Renal function affects the safety and efficacy of tirofiban in acute ischemic stroke thrombectomy patients

Abstract

Background

Acute ischemic stroke poses a significant health threat, and thrombectomy has become a routine treatment. Tirofiban has emerged as a promising adjunct therapy to minimize reocclusion after thrombectomy. We aimed to investigate whether renal function influences the safety and efficacy of tirofiban in patients undergoing endovascular therapy.

Methods

Patients' clinical data collected from the stroke unit were analyzed. The modified Rankin scale score and symptomatic intracranial hemorrhage (sICH) were used as outcome measures.

Results

A total of 409 patients (mean age: 66.5 years, 292 males [71.4%]) were included. Tirofiban significantly improved 3-month functional outcomes (adjusted odds ratio [aOR] = 2.408, 95% confidence interval [CI] 1.120–5.175), reduced 3-month mortality (aOR = 0.364, 95% CI 0.155–0.856), and decreased the incidence of sICH (aOR = 0.339, 95% CI 0.149–0.767) in patients with estimated glomerular filtration rate (eGFR) ≥ 90 mL/min/1.73 m². However, no significant improvement in prognosis was observed with tirofiban in patients with eGFR < 90 mL/min/1.73 m². Interaction analysis suggested a potential influence of renal function on tirofiban efficacy.

Conclusion

Renal function may impact the efficacy of tirofiban. Administration of tirofiban in direct thrombectomy patients with normal renal function is safe and improves prognosis. However, the prognostic benefits of tirofiban are limited in patients with impaired renal function.

Introduction

Acute ischemic stroke (AIS) is a significant health concern and remains a leading cause of death in China. ¹ Intravenous recombinant tissue plasminogen activator is the recommended first-line treatment for AIS within 4.5 h of onset, but it has limitations such as a narrow treatment time window and relatively low revascularization rates. ² In recent years, endovascular therapy (EVT) has emerged as an effective approach for improving functional outcomes in some AIS patients,^3–9 particularly for those with large vessel occlusion. ¹⁰ However, EVT procedures can potentially cause endothelial damage, platelet activation, thromboembolism, and limited reperfusion rates.^11,12 Approximately 20% of patients experience early reocclusion after successful recanalization. ¹³ Tirofiban, a highly selective glycoprotein (GP) IIb/IIIa receptor antagonist, has been shown to effectively inhibit platelet activation, preventing local platelet aggregation and reducing reocclusion when used after EVT treatment.^14,15 However, approximately 80% of tirofiban's metabolism occurs in the kidneys, and renal insufficiency can lead to reduced plasma clearance of tirofiban. ¹⁴ Clinical and animal studies have demonstrated an increased risk of cerebral hemorrhage with higher doses of tirofiban.^16,17 However, no study has yet investigated whether renal function affects the efficacy and safety of tirofiban in EVT patients. The objective of this study was to explore the relationship between renal function and the effectiveness of tirofiban in EVT patients.

Method

Participants

A prospective cohort study was designed to examine the impact of renal function on the efficacy of tirofiban in stroke patients undergoing thrombectomy. The study included patients who were admitted to the stroke unit of the hospital from December 2018 to February 2022 and received EVT within 24 h of stroke onset.

Data collection

The data of the patients were collected upon admission to the hospital and analyzed. Blood samples were taken at the same time, and estimated glomerular filtration rate (eGFR) was measured before EVT using the following formula: Egfr [mL/(min·1.73 m²)] = 141 × min (blood creatinine/κ, 1) α × max (blood creatinine/κ, 1) – 1.209 × 0.993 × age (years) (×1.018 female) (κ_female = 0.7, α_female = −0.329; κ_male = 0.9, α_male = −0.411; blood creatinine unit mg/dL). ¹⁸ A normal renal function was defined as an eGFR level above 90 ml/min/1.73 m². The National Institutes of Health Stroke Scale (NIHSS) score at admission was used to assess stroke severity at baseline and was obtained in the emergency department. ¹⁹ Stroke etiology was analyzed through diagnostic procedures including cerebral imaging, imaging of the brain's supplying arteries, cardiac imaging, and heart rhythm monitoring. The modified thrombolysis in cerebral infarction (mTICI) score was evaluated independently by two board-certified neuroradiologists. The adequacy of reperfusion was defined as an mTICI score of 2c or 3 in the anterior circulation and an mTICI score of 2b or 3 in the posterior circulation, following current recommendations. ²⁰ The treatment operation of thrombectomy procedures is derived from specific intraoperative records, and the procedures are categorized into the following three types: direct aspiration, stent-assisted thrombectomy, and stent-assisted thrombectomy followed by subsequent balloon angioplasty.

