adjusting for age, sex, diabetes mellitus, 24-hours systolic blood pressure, and smoking (P < 0.01). No differences in either outcome were observed between the adenoma and adrenal hyperplasia groups (both P > 0.05). Hypertensive patients with hyperaldosteronism appear to exhibit deteriorative effects on both vascular structure and function, independent of hypertension.

Indexed as

Brachial ArteryCarotid ArteriesCarotid Intima-Media ThicknessHyperaldosteronismHypertensionAldosteroneAntihypertensive AgentsCorrelation of DataEndothelium, VascularFemaleHumansMaleMiddle AgedAldosteroneAntihypertensive Agentsaldosteronecarotid intima-media thicknessendothelial dysfunctionflow-mediated dilationhypertensionprimary aldosteronism

Identifiers

PMID31187936
PMCPMC6771730
OpenAlexW2949533269

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.