scholarly journals Atrial Natriuretic Peptide Single Nucleotide Polymorphisms in Patients with Nonfamilial Structural Atrial Fibrillation

2013 ◽  
Vol 7 ◽  
pp. CMC.S12239 ◽  
Author(s):  
Pietro Francia ◽  
Agnese Ricotta ◽  
Alessandra Frattari ◽  
Rosita Stanzione ◽  
Anna Modestino ◽  
...  

Background Atrial natriuretic peptide (ANP) has antihypertrophic and antifibrotic properties that are relevant to AF substrates. The -G664C and rs5065 ANP single nucleotide polymorphisms (SNP) have been described in association with clinical phenotypes, including hypertension and left ventricular hypertrophy. A recent study assessed the association of early AF and rs5065 SNPs in low-risk subjects. In a Caucasian population with moderate-to-high cardiovascular risk profile and structural AF, we conducted a case-control study to assess whether the ANP -G664C and rs5065 SNP associate with nonfamilial structural AF. Methods 168 patients with nonfamilial structural AF and 168 age- and sex-matched controls were recruited. The rs5065 and -G664C ANP SNPs were genotyped. Results The study population had a moderate-to-high cardiovascular risk profile with 86% having hypertension, 23% diabetes, 26% previous myocardial infarction, and 23% left ventricular systolic dysfunction. Patients with AF had greater left atrial diameter (44 ± 7 vs. 39 ± 5 mm; P < 0.001) and higher plasma NTproANP levels (6240 ± 5317 vs. 3649 ± 2946 pmol/mL; P < 0.01). Odds ratios (ORs) for rs5065 and -G664C gene variants were 1.1 (95% confidence interval [CI], 0.7-1.8; P = 0.71) and 1.2 (95% CI, 0.3-3.2; P = 0.79), respectively, indicating no association with AF. There were no differences in baseline clinical characteristics among carriers and noncarriers of the −664C and rs5065 minor allele variants. Conclusions We report lack of association between the rs5065 and -G664C ANP gene SNPs and AF in a Caucasian population of patients with structural AF. Further studies will clarify whether these or other ANP gene variants affect the risk of different subpheno-types of AF driven by distinct pathophysiological mechanisms.

2010 ◽  
Vol 14 (6) ◽  
pp. 457-460 ◽  
Author(s):  
S. Giovannini ◽  
M. Cesari ◽  
E. Marzetti ◽  
C. Leeuwenburgh ◽  
M. Maggio ◽  
...  

2021 ◽  
Vol 28 (Supplement_1) ◽  
Author(s):  
N Kraenkel ◽  
A Koc ◽  
S Kaczmarek ◽  
K Lehnert ◽  
I Urbaneck ◽  
...  

Abstract Funding Acknowledgements Type of funding sources: Public grant(s) – National budget only. Main funding source(s): BMBF Background Patients with heart failure with reduced ejection fraction (HFrEF) have an increased inflammatory load and impaired cardiac oxidative lipid phosphorylation. Early dysregulations of pathophysiological alterations may not be detectable if patients are assessed under resting conditions. Purpose We exposed HFrEF patients to a physical exertion challenge by cardiopulmonary exercise testing (CPET) and determined inflammatory and metabolic parameters before, during and 2 hours after the test. Methods A symptom-limited CPET was performed in participants with HFrEF (n = 16) and age and sex matched controls (CON, n = 13). In addition to clinical and physiological parameters, we assessed blood counts of leukocyte subtypes, their morphology, aggregation with platelets and microvesicle release, as well as plasma cytokines and metabolites at baseline (T1), immediately after CPET (T2), and after 2 hours of rest (T3). Inflammatory and metabolic parameters were measured using the ThermoFischer ProcartaPlex Human Inflammation-Panel and Biocrates MxP® Quant 500 kit, respectively. Non-parametric tests were chosen and all multiple tests were adjusted by the Benjamini-Hochberg method. Results Cardiovascular risk profile of HFrEF and CON was similar. In agreement with the definition for HFrEF, these patients had a lower EF and a greater left ventricular enddiastolic diameter compared to CON. There were no differences between groups for leukocyte, cytokine or metabolic parameters at T1. Immediately after CPET, 20 parameters were significantly increased in both groups, including an increase of lactate, natural killer (NK) and NK T cell blood counts. In addition, 131 inflammatory and metabolic parameters were upregulated only in HFrEF, as compared to only 17 in CON. In HFrEF-platelet aggregates with NK cells, CD8+ cytotoxic T cells and "classical" CD14++CD16-monocytes, 58 different phosphatidylcholines and 21 triglycerides were upregulated immediately after exercise. At T3 almost all altered parameters returned to baseline in CON while in HFrEF blood counts and morphological markers of inflammatory effector cell types, including NK cells, CD8+ T cells and neutrophils, as well as genomic nuclear DNA, an indicator of cell death, remained elevated. Moreover, several triglycerides did not return to baseline in HFrEF after a 2-hour resting period. In these patients, but not in CON, the different lipids (i.e. phosphatidylcholine, triglycerides) strongly correlated with pro-inflammatory cytokines and NK cells. Conclusion Our data support the concept of impaired fatty acid utilization and inflammation-mediated metabolic dysregulation in HFrEF. However, the correlations between metabolic and inflammatory parameters were not detected at baseline in comparison to a control group with similar cardiovascular risk profile. Therefore, investigating patients in response to a physical or metabolic challenge might reveal early pathological changes.