Tirofiban treatment

After the completion of EVT, the patients received a continuous intravenous infusion of tirofiban at a rate of 0.1 μg/kg per minute for 48 h. The administration of tirofiban in patients followed the latest clinical guidelines and was tailored to the individual patient's overall condition. ²¹

Outcome assessment

The primary functional outcomes were assessed using the modified Rankin scale (mRS) and evaluated through a telephone follow-up after the third month of onset. A favorable clinical outcome was defined as a mRS score of 0–2 or a score that was equal to the patient's premorbid level. Conversely, an unfavorable outcome was defined as an mRS score of 3–6, with a score of 6 indicating death. ²² The secondary outcome of the study was symptomatic intracranial hemorrhage (sICH). The definition of sICH was based on the criteria outlined in the European Cooperative Acute Stroke Study-III study, which defines it as any apparent extravascular blood in the brain or within the cranium that is associated with clinical deterioration, as indicated by an increase of 4 points or more in the NIHSS score. ²³

Ethical approval

The study was conducted with the approval of the ethics committee, and all research procedures adhered to the principles outlined in the Declaration of Helsinki. Written informed consent was obtained from all patients or their authorized proxies prior to their participation in the study.

Statistical methods

Statistical analysis was conducted using IBM SPSS Statistics 26 software. The baseline information and risk factors of the patients were analyzed. Categorical variables were assessed using the chi-square test or Fisher's exact test and are presented as percentages. Continuous variables were reported as either mean ± standard deviation (SD) or median and interquartile range (IQR), depending on their distribution. Student's t-test or the Mann–Whitney test was used to compare continuous variables. For the data presented in Tables 2 and 3, binary logistic regression analysis was performed to determine whether tirofiban could independently predict favorable outcomes after stroke. Logistic regression was utilized for the interaction analysis presented in Figure 2. Propensity score matching was performed using the built-in functions in SPSS. Statistical significance was set at p < 0.05.

Table 2.

Binary logistic regression analysis in patients with different eGFR levels and p values of interaction model.

	Case		Unadjusted p value	Unadjusted OR	95% CI		Adjusted p value	Adjusted OR	95% CI
	Tirofiban	Without tirofiban			Lower Limit	Upper Limit			Lower limit	Upper limit
			Binary logistic regression in patients with normal renal function
3-month mRS0–2a	64 (42.4%)	23 (29.1%)	0.018*	2.041	1.131	3.681	0.024*	2.408	1.120	5.175
3-month mortalitya	25 (16.6%)	26 (32.9%)	0.012*	0.439	0.231	0.831	0.021*	0.364	0.155	0.856
sICHb	20 (13.2%)	20 (25.3%)	0.024*	0.450	0.225	0.900	0.009*	0.339	0.149	0.767
			Binary logistic regression in patients with impaired renal
3-month mRS0–2a	32 (31.1%)	22 (28.9%)	0.972	1.012	0.525	1.950	0.783	1.135	0.462	2.789
3-month mortalitya	33 (32.0%)	27 (35.5%)	0.427	0.773	0.409	1.460	0.970	0.984	0.420	2.305
sICHb	16 (15.5%)	11 (14.5%)	0.845	1.087	0.473	2.498	0.629	1.266	0.486	3.297
P value of interaction model (eGFR × tirofiban) = 0.091

CI: confidence interval; OTT: onset to treatment time; TOAST: Trial of Org 10,172 in acute stroke treatment; sICH: symptomatic intracerebral hemorrhage; NIHSS, National Institutes of Health Stroke Scale.

