뇌경색 환자에서 실로스타졸 투여 후 발생하는 두통과 경동맥 경직과의 연관성
Association Between Carotid Artery Stiffness and Headache Following Cilostazol Use in Cerebral Infarction Patients
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Background: Cilostazol leads to inhibition of platelet aggregation and to vasodilatation. It is widely used for the secondary prevention of cerebral infarction. However, headache is a well-known adverse effect of cilostazol, and these headaches may be caused by the vasodilation of the cerebral artery. The goal of our study was to assess the frequency and severity of headaches following cilostazol treatment and to evaluate factors related to the development of these headaches. Methods: Seventy patients with cerebral infarction were included in this study. We measured the carotid intima media thickness (IMT), the distensibility of the carotid artery (CAD), the brachial ankle index (ABI), and the brachial ankle pulse wave velocity (PWV) in order to quantify the degree of atherosclerosis and arterial stiffness. Patients were then given 100 mg of cilostazol in tablet form twice daily. For three days, we evaluated headache incidence and severity using a verbal rating scale (0-10). Results: Twenty three (32.9%) patients reported headache during cilostazol medication and 7 patients had severe headache. Women were more likely to develop headaches than men (p=0.03). In addition, the mean IMT was lower in subjects with cilostazol-induced headache than in the headache-free subjects (0.8±0.1 vs 1.01±0.2 mm, p=0.001), while CAD was higher in these subjects (0.3±0.1 vs 0.25±0.1, p=0.03). There was no difference in PWV and ABI. Conclusions: Lower carotid IMT, increased CAD, and female gender may be associated with the development of cilostazol-induced headache in patients with cerebral inafarction, but not the systemic arterial stiffness.
Abstract
Background: Cilostazol leads to inhibition of platelet aggregation and to vasodilatation. It is widely used for the secondary prevention of cerebral infarction. However, headache is a well-known adverse effect of cilostazol, and these headaches may be caused by the vasodilation of the cerebral artery. The goal of our study was to assess the frequency and severity of headaches following cilostazol treatment and to evaluate factors related to the development of these headaches. Methods: Seventy patients with cerebral infarction were included in this study. We measured the carotid intima media thickness (IMT), the distensibility of the carotid artery (CAD), the brachial ankle index (ABI), and the brachial ankle pulse wave velocity (PWV) in order to quantify the degree of atherosclerosis and arterial stiffness. Patients were then given 100 mg of cilostazol in tablet form twice daily. For three days, we evaluated headache incidence and severity using a verbal rating scale (0-10). Results: Twenty three (32.9%) patients reported headache during cilostazol medication and 7 patients had severe headache. Women were more likely to develop headaches than men (p=0.03). In addition, the mean IMT was lower in subjects with cilostazol-induced headache than in the headache-free subjects (0.8±0.1 vs 1.01±0.2 mm, p=0.001), while CAD was higher in these subjects (0.3±0.1 vs 0.25±0.1, p=0.03). There was no difference in PWV and ABI. Conclusions: Lower carotid IMT, increased CAD, and female gender may be associated with the development of cilostazol-induced headache in patients with cerebral inafarction, but not the systemic arterial stiffness.
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