Abstract 029: Experimental Modest Weight Gain Increases 24-h Blood Pressure in Lean Healthy Subjects: Implications of Increased Visceral Fat

Hypertension ◽  
2014 ◽  
Vol 64 (suppl_1) ◽  
Author(s):  
Naima Covassin ◽  
Prachi Singh ◽  
Fatima H Sert-Kuniyoshi ◽  
Abel Romero-Corral ◽  
Diane E Davison ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Body Composition ◽  
Weight Gain ◽  
Ambulatory Blood Pressure ◽  
Visceral Fat ◽  
Healthy Subjects ◽  
Blood Pressure Monitoring ◽  
Subcutaneous Fat ◽  
Normal Weight

Introduction: Obesity is linked with heightened vulnerability to cardiovascular diseases including hypertension. Nonetheless, mechanistic studies addressing the effects of experimental weight gain on blood pressure are lacking. We sought to examine whether experimental weight gain raises ambulatory blood pressure in healthy individuals and identify any relationship between changes in blood pressure and changes in regional fat distribution. Methods: Twenty-six normal weight subjects were randomized to a 8-week period of weight gain through overfeeding (N=16; age 30.4±6.6 years, BMI 23.5±3.5 kg/m 2 ) or weight maintenance (N=10; age 27.1±7.7 years, BMI 23.6±2.7 kg/m 2 ). Measurements of body composition by dual-energy X-ray absorptiometry and abdominal computed tomographic scans and 24-h ambulatory blood pressure monitoring were obtained at baseline and at follow-up. Results: Overfeeding resulted in an increase in body weight of 3.7±1.5 kg ( p <0.001) in weight gainers, with increments seen in total (21994±8247.4 to 25180.7±8563.1 gr, p <0.001), visceral (61.6±32.7 to 75.5±30.9 cm 2 , p =0.002) and subcutaneous fat (135.5±77.4 to 167.9±82.9 cm 2 , p <0.001). No changes occurred in the maintenance group. Weight gainers exhibited an increase in 24-h systolic blood pressure at follow-up (113.7±8 to 117.7±7.9 mmHg, p =0.009) and mean blood pressure (MAP) (85.1±4.9 to 86.8±5.1 mmHg, p =0.02), while blood pressure was unchanged in controls. Changes in MAP were positively correlated only with changes in visceral fat (rho=0.452, p =0.02) but not with changes in weight or any other body composition measure. Conclusion: Modest weight gain leads to marked elevation in 24-h blood pressure in lean healthy subjects. The association between increased MAP and abdominal visceral fat accumulation suggests that visceral deposition of adipose tissue may contribute specifically and mechanistically to the enhanced risk of hypertension associated with weight gain.

scholarly journals Experimental Weight Gain Increases Ambulatory Blood Pressure in Healthy Subjects: Implications of Visceral Fat Accumulation

2018 ◽  
Vol 93 (5) ◽  
pp. 618-626 ◽  
Author(s):  
Naima Covassin ◽  
Fatima H. Sert-Kuniyoshi ◽  
Prachi Singh ◽  
Abel Romero-Corral ◽  
Diane E. Davison ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Weight Gain ◽  
Ambulatory Blood Pressure ◽  
Visceral Fat ◽  
Healthy Subjects ◽  
Fat Accumulation ◽  
Visceral Fat Accumulation

scholarly journals Role of Ambulatory Blood Pressure Monitoring in Predicting Adverse Maternofetal Events in Pregnancy

2021 ◽  
Author(s):  
Satish Kumar Rao Vavilala ◽  
Indrani Garre ◽  
Sumalatha Beeram
Keyword(s):  
Blood Pressure ◽  
Logistic Regression ◽  
Standard Deviation ◽  
Ambulatory Blood Pressure ◽  
Blood Pressure Monitoring ◽  
Statistical Significance ◽  
Binary Logistic Regression ◽  
Pressure Monitoring ◽  
In Pregnancy

