https://orcid.org/0009-0008-6055-5725
Figures
Abstract
Background
N-terminal pro-brain natriuretic peptide (NT-proBNP) was identified as an important biomarker of cardiovascular disease, in ischemic stroke. This study intends to assess the association of NT-proBNP levels with clinical outcomes of patients ischemic stroke patients.
Methods
A comprehensive search of MEDLINE, Web of Science, ScienceDirect, and Cochrane CENTRAL electronic databases was done for papers published till April 2024 and reporting on the levels of NT-proBNP in patients with ischemic stroke. Outcomes of interest included mortality (all-cause and cardiovascular) and neurological, and functional outcomes. A random-effects meta-analysis model was used, and final estimates were reported as pooled odds ratio (OR) with 95% confidence interval (CI).
Results
Elevated NT-proBNP levels were significantly linked to increased all-cause (pooled OR = 2.322, 95% CI: 1.718 to 2.925) and cardiovascular mortality (pooled OR = 1.797, 95% CI: 1.161 to 2.433). Higher NT-proBNP levels were also related to poorer functional outcomes (pooled OR = 1.129, 95% CI: 1.041 to 1.217). Patients with higher NT-proBNP levels had somewhat worse neurological outcomes (pooled OR = 1.317, 95% CI: 0.859 to 1.774). Considerable heterogeneity was detected across the studies (I² > 40% in most analyses).
Conclusion
NT-proBNP levels may serve as a robust predictor of mortality and offer potential utility in predicting functional recovery in ischemic stroke patients. The integration of NT-proBNP measurement into clinical settings may be beneficial for risk stratification and management of stroke survivors.
Citation: Zhang Y, Zheng J, Xu F (2025) Association between N-terminal pro-brain natriuretic peptide levels and outcomes of ischemic stroke: A systematic review and meta-analysis. PLoS One 20(6): e0322816. https://doi.org/10.1371/journal.pone.0322816
Editor: Zhehao Dai, The University of Tokyo Graduate School of Medicine Faculty of Medicine, JAPAN
Received: January 28, 2025; Accepted: March 26, 2025; Published: June 27, 2025
Copyright: © 2025 Zhang et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Data Availability: All relevant data are within the manuscript and its Supporting Information files.
Funding: The author(s) received no specific funding for this work.
Competing interests: The authors have declared that no competing interests exist.
Introduction
Ischemic stroke is considered one of the major contributors to mortality and long-term disability worldwide [1]. Therefore, identification of biomarkers that can predict outcomes and guide therapeutic strategies in stroke patients is crucial [2].
N-terminal pro-brain natriuretic peptide (NT-proBNP) has been identified as a potential biomarker of considerable interest due to its function and association with cardiovascular diseases [3].
NT-proBNP is a prohormone produced primarily in the cardiac ventricles [4]. It is released in response to changes in heart wall stress, serving as a regulatory peptide that modulates blood pressure and fluid balance. In clinical practice, NT-proBNP is predominantly recognized as a marker for diagnosing and managing heart failure [4], since elevated levels of this peptide indicate an increased strain on the cardiac walls, which is commonly seen in conditions such as heart failure, acute coronary syndromes, and atrial fibrillation [4].
The connection between cardiovascular impairment and stroke also makes NT-proBNP a promising candidate marker of the risk of ischemic stroke [5]. Ischemic stroke occurs as a result of obstruction (due to a thrombus or embolism) that compromises blood supply to parts of the brain, resulting in neuronal injury [6]. In addition to local cerebral changes, this pathological state also leads to systemic physiological responses, including changes in cardiac function. Therefore, current research suggests that measuring NT-proBNP levels post-stroke may reflect not just concurrent cardiac pathology but also severity of stroke and the extent of neurohormonal activation triggered by the acute event [7].
