Androgen deprivation therapy reversibly increases endothelium-dependent vasodilation in men with prostate cancer

Paul L. Nguyen, Petr Jarolim, Shehzad Basaria, Jonah P. Zuflacht, Jessica Milian, Samoneh Kadivar, Powell L. Graham, Andrew Hyatt, Philip W. Kantoff, Joshua A. Beckman

Research output: Contribution to journalArticlepeer-review

18 Scopus citations


Background-Androgen deprivation therapy (ADT) is a standard treatment for patients with aggressive prostate cancer. AlthoughADT improves survival, it increases the risk of diabetes. Emerging evidence suggests that ADT increases adverse cardiovascularevents as early as 3 months after initiation in patients with cardiovascular disease, but the mechanism is unknown. Wehypothesized that ADT may impair endothelium-dependent vasodilation due to increases in lipids and insulin resistance and mayprovide a link for heightened cardiovascular risk in this population.Methods and Results-We prospectively evaluated conduit artery endothelium-dependent and -independent vasodilation, lipids,and insulin resistance in 16 consecutively treated men (mean age 66±7 years; 25% with diabetes) with prostate cancer before andafter 3 months of ADT. High-resolution B-mode ultrasound was used to assess flow-mediated (endothelium-dependent) andnitroglycerine-mediated (endothelium-independent) brachial artery vasodilation. ADT significantly increased insulin resistance, totalcholesterol, HDL, and LDL. Endothelium-dependent vasodilation was greater at 3 months than at baseline (10.8% [interquartilerange: 7.7% to 14.6%] versus 8.9% [interquartile range: 4.0% to 12.6%], respectively; P=0.046, allometric P=0.037). Nitroglycerinemediatedvasodilation did not change from baseline (P>0.2). The subset of participants on ADT for 6 months returned forreevaluation at 1 year. In this group, endothelium-dependent vasodilation increased from baseline to 3 months and returned tobaseline 6 months after ADT withdrawal (9.4% [interquartile range: 6.9% to 10.9%], 11.6% [interquartile range: 7.9% to 15.2%], and9.0% [interquartile range: 5.1% to 12.5%], respectively; P=0.05).Conclusions-In contrast to our expectation, ADT improved endothelium-dependent vasodilation and its cessation returnedendothelium-dependent vasodilation to baseline. Determining the mechanism of this change requires further investigation.

Original languageEnglish (US)
Pages (from-to)e001914
JournalJournal of the American Heart Association
Issue number4
StatePublished - 2015
Externally publishedYes


  • Androgen deprivation therapy
  • Endothelial function
  • Inflammation
  • Insulin resistance
  • Prostate cancer

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine


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