Abstract Aims To correlate the relationship between the ambulatory blood pressure parameters and the occurrence of the antenatal and postnatal adverse maternofetal events in pregnancy. Methods Observational study designed for 50 pregnant patients who had an appointment to the obstetrics with abnormal blood pressure (BP) measurements and for whom ambulatory blood pressure monitoring (ABPM) was studied between January 2019 and June 2019. Data about age, personal history, obstetrics, family, body mass index (BMI), weight gain in pregnancy, values of blood pressure in the appointment, values recorded in ABPM, delivery and newborn, pregnancy and postpartum events, and follow-up of woman and child. Data were analyzed using descriptive and inferential statistics with Minitab 17.0 for Windows. Results Patients demographic data, clinical history, and laboratory results, including the ABPM parameters, were compiled. Antenatal complications occurred in 22 patients (44%), and postpartum complications were found in 41 patients (82%) whose ABPM values were deranged. Antenatal complications were studied using the binary logistic regression analysis for calculating the role each factor played in the development of hypertension. In the sample studied, mean age was 24.980 with a standard deviation of 4.876 (p = 0.003; minimum age of 19 years and maximum age of 38 years), mean weight of patient was 63.71 with a standard deviation of 63.71 (p = 0.001), mean gravida was 1.780 with a standard deviation of 0.910 (p = 0.034), mean gestation weeks at presentation was 33.000 weeks with a standard deviation of 4.086 (p = 0.041), mean birth weight was 2.226 with a standard deviation of 0.797 (p = 0.000), mean maximum diastole was 109.22 with a standard deviation of 16.53 (p = 0.002), mean day maximum systole was 187.2 with a standard deviation of 203.5 (p = 0.009), mean day minimum diastole was 63.50 with a standard deviation of 12.99 (p = 0.013), all of which had statistical significance. It is found that the nighttime diastolic blood pressure (DBP) and daytime maximum systolic blood pressure (SBP) were the best predictors of adverse events. Among antenatal complications (ANC), the most common complication is intrauterine growth restriction (IUGR), noted in (n = 19, 86.36%) preterm delivery (n = 17, 77.27%) among the 17 babies who were delivered preterm; 12 (70.5%) needed neonatal intensive care unit (NICU) care of which 4 (25%) babies died because of prematurity; intrauterine death (IUD) was noted in 7 (31.81%) patients and eclampsia was seen in 5 (22.72%). Nondippers proðle had a worse survival rate at follow-up until delivery compared with those with a dipper proðle. Postnatal complications were seen in 41 patients; among them, 13 patients (31.7%) had abnormal fundus examination, 15 patients (36.58%) required usage of antihypertensive beyond first postpartum, 9 patients (21.95%) required blood transfusion for severe bleeding in the form of postpartum hemorrhage. Binary logistic regression for systolic dippers versus nondippers shows statistical significance in age (p = 0.023), weight (p = 0.038), and para (p = 0.045) (Table 3). Binary logistic regression for diastolic dippers versus nondippers shows statistical significance in age (p = 0.039), weight (p = 0.020), birth weight (p = 0.010), maximum heart rate (p = 0.043), and ANC (p = 0.007) Adverse events occurred most commonly in nondippers. Systole nondippers is noted in (n = 41, 82%). Dippers is noted in (n = 9, 18%), Diastole nondippers is noted in (n = 39, 78%) Dippers is noted in (n = 11, 22%). Conclusion ABPM recorded blood pressure is very precise. ABPM is the advised method for both diagnostic and therapeutic monitoring of hypertensive pregnancy diseases, mainly in situations like whitecoat hypertension, masked hypertension, nocturnal hypertension, and nondipping profile. In patients with high-risk pregnancy, elderly primigravida, and precious pregnancy, who have a high-risk of developing pregnancy-induced hypertension (PIH) and related complications, early use of ABPM predicts adverse maternofetal events, which when intervened at an earlier date can prevent antenatal and postnatal complications.

Abstract 3519: Modest Fat Gain Causes Endothelial Dysfunction In Lean Healthy Humans: A Randomized Blinded Controlled Trial

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Abel Romero Corral ◽  
Justo Sierra-Johnson ◽  
Marek Orban ◽  
Apoor S Gami ◽  
Fatima H Sert Kuniyoshi ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Weight Loss ◽  
Body Composition ◽  
Weight Gain ◽  
Endothelial Dysfunction ◽  
Endothelial Function ◽  
Brachial Artery ◽  
Controlled Trial ◽  
Subcutaneous Fat ◽  
Flow Mediated Dilation

Background: Endothelial dysfunction assessed by flow mediated dilation (FMD) of the brachial artery has been identified as an independent predictor of cardiovascular events. However, whether weight gain impairs endothelial function is unknown. Methods: A randomized blinded controlled-trial to assess the effects of weight gain on endothelial function. After a weight maintenance period supervised by an experience dietitian, volunteers were randomized to gain weight (4 kg) or maintain weight. We recruited lean (BMI 18.5–24.9 kg/m 2 ) healthy volunteers (no diseases, medications and non-smokers) from the community. Using ultrasound, endothelial function was measured by FMD and non-flow mediated dilation (NFMD) of the brachial artery in the early morning (6:30 a.m.). Endothelial function was measured at baseline, after fat gain at 8 weeks and after weight loss at 16 weeks for fat-gainers and at baseline and follow-up (8 weeks) for weight maintainers. Body composition techniques to measure body fat %, such as dual x-ray absorptiometry and abdominal CT scans were performed. Results: We recruited 35 fat-gainers and 8 weight maintainers. Mean age was 29 ± 6 years and 18 (42 %) were women. There were no differences in age, anthropometric and body composition measurements, blood pressure, heart rate or apnea hypopnea index at baseline between both groups. After an average gain of 4 kg, the fat-gainer group significantly increased their total, visceral and subcutaneous fat. Brachial artery FMD and NFMD remained unchanged in weight maintainers. However, it decreaed in fat-gainers (FMD=9.1 ± 3 vs. 7.6 ± 3.2, p=0.003 and NFMD=12.0 ± 4.9 vs. 10.1 ± 6.0, p=0.01), but recovered to baseline after subjects shed the gained weight (basleline vs. recovery: FMD=9.1 ± 3 vs. 9.0 ± 3, p=NS and NFMD =12.0 ± 4.9 vs.12.6 ± 5.0, p=NS). Visceral fat gain, but not subcutaneous fat gain was significantly correlated with the decrease in brachial artery FMD (rho =−0.42, p=0.004 and rho =−0.22, p=0.15, respectively). Conclusions: In lean healthy young subjects, modest weight gain results in impaired endothelial function, even in the absence of changes in blood pressure. Endothelial funcion recovers after weight loss. Viscerar rather than subcutaneous fat predicts endothelial dysfunction.

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