^aAdjusted for age, NIHSS score on admission, OTT, length of hospital stay, TOAST classification, occlusion site, and bridging venous thrombolysis.

^bAdjusted for age, NIHSS score on admission, OTT, TOAST classification, occlusion site, and bridging venous thrombolysis.

*p < 0.05, **p < 0.005, ***p < 0.001.

Table 3.

Binary logistic regression models by different grouping methods.

	Case		Unadjusted p value	Unadjusted OR	95% CI		Adjusted p value	Adjusted OR	95% CI
	Tirofiban	Without tirofiban			Lower limit	Upper limit			Lower limit	Upper limit
			Binary logistic regression in all EVT patients
3-month mRS0–2a	96 (40%)	45 (30.4%)	0.057	1.526	0.988	2.358	0.068	1.681	0.963	2.936
3-month mortalitya	58 (24.2%)	53 (35.8%)	0.014*	0.571	0.365	0.894	0.090	0.607	0.341	1.081
sICHb	36 (14.2%)	31 (20.0%)	0.124	0.661	0.389	1.120	0.075	0.582	0.321	1.056
			Binary logistic regression in direct thrombectomy patients
3-month mRS0–2a	72 (37.9%)	23 (21.5%)	0.006*	2.136	1.244	3.665	0.025*	2.156	1.102	4.219
3-month mortalitya	50 (26.3%)	45 (41.7%)	0.007*	0.500	0.303	0.825	0.034*	0.499	0.263	0.949
sICHb	26 (13.0%)	20 (18.0%)	0.234	0.680	0.360	1.284	0.107	0.542	0.257	1.141
			Binary logistic regression in direct thrombectomy patients with eGFR > 90 mL/min/1.73 m² e
3-month mRS0–2c	44 (39.3%)	13 (23.2%)	0.016*	2.467	1.185	5.134	0.040*	2.507	1.042	6.027
3-month mortalityd	19 (17.0%)	22 (39.3%)	0.005*	0.350	0.168	0.727	0.008*	0.246	0.088	0.689
sICHe	13 (11.6%)	14 (25.0%)	0.029*	0.394	0.171	0.910	0.031*	0.274	0.084	0.887

CI: confidence interval; OTT: onset to treatment time; TOAST: Trial of Org 10,172 in acute stroke treatment; sICH: symptomatic intracerebral hemorrhage; NIHSS: National Institutes of Health Stroke Scale; EVT: endovascular therapy.

^aAdjusted for age, NIHSS score on admission, OTT, length of hospital stay, TOAST classification, occlusion site, and bridging venous thrombolysis.

^bAdjusted for age, NIHSS score on admission, OTT, TOAST classification, occlusion site, and bridging venous thrombolysis.

^cAdjusted for age, diabetes, NIHSS score on admission, TOAST classification, and occlusion site.

^dAdjusted for age, NIHSS score on admission, diabetes, OTT, length of hospital stay, TOAST classification, and occlusion site.

^eAdjusted for age, gender, NIHSS score on admission, diabetes, atrial fibrillation, hypertension, TOAST classification, and OTT.

*p < 0.05, **p < 0.005, ***p < 0.001.

Figure 2.

Estimated glomerular filtration rate (eGFR) levels and tirofiban treatment predicted functional outcomes. Patients taking tirofiban were less likely to have a poor prognosis as eGFR levels increased. There was no similar relationship between eGFR levels and prognosis in patients who did not receive tirofiban (p = 0.091).

