Knockdown of CXCL13 Improves Vascular Remodeling, Reduces Blood Pressure and Protects the Heart in a Hypertensive rat Model by Regulating the PF4V1/NF-κB Signaling Pathway.

This paper aimed to unveil the diagnostic values of serum brain natriuretic peptide (BNP), pentraxin 3 (PTX3), and vascular endothelial growth factor (VEGF) in acute pulmonary embolism complicated by pulmonary artery hypertension (APE-PAH) and their correlations with severity of PAH. A total of 153 patients with APE were selected for our study and divided into the PAH and Non-PAH groups according to the measurement of pulmonary artery pressure by echocardiography. Serum BNP levels were measured by chemiluminescence immunoassay, and serum PTX3 and VEGF levels were appraised by ELISA. The predictive values of BNP, PTX3, and VEGF for APE-PAH were evaluated by applying the receiver operating characteristic (ROC) curve. Spearman test was implemented to correlate BNP, PTX3, and VEGF with the severity of PAH. Higher serum levels of BNP, PTX3, and VEGF were observed in the PAH group versus the Non-PAH group (p < .05). ROC curve analysis indicated that BNP, PTX3, and VEGF had acceptable diagnostic value for predicting APE-PAH. Higher serum levels of BNP, PTX3, and VEGF were witnessed in the moderate and severe PAH groups in contrast to the mild PAH group (p < .05), and the levels of these parameters were elevated in the severe PAH group versus the moderate PAH group (p < .05). Spearman correlation analysis signified that serum BNP (r = 0.377), PTX3 (r = 0.488), and VEGF (r = 0.575) levels were positively correlated with the severity of PAH in APE-PAH patients. Serum BNP, PTX3, and VEGF levels are significantly elevated in APE-PAH patients. Serum BNP, PTX3, and VEGF levels are of clinical value in the diagnosis of APE-PAH patients, and serum BNP, PTX3, and VEGF levels are positively correlated with the severity of PAH and can be used as predictors of the severity of PAH.

Correlations between B type natriuretic peptide and blood pressure in patients with type 2 diabetes mellitus

Objective To investigate the application value of urine brain natriuretic peptide (BNP) level in 131Ⅰ treatment of hyperthyroid heart disease.Methods One hundred and eleven hyperthyroidism patients who received 131Ⅰ therapy were divided into two groups,hyperthyroidism group(51 cases) and hyperthyroid heart disease group (60 cases),and 30 healthy subjects as control.Sixty patients in the hyperthyroid heart disease group all received ultrasonic cardiogram.The hyperthyroid heart disease group was divided into two subgroups according to New York Heart Association (NYHA) functional classification (hyperthyroid heart disease A subgroup and hyperthyroid heart disease B subgroup).The urine and serum BNP level and serum free triiodothyronine (FT3),free thyroxine (FT4) level were measured through chemiluminescence before and after therapy.Results The urine and serum BNP level before 131Ⅰ therapy of the hyperthyroid heart disease group were significantly higher than those of hyperthyroidism group (serum:t=8.98 and 9.52,both P＜0.01;urine:t=10.83 and 12.73,both P＜0.01)and the control group (serum:t=8.97 and 9.52,both P＜0.01; urine:t=9.21 and 5.64,both P＜0.01).The urine and serum BNP level before and 6,12 months after 131Ⅰ therapy of the hyperthyroid heart disease A subgroup were significantly higher than those of hyperthyroid heart disease B subgroup (serum:t=5.98,5.87 and 6.35,all P＜0.01; serum:t=4.33,4.09 and 5.02,all P＜0.01).The urine level of BNP was gradually increased with the severity of cardiac insufficiency and it was positively correlated with the serum level of BNP(r=0.829,P＜0.01),the NYHA functional classification (r=0.751,P＜0.01)and the serum level of FT3 and FT4 (FT3:r=0.635,P＜0.01; FT4:r=0.672,P＜0.01).Conclusions The urine BNP level of hyperthyroid heart disease patient increased with the severity of cardiac insufficiency.The urine BNP level could accurately reflect cardiac function of hyperthyroid heart disease patient,and could be used as objective indicator for clinical diagnosis,effective evaluation and prognosis evaluation.The urine BNP level has the same value as the serum BNP level. Key words: Hyperthyroid heart disease; Iodine Radioisotope; Natriuretic peptide; Brain; Urinalysis

