natriuretic-peptide--brain has been researched along with Constriction--Pathologic* in 10 studies
10 other study(ies) available for natriuretic-peptide--brain and Constriction--Pathologic
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Influence of cardiac biomarkers on predicting significant coronary artery disease in hypertrophic cardiomyopathy patients.
In this study, our aim was to investigate the role of cardiac biomarkers in predicting the presence of significant coronary artery disease in hypertrophic cardiomyopathy (HCM) patients.. The study population was composed of hypertrophic cardiomyopathy patients who underwent coronary angiography at a single center between June 2021 and March 2023, and whose cardiac biomarkers were evaluated before the procedure. HCM patients were screened retrospectively. Significant CAD was defined as > 50% stenosis of the left main coronary artery or > 70% stenosis in a major coronary vessel. Demographic, echocardiographic and cardiac biomarker values were compared between the two groups.. A total of 123 patients were evaluated. Significant CAD was detected in 39 (31.7%) patients. Patients with significant CAD had higher CK-MB values than those without CAD [2.8 (2.1-4.0) vs. 3.4 (2.8-4.6), p = 0.036], and a higher level of high-sensitivity troponin T (hs-TnT) than those without CAD (24 vs. 17.8, p = 0.022). the NT-proBNP/hs-TnT ratio was found to be significantly lower in patients with CAD than in those with CAD (31.4 vs. 21.4, p = 0.019). In multivariate anaylsis, NT-proBNP/hs-TnT was determined as an independent predictor for significant CAD. In ROC analysis, NT-proBNP/hs-TnT ratio lower than the cut-off value of 30.7 could detect the presence of significant CAD with 76.9% sensitivity and 53.6% specificity (AUC: 0.632, 95% CI: 0.528-0.736, p = 0.019).. To sum up, we suggest that cardiac biomarkers were valuable and simple parameters in terms of significant CAD in HCM patients. Topics: Biomarkers; Cardiomyopathy, Hypertrophic; Constriction, Pathologic; Coronary Artery Disease; Humans; Natriuretic Peptide, Brain; Peptide Fragments; Retrospective Studies; Troponin T | 2023 |
Biomarkers for Non-Invasive Stratification of Coronary Artery Disease and Prognostic Impact on Long-Term Survival in Patients with Stable Coronary Heart Disease.
Knowledge about cardiac and inflammatory biomarkers in patients with stable coronary artery disease (CAD) is limited. To address this, we analyzed 3072 patients (36% female) with a median follow-up of 10 years in the Leipzig LIFE Heart Study with suspected CAD with coronary angiography. Selected biomarkers included troponin T (hsTNT), N-terminal pro B-type natriuretic peptide (NT-proBNP), copeptin, C-reactive protein (hsCRP), and interleukin-6 (IL-6). Patients were stratified by CAD severity: CAD0 (no sclerosis), CAD1 (non-obstructive, i.e., stenosis < 50%), and CAD2 (≥one stenosis ≥ 50%). Group comparison (GC) included GC1: CAD0 + 1 vs. CAD2; GC2: CAD0 vs. CAD1 + 2. CAD0, CAD1, and CAD2 were apparent in 1271, 631, and 1170 patients, respectively. Adjusted for classical risk factors, hs-cTnT, NT-proBNP, and IL-6 differed significantly in both GC and hsCRP only in GC2. After multivariate analysis, hs-cTnT, NT-proBNP, and IL-6 remained significant in GC1. In GC2, hs-cTnT (p < 0.001) and copeptin (p = 0.014) reached significance. Ten-year survival in groups CAD0, CAD1, and CAD2 was 88.3%, 77.3%, and 72.4%. Incorporation of hs-cTnT, NT-proBNP, copeptin, and IL-6 improved risk prediction (p < 0.001). The studied cardiac and inflammatory biomarkers enable fast and precise non-invasive identification of mortality risk in CAD patients, allowing the tailoring of primary and secondary CAD prevention. Topics: Biomarkers; C-Reactive Protein; Constriction, Pathologic; Coronary Artery Disease; Female; Humans; Interleukin-6; Male; Natriuretic Peptide, Brain; Peptide Fragments; Prognosis | 2022 |
Ndufs1 Deficiency Aggravates the Mitochondrial Membrane Potential Dysfunction in Pressure Overload-Induced Myocardial Hypertrophy.
