The Clinical Noteworthiness of Plasma NT-ProBNP Standard in Sufferers with Cardiogenic Cerebral Embolism and Its Diagnostic Value for Such Sufferers.

In order to explore the clinical noteworthiness of plasma NT-proBNP standards in sufferers with cardiogenic cerebral embolism and its diagnostic value for such sufferers, a retrospective study is conducted by the clinical data of sufferers with cerebral embolism. 100 sufferers with cerebral embolism admitted to our hospital from January 2018 to December 2020 are selected. According to the heparin-like drug therapy of acute ischemic stroke test (TOAST) classification criteria, they are divided into cardiac sufferers with cerebral embolism set (43 cases) and noncardiac cerebral embolism set (57 cases). The analysis results show the correlation between serum NT-proBNP standard and neurological impairment score. The detection of-proBNP standard can be used as a diagnostic indicator of disease severity and prognosis for sufferers with cardiogenic cerebral embolism.

1. Introduction

Cerebral embolism refers to various emboli in the blood, such as mural thrombus in the heart, atherosclerotic plaque, fat, tumor cells, fibrocartilage, or air, which enter the cerebral artery with the blood flow and block the blood vessels. Once the collateral circulation cannot be compensated, it will lead to ischemic necrosis of the brain tissue in the blood supply area of the artery and focal neurological deficit. Cerebral embolism often occurs in the internal carotid artery system, and the vertebral basilar artery system is relatively rare. In addition, cerebral embolism accounts for about 15%–20% of ischemic stroke. Cerebral embolism can be divided into cardiogenic cerebral embolism and noncardiogenic cerebral embolism according to the source of emboli. Cardiogenic cerebral embolism is the most common form of cerebral embolism, and about 75% of cardiogenic cerebral embolism occurs in the brain. The common heart diseases associated with cerebral embolism include atrial fibrillation, heart valve disease, infective endocarditis, myocardial infarction, cardiomyopathy, cardiac surgery, congenital heart disease, and cardiac myxoma. Cardiogenic cerebral embolism accounts for a relatively lofty proportion, accounting for about 20% of ischemic stroke [1]. Sufferers usually have rapid onset, severe symptoms, poor prognosis, easy recurrence, and lofty mortality. Surviving sufferers are often accompanied by a certain degree of neurological impairment, which has a negative impact on the quality of life of sufferers, and also aggravate the life and economic burden of the sufferer's family. Therefore, early diagnosis of sufferers with cardiogenic cerebral embolism has important clinical noteworthiness for guiding therapy [2, 3]. Plasma N-terminal B-type brain natriuretic peptide (NT-proBNP) is widely distributed in the brain, heart, spinal cord, and other important organs. NT-proBNP is actually one of the chemical structures of BNP precursor after degradation, which can be understood as the metabolite of BNP. It has no biological activity and appears in the same amount as BNP with biological activity. The increase of its concentration can indirectly reflect the concentration of BNP in the blood. It has a long half-life, so it is important to determine whether there are recent heart failure events. NT-proBNP is mainly used to check whether patients have heart failure. If the patient comes to the hospital due to wheezing and dyspnea, it is necessary to judge whether it is cardiogenic or pulmonary. Because both heart and lung diseases are prone to dyspnea, it can be identified by NT-proBNP detection. If the measured NT-proBNP level is less than 450 pg/ml, cardiogenic dyspnea can be basically ruled out and respiratory problems can be considered. NT-proBNP is synthesized in the ventricle and can promote vasodilation. At present, it has been widely used as a diagnostic index for symptoms such as heart failure and myocardial infarction, and it also has important value in therapy and prognosis evaluation [4, 5]. However, there are few studies using NT-proBNP to diagnose cardiogenic cerebral thrombosis [6]. Therefore, this study retrospectively analyzed the clinical data of 100 sufferers with cerebral embolism in our hospital, and scanned the clinical noteworthiness of NT-proBNP standard in sufferers with cerebral embolism.

The remainder of this paper is organized as follows. Section 2 discusses the related work. The general information and proposed method in presented in Section 3. The results and analysis are discussed in Section 4. Section 5 concludes the paper with a summary.