Results

Participants

Between December 2018 and February 2022, a total of 543 stroke patients were enrolled in the stroke unit of the hospital. Among them, 134 patients did not receive EVT and were excluded from the study. After the exclusion process, 409 patients were included in the analysis (Figure 1). Of these, 254 (62.1%) patients received tirofiban treatment, while the remaining 155 (37.9%) patients did not receive tirofiban. During the 3-month follow-up period, 21 patients were lost to follow-up. It was observed that the tirofiban-treated group had a lower 3-month mortality rate compared to the non-tirofiban group (58 [24.2%] vs. 53 [35.8%], p = 0.014). However, there was no statistically significant difference in the 3-month good outcome (96 [40.0%] vs. 45 [30.5%], p = 0.056) and the occurrence of sICH (36 [14.2%] vs. 31 [20.0%], p = 0.122) between the two groups. Further details can be found in Supplemental material 1.

Figure 1.

Condition of inclusion and exclusion of AIS patients. A total of 543 patients with AIS, 134 of whom were not treated with EVT were excluded and 409 patients were included in the study. Of these patients, 21 were lost to follow-up, 141 had a favorable outcome (mRS 0–2), and 247 had an unfavorable outcome (111 had died at follow-up).

AIS: acute ischemic stroke; EVT: endovascular therapy.

Baseline characteristics of patients grouped according to level of renal function and whether using tirofiban or not

The demographic and clinical characteristics of the patients are summarized in Table 1. Among the patients with normal renal function (eGFR ≥ 90 mL/min/1.73 m²), 65.7% (151 out of 230) received tirofiban treatment. In the group of patients with impaired renal function, the percentage of patients receiving tirofiban was 57.5% (103 out of 179).

Table 1.

Comparisons of baseline characteristics of patients grouped by renal function level and whether using tirofiban or not.

	Normal renal function (230)			Impaired renal (179)
	Tirofiban (151)	Without tirofiban (79)	p value	Tirofiban (103)	Without tirofiban (76)	p value
Age, years (median, IQR)	62 (53–71)	67 (59–73)	0.011*	72 (65–78)	75 (70–81)	0.017*
Male, n (%)	115 (76.2%)	61 (77.2%)	0.858	64 (62.1%)	52 (68.4%)	0.430
Hypertension, n (%)	93 (61.6%)	42 (53.2%)	0.176	73 (70.9%)	54 (71.1%)	0.940
Diabetes, n (%)	25 (16.6%)	14 (17.7%)	0.857	25 (24.3%)	16 (21.1%)	0.596
Atrial fibrillation, n (%)	26 (17.2%)	24 (30.4%)	0.030*	31 (30.1%)	30 (39.5%)	0.264
Coronary artery disease, n (%)	7 (4.6%)	6 (7.6%)	0.550	11 (10.7%)	12 (15.8%)	0.370
Currently smoking, n (%)	66 (43.7%)	30 (38.0%)	0.398	38 (36.9%)	25 (32.9%)	0.634
Previous stroke, n (%)	20 (13.2%)	7 (8.9%)	0.391	8 (7.8%)	12 (15.8%)	0.099
SBP, mmHg (mean ± SD)	153.8 (127.8–179.9)	150.3 (120.0–180.6)	0.360	161.1 (129.7–192.6)	162.9 (131.9–193.9)	0.711
DBP, mmHg (mean ± SD)	87.2 (72.3–102.0)	87.1 (69.1–105.2)	0.992	89.0 (69.2–108.8)	89.5 (73.6–105.3)	0.864
Glucose, mmol/L (mean ± SD)	7.9 (5.1–10.7)	7.9 (4.8–11.0)	0.976	8.5 (5.2–11.9)	7.8 (5.5–10.0)	0.088
Platelet count, 109/L (mean ± SD)	205.7 (152.0–259.4)	209.8 (136.1–283.5)	0.683	220.7 (148.6–292.9)	195.0 (137.7–252.2)	0.017*
NIHSS score on admission (median, IQR)	13.0 (10.0–15.0)	13.0 (13.0–17.0)	0.017*	13.0 (11.0–17.0)	11.0 (13.0–15.0)	0.879
OTT, min (median, IQR) Bridging venous thrombolysis, n (%)	354.5 (270.3–501.3) 36 (23.8%)	328.0 (257.0–460.0) 23 (29.1%)	0.237 0.428	360.0 (259.0–468.0) 18 (17.5%)	329.0 (269.3–420.8) 21 (27.6%)	0.342 0.142
TOAST classification			0.003**			0.000***
Large artery atherosclerosis	90 (59.6%)	31 (39.2%)		52 (50.5%)	17 (22.4%)
Cardioembolism	43 (28.5%)	42 (53.2%)		43 (41.7%)	55 (72.4%)
Unknown etiology	11 (7.3%)	4 (5.1%)		6 (5.8%)	0 (0%)
Other	6 (4.0%)	2 (2.5%)		2 (1.9%)	4 (5.3%)
Occlusion site			0.105			0.686
Anterior circulation	117 (77.5%)	69 (87.3%)		77 (74.8%)	61 (80.3%)
Posterior circulation	27 (17.9%)	8 (10.1%)		20(19.4%)	11(14.5%)
Both circulation	7 (4.6%)	1 (1.3%)		4 (3.9%)	3 (3.9%)
Treatment operation			0.717			0.160
Aspiration only MT	8 (5.4%)	4 (5.3%)		4 (3.9%)	3 (3.9%)
Stent-assisted MT	125 (83.9%)	61 (80.3%)		91 (89.2%)	61 (80.3%)
Stent-assisted MT with Balloon angioplasty	16 (10.7%)	11 (14.5%)		7 (6.9%)	12 (15.8%)
mTICI ≥ 2b	145 (96.0%)	75 (94.9%)	0.722	94 (91.3%)	70 (92.1%)	0.841
Length of hospital stay (day) (median, IQR)	13.0 (9.0–22.3)	11.0 (7.0–18.0)	0.077	12.0 (7.0–18.0)	9.0 (5.0–13.0)	0.074