Several observational studies have reported associations between elevated NT-proBNP levels and poor outcomes in stroke patients, such as higher mortality rates, increased risk of complications, and diminished functional recovery [8–11]. These outcomes may be mediated through NT-proBNP’s relationship with left ventricular dysfunction, atrial fibrillation, and the extent of brain damage, all of which are critical determinants of prognosis after stroke. Furthermore, as shown by recent research, neuroendocrine stress caused by acute stroke may lead to increased NT-proBNP levels. NT-proBNP levels, therefore, may serve as a measure of the intensity of physiological stress response [12].
However, despite accumulating evidence, the prognostic value of NT-proBNP in the management of stroke patients remains unclear, potentially due to high that stems from differences in study design, timing of biomarker measurement, patient demographics, and the presence of concomitant cardiac conditions.
This review investigated the association between NT-proBNP and the outcomes of ischemic stroke to assess the prognostic value of NT-proBNP in this group of patients.
Methods
Eligibility criteria
Experimental trials and/or case-control, cohort, and cross-sectional observational studies that investigate the relationship between the levels of NT-proBNP and outcomes of ischemic stroke were eligible for inclusion. Full-text articles were included, while publications that were available solely as abstracts or unpublished data were excluded. Only studies that compared the effects of varying levels of NT-proBNP in patients undergoing treatment for ischemic stroke were eligible. The included studies were required to meet the following criteria:
Study population
Adults diagnosed with ischemic stroke, that had measurements of NT-proBNP taken during their treatment course.
Exposure
Observational data on NT-proBNP levels, without specific interventions that may alter these levels.
Outcomes of interest
Cardiovascular mortality.
Number of deaths specifically attributed to cardiovascular causes post-stroke.
Search strategy
Literature search was performed across MEDLINE, Web of Science, ScienceDirect, and Cochrane CENTRAL databases from the inception to 30 April 2024, with no language restrictions. Search terms and combinations used were: “N-terminal pro-brain natriuretic peptide,” “NT-proBNP,” “ischemic stroke,” “stroke outcomes,” “biomarkers in stroke,” and “neurological assessment.” Manual searches of bibliographies from selected studies were conducted to identify additional relevant articles.
Study registration
The protocol of this systematic review was registered at PROSPERO, with the number: CRD42024547558. Only publicly available studies were utilized for this meta-analysis and no ethical approval was required.
Study selection procedure
Two independent reviewers performed study selection. Initially, each reviewer conducted a separate search and then collaboratively reviewed titles and abstracts to shortlist preliminary eligible articles. Subsequently, full texts of selected studies were independently assessed by each reviewer to confirm eligibility based on the established criteria. In cases of disagreement, discussion between the authors or consultation with additional reviewer were used to reach consensus. List of excluded studies with reasons are attached as S1 File.
Data collection
A structured data collection framework was implemented under the guidance of the lead researcher. Retrieved data included date of data extraction, study title, author information, study design details, descriptions of the study population and setting, sample size for each group, baseline participant characteristics, and outcomes assessed. Additionally, information on the inclusion and exclusion criteria, descriptions of the groups based on NT-proBNP levels (high, normal, or not measured), follow-up duration, and key outcomes such as all-cause mortality, cardiovascular mortality, functional status, neurological outcomes, and incidences of haemorrhagic transformation were also extracted and catalogued.
Risk of bias assessment
Study quality was evaluated by two independent reviewers using the Newcastle-Ottawa Scale (NOS) that assesses quality of non-randomized, observational studies [13]. The NOS provides a framework for evaluating potential bias in three critical areas: selection of participants, comparability of study groups, and the accuracy of the outcome or exposure measurement reported. Studies scoring 7–9 were deemed to have a ‘low’ risk of bias, those scoring 4–6 as having a ‘moderate’ risk of bias, and studies with scores from 0 to 3 had a ‘high’ risk of bias.
Statistical analysis
A random-effects model through the inverse variance method of analysis was used [14] to accommodate differences among the included studies. For each study, odds ratios (ORs) with 95% confidence intervals (CIs) were calculated for both adjusted and unadjusted results. The pooled estimates were visually represented using Forest plots.
