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Chemotherapy-induced Vascular Toxicity - Real-time In vivo Imaging of Vessel Impairment
Published on: January 7, 2015
Anthracyclines cause endothelial injury in pediatric cancer patients: a pilot study
Amy Y Chow1, Clifford Chin, Gary Dahl
1Department of Pediatrics, Lucile Salter Packard Children's Hospital, Stanford University, Stanford, CA 94304, USA.
Insights
Anthracycline chemotherapy in pediatric cancer patients significantly impairs arterial vasodilation, indicating a new form of endothelial toxicity. This finding suggests potential long-term cardiovascular risks, requiring further investigation.
Area of Science:
- Cardiovascular Medicine
- Pediatric Oncology
- Pharmacology
Background:
- The vascular endothelium regulates arterial tone via nitric oxide-mediated vasodilation.
- Anthracyclines are known to cause endothelial damage in animal models.
- Human data on anthracycline-induced endothelial toxicity are limited.
Purpose of the Study:
- To assess endothelial toxicity in pediatric cancer patients treated with anthracyclines.
- To evaluate the impact of anthracyclines on brachial artery reactivity (BAR).
Main Methods:
- Compared 14 pediatric cancer survivors (4-21 years) treated with anthracyclines to 14 controls.
- Measured brachial artery diameter using high-resolution ultrasound.
- Calculated BAR as the percentage change in brachial artery diameter after cuff occlusion and deflation.
Main Results:
- Baseline characteristics were similar between groups.
- Anthracycline-treated patients showed significantly reduced BAR (3.8%) compared to controls (6.7%, P < .05).
- This indicates impaired vasomotor reactivity in patients who received anthracyclines.
Conclusions:
- Anthracyclines appear to cause impaired endothelial function, a novel toxicity.
- Endothelial dysfunction is an early step in atherogenesis, suggesting potential clinical implications.
- Further research in a larger cohort is needed to confirm these preliminary findings.
Purpose:
The vascular endothelium plays a central role in the regulation of arterial vasomotor tone, releasing nitric oxide for vasodilation. Endothelial-dependent vasodilation can be assessed in vivo, using high resolution ultrasound to measure changes in diameter of the brachial artery. Animal studies have demonstrated that anthracyclines can damage the endothelium and impair the vasodilatory response of arteries; however, there are no comparable data in humans. This is a pilot study assessing endothelial toxicity from anthracyclines in pediatric cancer patients.
Patients And Methods:
Fourteen control patients and 14 cancer patients (4 to 21 years) were studied. Cancer patients had completed chemotherapy containing no less than 300 mg/m2 of anthracyclines 2 to 60 months before study. Brachial artery diameters were measured at rest and 1 minute after blood pressure cuff occlusion. Brachial artery reactivity (BAR) was calculated as percent change between baseline and after cuff deflation measurements. Results were compared using unpaired, two-tailed t-test.
Results:
Baseline characteristics, including age, percentage of females, blood pressure, and resting vessel diameters were similar between the two groups. BAR in the controls averaged 6.7% with a standard deviation (SD) of 3.3%, while BAR in patients receiving anthracyclines averaged 3.8% with an SD of 3.4%, demonstrating a significant decrease (P < .05) in vasomotor reactivity in the treated group.
Conclusion:
These results suggest that anthracyclines cause impaired endothelial function, an important and newly recognized toxicity. Since endothelial dysfunction is an early event in atherogenesis, there may be important clinical implications from these findings. Further study is required to confirm these preliminary results in a larger cohort.
