Effect of tirofiban in treating patients with progressive ischemic stroke.

OBJECTIVE

Our aim is to investigate the efficacy and safety of tirofiban in the treatment of patients experiencing progressive ischemic stroke (PIS).

PATIENTS AND METHODS

A retrospective analysis was performed on the clinical data of 150 patients with ischemic stroke admitted to our hospital from May 2018 to December 2019. All the patients were divided into two groups according to different treatment methods. In Control group, conventional comprehensive treatment and antiplatelet therapy with aspirin + clopidogrel were conducted, while tirofiban was administered in Tirofiban group in addition to the treatments in Control group. Neurological deficits were scored by means of the National Institutes of Health Stroke Scale (NIHSS) at the time of progression and 30 d after treatment, and the modified Rankin Scale (mRS) and Activity of Daily Living (ADL) scale were employed to assess prognosis at 90 d after treatment. Thereafter, the platelet aggregation rate, platelet adhesion rate, plateletcrit (PCT), platelet distribution width (PDW), and platelet inhibition rate were measured before and after treatment. Finally, the patients were followed up, and the occurrence of hemorrhage events during treatment and within 90 d after discharge was recorded.

RESULTS

After treatment, all the patients had significantly lower NIHSS and mRS scores and a dramatically higher Barthel index (BI) than those before treatment (p<0.001). At 90 d after treatment, Tirofiban group exhibited significantly higher BI (p<0.001) and lower mRS score than Control group (p=0.011). In addition, at 14 d after treatment, the clinical efficacy was assessed for all the patients. It was found that the overall response rate in Tirofiban group was substantially higher than that in Control group [82.7% (62/75) vs. 64.0% (48/75), p=0.009]. At 7 d after treatment, the PCT and adenosine diphosphate (ADP) platelet inhibition rate in Tirofiban group were markedly higher than those in Control group (p=0.006, p<0.001), and Tirofiban group had remarkably lower measured values of platelet aggregation rate, platelet adhesion rate and PDW than Control group (p=0.007, p=0.021, p<0.001). After treatment, the levels of serum IL-6 and hs-CRP declined notably in the two groups of patients, and the differences in their levels at 2 and 14 d after treatment between the two groups were statistically significant (p<0.05). During treatment and within 90 d after discharge, both groups of patients had no cerebral hemorrhage, gastrointestinal hemorrhage, and severe hemorrhage adverse events requiring blood transfusion, but they experienced subcutaneous ecchymosis, epistaxis, gingival hemorrhage, and hemorrhage around the infarct, which were improved after symptomatic treatment. Moreover, the occurrence rate of hemorrhage in Tirofiban group was higher than that in Control group, showing no statistically significant difference (p>0.05).

CONCLUSIONS

Tirofiban combined with conventional basic treatment can greatly improve neurological deficits and disease outcomes, alleviate platelet adhesion, and reduce platelet activation without increasing the risk of hemorrhage in PIS patients.