Abstract 062: Aortic Stiffness, Blood Pressure Progression and Incident Hypertension: The Framingham Heart Study

Circulation ◽  
2012 ◽  
Vol 125 (suppl_10) ◽  
Author(s):  
Bernhard M Kaess ◽  
Jian Rong ◽  
Martin G Larson ◽  
Naomi M Hamburg ◽  
Joseph A Vita ◽  
...  

Background: Increased vascular stiffness and excessive blood pressure (BP) pulsatility are important risk factors for age-related morbidity. Vascular stiffness and BP pulsatility are related, with a prevailing view that hypertension antedates and contributes to premature vascular aging and a secondary increase in vascular stiffness. However, temporal relations between comprehensive vascular measures and BP elevation have not been fully delineated in a large community-based sample. Methods: We examined longitudinal relations of BP and 3 measures of vascular stiffness and pressure pulsatility derived from arterial tonometry (carotid-femoral pulse wave velocity [CFPWV], forward wave amplitude and augmentation index) over a 7-year period in 1,898 Framingham Offspring participants (mean age 60 yrs, 1,057 women). We also examined relations between measures of microvascular and endothelial function derived from brachial artery Doppler and future progression of BP or vascular stiffness. Results: In multivariable-adjusted regression models, baseline tonometry measures were separately and jointly associated with higher systolic and pulse pressure and incident hypertension ( Table ). Conversely, higher baseline BP was associated with higher forward wave amplitude and augmentation index (all p<0.05) but not CFPWV at follow-up. Higher baseline resting brachial artery flow and lower flow-mediated dilation were associated with incident hypertension in models that included BP and tonometry measures ( Table ). Conclusion: Higher aortic stiffness (CFPWV), pressure pulsatility (forward wave amplitude), and wave reflection (augmentation index) and lower flow-mediated dilation are associated with blood pressure progression and incident hypertension. Our findings support the notion of aortic stiffness as a precursor of hypertension and further suggest a vicious cycle of increasing pressure pulsatility with advancing age. Table. Correlates of incident hypertension. Predictor Variables (baseline) OR 95% CI P Systolic BP 3.24 (2.17; 4.84) <0.0001 Diastolic BP 1.47 (1.13; 1.92) 0.0042 CFPWV 1.30 (1.02; 1.67) 0.037 Forward wave amplitude 1.66 (1.32; 2.09) <0.0001 Augmentation index 1.78 (1.45; 2.17) <0.0001 Brachial artery baseline flow 1.23 (1.05; 1.45) 0.013 Flow-mediated dilation 0.83 (0.70; 0.98) 0.029 Results of a single multivariable model that further adjusted for age,sex, BMI, height and triglycerides in 1,019 participants free of hypertension at baseline who experienced 337 cases of incident hypertension during follow-up. OR expressed per 1 SD of the independent variable.

Circulation ◽  
2014 ◽  
Vol 129 (suppl_1) ◽  
Author(s):  
Connie W Tsao ◽  
Asya Lyass ◽  
Martin G Larson ◽  
Gary F Mitchell ◽  
Ramachandran S Vasan

Background: The structure and function of the aorta and left ventricle are closely coupled, but the relations of arterial stiffness, pressure pulsatility, and wave reflection to clinical heart failure (HF) are not well described. Methods: We evaluated 2904 Framingham Heart Study participants (mean age 64+11 yrs, 56% F) who were free of clinical HF and myocardial infarction (MI). Carotid-femoral pulse wave velocity (CFPWV), central pulse pressure, forward wave amplitude, and augmentation index were assessed by applanation tonometry. Cox proportional hazards models accounted for competing risk of death and adjusted for age, sex, body mass index, mean arterial pressure, total and HDL cholesterol, use of hypertensive medications, prevalent diabetes, current smoking, and prevalent cardiovascular disease. Results: On follow-up (mean 9.2 years, limits 0.04-13 years), 170 participants developed new-onset HF while 106 experienced an MI. The incidence of HF rose across CFPWV tertiles ( Figure ). Each standard deviation (SD) higher CFPWV conferred a 50% (95% CI 1.21-1.85, p=0.0002) and 30% (95% CI 1.02-1.64, p=0.037) increased risk of incident HF in age- and sex-adjusted and multivariable-adjusted analyses, respectively. CFPWV was associated with increased risk of MI (hazards ratio [HR] per SD 1.46, 95% CI 1.01-2.12, p=0.04). The inclusion of interim MI in multivariable models attenuated the association of CFPWV with HF incidence (HR per SD 1.26, 95% CI 0.99-1.60, p=0.061). Central pulse pressure, forward wave amplitude, and augmentation index were not associated with incident HF in multivariable-adjusted models. Conclusions: Higher aortic stiffness as assessed by CFPWV is associated with increased risk of incident HF, mediated in part by the increased risk of interim MI associated with vascular stiffness. These findings illustrate the importance of ventricular-vascular coupling, and underscore the need for studies to examine the benefit of therapies that modify aortic stiffness for lowering the population burden of MI and HF.