Mitochondrial dysfunction has been suggested to be the key factor in the development and progression of cardiac hypertrophy. The onset of mitochondrial dysfunction and the mechanisms underlying the development of cardiac hypertrophy (CH) are incompletely understood. The present study is based on the use of multiple bioinformatics analyses for the organization and analysis of scRNA-seq and microarray datasets from a transverse aortic constriction (TAC) model to examine the potential role of mitochondrial dysfunction in the pathophysiology of CH. The results showed that NADH:ubiquinone oxidoreductase core subunit S1- (Ndufs1-) dependent mitochondrial dysfunction plays a key role in pressure overload-induced CH. Furthermore, Topics: Angiotensin II; Animals; Atrial Natriuretic Factor; Biomarkers; Cardiomegaly; Constriction, Pathologic; Down-Regulation; Male; Membrane Potential, Mitochondrial; Mice, Inbred C57BL; Mitochondria, Heart; Myocardium; Myocytes, Cardiac; Myosin Heavy Chains; NADH Dehydrogenase; Natriuretic Peptide, Brain; Pressure; Rats; RNA-Seq; Single-Cell Analysis | 2021 |
Serial evaluation of cardiac biomarker NT-proBNP with speckle tracking echocardiography in a 6-year-old Golden Retriever dog with subaortic stenosis and dilated cardiomyopathy.
Topics: Animals; Biomarkers; Cardiomyopathy, Dilated; Constriction, Pathologic; Dog Diseases; Dogs; Echocardiography; Male; Natriuretic Peptide, Brain; Peptide Fragments | 2020 |
Bakuchiol protects against pathological cardiac hypertrophy by blocking NF-κB signaling pathway.
Bakuchiol (Bak), a monoterpene phenol isolated from the seeds of Psoralea corylifolia, has been widely used to treat a large variety of diseases in both Indian and Chinese folkloric medicine. However, the effects of Bak on cardiac hypertrophy remain unclear. Therefore, the present study was designed to determine whether Bak could alleviate cardiac hypertrophy. Mice were subjected to aortic banding (AB) to induce cardiac hypertrophy model. Bak of 1 ml/100 g body weight was given by oral gavage once a day from 1 to 8 weeks after surgery. Our data demonstrated for the first time that Bak could attenuate pressure overload-induced cardiac hypertrophy and could attenuate fibrosis and the inflammatory response induced by AB. The results further revealed that the effect of Bak on cardiac hypertrophy was mediated by blocking the activation of the NF-κB signaling pathway. Topics: Administration, Oral; Angiotensin II; Animals; Aorta; Atrial Natriuretic Factor; Cardiomegaly; Cardiotonic Agents; Collagen; Connective Tissue Growth Factor; Constriction, Pathologic; Gene Expression Regulation; Male; Mice; Mice, Inbred C57BL; Myocytes, Cardiac; Natriuretic Peptide, Brain; NF-kappa B; Phenols; Plant Extracts; Primary Cell Culture; Psoralea; Signal Transduction | 2018 |
Alterations in cardiac structure and function in a modified rat model of myocardial hypertrophy.
This study was aimed to establish a stable animal model of left ventricular hypertrophy (LVH) to provide theoretical and experimental basis for understanding the development of LVH. The abdominal aorta of male Wistar rats (80-100 g) was constricted to a diameter of 0.55 mm between the branches of the celiac and anterior mesenteric arteries. Echocardiography using a linear phased array probe was performed as well as pathological examination and plasma B-type natriuretic peptide (BNP) measurement at 3, 4 and 6 weeks after abdominal aortic constriction (AAC). The results showed that the acute mortality rate (within 24 h) of this modified rat model was 8%. Animals who underwent AAC demonstrated significantly increased interventricular septal (IVS), LV posterior wall (LVPWd), LV mass index (LVMI), cross-sectional area (CSA) of myocytes, and perivascular fibrosis; the ejection fraction (EF), fractional shortening (FS), and cardiac output (CO) were consistently lower at each time point after AAC. Notably, differences in these parameters between AAC group and sham group were significant by 3 weeks and reached peaks at 4th week. Following AAC, the plasma BNP was gradually elevated compared with the sham group at 3rd and 6th week. It was concluded that this modified AAC model can develop LVH, both stably and safely, by week four post-surgery; echocardiography is able to assess changes in chamber dimensions and systolic properties accurately in rats with LVH. Topics: Animals; Aorta, Abdominal; Constriction, Pathologic; Disease Models, Animal; Echocardiography; Enzyme-Linked Immunosorbent Assay; Heart; Hypertrophy, Left Ventricular; Male; Myocardium; Natriuretic Peptide, Brain; Rats, Wistar; Time Factors | 2014 |
Recombinant B-type natriuretic peptide nesiritide attenuates vascular remodelling by reducing plasma aldosterone in rabbits.