2017 ◽  
Vol 06 (01) ◽  
Author(s):  
Eddy Jean-Baptiste ◽  
Philippe Larco ◽  
Rodolphe Paul ◽  
Bello Jérôme ◽  
Nancy Charles Larco ◽  
...  

Hypertension ◽  
2020 ◽  
Vol 76 (Suppl_1) ◽  
Author(s):  
Nayara A Cruz ◽  
Lilian C Oliveira ◽  
Fernanda B Fernandes ◽  
Dulce E Casarini

Angiotensin converting enzyme (ACE) plays a dominant role in renal and cardiovascular diseases, obesity and diabetes. The somatic ACE (130-190 kDa) is composed of two homologous N- and C- domains. Two soluble N-domain isoforms have been described in human urine with 65 and 90KDa. Studies have supported that N-domain ACE with 90KDa is a biomarker for hypertension, pre-eclampsia and inflammation. We analyzed the expression of somatic and soluble N-domain ACE isoforms in urine of children and adolescents with different nutritional status and cardiovascular risk profile. The volunteers aged from 6 to 19 years were classified into four groups according to their BMI percentile; underweight (n=51), normal weight (n = 53), overweight (n=53) and obese (n=49). Waist-height-ratio (WHtR) was used to assess cardiovascular risk profile dividing the participants into normal risk (n=105) and high risk (n=101). The urines were concentrated 10-fold and dialyzed with Tris-HCl pH 8 and pure water. Then, we performed western blot analysis using 50μg of lyophilized urinary protein, using the ACE polyclonal antibody Y1. Protein detection was performed by chemiluminescent and analysis in Image Lab software utilizing total protein stain for normalization. ACE expression is augmented in obese children when compared with normal weight children ( 0.09 vs 0.53 arbitrary units, p=0,04 ). The higher cardiovascular risk group also presented increased expression of ACE ( 0.27 vs 0.09 arbitrary units, p=0.046 ). The 90KDa N-domain isoform is frequently found in the high cardiovascular risk children ( p= 0.02 ). According to Spearman correlation test, the expression of 90 kDa N-domain ACE correlates positively with waist circumference, WHtR, BMI percentile and Z-score of BMI. Increased ACE expression in obese children contributes to higher cardiovascular risk once this enzyme biosynthesizes Angiotensin II which promotes blood pressure increase, sympathetic nervous system activation and release of glucocorticoids from adrenal gland. ACE expression is also augmented in children with high cardiovascular risk. Presence of 90 KDa N-domain ACE in urine of children and adolescents is a biomarker of poor prognostic for cardiovascular disease in childhood obesity.


2013 ◽  
Vol 124 (1) ◽  
pp. 306-310 ◽  
Author(s):  
Tobias E. Herrscher ◽  
Britt Overland ◽  
Leiv Sandvik ◽  
Arne S. Westheim ◽  
Harriet Akre

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