DBP: diastolic blood pressure; IQR: interquartile range; mTICI: modified thrombolysis in cerebral infarction; NIHSS: National Institutes of Health Stroke Scale; OTT: onset to treatment time; eGFR: estimated glomerular filtration rate; SBP: systolic blood pressure; SD: standard deviation; sICH: symptomatic intracranial hemorrhage; HDL: high-density lipoprotein; LDL: low-density lipoprotein; MT: mechanical thrombectomy; TOAST: Trial of Org 10,172 in acute stroke treatment.

*p < 0.05, **p < 0.005, ***p < 0.001.

Efficacy and safety of tirofiban in subgroups based on renal function

In patients with normal renal function (eGFR ≥ 90 mL/min/1.73 m²), tirofiban treatment was associated with a better 3-month prognosis (64 [42.4%] vs. 23 [29.1%], p = 0.018), lower 3-month mortality (25 [16.6%] vs. 26 [32.9%], p = 0.012), and fewer cases of sICH (20 [13.2%] vs. 20 [25.3%], p = 0.024). However, tirofiban treatment did not significantly affect the prognosis in patients with impaired renal function (Table 2).

The binary logistic regression analysis revealed a connection between tirofiban treatment and prognosis in patients with different eGFR levels (Table 2). Among patients with normal renal function, the use of tirofiban was associated with improved 3-month functional outcomes (OR = 2.041, 95% confidence interval [CI] = 1.131–3.681, p = 0.018), reduced mortality (OR = 0.439, 95% CI = 0.231–0.831, p = 0.012), and a lower incidence of sICH (OR = 0.450, 95% CI = 0.225–0.900, p = 0.024). These significant differences persisted after adjusting (Table 2). Tirofiban treatment was still associated with improved 3-month functional outcomes (adjusted odds ratio [aOR] = 2.408, 95% CI = 1.120–5.175, p = 0.024), reduced mortality (aOR = 0.364, 95% CI = 0.155–0.856, p = 0.020), and a lower incidence of sICH (aOR = 0.339, 95% CI = 0.149–0.767, p = 0.009). However, in the group of patients with impaired renal function, there were no statistically significant differences in the odds ratios (ORs) before and after adjustment (Table 2).