2. Related Work

Cerebral embolism refers to the obstruction phenomenon caused by various emboli in the blood system entering the cerebral arteries with the blood circulation, resulting in the narrowing of the cerebral arteries and poor blood circulation [7, 8]. The central source of cerebral embolism refers to the emboli from the heart, including the atrium, ventricular wall thrombus, heart valve vegetation, or atrial myxoma [9]. Cardiogenic cerebral embolism has a lofty incidence and rapid onset, usually peaking in a short period of time, and some sufferers have a step-like progression of symptoms. The disease has lofty mortality, morbidity, and recurrence rates [10]. The serum NT-proBNP standard is widely used in clinical practice as an important indicator for predicting stroke. Some studies have pointed out that the onset of acute stroke can cause a strong stress response, activate the protective mechanism of the central nervous system in the body, and increase the body's BNP. The secretion of NT-proBNP is the cleavage product of BNP, and the two have extensive homology [11]. At the same time, the half-life of NT-proBNP is longer, and its detection sensitivity is loftier than that of BNP. Therefore, the detection of NT-proBNP standards in sufferers has a more extensive advantage in the diagnostic value and prognosis evaluation of cardiogenic cerebral embolism [12].

In addition to NT-proBNP standards, hemoglobin, CRP, and Hcy standards were also notoriously different between the severe set and the other two sets. Lofty standards of Hcy will have an impact on vascular regulation, leading to atherosclerosis, vascular stenosis, and cerebral embolism [13]. As an inflammatory factor, CRP will increase in standard when blood vessels are damaged. Also, low standards of hemoglobin can easily induce cerebral embolism [14]. Comparatively, according to the clinical data of cardiogenic cerebral embolism group and noncardiogenic cerebral embolism group, the hemoglobin and serum NT-proBNP standards of cardiogenic cerebral embolism group were significantly higher than those of noncardiogenic cerebral embolism group. According to the ROC curve of serum NT-proBNP standard in the diagnosis of cardiogenic cerebral embolism, the AUC was 0.9343, indicating that the serum NT-proBNP standard has an extensive effect on the diagnosis of cardiogenic cerebral embolism. Studies by many scholars have shown that the serum NT-proBNP standard in sufferers with cardiogenic cerebral embolism is loftier than that in other types of stroke sufferers, and when the serum NT-proBNP standard is >360 pg/mL, its correlation with cardiogenic cerebral embolism is the most obvious [15, 16]. In the setting according to the prognosis, the serum NT-proBNP standard of sufferers in the good prognosis set with less nervous system damage was lower than that in the poor prognosis set. It can also be clearly seen from the ROC curve that the serum NT-proBNP standard is related to the prognosis of sufferers with cerebral embolism. The situation has extremely lofty sensitivity and specificity, which further proves the prognostic value of serum NT-proBNP standards in sufferers with cerebral embolism.

In this study, the sufferers were divided into mild, moderate, and severe sets according to their conditions. The clinical data of the three sets of sufferers were in contrast, and it was found that, among various indicators, the standards of NT-proBNP were notoriously different, and the severe set and the moderate set had the loftiest value. The sufferers in the mild set were the second and had the lowest value. In the current clinical examination, some scholars speculate on the relationship between the severity of cerebral embolism and the increase of NT-proBNP standard in sufferers with cerebral embolism. During the onset of cerebral embolism, the increase of intracranial pressure and ischemia in sufferers leads to bad things in the brain tissue and also leads to abnormal secretion system. It increases the secretion of NT-proBNP. In this examination, cerebral embolism was severe in sufferers with severe cerebral ischemia, and the area of cerebral ischemia was extensive than that of the other two sets, so the standard of NT-proBNP increased, which is consistent with the current examination results [17].