Brain Natriuretic Peptide in Acute Ischemic Stroke

&lt;p&gt;Background: Hypertension is a major risk factor for cardiovascular disease (CVD), which is the number one cause of global mortality. The potential use of natural products to alleviate high blood pressure has been demonstrated to exert a cardioprotective effect. Centella asiatica (L.) Urb. belongs to the plant family Apiaceae (Umbelliferae). It contains a high amount of triterpenoid and flavonoid that have antioxidant properties and are involved in the renin-angiotensin-aldosterone system which is an important hormonal system for blood pressure regulation.&lt;/p&gt;&lt;p&gt;Objective: This study aimed to investigate the effects of C. asiatica ethanolic extract on blood pressure and heart in a hypertensive rat model, which was induced using oral N(G)-nitro-l-arginine methyl ester (l-NAME).&lt;/p&gt;&lt;p&gt;Methods: Male Sprague-Dawley rats were divided into five groups and were given different treatments for 8 weeks. Group 1 only received deionized water. Groups 2, 4, and 5 were given l-NAME (40 mg/kg, orally). Groups 4 and 5 concurrently received C. asiatica extract (500 mg/kg, orally) and captopril (5 mg/kg, orally), respectively. Group 3 only received C. asiatica extract (500 mg/kg body weight, orally). Systolic blood pressure (SBP) was measured at weeks 0, 4, and 8, while serum nitric oxide (NO) was measured at weeks 0 and 8. At necropsy, cardiac and aortic malondialdehyde (MDA) contents, cardiac angiotensin-converting enzyme (ACE) activity, and serum level of brain natriuretic peptide (BNP) were measured.&lt;/p&gt;&lt;p&gt;Results: After 8 weeks, the administrations of C. asiatica extract and captopril showed significant (p &lt; 0.05) effects on preventing the elevation of SBP, reducing the serum nitric oxide level, as well as increasing the cardiac and aortic MDA content, cardiac ACE activity, and serum brain natriuretic peptide level.&lt;/p&gt;&lt;p&gt;Conclusion:C. asiatica extract can prevent the development of hypertension and cardiac damage induced by l-NAME, and these effects were comparable to captopril.&lt;/p&gt;

P28-5 - The Impact of Pulse Pressure on Silent and Ongoing Myocardial Damage in the General Population

CONTEXT: Plasma brain natriuretic peptide (BNP) levels are elevated in patients with acute ischemic stroke, particularly when accompanied by atrial fibrillation (AF). Plasma BNP might be a useful marker of vulnerability to thromboembolism in non-valvular AF patients. AIM: The aim of the present study was to assess whether the BNP level can serve as a biomarker of the left atrial (LA) thrombus in AF patients with acute ischemic stroke. SETTINGS AND DESIGN: This was a multicenter prospective cohort study. PATIENTS AND METHODS: Thirty AF patients with acute ischemic stroke were included in the study. Their transesophageal echocardiography (TEE) and BNP were assessed. RESULTS: There was a positive significant relation between serum BNP levels and LA thrombus detection by TEE. BNP with a cutoff value &gt;498 pg/l can be used as a diagnostic biomarker for the presence of the LA thrombus. A significant positive correlation existed between serum BNP and LA diameter. Furthermore, a statistically significant positive correlation between serum BNP and AF rate and duration was found in all patients. In addition, a statistically significant inverse correlation was detected between serum BNP and direct bilirubin, international normalized ratio, and albumin. A statistically significant positive correlation existed between serum BNP and prothrombin concentration. CONCLUSION: BNP can be a good diagnostic biomarker for the detection of the LA thrombus in chronic AF patients with acute ischemic stroke.

Background: Hypertension is a major risk factor for cardiovascular disease (CVD), which is the number one cause of global mortality. The potential use of natural products to alleviate high blood pressure has been demonstrated to exert a cardioprotective effect. Centella asiatica (L.) Urb. belongs to the plant family Apiaceae (Umbelliferae). It contains a high amount of triterpenoid and flavonoid that have antioxidant properties and are involved in the renin-angiotensin-aldosterone system which is an important hormonal system for blood pressure regulation. Objective: This study aimed to investigate the effects of C. asiatica ethanolic extract on blood pressure and heart in a hypertensive rat model, which was induced using oral N(G)-nitro-l-arginine methyl ester (l-NAME). Methods: Male Sprague-Dawley rats were divided into five groups and were given different treatments for 8 weeks. Group 1 only received deionized water. Groups 2, 4, and 5 were given l-NAME (40 mg/kg, orally). Groups 4 and 5 concurrently received C. asiatica extract (500 mg/kg, orally) and captopril (5 mg/kg, orally), respectively. Group 3 only received C. asiatica extract (500 mg/kg body weight, orally). Systolic blood pressure (SBP) was measured at weeks 0, 4, and 8, while serum nitric oxide (NO) was measured at weeks 0 and 8. At necropsy, cardiac and aortic malondialdehyde (MDA) contents, cardiac angiotensin-converting enzyme (ACE) activity, and serum level of brain natriuretic peptide (BNP) were measured. Results: After 8 weeks, the administrations of C. asiatica extract and captopril showed significant (p < 0.05) effects on preventing the elevation of SBP, reducing the serum nitric oxide level, as well as increasing the cardiac and aortic MDA content, cardiac ACE activity, and serum brain natriuretic peptide level. Conclusion: C. asiatica extract can prevent the development of hypertension and cardiac damage induced by l-NAME, and these effects were comparable to captopril.