An interaction study of eGFR levels with tirofiban showed that the effectiveness of tirofiban in improving prognosis was influenced by eGFR levels. The use of tirofiban in patients with impaired renal function made the prognosis worse, this trend was not observed in patients who did not receive tirofiban treatment (p = 0.091) (Figure 2).

A significant difference in baseline information between patients with and without tirofiban in patients with normal renal function. Of these differing baseline profiles, age, and admission NIHSS score, both may influence prognosis. We reallocated patients by propensity score matching, age, and admission NIHSS score were not statistically different after matching (Supplemental material 2), showed that the use of tirofiban in patients with normal renal function improved functional prognosis and reduced the risk of SICH and death (Supplemental material 2).

Efficacy and safety of tirofiban in different subgroups

Different grouping methods and models were performed to examine the factors influencing the efficacy of tirofiban in EVT patients. We performed binary logistic regression analyses for all EVT patients, direct thrombectomy patients, and direct thrombectomy patients with eGFR > 90 mL/min/1.73 m².

For all EVT patients, the univariate analysis revealed that tirofiban was associated with lower 3-month mortality (OR = 0.571, 95% CI = 0.365–0.894, p = 0.014). However, after adjusting for other factors, this difference became non-significant (aOR = 0.607, 95% CI = 0.341–1.081, p = 0.090) (Table 3).

In the model focusing on direct thrombectomy patients, the univariate analysis showed that tirofiban use was associated with a better 3-month functional prognosis (aOR = 2.136, 95% CI = 1.244–3.665, p = 0.006) and lower 3-month mortality (aOR = 0.500, 95% CI = 0.303–0.825, p = 0.007). After adjusting for other factors, tirofiban use remained associated with a better 3-month functional prognosis (aOR = 2.136, 95% CI = 1.123–4.064, p = 0.021) and lower 3-month mortality (aOR = 0.448, 95% CI = 0.237–0.848, p = 0.014).

The regression analysis for direct thrombectomy patients with eGFR > 90 mL/min/1.73 m² revealed that before adjustment, tirofiban was associated with a better 3-month functional prognosis (OR = 2.467, 95% CI = 1.185–5.134, p = 0.016), lower 3-month mortality (OR = 2.861, 95% CI = 1.376–5.947, p = 0.005), and lower incidence of sICH (OR = 0.394, 95% CI = 0.171–0.910, p = 0.029). After adjusting for other factors, these differences remained significant. Tirofiban was still associated with a better 3-month functional prognosis (aOR = 2.507, 95% CI = 1.042–6.027, p = 0.040), lower 3-month mortality (aOR = 0.246, 95% CI = 0.088–0.689, p = 0.008), and a lower incidence of sICH (aOR = 0.274, 95% CI = 0.084–0.887, p = 0.031).

Discussion

Our study is the first to explore the link between tirofiban treatment and eGFR in EVT patients. We found that using tirofiban in patients with normal eGFR (>90 mL/min/1.73 m²) improves the prognosis at 3 months, reduces sICH, and lowers 3-month mortality but has no impact on prognosis in patients with eGFR < 90 mL/min/1.73 m². Our regression modeling and propensity score matching confirmed these results. We observed that tirofiban may be less effective in patients undergoing bridging thrombectomy (Supplemental material 3). The interaction analysis between eGFR and tirofiban usage showed a potential trend, suggesting that the improvement in functional outcome with tirofiban might be influenced by eGFR levels (p = 0.091).

