Cortisol in cardio-kidney-metabolic disease

Clicks: 11
ID: 337324
2026
Free PDF
Article Quality & Performance Metrics
Overall Quality
Not rated
Combines reader engagement with the AI quality analysis. This article has not been analysed, so there is no overall score — reader engagement is measured and shown alongside.
AI Quality Assessment
Not analyzed
Readership in this journal
Emerging

Ranked #350 of 374 articles by views in european heart journal

Most read Least read

Bar heights use a square-root scale. Only the 120 most-read articles are drawn; the journal has 374 in total.

Mint this article as an NFT
Not yet minted

Create a permanent, verifiable on-chain record of this article on the Scimatic Network. The NFT is held in your Journament account, and you can withdraw it to your own wallet at any time.

5 SUSD one-off · no wallet required
Sign in to mint
Abstract
Abstract Despite guideline-directed therapy, many patients with cardio-kidney-metabolic (CKM) disease remain uncontrolled due to therapeutic inertia, adherence barriers, and underrecognized secondary causes. Hypercortisolism, ranging from mild autonomous cortisol secretion (MACS) to overt Cushing syndrome, is an increasingly recognized contributor. MACS is associated with a 2.5-fold higher risk of cardiovascular death and increased prevalence of hypertension, type 2 diabetes mellitus (T2DM), and kidney impairment. Cortisol excess promotes muscle insulin resistance, hepatic gluconeogenesis, β-cell dysfunction, sodium retention, and vascular remodelling, worsening glycaemia and blood pressure, leading to poor CKM outcomes. Recent prospective studies suggest that hypercortisolism is more prevalent than previously suspected in selected CKM phenotypes, including 24% in patients with difficult-to-control T2DM in CATALYST and 27% in patients with resistant hypertension in MOMENTUM. The overnight 1 mg dexamethasone suppression test remains the diagnostic test of choice. Therapeutic strategies include adrenal steroidogenesis inhibitors, glucocorticoid receptor antagonists, and pituitary-directed therapies in selected cases, while surgery remains the first-line treatment for surgically remediable disease. This review summarizes the epidemiology and mechanisms linking cortisol excess to CKM dysfunction, and also highlights the need for clinical trials, standardized diagnostic thresholds, and assays to enable integration of cortisol-targeted therapies into management pathways to mitigate residual CKM risk. This review will serve as a practical guide for cardiologists to manage a potentially reversible contributor to poor CKM control.
Reference Key
openalex_W7223954898 Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors Muhammad Shahzeb Khan, Muhammad Sameer Arshad, Deepak L. Bhatt, David Z.I. Cherney, Ralph A. DeFronzo, Jennifer B. Green, Yehuda Handelsman, Tariq Shafi, Jeffrey Moore Testani, Javed Butler
Are you one of these authors? Claim your profile
Journal european heart journal
Year 2026
DOI
10.1093/eurheartj/ehag827
URL
https://doi.org/10.1093/eurheartj/ehag827
Keywords Keywords not found

Citations

No citations found. To add a citation, contact the admin at info@scimatic.org

Comments

No comments yet. Be the first to comment on this article.