In addition, this examination found that the area under the curve (AUC) of the relationship between serum NT-proBNP standards and neurological impairment in sufferers was 0.947, indicating that the indicator had lofty specificity and sensitivity. The relationship between serum NT-proBNP standards and neurological impairment scores shows that there was an extensive positive correlation (r = 0.845, P < 0.001) because BNP is a neurohormone secreted by ventricular myocytes, initially synthesized as a precursor of the brain natriuretic peptide and then cracked into biologically inactive NT-proBNP and biologically active BNP. Bioactive BNP and NT-proBNP, both of which have the same clinical noteworthiness, but NT-proBNP has a longer half-life than BNP, so it has more tabulations in the plasma [18]. When brain cells are insufficient, cerebral vasodilation can lead to the rapid release of NT-proBNP in brain cells into the blood, thereby regulating cerebrovascular function. Therefore, the determination of NT-proBNP in the plasma can predict brain cell damage. In this examination, the serum NT-proBNP standard in the cerebral infarction set was notoriously loftier than that in the contrast set, and the loftier the NIHSS score, the loftier the serum HCY standard in the stroke sufferers; the extensive the infarct size, the loftier the serum HCY standard in the stroke sufferers, indicating that NT-proBNP standard can be used as a predictor of the occurrence and progression of stroke sufferers [19, 20]. This may be due to the increased intracranial pressure caused by the cerebral edema in sufferers with acute stroke, and the increased intracranial pressure will affect the hypothalamic-pituitary system and lead to abnormal secretion of neurotransmitters, resulting in increased secretion of NT-proBNP.

3. Our Proposed Method

3.1. General Information

A retrospective examination was performed on 100 sufferers with cerebral embolism admitted to our hospital from January 2018 to December 2020 including 44 males and 56 females with an average age of 75.38 ± 12.24 years. The weight of the sufferers was 43.37–72.58 kg, and the average weight was 55.29 ± 1.23 kg. The setting method specifically considers the following aspects: (1) etiology setting: according to the classification criteria of heparin-like drug therapy of acute ischemic stroke test (TOAST), the patients were divided into cardiogenic cerebral embolism group (43 cases) and noncardiogenic cerebral embolism group (57 cases); (2) condition settings: according to the National Institutes of Health Stroke Scale (NIHSS), the patients were divided into two groups: 0–4 mild group (24 cases), 4–15 moderate group (48 cases), and 28 severe group (more than 15 points); and (3) prognosis settings: all sufferers were treated, and they were followed up by outsufferer or telephone after 14 days to evaluate the prognosis of sufferers, and the modified Rankin scale was used to score (modified Rankin Scale, mRS), in which mRS score ≤2 indicates good prognosis, >2 indicates poor prognosis, and loftier scores indicate worse prognosis. mRS ≤2 means good prognosis (60 cases) and mRS >2 means poor prognosis (40 cases).

Inclusion criteria include the following: (1) sufferers diagnosed with cerebral embolism in our hospital; (2) sufferers with first onset; (3) admission within 24 hours after onset; and (4) sufferers with complete clinical data.

Exclusion criteria include the following: (1) sufferers whose condition deteriorated suddenly during the examination process; (2) sufferers whose other diseases affected the examination results; (3) sufferers who had unexpected circumstances during the examination process and made it difficult to continue the examination; and (4) sufferers with severe diseases during the examination process and sufferers affecting other examinations.

3.2. Methods

The blood routine, diastolic blood pressure (SBP), and systolic blood pressure (DBP) of the sufferers were detected after admission, and fasting venous blood samples were collected from the sufferers to collect the total cholesterol (TC), triglyceride (TG), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), C-reactive protein (CRP), homocysteine (Hcy), hemoglobin, fibrinogen (FIB), and D-dimer were detected. 5 ml of cubital venous blood was drawn from all the participating examinees in the fasting state in the morning, centrifuged at 3 500 r/min for 10 min, the centrifugation radius was 10 cm, and the serum was collected for testing. The standard of NT-proBNP in the serum of sufferers was detected by electrochemiluminescence, and the kit was purchased from Roche Diagnostics Co.

3.3. Observation Indicators and Inspection Standards

The observation indicators and inspection standards are as follows:

Contrast of clinical indicators of sufferers with mild disease set, moderate disease set, and severe disease set.

Contrast of clinical data between the cardiogenic cerebral embolism set and the non-cardiogenic cerebral embolism set.