Heterogeneity among the studies was measured by chi-square tests and the I2 statistic. A chi-square test p-value below 0.05 and an I2 statistic exceeding 50% were used as indicators of significant heterogeneity [14]. Additional subgroup analysis and meta-regression was performed to identify the source of heterogeneity.
Funnel plots and Egger’s test were used to assess potential publication bias [14]. STATA software, version 16 was used for analyses. The dataset is available as S2 File.
Results
Search results
Systematic literature search of the databases identified 4,173 articles. Of them, 2,851 records remained after deduplication. After thorough assessment for eligibility, 2,119 records were excluded primarily due to not reporting data on NT-proBNP, not focusing on ischemic stroke, or due to the lack of relevant outcome data. Finally, 24 studies were included in the review (Fig 1) [8–11,15–34].
Characteristics of the included studies
Most included studies were prospective, and conducted across various countries including China, Austria, England, Slovenia, Denmark, Korea, Spain, Thailand, UK, and the USA (Table 1). Sample sizes ranged notably, from 67 to 6,315 participants. Most studies reported mean age of participants, often in the late sixties to early seventies. The studies explored outcomes such as mortality, functional status, and haemorrhagic transformation post-stroke, with follow-up periods varying from the duration of hospitalization to up to 14 months. In most studies, functional outcomes were assessed as measures of post-stroke disability or independence. Commonly used instruments included the modified Rankin Scale (mRS) and the Barthel Index. For example, several studies dichotomized functional outcome using mRS (with cutoffs such as mRS ≤ 2 or ≤3 to indicate favourable recovery), while others used alternative scales or categorization methods. Despite these minor differences, the underlying construct—namely, the degree of functional independence or disability—remained consistent across studies.
In contrast, neurological outcomes were generally defined as the evaluation of neurological impairment post-stroke. Although many studies relied on established clinical scales (such as the National Institutes of Health Stroke Scale, NIHSS), the specific thresholds or time points for assessment varied. For instance, one study might have defined neurological outcome in terms of early neurological deterioration (END) during the acute phase, whereas another assessed neurological status at a later follow-up. This heterogeneity in assessment tools and timing reflects the absence of a universally adopted definition for neurological outcomes in the context of stroke studies. As identified by the NOS score, 11 studies had a high risk of bias, 9 had a moderate risk, and 4 studies had a high risk of bias (Table 2).
Mortality
Nine studies assessed the link between NT-proBNP levels and mortality in ischemic stroke patients, using unadjusted odds ratios. The pooled OR of 2.322 (95% CI: 1.718 to 2.925) pointed to a significant association (p-value < 0.001), with moderate heterogeneity (I² of 47.8%; Fig 2).
Fourteen studies reported the link between adjusted NT-proBNP levels and mortality in ischemic stroke patients using adjusted odds ratios. The analysis revealed a pooled adjusted OR of 1.591 (95% CI: 1.376 to 1.806), demonstrating a statistically significant association (p < 0.001) (Fig 3), with low (I² = 28.4%) heterogeneity. Funnel plot was asymmetrical (S1 Fig), which was confirmed by significant Egger’s test (p = 0.001). A trim-and-fill analysis was conducted to address potential publication bias. The original random-effects model based on 14 studies estimated a pooled effect of 1.591 (95% CI: 1.376–1.806). After imputing 6 missing studies (for a total of 20 studies), the adjusted pooled effect was 1.555 (95% CI: 1.315–1.795), indicating only a modest attenuation of the effect size due to publication bias.
Subgroup analysis using adjusted estimates stratified by study design showed that the results pooled from 12 prospective studies had adjusted OR of 1.553 (95%CI: 1.321 to 1.784), while two retrospective studies provided a combined adjusted OR of 1.944 (95% CI: 1.057 to 2.831). There was no difference in estimates between the subgroups (p = 0.403) (Fig 4).