Abstracts

BackgroundCardiac re-expression of fetal genes in patients with heart failure (HF) suggests the presence of low cardiac tissue thyroid hormone (TH) function. However, serum concentrations of T3 and T4 are often normal or subclinically low, necessitating an alternative serum biomarker for low cardiac TH function to guide treatment of these patients. The clinical literature suggests that serum Brain Natriuretic Peptide (BNP) levels are inversely associated with serum triiodo-L-thyronine (T3) levels. The objective of this study was to investigate BNP as a potential serum biomarker for TH function in the heart.MethodsTwo animal models of thyroid hormone deficiency: (1) 8-weeks of propyl thiouracil-induced hypothyroidism (Hypo) in adult female rats were subsequently treated with oral T3 (10 μg/kg/d) for 3, 6, or 14 days; (2) HF induced by coronary artery ligation (myocardial infarction, MI) in adult female rats was treated daily with low dose oral T3 (5 μg/kg/d) for 8 or 16 wks.ResultsSix days of T3 treatment of Hypo rats normalized most cardiac functional parameters. Serum levels of BNP increased 5-fold in Hypo rats, while T3 treatment normalized BNP by day 14, showing a significant inverse relationship between serum BNP and free or total T3 concentrations. Myocardial BNP mRNA was increased 2.5-fold in Hypo rats and its expression was decreased to normal values by 14 days of T3 treatment. Measurements of hemodynamic function showed significant dysfunction in MI rats after 16 weeks, with serum BNP increased by 4.5-fold and serum free and total T3 decreased significantly. Treatment with T3 decreased serum BNP while increasing total T3 indicating an inverse correlation between these two biologic factors (r2 = 0.676, p < 0.001). Myocardial BNP mRNA was increased 5-fold in MI rats which was significantly decreased by T3 over 8 to 16 week treatment periods.ConclusionsResults from the two models of TH dysfunction confirmed an inverse relationship between tissue and serum T3 and BNP, such that the reduction in serum BNP could potentially be utilized to monitor efficacy and dosing of T3 treatment. Thus, serum BNP may serve as a reliable biomarker for cardiac TH function.

Serum brain natriuretic peptide (BNP) is elevated after subarachnoid hemorrhage (SAH), causes diuresis and natriuresis (cerebral salt wasting), and may exacerbate delayed ischemic neurological deficits. We examined the temporal relationship between serum BNP elevation, hyponatremia, and the onset of delayed ischemic neurological deficits and determined whether serum BNP levels correlated with the 2-week outcome after SAH. Serum BNP and sodium were measured prospectively every 12 hours for 14 days in 40 consecutive patients admitted with SAH. All patients remained euvolemic, underwent transcranial Doppler assessment every 48 hours, and underwent angiography at the onset of delayed neurological deficits. New-onset neurological deficits were attributed to vasospasm only in the absence of other causes and when supported by transcranial Doppler or cerebral angiography. Sixteen patients (40%) experienced symptomatic cerebral vasospasm after SAH. A more than threefold increase in admission serum BNP was associated with the onset of hyponatremia (P < 0.05). Mean BNP levels were similar between vasospasm and nonvasospasm patients fewer than 3 days after SAH (126 +/- 39 pg/ml versus 154 +/- 40 pg/ml; P = 0.61) but were elevated in the vasospasm cohort 4 to 6 days after SAH (285 +/- 67 pg/ml versus 116 +/- 30 pg/ml; P < 0.01), 7 to 9 days after SAH (278 +/- 72 pg/ml versus 166 +/- 45 pg/ml; P < 0.01), and 9 to 12 days after SAH (297 +/- 83 pg/ml versus 106 +/- 30 pg/ml; P < 0.01). BNP level remained independently associated with vasospasm adjusting for Fisher grade and Hunt and Hess grade (odds ratio, 1.28; 95% confidence interval, 1.1-1.6). In patients in whom vasospasm developed, mean serum BNP increased 5.4-fold within 24 hours after vasospasm onset and 11.2-fold the first 3 days after vasospasm onset. Patients with increasing BNP levels from admission demonstrated no change (0 +/- 3) in Glasgow Coma Scale score 2 weeks after SAH versus a 3.0 +/- 2 (P < 0.05) improvement in Glasgow Coma Scale score in patients without increasing serum BNP levels. Increasing serum BNP levels independently were associated with hyponatremia, significantly increased the first 24 hours after onset of delayed ischemic neurological deficits, and predicted the 2-week Glasgow Coma Scale score.