This study was designed to investigate the effect of nesiritide, a recombinant B-type natriuretic peptide (BNP), on plasma aldosterone and vascular remodelling following balloon-induced endothelial injuries to the iliac arteries.. Twenty-four male New Zealand rabbits were divided into nesiritide (0.1mg/kg/day, sc, for 4 weeks, n=12) and saline-treated control group (n=12). A balloon catheter was inserted to the right iliac artery to induce endothelia injuries. Plasma aldosterone was measured before and 28 days after the treatment by radioimmunoassay.. The area under internal elastic membrane (657.1±129.6 vs 486.7±124.0μm(2), P=0.02) and the area under external elastic membrane (1506.2±188.3.9 vs 1185.0±202.9μm(2), P=0.02) in the nesiritide group were greater than in the control group. The stenosis ratio in the nesiritide group was lower than in the control group (20.1±6.2% vs 39.6±9.5%, P=0.01). The plasma levels of aldosterone (2.03±0.31 vs 3.00±0.29ng/L, P<0.01) in the nesiritide group was lower than in the control group. Pearson's correlation analysis showed a positive correlation between the levels of plasma aldosterone and the stenosis ratio of the injured right iliac arteries (r=0.622, P=0.002).. Nesiritide treatment reduced stenosis ratio of the rabbit iliac artery following balloon-induced endothelial injuries, and the reduced stenosis ratio was associated with a reduction in the plasma aldosterone concentrations. Topics: Aldosterone; Animals; Constriction, Pathologic; Iliac Artery; Male; Natriuretic Peptide, Brain; Rabbits; Recombinant Proteins | 2012 |
Treatment with nesiritide, a recombinant B-type natriuretic Peptide, reduces vascular remodeling following balloon-induced endothelial injuries in rabbits.
Re-stenosis or remodeling of coronary and peripheral arteries remains a major complication following balloon-angioplasty or stenting. This study was designed to investigate the effect of nesiritide, a recombinant B-type natriuretic peptide (BNP), on vascular remodeling following balloon-induced endothelial injuries. Twenty-eight male New Zealand rabbits were divided into nesiritide-treated (0.1 mg/kg/day, sc, for 4 weeks, n = 10), saline-treated control (n = 10) and sham-operated groups (n = 8). In the nesiritide and control groups, a balloon catheter was inserted to the right iliac artery to induce injuries. Vascular endothelial growth factor (VEGF) was measured by immunohistochemistry. The area under internal elastic membrane of the arterial wall (643.2 ± 134.1 vs 493.7 ± 139.3 µm(2), p < 0.05) and the area under external elastic membrane (1495.1 ± 204.9 vs 1265.9 ± 232.6 µm(2), p < 0.05) in the nesiritide group were greater than those in the control group, but were smaller than those in the sham-operated group (p < 0.05). The stenosis ratio was lower in the nesiritide group than in the control group (18.7 ± 7.7% vs 38.0 ± 8.3%, p < 0.01). Importantly, the VEGF expression rate was significantly lower in the nesiritide group than in the control group (42.2 ± 8.8% vs 56.1 ± 13.1%, p < 0.05), while there were no signs of VEGF expression in the non-injured arteries of the three groups. In conclusion, nesiritide treatment reduces the stenosis of the rabbit iliac artery following balloon-induced endothelial injuries probably by decreasing VEGF expression. Topics: Angioplasty, Balloon; Animals; Blood Vessels; Constriction, Pathologic; Drug Evaluation, Preclinical; Endothelium, Vascular; Iliac Artery; Male; Natriuretic Agents; Natriuretic Peptide, Brain; Rabbits; Recombinant Proteins; Vascular Diseases; Vascular Endothelial Growth Factor A | 2010 |
B-type natriuretic peptide levels and insulin resistance in patients with severe ischemic myocardial dysfunction.