2021 ◽  
Vol 36 (Supplement_1) ◽  
Author(s):  
Aya Lafta ◽  
Aminu Bello ◽  
Sara Davison ◽  
Stephanie Thompson ◽  
Branko Braam

Abstract Background and Aims Fluid overload and vascular stiffness are two independent predictors of cardiovascular events in hemodialysis (HD) patients. To date, observational and interventional studies that investigated the effect of inter- and intradialytic fluid overload changes on vascular stiffness in HD patients are very limited. We performed a scoping review to explore existing reports about effects of fluid overload on vascular stiffness in adults receiving HD treatment and to identify knowledge gaps for future research. Method We followed the framework originally developed by Arksey and O’Malley. We searched Medline, Embase, CINAHL, and Cochrane Database of systematic reviews from inception to October 29, 2019. References of review papers were screened for relevant studies not identified from the initial search until saturation is achieved. Results Of 666 eligible studies, nineteen studies met the inclusion criteria. These included clinical observational studies (n=16) and randomized controlled trials (n=3). In general, most of the identified studies had small sample size and short term of follow up. Studies use different definitions of fluid overload and vascular stiffness. Measures of relative fluid overload like the ratio of extracellular fluid/intracellular fluid, fluid overload/extracellular fluid, and/or extracellular fluid/total body fluid were used as a representative of fluid status. Pulse wave velocity and augmentation index were used interchangeably as vascular stiffness measures. The accumulated findings were inconsistent and inconclusive. There was no consensus whether intradialytic fluid volume changes affected vascular stiffness. In the majority of the observational studies, a decrease in pulse wave velocity or augmentation index correlated with a decrease in blood pressure after fluid correction by HD treatment. The randomized clinical trials used different methods and technologies for the correction of fluid overload, thereby, results were conflicting. Conclusion Current literature is insufficient to justify whether fluid overload changes have a direct effect on vascular stiffness in HD patients. The findings were conflicting which limits the comparisons of studies and generalization of findings. These knowledge gaps urge the need for further clinical studies to enhance the understanding and to improve the quality of research in this topic. This includes standardized definitions and methodologies as well as longer term of follow up.


Circulation ◽  
2020 ◽  
Vol 141 (Suppl_1) ◽  
Author(s):  
Allana T Forde ◽  
Mario Sims ◽  
Paul Muntner ◽  
Tené Lewis ◽  
Amanda Onwuka ◽  
...  

Background: African Americans have a higher risk for hypertension compared to other racial or ethnic groups in the United States. One possible explanation for this health disparity is perceived discrimination. Few studies have prospectively examined the association between discrimination and the incidence of hypertension. Methods: We examined the associations of everyday, lifetime, and stress from lifetime discrimination with incident hypertension and whether these associations differed by sex, discrimination attribution (i.e. the main reason for the discrimination event), and coping responses to discrimination among African Americans enrolled in the Jackson Heart Study. Discrimination was self-reported by 1845 African Americans aged 21 to 85 years without hypertension at baseline (2000-2004). Participants completed two follow-up study visits from 2005-2008 and 2009-2013. We used interval-censored Cox regression to estimate associations of discrimination with incident hypertension (antihypertensive medication use; and/or systolic blood pressure ≥ 140 mm Hg and diastolic blood pressure ≥ 90 mm Hg at follow-up visits 2 or 3) after adjustment for confounding variables. Results: Overall, 52% (954 of 1845) of participants developed hypertension over the follow-up period. After adjustment for age, sex, education and hypertension risk factors (body mass index, alcohol use, smoking, diet and physical activity), medium versus low levels of lifetime discrimination (hazard ratio-HR: 1.45, 95% confidence interval-CI: 1.15-1.82) and high versus low levels of lifetime discrimination (HR: 1.35, CI: 1.08-1.68) were associated with a higher incidence of hypertension. High versus low stress from lifetime discrimination was associated with hypertension risk after adjustment for demographics (HR: 1.20, CI: 1.02-1.41), but the association was attenuated after adjustment for hypertension risk factors (HR: 1.14, CI: 0.97-1.35). Lifetime discrimination and stress from discrimination were associated with an increased hypertension risk among females, but not males. No interactions with age, attribution or coping were present for any type of discrimination. Conclusions: Findings from this study support an association between lifetime discrimination and incident hypertension in African Americans.