No clinical studies have been conducted to elucidate the impact of eGFR on the efficacy of Tirofiban in EVT patients. However, we hypothesize that the variation in tirofiban plasma drug concentrations due to eGFR levels may contribute to the disparate prognoses observed in patients treated with tirofiban. Approximately 80% of tirofiban is eliminated through the kidneys in its prototype form. ¹⁴ Consequently, patients with severe renal insufficiency may experience a reduction of more than 50% in plasma clearance of tirofiban. ¹⁴ Abnormal renal function hampers tirofiban excretion and increases its concentration, thereby elevating the risk of intracerebral hemorrhage and adverse outcomes. This conclusion is supported by previous studies that demonstrate a dose-dependent increase in cerebral hemorrhage with tirofiban.^16,17 Furthermore, research has indicated that renal insufficiency extends bleeding time in patients being treated with GP IIb/IIIa antagonists. ²⁴ Animal studies have shown that reducing the dose of tirofiban from the full dose to 10% of the full dose can decrease the probability of intracranial hemorrhage from 50% to 0%. ¹⁷ Full-dose administration of intra-arterial tirofiban (10 µg/kg) resulted in 22.2% sICH, whereas reducing the tirofiban concentration to one-third of the full dose lowered the incidence of SICH to 5.6%. ¹⁶ These findings support that eGFR may influence drug efficacy by affecting tirofiban blood concentrations.

Previous studies have established a correlation between the pre-thrombectomy eGFR level and the prognosis of patients three months after the onset of In AIS patients, an eGFR below 60 mL/min/1.73 m² is associated with a poor prognosis.^25,26 Diminished renal function negatively impacts the function of vascular endothelial cells.^27,28 Impaired renal function also affects the number and function of endothelial progenitor cells,^29,30 compromising the integrity of the vascular endothelium and increasing the risk of bleeding. Our study suggests that treatment with tirofiban may not be effective in patients with low eGFR levels.

The association between tirofiban and the risk of sICH following thrombectomy in AIS patients has been a subject of debate. The risk of bleeding is influenced by both the dosage and the method of administration, whether intra-arterial or intravenous. Asian countries, such as China, have a higher prevalence of intracranial atherosclerosis compared to Western countries.^31,32 In China, the primary pathogenesis in patients with AIS is large artery atherosclerosis (LAA). ³³ Tirofiban has been found to be more effective in LAA AIS compared to cardiogenic AIS. ³⁴ As a result, studies examining the therapeutic efficacy of tirofiban have yielded different results in various countries and regions. Our findings suggest that tirofiban reduces the risk of sICH in thrombectomized patients with normal eGFR. However, this protective effect was not observed in patients with impaired renal function. We observed that the subgroup of patients with normal renal function who did not receive tirofiban had the highest incidence of sICH. This may be attributed to the fact that these patients presented with higher NIHSS scores upon admission, as demonstrated in Table 1. The severity of symptoms at admission could potentially influence the therapeutic effects of tirofiban or the risk of adverse events such as bleeding. However, the specific relationship requires further clinical investigation.

Several limitations should be acknowledged in our study. Firstly, our data are derived from a single center, and the study would have benefited from a larger sample size. Additionally, statistically significant differences in baseline information can cause bias. To mitigate these limitations, we conducted logistic regression analysis and propensity score matching. Another limitation is the lack of sufficient evidence to differentiate the causes of eGFR abnormalities during hospitalization, as well as the inability to distinguish between transient eGFR impairment and chronic renal insufficiency.

Despite its limitations, our study indicates that tirofiban is safe and effective for thrombectomy in patients with normal renal function. This research provides crucial guidance on the safe and effective utilization of tirofiban, particularly in EVT patients. Tirofiban demonstrates varying efficacy across patients with different renal functions, underscoring the importance of tailoring treatment based on individual renal conditions. We strongly recommend routine assessment of renal function in stroke patients before undergoing EVT treatment and the evaluation of potential history of chronic kidney disease. However, the specific mechanisms involved require further investigation, and clinical trials with larger sample sizes and well-controlled designs will contribute to providing more definitive evidence for the use of tirofiban in specific patient subgroups.

Conclusion

Renal function can impact the effectiveness of tirofiban. The use of tirofiban in patients with normal renal function appears to be safe and associated with a better prognosis. However, tirofiban has limited prognostic benefits in patients with impaired renal function.