FM Combined With NIHSS Score Contributes to Early AIS Diagnosis and Differential Diagnosis of Cardiogenic and Non-Cardiogenic AIS

Abstract

A growing researchers have suggested that fibrin monomer (FM) plays an important role in early diagnosis of thrombotic diseases. We explored the application of FM in the diagnosis and classification of acute ischemic stroke (AIS). The differences in FM, D-dimer, and NIHSS scores between different TOAST (Trial of ORG 10172 in Acute Stroke Treatment) types were analyzed with one-way ANOVA; the correlation between FM, D-dimer and NIHSS score in patients with different TOAST classification was analyzed by Pearson linear correlation. The ROC curve was utilized to analyze the diagnostic performance. 1. FM was more effective in diagnosing patients with AIS than D-dimer. 2. The FM level in cardiogenic AIS was significantly different from that in non-cardiogenic patients ( P < 0.05); the NIHSS score in cardiogenic stroke was significantly higher than in atherosclerotic and unexplained stroke group. Whereas, no statistical difference was observed in the D-dimer level between these groups ( P > 0.05). 3. The correlation between FM and NIHSS scores in the cardiogenic (r = 0.3832) and atherosclerotic (r = 0.3144) groups was statistically significant. 4. FM exhibited the highest diagnostic efficacy for cardiogenic AIS; furthermore, FM combined with the NIHSS score was more conducive to the differential diagnosis of cardiogenic and non-cardiogenic AIS. FM detection contributes to the early diagnosis of AIS, and is important for the differential diagnosis of different TOAST types of AIS. Moreover, FM combined with the NIHSS score is valuable in the differential diagnosis of cardiogenic and non-cardiogenic AIS.

Nomogram prediction model for the risk of intracranial hemorrhagic transformation after intravenous thrombolysis in patients with acute ischemic stroke

“…Similar results were obtained by H Y et al, who suggested that increased SBP mediates brain-blood barrier damage and upregulation of aquaporin Protein-4 via oxidative stress, leading to an increased risk of neurological deterioration (18). Meanwhile, hypertension impairs collateral circulation, reduces the ability of brain tissue to maintain adequate oxygenation during cerebral artery occlusion, and promotes the accumulation of reactive oxygen species and the release of in ammatory factors, leading to further damage to the blood-brain barrier, which in turn leads to hemorrhagic transformation after thrombolysis (19).…”

Correlation of LP-PLA2 and MMP-9 with the occurrence of early neurological deterioration in patients with acute ischemic stroke

“…Secondly, patients with cardiogenic embolism also have a larger cerebral infarct area and a more rapid progression of the disease due to the sudden onset of the disease and the fact that collateral circulation has not yet formed at the infarct site. [30] The occurrence of AIS causes cerebral edema, which exacerbates the patient's condition and promotes an increase in intracranial pressure, exacerbating neurological impairment. However, the correlation between cardiogenic embolism and the occurrence of END after AIS was not found in this study, and it is considered that due to the inclusion of a small sample size of cardiogenic embolism (n = 73), further multicenter studies with large data samples are needed for validation.…”

Nomogram prediction model for the risk of intracranial hemorrhagic transformation after intravenous thrombolysis in patients with acute ischemic stroke

“…Similar results were obtained by He et al who suggested that increased SBP mediates brain–blood barrier damage and upregulation of aquaporin Protein-4 via oxidative stress, leading to an increased risk of neurological deterioration ( 19 ). Meanwhile, hypertension impairs collateral circulation, reduces the ability of brain tissue to maintain adequate oxygenation during cerebral artery occlusion, and promotes the accumulation of reactive oxygen species and the release of inflammatory factors, leading to further damage to the blood–brain barrier, which in turn leads to hemorrhagic transformation after thrombolysis ( 20 ).…”