2020 ◽  
Vol 29 ◽  
Author(s):  
Sang Won Jeon ◽  
Yoosoo Chang ◽  
Se-Won Lim ◽  
Juhee Cho ◽  
Han-Na Kim ◽  
...  

Abstract Aims To evaluate the bidirectional relationship between blood pressure (BP) and depressive symptoms using a large prospective cohort study. Methods Prospective cohort study was performed in 276 244 adults who participated in a regular health check-up and were followed annually or biennially for up to 5.9 years. BP levels were categorised according to the 2017 American College of Cardiology and American Heart Association hypertension guidelines. Depressive symptoms were assessed using Centre for Epidemiologic Studies-Depression (CESD) questionnaire and a cut-off score of ≥25 was regarded as case-level depressive symptoms. Results During 672 603.3 person-years of follow-up, 5222 participants developed case-level depressive symptoms. The multivariable-adjusted hazard ratios (HRs) [95% confidence interval (CI)] for incident case-level depressive symptoms comparing hypotension, elevated BP, hypertension stage 1 and hypertension stage 2 to normal BP were 1.07 (0.99–1.16), 0.93 (0.82–1.05), 0.89 (0.81–0.97) and 0.81 (0.62–1.06), respectively (p for trend <0.001). During 583 615.3 person-years of follow-up, 27 787 participants developed hypertension. The multivariable-adjusted HRs (95% CI) for incident hypertension comparing CESD 16–24 and ⩾25 to CESD < 16 were 1.05 (1.01–1.11) and 1.12 (1.03–1.20), respectively (p for trend <0.001) and in the time-dependent models, corresponding HRs (95% CI) were 1.12 (1.02–1.24) and 1.29 (1.10–1.50), respectively (p for trend <0.001). Conclusions In this large cohort study of young and middle-aged individuals, higher BP levels were independently associated with a decreased risk for developing case-level depressive symptoms and depressive symptoms were also associated with incident hypertension. Further studies are required to elucidate the mechanisms underlying the bidirectional association between BP levels and incident depression.


Hypertension ◽  
2021 ◽  
Vol 77 (1) ◽  
pp. 241-251
Author(s):  
Sarah C. Couch ◽  
Brian E. Saelens ◽  
Philip R. Khoury ◽  
Katherine B. Dart ◽  
Kelli Hinn ◽  
...  

This randomized control trial assessed the post-intervention and 18-month follow-up effects of a 6-month dietary approaches to stop hypertension (DASH)-focused behavioral nutrition intervention, initiated in clinic with subsequent telephone and mail contact, on blood pressure (BP) and endothelial function in adolescents with elevated BP. Adolescents (n=159) 11 to 18 years of age with newly diagnosed elevated BP or stage 1 hypertension treated at a hospital-based clinic were randomized. DASH participants received a take-home manual plus 2 face-to-face counseling sessions at baseline and 3 months with a dietitian regarding the DASH diet, 6 monthly mailings, and 8 weekly and then 7 biweekly telephone calls focused on behavioral strategies to promote DASH adherence. Routine care participants received nutrition counseling with a dietitian consistent with pediatric guidelines established by the National High Blood Pressure Education Program. Outcomes, measured pre- and post-intervention and at 18-months follow-up, included change in BP, change in brachial artery flow-mediated dilation, and change in DASH score based on 3-day diet recalls. Adolescents in DASH versus routine care had a greater improvement in systolic BP (–2.7 mm Hg, P = 0.03, –0.3 z-score, P =0.03), flow-mediated dilation (2.5%, P =0.05), and DASH score (13.3 points, P <0.0001) from baseline to post-treatment and a greater improvement in flow-mediated dilation (3.1%, P =0.03) and DASH score (7.4 points, P =0.01) to 18 months. The DASH intervention proved more effective than routine care in initial systolic BP improvement and longer term improvement in endothelial function and diet quality in adolescents with elevated BP and hypertension. Registration: URL: https://www.clinicaltrials.gov ; Unique identifier: NCT00585832.