B-type natriuretic peptide (BNP) is an important clinical parameter of severity in congestive heart failure (CHF). Recent findings suggest a close relation between lipid and glucose metabolism and the natriuretic peptide axis, even if conflicting data exist on the relationship between natriuretic peptide levels and insulin resistance (IR). Thus, we sought to investigate potential relations between BNP level and IR in 134 patients with severe ischemic myocardial dysfunction [mean+/-SD: age =64.8+/-9.6 yr, male/female =104/30; body mass index (BMI) =25.5+/-4.05 kg/m2, 26.1% diabetics; ejection fraction (EF) = 30.2+/-7.7%]. In univariate analysis, an inverse relationship between BNP levels and EF% was observed (R=-0.43, p=0.0006). Moreover, we found an inverse association between BNP levels and BMI (R=-0.27, p=0.036), and also between BNP and homeostasis model assessment of insulin resistance (HOMA-IR) (R=-0.27, p=0.039). In multivariate analysis, EF% and HOMA-IR were significantly and independently associated with logarithmically transformed BNP levels (beta=-0.40, p=0.019 and beta=-0.26, p=0.042, respectively; R2=0.36). In conclusion, in patients with severe ischemic myocardial dysfunction EF and IR are independently associated with BNP levels explaining about 1/3 of the variability of this parameter. Multiple potential mechanisms may underlie this association, but it seems now clinically important to take into account also metabolic features when interpreting plasma natriuretic peptide concentrations obtained for diagnostic or prognostic purposes. Topics: Aged; Analysis of Variance; Blood Glucose; Body Mass Index; Constriction, Pathologic; Coronary Angiography; Diabetes Mellitus; Female; Humans; Immunoassay; Insulin; Insulin Resistance; Male; Middle Aged; Myocardial Ischemia; Natriuretic Peptide, Brain; Patient Selection; Ultrasonography | 2009 |
Mechanical stress enhances serotonin 2B receptor modulating brain natriuretic peptide through nuclear factor-kappaB in cardiomyocytes.
Serotonin via serotonin 2B receptors (SR2BR) regulates cardiac embryonic development and adult heart functions. However, the role of SR2BR in the failing heart due to pressure overload is not well understood.. Wistar rats of aortic banding and neonatal cardiomyocyte with mechanical stretch were used as cardiomyopathy models.. After two weeks of aortic banding surgery, serum serotonin, mRNA and protein expression of SR2BR increased significantly. The selective SR2BR antagonist, SB215505 (SB), significantly reduced the increase in heart weight, decreased heart wall thickness, left ventricular mass and the expression of the brain natriuretic peptide (BNP) but did not attenuate the up-regulation of SR2BR protein expression in rats after aortic banding for three weeks. After following in vitro mechanical stretch of cardiomyocytes and incubation with serotonin 1 muM, the level of SR2BR and BNP protein increased time-dependently. When transfected by specific siRNA of SR2BR or pretreated with caffeic acid phenethyl ester in cardiomyocytes, the increase of nuclear factor-kappaB (NF-kappaB) translocation and BNP protein induced by serotonin incubation plus mechanical stretch were both reversed.. SR2BR expression is involved in pressure-induced cardiomyopathy and its downstream signaling may involve NF-kappaB to modulate BNP expression in cardiomyocyte. Topics: Animals; Animals, Newborn; Aorta; Caffeic Acids; Constriction, Pathologic; Heart Failure; Hypertrophy, Left Ventricular; Indoles; Models, Animal; Myocytes, Cardiac; Natriuretic Peptide, Brain; NF-kappa B; Phenylethyl Alcohol; Quinolines; Rats; Rats, Wistar; Receptor, Serotonin, 5-HT2B; RNA Interference; RNA, Small Interfering; Serotonin; Serotonin 5-HT2 Receptor Antagonists; Stress, Mechanical; Ventricular Remodeling | 2006 |