The recommended and widely accepted standard conservative treatment for VSP includes prophylactic administration of nimodipine, triple-H therapy (hypertension, hypervolemia, and hemodilution; without hypervolemia [16]) and cerebrospinal fluid drainage [7]. If these standard treatments fail, intraarterial injection of vasodilators such as verapamil [14], papavarine [11], nimodipine [6], nicardipine [5], or balloon angioplasty with or without additional intraarterial vasodilators [8] have been proposed as rescue therapies. Several alternative substances such as fasudil [20], mainly used in Japan, and colforsin daropate [21] for local endovascular as well as systemic intraarterial or intravenous administration have also been tried. A main problem with all the interventional techniques remains the reversibility of the vasodilation and, thus, clinical treatment effects. Using balloon angioplasty, there is even a potential for serious life-threatening complications, including vessel rupture, branch occlusion, displacement of surgical clips, and rupture of untreated aneurysms despite improved techniques and catheters [22]. The first randomized controlled trial, the IMCVS trial (ClinicalTrials.gov Identifier: NCT01400360), using mainly balloon angioplasty with or without intraarterial application of vasodilators, was interrupted because of statistical significant higher mortality in the interventional group as compared with the conservative treatment group [23].

Therefore, researchers are seeking approaches that are new and more effective. Milrinone, widely used in cardiology for heart failure, has vasodilating effects in addition to positive inotrope and antiinflammatory effects. As described by Lannes et al. [13] in detail, milrinone is a potent selective phosphodiesterase III (PDE III) inhibitor that affects cyclic adenosine monophosphate (cAMP) pathways with both inotropic and vasodilatory effects [24]. Milrinone has also antiinflammatory effects through the inhibition of interleukin 1B and interleukin 6 [10]. Thus, several authors have used milrinone in smaller cohorts, but without aggressive reintervention indications [4, 9, 13, 17–19].

In this preliminary series, we used milrinone supplementary to the more commonly used nimodipine. To minimize the effects of postinterventional VSP recurrence, we indicated reinterventions aggressively in cases with persistent neurological deficits or persistent high mean TCD >180 cm/s. The baseline data show a representative patient cohort with typical age, gender, aneurysm location, and clinical severity distribution. Only the high rate of clipped patients may be atypical. With the present algorithm, we could reach a very low mortality of 6.25 % as compared with the up to 15 % mortality in the literature for conservative treatment alone and contradictory to the negative results of the IMCVS trial [7]. Clinical improvement at a mean of 4.5 months was observed in 68.5 % of patients. Very good and good clinical outcomes with mRS ≤ 2 were reached in 68.5 % of patients. This is in the higher range when compared with the literature, with mRS ≤ 2 rates between 57 % [3] and 75 % [13]. Interestingly, milrinone showed a clear supplementary vasodilating effect over nimodipine in all interventions, leading to 87.5 % DSA improvement. We did not observe any negative side effects of multiple interventions, nor did we find severe cardiovascular adverse events of milrinone, because we used relatively low doses.