Subgroup analysis based on follow-up duration revealed that the results pooled from eight studies with short-term follow-up had an adjusted OR of 1.580 (95% CI: 1.163 to 1.997), while five studies with long-term follow-up provided a combined adjusted OR of 1.639 (95% CI: 1.341 to 1.936). Estimates of the short-term and long-term follow-up subgroups were comparable (p = 0.823) (Fig 5). Each subgroup analysis demonstrated significant effects (Short-term: p < 0.001; Long-term: p < 0.001), indicating that NT-proBNP levels consistently predict mortality across different follow-up durations (Table 3).
We further conducted subgroup analyses to explore whether the timing of NT-proBNP measurement and study quality influenced the association with adjusted mortality. For the timing-based analysis, studies were categorized into two groups: “Admission” and “<24 hours.” In the “Admission” subgroup, pooled adjusted OR was 1.442 (95% CI: 1.188–1.697) with minimal heterogeneity (Cochran’s Q = 0.64, p = 0.425; I² = 0.0%) (S2 Fig). In contrast, the “<24 hours” subgroup—which included eight studies yielded a pooled adjusted OR of 1.559 (95% CI: 1.302–1.816) with moderate heterogeneity (Cochran’s Q = 10.33, p = 0.171; I² = 32.2%) (S3 Fig). Additionally, subgroup analysis by risk of bias stratified studies into low, moderate, and high risk groups. The low risk subgroup (n = 7 studies) demonstrated a pooled adjusted OR of 1.594 (95% CI: 1.229–1.958); the moderate risk subgroup (n = 5 studies) had a pooled adjusted OR of 1.562 (95% CI: 1.301–1.823); and the high risk subgroup (n = 2 studies) showed a pooled adjusted OR of 1.824 (95% CI: 0.562–3.087) (S4 Fig). Meta-regression was performed with all the variables used in subgroup analysis and NTproBNP cut-off value (as continuous variable). However, none of the variables were able to explain heterogeneity associated with this outcome with every univariable meta-regression model giving a p-value more than 0.05.
Cardiovascular mortality
Three studies examined the link between NT-proBNP levels and cardiovascular mortality in ischemic stroke patients, with a pooled adjusted OR of 1.797 (95%CI: 1.161 to 2.433; p < 0.001) (Fig 6), with moderate (I² = 41.4%) heterogeneity. No subgroup analysis or publication bias assessment were done due to limited number of studies.
Neurological outcome
As shown in Fig 7, 3 studies that investigated the link between NT-proBNP levels and neurological outcomes post-stroke, reported insignificant (p > 0.05) pooled OR of 1.317 (95%CI: 0.859 to 1.774). This finding suggests that higher NT-proBNP levels may be associated with poorer neurological outcomes post-stroke. The heterogeneity was considerable, with an I² of 59.2%. Subgroup analysis and publication bias assessment were not done due to small number of studies.
Haemorrhagic transformation
Two studies investigated the association between NT-proBNP levels and haemorrhagic transformation, and reported pooled adjusted OR of 1.192 (95%CI: 0.793 to 1.591), which indicates no significant relationship (p > 0.05) (Fig 8), with substantial heterogeneity (I² of 88.7%).
Functional outcome
Nine studies explored the association between NT-proBNP levels and unadjusted functional outcomes following ischemic stroke. The pooled unadjusted OR was 1.155 (95%CI: 0.883 to 1.427) (Fig 9). However, the heterogeneity among the included studies was extremely high, with an I² of 95.0%
Ten studies assessed the association between NT-proBNP levels and adjusted functional outcomes following ischemic stroke, with the pooled adjusted OR of 1.129 (95%CI: 1.041 to 1.217), a statistically significant effect (p < 0.001) (Fig 10). There was a considerable heterogeneity (I² = 72.1%), and Funnel plot was asymmetrical with significant Egger’s test (p = 0.001) (S5 Fig). The original random-effects meta-analysis based on 10 studies estimated a pooled effect of 1.129 (95% CI: 1.041–1.217). After imputing 5 potentially missing studies (increasing the total to 15 studies), the adjusted pooled effect was 1.098 (95% CI: 1.000–1.196). Although the effect size was modestly attenuated, the association remains statistically significant, suggesting that publication bias may slightly overestimate the effect but does not substantially alter the overall findings.
