Evidence map›Paper›PMID 42329476›Full record

ArticleBreast cancer research and treatment2026

Is endothelial dysfunction induced by aromatase inhibitors reversible after treatment?

Mohamed S Dabour, Adnan Shaaban, Daniel A Duprez, Beshay N Zordoky, Anne H Blaes

Abstract read
In one paragraph

Article in Breast cancer research and treatment, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Mohamed S DabourDepartment of Experimental and Clinical Pharmacology, College of Pharmacy, University of Minnesota, Minneapolis, MN, USA.
Adnan ShaabanDivision of Cardiology, AdventHealth Orlando, Orlando, FL, USA.
Daniel A DuprezDivision of Cardiology, University of Minnesota, Minneapolis, MN, USA.
Beshay N ZordokyDepartment of Experimental and Clinical Pharmacology, College of Pharmacy, University of Minnesota, Minneapolis, MN, USA.
Anne H BlaesDivision of Hematology/Oncology/Transplantation, Medical School, University of Minnesota, 909 Fulton St SE, Minneapolis, MN, 55455, USA. blaes004@umn.edu.ORCID https://orcid.org/0000-0002-5433-4810

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeAromatase inhibitors (AIs) are standard therapy for postmenopausal women with hormone receptor-positive breast cancer. However, prolonged AI use is associated with increased cardiovascular (CV) risk, including hypertension, and endothelial dysfunction. This study evaluated the longitudinal changes in endothelial function during AI therapy, and whether AI-induced endothelial dysfunction is reversible post-discontinuation.

methodsPatients were recruited before or within one month of AI initiation (Pre/early AI), during AI therapy, and after discontinuation (Post-AI) from two prospective studies. Patients with hypertension, hyperlipidemia, diabetes, or tobacco use were excluded. Vascular assessments included peripheral arterial tonometry (EndoPAT) for endothelial function (abnormal if ratio < 1.67) and artery elasticity indices. Estradiol, lipid profiles, and inflammatory markers were also measured.

resultsThe study included 12 Pre/early AI patients, 67 visits from 41 patients during AI (median 2.89 years on AI), and 9 Post-AI patients (median 4.17 years follow-up). EndoPAT ratio was significantly impaired during AI therapy compared to the Pre/early AI (median: 0.86 vs 2.19). The EndoPAT ratio declined as early as six months and showed a progressive decline over time. Post-discontinuation, the EndoPAT ratio was only partially and not significantly restored (median: 1.08) despite full estradiol restoration and long follow-up. Arterial elasticity showed no significant changes. Systolic blood pressure increased modestly during AI therapy and returned to baseline after discontinuation, while diastolic pressure remained unchanged. Circulating interleukin-6 and tumor necrosis factor-α significantly decreased following AI discontinuation.

conclusionsAI therapy is associated with significant and progressive endothelial dysfunction, which does not fully recover after treatment cessation, highlighting the importance of CV monitoring in patients receiving long-term AI therapy.

Indexed as

Aromatase InhibitorsBreast NeoplasmsEndothelium, VascularAgedEstradiolFemaleHumansMiddle AgedPostmenopauseProspective StudiesAromatase InhibitorsEstradiolAromatase inhibitorsBreast cancer survivorshipCardiovascular toxicityEndoPATEndothelialVascular function

Identifiers

PMID42329476
PMCPMC13287299

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.