scholarly journals Effects of Potassium Chloride and Potassium Bicarbonate on Endothelial Function, Cardiovascular Risk Factors, and Bone Turnover in Mild Hypertensives

Hypertension ◽  
2010 ◽  
Vol 55 (3) ◽  
pp. 681-688 ◽  
Author(s):  
Feng J. He ◽  
Maciej Marciniak ◽  
Christine Carney ◽  
Nirmala D. Markandu ◽  
Vidya Anand ◽  
...  
PLoS ONE ◽  
2014 ◽  
Vol 9 (7) ◽  
pp. e103444 ◽  
Author(s):  
Ruth Clapauch ◽  
André Felipe Mourão ◽  
Anete S. Mecenas ◽  
Priscila A. Maranhão ◽  
Ana Rossini ◽  
...  

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Karina P Martins ◽  
Sandhi Barreto ◽  
Daniel Bos ◽  
JESIANA PEDROSA ◽  
Douglas Mesquita ◽  
...  

Introduction: Epicardial fat has been related to coronary artery disease (CAD) independent of visceral or subcutaneous fat. The mechanism responsible for this association has not yet been elucidated. Our objective was to evaluate the association between automatically measured epicardial fat volume (EFV), cardiovascular risk factors, coronary artery calcium (CAC) and endothelial function in participants of ELSA-Brasil. Methods and Results: The sample comprised 470 (mean age 55± 8y, 52.3% men) participants from ELSA-MG, one of the Investigation Centers of the cohort, who had valid computed tomography scans and endothelial function evaluated by peripheral arterial tonometry (PAT). The mean EFV was 111 (IQ 86-144) mL. CAC=0 was detected in 55% of participants. In the multivariable analyses between cardiovascular risk factors and EFV, the following associations were observed with higher EFV: female sex; and increased age, waist circumference and triglycerides (p <0.001 for all). In multivariable analyses, higher EFV remained associated with worse endothelial function - basal pulse amplitude (q2=1.22, CI95% 1.07-1.40, p=0.004; q3=1.50, CI95% 1.30-1.74, p<0.001; q4=1.50, CI95% 1.28-1.79, p<0.001) and PAT ratio (q2=0.87, CI95% 0.81-0.95, p<0.001; q3=0.86, CI95% 0.79-0.94, p<0.001; q4=0.80, CI95% 0.73-0.89, p<0.001), but not with CAC. Conclusions: Higher EFV was associated with impaired endothelial function, but not with higher CAC. Our results suggest that the mechanism by which epicardial fat deposits relates to CAD may be different from the pathway of CAC, which relates to calcified plaques. A possible mechanism may be through the enhancement of endothelial dysfunction, microvascular disease and predominantly lipidic non-calcified plaques.


2019 ◽  
Vol 13 (2) ◽  
pp. 1387-1391 ◽  
Author(s):  
Alireza Sedaghat ◽  
Hajieh Shahbazian ◽  
Afshin Rezazadeh ◽  
Fatemeh Haidari ◽  
Alireza Jahanshahi ◽  
...  

2011 ◽  
Vol 31 (10) ◽  
pp. 2353-2359 ◽  
Author(s):  
Junko Soga ◽  
Kensuke Noma ◽  
Takaki Hata ◽  
Takayuki Hidaka ◽  
Yuichi Fujii ◽  
...  

2016 ◽  
Vol 26 ◽  
pp. 301-308 ◽  
Author(s):  
Gustavo Vieira de Oliveira ◽  
Marina Morgado ◽  
Anna Paola Pierucci ◽  
Thiago Silveira Alvares

Circulation ◽  
2001 ◽  
Vol 103 (11) ◽  
pp. 1497-1502 ◽  
Author(s):  
Sarah C. Clarke ◽  
Peter M. Schofield ◽  
Andrew A. Grace ◽  
James C. Metcalfe ◽  
Heide L. Kirschenlohr

2016 ◽  
Vol 101 (9) ◽  
pp. 3401-3408 ◽  
Author(s):  
Matthieu Roustit ◽  
Jordan Loader ◽  
Carly Deusenbery ◽  
Dimitrios Baltzis ◽  
Aristidis Veves

Abstract Context: Cardiovascular risk factors are well-known predictors of the development of diabetic peripheral neuropathy (DPN), which has traditionally been considered as a manifestation of diabetes-associated microangiopathy. Because endothelial dysfunction is strongly associated with all cardiovascular risk factors, we hypothesized that it may be a link between cardiovascular risk factors and DPN. Objective: The primary objective of this study was to test whether endothelial dysfunction is a predictor of DPN. Design and Setting: This is a cross-sectional analysis of a cohort composed of patients followed at the Microcirculatory Laboratory, Beth Israel Deaconess Medical Center. Patients: Participants with diabetes without DPN (n = 192) and with DPN (n = 166), subjects with prediabetes (n = 75), and nondiabetic controls (n = 59) were included. Interventions: Endothelial function was assessed with flow-mediated dilation (FMD) of the brachial artery. Inflammatory cytokines and biomarkers of endothelial function (soluble intercellular and vascular cell adhesion molecules) were quantified using a multiplex bead-based immunoassay. Neurological assessment included the neuropathy disability score (NDS). Main Outcome Measure: The relationship between FMD and NDS assessed using multiple linear regression. Results: In addition to already known risk factors of DPN, FMD was strongly associated with NDS (β = −0.24; P &lt; .001). Sensitivity analysis that removed FMD from the model provided similar results for soluble intercellular cell adhesion molecule-1, another biomarker of endothelial function. Confirmatory factor analysis further showed that endothelial dysfunction is a significant mediator between glycosylated hemoglobin and diabetes duration and diabetic complications. Conclusions: This study shows that endothelial dysfunction occurs early in the pathophysiology of diabetes and is a link between cardiovascular risk factors and DPN.


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