Objectives: To analyze the outcome of monosymptomatic primary nocturnal enuresis (MPNE) after adenotonsillectomy in children with obstructive sleep apnea syndrome (OSAS). Methods: The study included 74 MPNE children with OSAS qualified for an adenotonsillectomy procedure. MPNE was assessed prior to surgical procedure as well as 3 and 6 months after surgery. In addition to polysomnographic parameters, serum antidiuretic hormone (ADH) and brain natriuretic peptide (BNP) levels were measured preoperatively and 3 months postoperatively. Results: The mean age was 9.8 years and the mean number of nocturnal wetting weekly was 4.1. Thirty-eight percent of patients had family history of MPNE. All the patients underwent a successful adenotonsillectomy. Nocturnal enuresis was still reported in 18% of children 6 months after adenotonsillectomy. An increased risk of MPNE was significantly demonstrated in children with high obstructive apnea-hypopnea index (O-AHI), high oxygen desaturation index (ODI), high frequent nocturnal enuresis and family history. After surgery, ADH levels were significantly lower, whereas BNP levels were significantly higher in non-resolution children. Univariate analysis showed that higher O-AHI, higher ODI, severe enuresis, low serum ADH and higher serum BNP levels were indicative of persistent nocturnal enuresis. Multivariate analysis showed that higher ODI and higher BNP levels are independent prognostic markers for MPNE. Conclusions: Adenotonsillectomy in MPNE children with OSAS is an effective treatment for resolution of MPNE. Also, higher ODI caused by apnea and elevated serum BNP levels are the most important factors affecting the outcome of MPNE patients. Level of evidence: Not applicable for this multicentre audit.

BackgroundObstructive sleep apnea-hypopnea syndrome (OSAHS) is associated with cardiovascular morbidity and mortality, which can be improved by using continuous positive airway pressure (CPAP) therapy. However, the pathophysiological links between the two kinds of disease and the mechanism of the CPAP effect remain incompletely understood. We aimed to inquire into the myocardial involvement in this relationship. We suggested that serum brain natriuretic peptide (BNP) is sensitive enough to detect myocardial stress caused by OSAHS.Design and methodsSixty-four subjects without cardiovascular disease (21 controls, 24 normotensive OSAHS patients, and 19 hypertensive OSAHS patients) were analyzed for serum BNP at baseline and serially over 6 months. CPAP was applied to 23 patients with severe OSAHS.ResultsAt baseline, the serum BNP levels were significantly higher (p=0.0001) in the OSAHS group (22.3±14.79 pg/ml) than in the control group (9.2±6.75 pg/ml). Increased serum BNP levels were significantly associated with mean transcutaneous oxygen saturation (SpO2) (p<0.0001), minimal SpO2 (p=0.002), oxygen desaturation index (p=0.001), and total sleep time spent with SpO2 lower than 90% (p=0.002). All patients with elevated BNP levels (≥37 pg/ml) had moderate or severe OSAHS (11/43 OSAHS patients). The more severe the OSAHS, the higher the BNP levels were. However, only the difference between severe and mild OSAHS was statistically significant (p=0.029). Hypertensive OSAHS patients had the highest baseline BNP levels (27.7±16.74 pg/ml). They were significantly higher (p=0.001) than in normotensive OSAHS patients (18±11.72 pg/ml) (p=0.039) and the controls (9.2±6.75 pg/ml). As compared with baseline, treatment with CPAP significantly decreased BNP levels in both hypertensive and normotensive OSAHS patients (respectively, from 36±16.10 to 29.7±14.29 pg/ml, p<0.001, and from 20±10.09 to 16±8.98 pg/ml, p<0.001). In contrast, the BNP levels slightly increased in the controls (from 9.2±6.75 to 9.5±7.02 pg/ml, p=0.029), but there was no statistically significant difference in comparison with the baseline value. The effect of CPAP on BNP levels was more marked in patients with higher baseline BNP levels and those with the most prolonged nocturnal desaturation (p=0.001, r=0.65). It was also more marked in hypertensive OSHAS patients (p=0.015, r=0.72) in comparison with normotensive OSAHS patients (p=0.03, r=0.62).ConclusionBNP seems to be sensitive enough to detect myocardial stress caused by OSAHS. As such, it is a potential marker for screening of preclinical cardiovascular damage in patients with untreated OSAHS. Application of CPAP decreases levels significantly in normotensive and particularly in hypertensive OSAHS. These findings are consistent with previous results suggesting the potential benefits of CPAP on cardiovascular outcome in OSAHS patients.