To scan the clinical value of NT-proBNP standard in predicting the prognosis of sufferers with cardiogenic cerebral embolism set, including sensitivity, specificity, cut-off value, and area under the ROC curve (AUC).

To scan the correlation between serum NT-proBNP standard and neurological impairment score.

3.4. Statistical Methods

SPSS26.0 statistical software was used to scan the data of this examination. The measurement data was expressed as (x ± s), and the t test was used for the contrast of two samples. The count data was expressed as the number of cases and percentage, and the X test was used. Pearson coefficient was used to scan the correlation of indicators. The ROC curve was used to make comparison of the diagnostic effect, and P < 0.05 was considered statistically extensive.

4. Results and Analysis

4.1. Contrast of Clinical Indicators of Sufferers with Mild Disease, Moderate Disease, and Severe Disease

The blood pressure (SBP and DBP) and blood lipids (TC, TG, HDL-C, and LDL-C) standards in the clinical data of the three sets of sufferers had little disparity, and there was no statistical noteworthiness (P > 0.05). The severe set was notoriously lower than the other two sets of sufferers; the standards of CRP, Hcy, and NT-proBNP in the severe set were loftier than those in the other two sets; the standards of Hcy, CRP, and NT-proBNP in the moderate set were loftier than those in the mild set, with extensive disparities. There is statistical noteworthiness (P < 0.05), as shown in Table 1. The difference is statistically significant: P < 0.05, contrast with the mild set; #P < 0.05, contrast with the moderate set. 1 mmHg = 0.133 kPa.

Table 1

Contrast of clinical indicators of sufferers with mild disease, moderate disease, and severe disease.

Set	Mild set (n = 24)	Moderate set (n = 48)	Severe set (n = 28)	t	P
SBP (mmHg)	139.41 ± 13.21	149.23 ± 13.94	156.24 ± 16.81	2.152	0.135
DBP (mmHg)	91.35 ± 10.32	92.51 ± 9.31	93.13 ± 6.91	0.312	0.818
TC (mmoL/L)	4.03 ± 0.56	4.36 ± 0.65	4.68 ± 0.63	1.351	0.182
TG (mmoL/L)	1.89 ± 0.31	1.90 ± 0.29	1.97 ± 0.33	0.491	0.623
HDL-C (mmoL/L)	1.23 ± 0.26	1.21 ± 0.21	1.26 ± 0.23	0.210	0.791
LDL-C (mmoL/L)	2.86 ± 0.79	2.98 ± 0.69	3.03 ± 0.49	1.642	0.196
Hemoglobin (g/dL)	13.12 ± 4.61	12.51 ± 5.13	9.31 ± 3.15∗#	3.150	0.041
FIB (g/L)	3.16 ± 1.29	3.09 ± 1.31	3.10 ± 0.99	0.813	0.461
D-dimer	0.97 ± 0.12	0.98 ± 0.13	1.01 ± 0.11	1.931	0.154
Hcy (μmoL/L)	14.91 ± 3.14	17.51 ± 5.13∗	18.13 ± 4.21∗	4.971	0.009
CRP (mg/L)	3.21 ± 1.23	4.20 ± 3.16∗	6.42 ± 3.12∗#	12.142	<0.001
Serum NT-proBNP	412.54 ± 81.31	557.46 ± 214.51∗	832.51 ± 185.31∗#	31.612	<0.001

4.2. Contrast of Clinical Indicators between the Cardiogenic Cerebral Embolism Set and the Noncardiogenic Cerebral Embolism Set

In the two sets of sufferers, the hemoglobin standard in the cardiogenic cerebral embolism set was lower than that in the noncardiogenic cerebral embolism set, and at the same time, the NT-proBNP standard was loftier than that in the noncardiogenic cerebral embolism set, and the disparity was statistically extensive (P < 0.05), as shown in Table 2.

Table 2

Contrast of clinical indicators of sufferers with cardiogenic cerebral embolism set and noncardiogenic cerebral embolism set.