Subgroup analysis based on study design showed that seven prospective studies contributed to a pooled adjusted OR of 1.161 (95%CI: 0.976 to 1.346) (Table 3). Three retrospective studies showed a combined adjusted OR of 1.320 (95% CI: 0.964 to 1.676) (S6 Fig). The analysis highlighted no significant difference in effect sizes between the prospective and retrospective study designs (p = 0.436), suggesting that NT-proBNP’s predictive value for functional outcomes post-stroke is consistent across different study methodologies.
We performed a subgroup meta‐analysis including only studies where NT-proBNP was measured within 24 hours of stroke onset. This analysis, which included six studies, yielded a pooled adjusted OR of 1.191 (95% CI: 1.023–1.359) (S7 Fig). The effect was statistically significant (z = 13.87, p < 0.001). However, there was substantial heterogeneity among these studies, with Cochran’s Q = 17.10 (p = 0.004), an I² of 70.8%, and a between-study variance (tau²) of 0.0233. We further stratified the analysis of functional outcomes by the risk of bias. In the low risk subgroup, the pooled adjusted OR was 1.153 (95% CI: 0.791–1.514). For the moderate risk subgroup, the pooled adjusted OR was 1.240 (95% CI: 1.020–1.460). In the high risk subgroup, adjusted OR was 1.360 (95% CI: 1.160–1.590) (S8 Fig). Analysis based on the follow-up duration could not be done due to limitation of information related to follow-up time for the outcome in the included studies.
Discussion
Our analysis demonstrated that NT-proBNP levels are significantly associated with both unadjusted and adjusted mortality in ischemic stroke patients. Specifically, higher NT-proBNP levels correlated with increased mortality rates, with unadjusted odds ratios showing a more pronounced effect compared to adjusted ratios. There was also a marked association between elevated NT-proBNP levels and higher risk of cardiovascular mortality, emphasizing the relevance of this biomarker in predicting severe post-stroke outcomes. Our results are in agreement with previous research that have identified NT-proBNP as a strong prognostic marker of cardiovascular conditions and post-stroke outcomes [35,36]. Numerous reports have consistently demonstrated that high NT-proBNP levels are indicative of cardiac stress and damage, which can also be extrapolated to the cerebrovascular events examined in our review [35–37].
The included studies suggest that higher NT-proBNP levels may be linked to poorer functional and neurological outcomes, although these associations were not statistically significant in all analyses. Therefore, NT-proBNP may potentially serve as a marker for the severity of stroke and patient’s prognosis. The link between NT-proBNP levels and haemorrhagic transformation after the stroke were not statistically significant. This implies that while NT-proBNP is indicative of other severe outcomes, it may not be as reliable for predicting these specific complications.
The significant association between NT-proBNP levels and various stroke outcomes can be understood through several physiological mechanisms. NT-proBNP is released in response to ventricular strain, which may occur as a result of acute neurological injury like stroke [38]. The brain-heart axis suggests that stroke-induced neurological impairment can lead to cardiac dysfunction, which in turn is reflected by elevated NT-proBNP levels [39]. Stroke can lead to disruption of the blood-brain barrier, promoting inflammation and neurohormonal activation that might stimulate NT-proBNP release [40]. Higher NT-proBNP levels could thus indicate more severe cerebral injury. Elevated NT-proBNP levels have been linked to poorer outcomes in various cardiac conditions due to their association with underlying cardiovascular diseases, which are also risk factors for worse outcomes in stroke patients.