BackgroundThyroid disorders are the second most common endocrine disorders after type 2 diabetes mellitus. Copeptin, the C-terminal part of pre-pro arginine vasopressin, and brain natriuretic peptide (BNP) are new markers of cardiac and endothelial diseases. The relationship between thyroid status and copeptin has not been studied yet. Serum BNP levels are also affected by thyroid function status; however, its value in the presence of thyroid dysfunction has been recently questioned.Aim of the workThe aim of this work was to assess the alteration of serum copeptin and BNP in patients with thyroid dysfunction and the relationship between this alteration and cardiovascular performance in patients with thyroid dysfunction.Materials and methodsThis study included 60 patients who were divided into two groups: group 1 included 30 patients with hyperthyroidism and group 2 included 30 patients with primary hypothyroidism. A total of 20 healthy euthyroid individuals served as the control group (group 3). All patients and controls were subjected to estimation of serum and urine osmolarity and electrolyte study and evaluation of T3, T4, thyroid-stimulating hormone, serum copeptin, and serum BNP using enzyme-linked immunosorbent assay. Echocardiographic study was conducted to assess left ventricle (LV) systolic and diastolic functions. In addition, endothelial function was assessed by measuring flow-mediated dilatation of the brachial artery.ResultsIn patients with hyperthyroidism, serum copeptin was significantly lower than that in controls (mean = 2.24 ± 1.68 vs. 3.34 ± 2.93 pmol/l, P = 0.03). However, it was significantly higher in hypothyroid patients in comparison with controls (mean = 18.78 ± 11.29 vs. 3.34 ± 2.93 pmol/l, P = 0.0001). Serum BNP in the hypothyroid group was significantly higher than that in the control group (mean = 15.02 ± 6.9 vs. 3.60 ± 1.38 ng/l, P = 0.028). E′/ A′ was significantly lower in hypothyroid patients in comparison with the control group (mean = 1.15 ± 0.72 vs. 1.48 ± 0.48, P = 0.03), and more than half of the patients (53%) had E′/ A′ less than 1, suggesting the presence of diastolic dysfunction in hypothyroid patients. There was a significant negative correlation between ejection fraction (P = 0.002), fractional shortening (P = 0.01), and copeptin in the hypothyroid group. There was a significant positive correlation between copeptin and flow-mediated dilatation (P = 0.01) in the hyperthyroid group.ConclusionSerum copeptin and BNP were significantly increased in hypothyroid patients, whereas serum copeptin was significantly decreased in hyperthyroid patients. In hyperthyroid patients, LV systolic function was increased. More than half of the hypothyroid patients with high serum copeptin levels had impaired LV filling.

Objective Brain natriuretic peptide (BNP) before and after thrombolysis in the patients with ST-elevated myocardial infarction(STEMI) were measured to explore their change characteristics and clinical significance.Methods 60 patients with a first ST -elevated myocardial infarction were divided into three groups :A group (non- thrombolysis n=18), B g-roup (non- reperfusion n=11) and C group (reperfusion n=31).the serum BNP at the hospitalized time,on24th hour and on the 5th day after ons-et of AMI wered measured with a immmunofluorescence assay provided by Triage Biosite, and then the consequences were compared between and in the groups. Results in the three groups :The levels of serum BN-P on the 24th hour and the 5th day were higher than those at the hos-pitalized time (P＜ 0.05), In the A and B groups,the serum BNP levels on the 5th day I were not different from those on 24th hour ,but in the -C group ,The levels of serum BNP on the 5th day were decreased sig-niticantly (P＜ 0.05) .between the groups: there are no diference in the the serum BNP levels at the hospitalized time.between the A and B grou-ps, the serum BNP levels both on the 24th hour and on the 5thday w-ere not diferent,but the serum BNP levels on the 24th hour and the 5th day of the two groups were higher than those of the reperfusion group(P＜ 0.05), Conclusion BNP measureme nt may help us evaluate the effi-cacy of thrombolysis,so it can offer evidence for assessing their condition, further treatment and the prognosis of AMI. Key words: Acute myocardial infarction (AMI); Thrombolysis; Brain natriuretic peptide(BNP)