Increment In Systolic Blood Pressure Research Articles

Effect of Right Nostril Breathing on Cardiorespiratory Parameters and Reaction Time in Young, Healthy Humans: An Interventional Study.

Yogic breathing helps in reduction of stress and strain in the body. Right and left nostril breathings (RNB and LNB, respectively) have different effects on cardiorespiratory parameters. The study was performed to examine the effect of RNB exercise on cardiorespiratory parameters and reaction time in young, healthy human volunteers. In this prospective, interventional study, 110 young healthy volunteers underwent systolic blood pressure (SBP), diastolic blood pressure (DBP), pulse rate (PR), respiratory rate (RR), vital capacity (VC), peak expiratory flow rate (PEFR), and reaction time (RT) examination before and after 2 weeks of performing 45 min of RNB exercise daily. There was notable increment in SBP (113.39 ± 17.72 vs. 117.74 ± 10.83 mmHg, P = 0.002) and DBP (67.64 ± 10.32 vs. 71.27 ± 8.68 mmHg, P = 0.002). PR increased nonsignificantly (86.44 ± 12.65/min vs. 87.32 ± 13.43/min, P = 0.476). Significant decrease in RR (14.40 ± 2.48/min vs. 12.31 ± 2.23/min, P < 0.0001) was observed. VC (3.57 ± 0.57 vs. 3.82 ± 0.55 L/min, P < 0.0001) and PEFR (441.36 ± 50.22 vs. 468.91 ± 53.66 L/min, P < 0.0001) also increased significantly. Substantial reduction in auditory reaction time (ART) (165.58 ± 32.18 vs. 147.42 ± 23.39 ms, P < 0.0001) and visual reaction time (VRT) (191.04 ± 37.94 vs. 165.86 ± 28.74 ms, P < 0.0001) was seen. After engaging in cardiorespiratory exercise, the maximal heart rate (MHR) remained unchanged (P = 0.929). RNB results in increase in blood pressure, heart rate, VC, and PEFR and decrease in ART and VRT. Further studies in patients with cardiorespiratory diseases are necessary to understand its clinical utility.

Effect of Three-Month Weight Training Program on Resting Heart Rate and Blood Pressure in Healthy Young Adult Males.

Background A planned and structured physical activity is the cornerstone of improving and sustaining body fitness. The underlying reason for exercise is personal interest, maintaining good health, or improving endurance for sports. Furthermore, exercise may be either isotonic or isometric. In weight training, different types of weight are being used and are lifted against gravity, and this type of exercise is of isotonic type. Objective The objective of this study was to observe the changes in heart rate (HR) and blood pressure (BP) after a three-month weight training intervention in healthy young adult males and to compare them with age-matched healthy control. Materials and methods We initially recruited a total of 25 healthy male volunteers for the study and 25 age-matched participants in the control group. Research participants were screened for any existing diseases and suitability for participation by the Physical Activity Readiness Questionnaire. We lost one participant from the study group and three participants from the control group in the follow-up. A structured weight training program (five days a week for three months) was applied for the study group with direct instruction and supervision in a controlled environment. A single expert clinician measured baseline and post-program (after three months) HR and BP (measured after 15 minutes, 30 minutes, and 24 hours of rest after exercise) to reduce any possible inter-observer variation. For comparing the pre-exercise and post-exercise parameters, we considered the post-exercise measurement, which was done after 24 hours of exercise. Mann-Whitney Utest, Wilcoxon signed-rank test, and Friedman test compared the parameters. Result A total of 24 males with a median age of 19 years (Q1-Q3: 18-20) participated as the study group and 22 males with the same median age were the control group. At the end of the three-month weight training exercise program, there was no significant change in the HR (median 82 versus 81 bpm, p = 0.27) in the study group. The systolic BP was increased (median 116 versus 126 mmHg, p <0.0001) after three months of the weight training program. In addition, pulse pressure and mean arterial BP was also increased. However, diastolic (median 76 versus 80 mmHg, p = 0.11) BP was not significantly increased. There was no change in HR, systolic and diastolic BP in the control group. Conclusion A structured weight training program (used in this study) for three months may sustain an increase in systolic BP at rest in young adult males while diastolic BP remains the same. The HR remains unchanged before and after the exercise program. Hence, those enrolling in such an exercise program should be monitored frequently for changes in BP over time for any timely intervention appropriate for the candidate. However, being a small-scale study, the result of this study would be validated by further observing the underlying causes of the increment of systolic blood pressure.