Set	Noncardiogenic cerebral embolism set (n = 57)	Cardiogenic cerebral embolism set (n = 43)	t	P
SBP (mmHg)	149.13 ± 12.91	154.63 ± 14.17	1.252	0.215
DBP (mmHg)	91.97 ± 10.14	90.51 ± 9.41	0.731	0.458
TC (mmoL/L)	4.33 ± 0.65	4.57 ± 0.71	0.231	0.732
TG (mmoL/L)	1.83 ± 0.29	2.01 ± 0.30	0.991	0.321
HDL-C (mmoL/L)	1.21 ± 0.16	1.18 ± 0.22	0.813	0.392
LDL-C (mmoL/L)	2.91 ± 0.73	2.93 ± 0.79	0.242	0.763
Hemoglobin (g/dL)	11.92 ± 4.59	9.71 ± 3.24	2.261	0.039
FIB (g/L)	3.22 ± 1.34	3.15 ± 1.27	0.538	0.572
D-dimer	0.98 ± 0.32	1.08 ± 0.34	0.341	0.854
Hcy (μmoL/L)	15.93 ± 4.17	16.73 ± 3.93	0.941	0.309
CRP (mg/L)	4.24 ± 2.53	5.19 ± 2.96	1.742	0.201
Serum NT-proBNP	512.34 ± 169.11	767.63 ± 262.61	4.922	<0.001

4.3. The Role of Serum NT-ProBNP Standard in the Diagnosis of Cardiogenic Cerebral Obstruction

The area under the curve (AUC) of serum NT-proBNP standard in the diagnosis of cardiogenic cerebral embolism was 0.934, and the indicator had lofty specificity and sensitivity, as shown in Figure 1 and Table 3.

Figure 1

ROC curve of serum NT-proBNP standard in the diagnosis of cardiogenic cerebral obstruction.

Table 3

The diagnostic effect of serum NT-proBNP standard on cardiogenic cerebral obstruction.

Index	Accuracy	Sensitivity	Specificity	AUC	95% CI	Youden index
NT-proBNP detection	83.33	80.00	85.00	0.934	0.857 ∼ 0.959	0.633

4.4. The Relationship between Serum NT-ProBNP Standard and Neurological Impairment in Sufferers

The serum NT-proBNP standard of sufferers in the good prognosis set was notoriously lower than that in the poor prognosis set, and the disparity was statistically extensive (P < 0.05), as shown in Table 4. The area under the curve (AUC) of the relationship between the serum NT-proBNP standard and the sufferer's neurological impairment was 0.947, and the indicator had lofty specificity and sensitivity. There was an extensive positive correlation between the serum NT-proBNP standard and the neurological impairment score (r = 0.845, P < 0.001), as shown in Table 5 and Figures 2 and 3.

Table 4

Relationship between serum NT-proBNP standards and neurological impairment scores.

Rankin score	Number of cases (n)	Serum NT-proBNP standard (ng/L)
mRS ≤ 2 score	60	539.71 ± 234.19
mRS > 2 score	40	843.34 ± 193.91
T		5.342
P		<0.001

Table 5

The role of serum NT-proBNP standards in the diagnosis of neurological damage.

Index	Accuracy	Sensitivity	Specificity	AUC	95% CI	Youden index
NT-proBNP	85.00	82.00	84.00	0.947	0.894 ∼ 0.986	0.660

Figure 2

ROC curve of serum NT-proBNP standard and neurological impairment in sufferers.

Figure 3

Relationship between serum NT-proBNP standard and neurological impairment scores in sufferers.

5. Conclusions

In this study, a retrospective study is conducted to explore the clinical noteworthiness of plasma NT-proBNP standards in sufferers with cardiogenic cerebral embolism and its diagnostic value for such sufferers. For sufferers with cerebral embolism, serum NT-proBNP standard detection can be used as a diagnostic index for disease severity and prognosis, and it is worthy of clinical application and promotion.

The research still has some limitations: as a retrospective check, there may be errors in the data collection process, resulting in certain degree of analysis deviation. Therefore, the number of samples should be further expanded in the future work. In addition, we need to further explore the correlation between NT-proBNP level changes and cardiogenic cerebral embolism.