Fasudil was originally designed as an intracellular calcium antagonist, with the intent of achieving vasodilation. Despite extensive investigations, the precise mechanism of action of fasudil remains unclear. A possible more clinically significant role for fasudil in vasospasm might be its role in Rho kinase II inhibition, thereby preventing the activation of pathways that promote vascular smooth muscle cell contraction and proliferation. Rho Kinase is thought to play a critical role in ET-1-mediated vasoconstriction and proliferation.

The first clinical trial using fasudil was reported from Japan in 1992; 267 patients with Hunt and Hess grades I to IV were randomized to either receive fasudil or placebo (55). The groups were matched clinically and demographically. Fasudil reportedly reduced angiographic vasospasm by 23% (61% vs. 38%, p =0.0023), ischemic CT lesions by 22% (38% vs. 16%, p = 0.0013), and symptomatic vasospasm by 15% (50% vs. 35%, p =0.0247). More importantly, the authors report that treated patients had improved rate of good GOS scores (26% vs. 12%, p =0.0152) (55). This study promoted the widespread use of fasudil in Japan to reduce the rate of vasospasm and its pathophysiologic consequences.

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