Our analyses revealed that the association between elevated NT-proBNP levels and mortality is notably stronger compared to its association with functional and neurological outcomes. One potential explanation for this discrepancy is that NT-proBNP primarily reflects systemic hemodynamic stress and underlying cardiovascular pathology rather than direct neurovascular injury. NT-proBNP is released in response to increased cardiac wall stress, and its elevation may be more indicative of systemic factors—such as pre-existing heart failure, atrial fibrillation, or other cardiovascular conditions—that contribute to overall mortality risk. In contrast, functional and neurological outcomes post-stroke are influenced by a broader spectrum of factors, including the extent of cerebral injury, collateral circulation, and post-stroke rehabilitation efforts, which might not be directly captured by NT-proBNP levels. This suggests that while NT-proBNP is a robust predictor of mortality, its utility in predicting long-term functional or neurological recovery may be limited. Future studies could explore combining NT-proBNP with more neuro-specific biomarkers to improve prognostication in these domains.
Understanding the mechanisms by which NT-proBNP levels influence stroke outcomes might open new therapeutic avenues aimed at mitigating neurocardiac effects in stroke survivors.
Our findings support the prognostic value of NT-proBNP in ischemic stroke; however, translating these results into routine clinical practice presents several challenges. First, a universal cutoff for NT-proBNP is unlikely to be applicable given the substantial heterogeneity in patient characteristics—such as age, renal function, and pre-existing cardiac conditions—that can influence baseline NT-proBNP levels. Instead, NT-proBNP should be integrated into multifactorial risk stratification models rather than used as a stand-alone indicator.
Furthermore, evidence suggests that biological variability accounts for approximately 40% of NT-proBNP alterations [41], which further complicates its use in clinical decision-making. This high degree of inherent variability implies that single measurements may not reliably reflect a patient’s true risk. Serial measurements and monitoring trends over time might offer more clinically relevant insights. Clinicians should interpret NT-proBNP levels in the context of other clinical findings and biomarkers, tailoring risk assessments to the individual patient profile.
NT-proBNP levels are known to be influenced by underlying cardiovascular conditions, such as atrial fibrillation and heart failure. To mitigate this potential confounding, many of the included studies adjusted for these factors in their multivariable models. Although the specific covariates varied across studies, several common adjustments were noted. Most studies controlled for demographic factors (e.g., age and sex) and traditional cardiovascular risk factors, including hypertension, diabetes, and hyperlipidemia. In addition, many studies specifically adjusted for a history of cardiovascular conditions (e.g., atrial fibrillation, heart failure) to better isolate the prognostic value of NT-proBNP in the context of ischemic stroke.
Moreover, several investigations further incorporated measures of stroke severity—such as the National Institutes of Health Stroke Scale (NIHSS)—and other acute stroke-related parameters (e.g., time from symptom onset to NT-proBNP measurement) into their adjusted models. Although the list of covariates was not uniform across studies, these adjustments consistently aimed to account for the influence of pre-existing cardiovascular pathology. This variability in adjustment strategies may partially contribute to heterogeneity in the reported effect sizes, and future research would benefit from a more standardized approach to covariate selection.
This review has certain limitations. There was significant heterogeneity in our meta-analyses, which could be due to differences in study populations, NT-proBNP measurement timing, and stroke severity. Variability in how studies utilized and categorized the biomarker of interest was another limitation. Some studies divided levels using categorical thresholds, others employed quintiles or quartiles, while some analyzed it as a continuous variable. This lack of standardized cutoff values poses challenges in translating findings into clinical practice, as it limits the biomarker’s applicability and reliability for routine clinical use.
Another limitation of this study is the potential influence of hemodynamic status on NT-proBNP levels, which was not consistently described or controlled for in most of the included studies. Hemodynamic factors, such as volume status, cardiac output, and blood pressure, are known to significantly impact NT-proBNP levels, potentially confounding the observed associations with stroke outcomes. The absence of systematic reporting and adjustment for these factors limits the ability to generalize the findings across diverse clinical contexts. Despite the overall robustness of our findings, asymmetry observed in funnel plots and significant Egger’s test indicate presence of potential publication bias. This bias may arise because studies reporting non-significant or negative associations between NT-proBNP levels and ischemic stroke outcomes are less likely to be published. Consequently, pooled effect estimates in our analysis could be overestimated, thereby affecting the reliability of conclusions drawn. Although sensitivity analyses and subgroup assessments (e.g., by timing and risk of bias) consistently demonstrated significant associations, the possibility of publication bias suggests that these results should be interpreted with caution. Future studies, including the incorporation of unpublished data and prospective trial registration, are warranted to further clarify and validate these associations.
