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Ultrasound Assessment of Endothelial Function: A Technical Guideline of the Flow-mediated Dilation Test
Published on: April 27, 2016
The Effect of Cilostazol on Endothelial Function as Assessed by Flow-Mediated Dilation in Patients with Coronary
Hiroyoshi Mori1, Atsuo Maeda, Kohei Wakabayashi
1Department of Cardiology, Showa University Fujigaoka Hospital.
Insights
Cilostazol did not improve flow-mediated dilation (FMD) in patients with coronary artery disease. However, cilostazol treatment led to significant increases in brachial artery diameter, suggesting potential cardiovascular benefits.
Area of Science:
- Cardiovascular Medicine
- Vascular Biology
- Pharmacology
Background:
- The vascular endothelium is crucial in atherosclerosis development.
- Endothelial function can be assessed using flow-mediated dilation (FMD).
- Cilostazol, an antiplatelet agent, may enhance endothelial function.
Purpose of the Study:
- To evaluate the effect of cilostazol on endothelial function in coronary artery disease (CAD) patients.
- To assess changes in FMD with cilostazol treatment.
Main Methods:
- Fifty-one CAD patients were divided into two groups: cilostazol (n=27) and control (n=24).
- Both groups received dual antiplatelet therapy; the cilostazol group also received 100 mg/day cilostazol.
- Flow-mediated dilation (FMD) was measured at baseline and after 6-9 months.
Main Results:
- No significant difference in FMD was observed between the cilostazol and control groups.
- The cilostazol group showed a trend towards increased baseline and maximal brachial artery diameters.
- Significant differences in the rates of change for baseline and maximal brachial artery diameters were found between groups.
Conclusions:
- Cilostazol did not alter FMD in CAD patients.
- Cilostazol significantly increased brachial artery diameters, indicating a potential positive impact on cardiovascular health.
Aim:
The vascular endothelium plays a key role in the pathophysiology of atherosclerosis. Flow-mediated dilation (FMD) is a novel way of assessing endothelial function. Cilostazol is a unique antiplatelet drug that also has the potential to improve endothelial function. The objective of this present study was to investigate the effects of cilosatzol on endothelial function as assessed by FMD.
Methods:
Fifty-one patients with coronary artery disease (CAD) were assigned to one of two groups: the Cilostazol(+) group (with cilostazol) and Cilostazol(-) group (without cilostazol). In addition to conventional dual antiplatelet therapy with aspirin and clopidogrel/ticlopidine, the Cilostazol(+) group (n=27) was also given cilostazol (100 mg/day). The Cilostazol(-) group (n=24) did not receive cilostazol. FMD was assessed at enrollment and after 6-9 months.
Results:
The FMD of both the Cilostazol(+) and Cilostazol(-) groups remained similar at 5.2 (interquartile range: 3.8-8.5) to 5.4 (interquartile range: 4.2-6.7) (P=0.29) and 5.0 (interquartile range: 3.6-6.4) to 4.9 (interquartile range: 4.0-7.0) (P=0.38), respectively. However, the diameters of the baseline and maximal brachial arteries tended to increase in the Cilostazol(+) group (baseline: 4.2±0.7 to 4.4±0.7, P=0.18; maximal: 4.5±0.7 to 4.6±0.7 P=0.22), whereas that of the Cilostazol(-) group tended to decrease (baseline: 4.1±0.6 to 3.9±0.5, P=0.10; maximal: 4.3±0.7 to 4.1±0.5, P=0.05). The rates of change in the baseline diameter (Cilostazol(+): 3.7±9.8% vs. Cilostazol(-): -3.8±12.2%, P=0.03) and maximal diameter (Cilostazol(+): +3.1±8.9% vs. Cilostazol(-): -4.4±12.0%, P=0.02) were significantly different.
Conclusion:
Although cilostazol didn't affect the FMD, there was a significant difference in the rates of change in baseline and maximal brachial artery diameter. This may have a beneficial effect in patients with cardiovascular disease.
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