2020 ◽  
Author(s):  
Alessandro Giollo ◽  
Giovanni Cioffi ◽  
Federica Ognibeni ◽  
Giovanni Orsolini ◽  
Andrea Dalbeni ◽  
...  

Abstract Background. Major cardiovascular disease (CVD) benefits of disease-modifying anti-rheumatic drugs (DMARDs) therapy occur in early RA patients with treat-to-target strategy. However, it is unknown whether long-term DMARDs treatment in established RA could be useful to improve CVD risk profile.Methods. Ultrasound aortic stiffness index (AoSI) has to be considered a proxy outcome measure in established RA patients. We measured AoSI in a group of RA patients on long-term treatment with tumour necrosis factor inhibitors (TNFi) or conventional synthetic DMARDs (csDMARDs). Eligible participants were assessed at baseline and after 12 months; changes in serum lipids, glucose and arterial blood pressure were assessed. All patients were on stable medications during the entire follow-up. Results. We included 107 (64 TNFi and 43 csDMARDs) RA patients. Most patients (74%) were in remission or low disease activity and had some CVD risk factors (45.8% hypertension, 59.8% dyslipidemia, 45.3% smoking). The two groups did not differ significantly for baseline AoSI (5.95±3.73% vs 6.08±4.20%, p=0.867). Follow-up AoSI was significantly increased from baseline in the csDMARDs group (+1.00%; p<0.0001) but not in the TNFi group (+0.15%, p=0.477). Patients on TNFi had significantly lower follow-up AoSI from baseline than the csDMARD group (-1.02%, p<0.001; ANCOVA corrected for baseline AoSI, age and systolic blood pressure). Furthermore, follow-up AoSI was significantly lower in TNFi users with 1-2 or >2 CVD risk factors than in those without. Conclusion. Long-term treatment with TNFi was associated with reduced aortic stiffness in patients with established RA and several CVD risk factors.


2020 ◽  
pp. 204748732094299
Author(s):  
Tobias Holmlund ◽  
Björn Ekblom ◽  
Mats Börjesson ◽  
Gunnar Andersson ◽  
Peter Wallin ◽  
...  

Aims To explore how change in cardiorespiratory fitness is associated with incident hypertension in adults, and whether the association varies between sex, age, body mass index, cardiorespiratory fitness at baseline and follow-up time. A second aim is to study how change in other lifestyle-related variables affects the results. Methods A total of 91,728 participants (48% women), normotensive at baseline, with two examinations from occupational health service screenings between 1982 and 2019 (mean duration 4.3 years) were included. Cardiorespiratory fitness was assessed as estimated maximal oxygen consumption using submaximal cycle testing. Change in cardiorespiratory fitness was expressed as the percentage change per year. Incident hypertension was defined as systolic blood pressure of 140 mmHg or greater or diastolic blood pressure of 90 mmHg or greater, or self-reported physician-diagnosed hypertension, at second examination. Results A large increase (≥3% annual change) in cardiorespiratory fitness was associated with a 11% lower risk of incident hypertension compared with maintainers (–1 to +1%), after multi-adjustment including change in smoking, body mass index, diet, stress and exercise habits. On the contrary, a small (–1 to −<3%) and large (≥–3%) decrease in cardiorespiratory fitness associated with a 21% and 25% higher risk compared with maintainers. Longer duration between the examinations was associated with stronger risk associations. Preserving, or changing to, risk level for the other lifestyle variables was associated with a higher risk of incident hypertension. However, a simultaneous maintenance of or increase in cardiorespiratory fitness attenuated the risk associated with smoking, and stress. Conclusion Preserving or increasing cardiorespiratory fitness should be part of any long-term strategy to decrease the risk of incident hypertension.


Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Abel Romero Corral ◽  
Justo Sierra-Johnson ◽  
Marek Orban ◽  
Apoor S Gami ◽  
Fatima H Sert Kuniyoshi ◽  
...  

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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