NT-proBNP could be used as a biomarker for risk stratification in stroke patients. Identifying high-risk patients early could help in tailoring aggressive therapeutic strategies to prevent severe outcomes. Regular monitoring of NT-proBNP levels in stroke patients could provide insights into their recovery trajectory and help in adjusting management plans accordingly.
By predicting functional and neurological outcomes, NT-proBNP levels could guide rehabilitation efforts, focusing resources on patients who are at higher risk of poor recovery.
Future research should aim to establish standardized protocols for NT-proBNP measurement in the acute and subacute phases of stroke and explore its incorporation into existing clinical scoring systems. By doing so, NT-proBNP could contribute to more precise risk stratification and targeted management strategies, ultimately improving the care and outcomes of stroke patients. More long-term longitudinal studies are needed to observe the progression of NT-proBNP levels from acute to chronic phases of stroke recovery and to assess how changes in these levels correlate with patient outcomes over time. Investigating the biological mechanisms through which NT-proBNP influences stroke outcomes can help clarify its role as a biomarker. Such studies could explore the impact of stroke event on neurocardiac interactions, particularly in patients with pre-existing cardiovascular conditions. Future research should also focus on standardizing timing and methods of NT-proBNP measurement after the stroke to reduce heterogeneity across studies, and making findings more comparable. Exploring NT-proBNP in conjunction with other biomarkers could provide a more comprehensive prognostic model to more accurately predict stroke outcomes.
Conclusion
The review has underscored significant prognostic value of NT-proBNP for various outcomes in ischemic stroke patients, including mortality, cardiovascular mortality, and functional recovery. The consistent association across multiple studies highlights the potential of NT-proBNP as a reliable biomarker for assessing stroke severity and predicting patient outcomes.
Supporting information
S2 Fig. Subgroup analysis based on NT-proBNP measurement at the time of admission for the association between N-terminal pro brain natriuretic peptide levels and mortality amongst ischaemic stroke patients.
https://doi.org/10.1371/journal.pone.0322816.s002
(JPG)
S3 Fig. Subgroup analysis based on NT-proBNP measurement at < 24 hours for the association between N-terminal pro brain natriuretic peptide levels and mortality amongst ischaemic stroke patients.
https://doi.org/10.1371/journal.pone.0322816.s003
(JPG)
S4 Fig. Subgroup analysis based on risk of bias for the association between N-terminal pro brain natriuretic peptide levels and mortality amongst ischaemic stroke patients.
https://doi.org/10.1371/journal.pone.0322816.s004
(JPG)
S6 Fig. Subgroup analysis based on study design showing the association between N-terminal pro brain natriuretic peptide levels and functional outcomes amongst ischaemic stroke patients.
https://doi.org/10.1371/journal.pone.0322816.s006
(TIF)
S7 Fig. Subgroup analysis based on NT-proBNP measurement at < 24 hours for the association between N-terminal pro brain natriuretic peptide levels and functional outcomes amongst ischaemic stroke patients.
https://doi.org/10.1371/journal.pone.0322816.s007
(JPG)
S8 Fig. Subgroup analysis based on risk of bias for the association between N-terminal pro brain natriuretic peptide levels and functional outcomes amongst ischaemic stroke patients.
https://doi.org/10.1371/journal.pone.0322816.s008
(JPG)
S1 File. List of excluded studies with reasons.
https://doi.org/10.1371/journal.pone.0322816.s009
(XLSX)
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