Association of pre-admission use of sartans and calcium channel antagonists with outcomes after spontaneous intracerebral hemorrhage: A retrospective cohort study

Spontaneous intracerebral hemorrhage (ICH) is a severe stroke subtype associated with high morbidity and mortality. Preclinical studies suggest that angiotensin Ⅱ-type 1 receptor blockers such as sartans and calcium channel antagonists (CCAs) may confer neuroprotective effects in cerebrovascular disease through anti-inflammatory actions, improving microcirculation, and mitigating cerebral vasospasm. These effects were of particular interest in patients suffering subarachnoid hemorrhage (SAH). This study aimed to evaluate whether these medications confer similar benefits in patients with ICH.

We performed a retrospective single-center cohort study including 326 patients with spontaneous ICH between December 2017 and June 2021. The primary endpoint was functional independence (mRS 0–2 at 90 days); an exploratory ordinal mRS-shift analysis was additionally conducted. 155 patients with documented antihypertensive therapy were included and stratified into four groups: sartans (n = 39), CCA (n = 36), sartan + CCA (SC; n = 17) and other antihypertensive medications (OAM; n = 63). 171 patients had to be excluded due to missing antihypertensive drug data. Clinical and radiographic data (including 3D-volumetric ICH measurements) were collected. Hematoma volume was measured using volumetric imaging (Brainlab AG, Germany). Functional outcome was assessed via the modified Rankin Scale (mRS) at discharge and at 1-, 3-, 6-, and 12-month follow-up. The 1-month follow-up was performed in person, whereas the 3-, 6- and 12-month follow-up were obtained via structured telephone interviews. Group differences were analyzed using chi-square/Fisher’s tests and ANOVA/Kruskal-Wallis tests as appropriate (two sided P < 0.05).

Groups were similar in age, sex, admission GCS, NIHSS, blood pressure, ICH location, and initial hemorrhage volume. The only significant baseline difference was BMI: the sartan group had a significantly higher BMI than the CCA and OAM groups (overall P = 0.039; post-hoc P = 0.028 and P = 0.019, respectively). There was no significant difference in the proportion of patients achieving functional independence (mRS 0–2) at any follow-up, nor in the ordinal mRS-shift analysis and no trend toward improved outcomes in patients on sartans or CCAs. Sartans were administered to 39 patients (25.2%), CCA to 36 (23.2%), both combined to 17 (11.0%), and OAM to 63 (40.6%). Functional outcomes at all follow-up intervals showed no significant variation among the groups.

Our study did not demonstrate a neuroprotective effect of sartans or CCAs resulting in improved functional outcomes after ICH. The limited sample size, especially in the group with combined use of sartan and CCA (n = 17) and the retrospective design, limit causal inference. While our data did not show a neuroprotective effect of sartans or CCA in ICH, prospective studies and subgroup analyses in larger cohorts are warranted to clarify whether specific agents, timing, or subgroups might benefit, especially in light of the existing supportive literature.