Cilostazol Therapy for Subarachnoid Hemorrhage

Mechanism of Action

Cilostazol functions through phosphodiesterase-3 inhibition, which increases intracellular cyclic AMP levels, leading to vasodilation and antiplatelet effects, as reported by the American College of Chest Physicians 1
The increase in intracellular cAMP leads to vasodilation of cerebral arteries, although the specific effect on cerebral arteries is not further detailed in the provided citations 1
Cilostazol inhibits platelet aggregation through cAMP-dependent mechanisms, with a half-life of approximately 11 hours, as noted by the American Heart Association 1, 2

Cilostazol inhibits vascular smooth muscle cell proliferation, reducing neointimal hyperplasia after endothelial injury, as observed in studies cited by the American College of Cardiology 1, 2
It also inhibits expression of vascular cell adhesion molecule-1, which plays a role in the inflammatory response, according to research published in Circulation 2

Cilostazol is contraindicated in patients with heart failure due to the potential for ventricular tachycardia, as warned by the American College of Cardiology 1, 2
Use caution in patients with severe renal impairment due to the prolonged half-life of cilostazol, as advised by the American College of Chest Physicians 1
Common side effects include headache, GI side effects, diarrhea, palpitations, and dizziness, as reported by the American College of Chest Physicians 1

Cilostazol is typically administered at 100 mg twice daily after aneurysm clipping or coiling, although the optimal dosage may vary depending on the patient's condition 1
The duration of treatment is usually 14 days or longer after subarachnoid hemorrhage, as recommended by the American College of Chest Physicians 1