Distinct causal effects of body fat distribution on cardiometabolic traits among children: Findings from the BCAMS study

Background and aimsObservational studies reveal that different body fat measures are associated with cardiometabolic disease with different effects. However, causality is not reflected by such observations. To explore and compare the causal relationships of general obesity (measured by body mass index (BMI)), adipose obesity (measured by fat mass percentage (FMP)) and central obesity (measured by waist-to-height ratio (WHtR)) with cardiometabolic traits among children. Methods and resultsWe conducted one sample Mendelian randomization (MR) analysis in 3266 children from Beijing Children and Adolescents Metabolic Syndrome Study. Genetic instruments based on 28 SNPs were performed to explore and compare the causal associations of genetically BMI, FMP and WHtR with cardiometabolic traits. The genetic instruments were robustly correlated with observed BMI, FMP and WHtR. Each genetically 1-SD increment in BMI, FMP and WHtR were causally associated with increment in systolic blood pressure (SBP), diastolic blood pressure (DBP), log-transformed fasting plasma glucose (FPG), log-transformed HOMA-β, and decrease in log-transformed high-density lipoprotein cholesterol (HDL), respectively (all P < 0.05 after Bonferroni correction). The receiver operating characteristic curve indicated that BMI and FMP showed stronger effects on SBP, DBP, HOMA-β and HDL than WHtR (all P < 0.05). We also observed causal associations of BMI and FMP with log-transformed fasting insulin and HOMA-IR. ConclusionsThe MR analysis based on population-based cohort indicated a causal relationship of adiposity and body fat distribution with cardiometabolic traits. When compared with central obesity, general obesity and adipose obesity might own stronger effects on blood pressure and blood lipids among children.

Association between blood pressure and short-term exposure to ambient air pollutants in Beijing, China

Substantial evidences have pointed to a link between hypertension and air pollution. This explored the link between blood pressure and short-term exposure to ambient atmospheric pollutants in a heavily polluted city. A monitoring program was designed to continuously record physical examination data of 1796 participants in Beijing, China from 2013 to 2018, and the individual-level exposure of atmospheric pollutants (PM2.5, PM10, NO2, CO, O3, and SO2) was estimated using land use regression model. A generalized additive mixed-effects model was applied within the investigation of the acute impacts of air pollutants on blood pressure, including systolic blood pressure, diastolic blood pressure, pulse pressure, and mean arterial pressure. Air pollutant concentrations were found to be positively correlated with blood pressure levels after their adjustment for a number of demographic and meteorological elements, e.g. each 10 μg/m3 increment of NO2 resulted in an increment in systolic blood pressure of 0.351 mm Hg (95th percentile confidence interval: 0.001, 0.701; p < 0.05). In addition, stronger associations were found among males and patients with hypertension, and the blood pressure level of outdoor workers was more susceptible to the changes in NO2 concentration. Generally, elevated concentrations of air pollutants contributed to increased levels of blood pressure.

Abstract 033: Epigenetic Clocks And Incident Heart Failure: The Atherosclerosis Risk In Communities (aric)

Background: DNA methylation (DNAm)-based measures of aging, termed epigenetic clocks (EC), are associated with aging-related outcomes including cardiovascular disease (CVD) and all-cause mortality. Associations of ECs with heart failure (HF) are unclear. We tested whether ECs were positively associated with risk of incident HF in the Atherosclerosis Risk in Communities (ARIC) study and evaluated whether adding ECs to Pooled Cohort Equation (PCE) variables improved risk prediction. Methods: We measured DNAm in peripheral blood leukocytes in 2,263 African American (mean age=56.3 years) and 925 European American (mean age=59.5 years) participants using the Illumina HM450K and calculated 7 ECs: Horvath, Hannum, extrinsic (EEAA) and intrinsic (IEAA) epigenetic age acceleration, Hannum, PhenoAge, and GrimAge. HF was ascertained by ICD- 9 code 428 and adjudication by an expert panel. We carried out race stratified proportional hazards regression to test associations ECs with incident HF, adjusting for PCE variables: age, sex, smoking, total cholesterol, HDL, systolic blood pressure (SBP), antihypertensive medication use, and diabetes. We calculated area under the curve (AUC) and integrated discrimination index (IDI) to evaluate improvement in risk prediction when adding the ECs to PCE variables. Results: The number of incident HF events and mean follow-up time in African Americans and European Americans were 640 (189 in the first 10 years) and 19.3 years, and 191 and 21.7 years, respectively. All 7 ECs were positively associated with HF in both African Americans and European Americans. In African Americans with follow-up restricted to the first 10 years, the HR for a one SD increment in GrimAge (5.64 years) was 1.57 (95% CI=1.31, 1.88), comparable to that for a one-SD (5.82 years) increment in age (HR=1.58, 95% CI=1.36, 1.83) and greater than that for a one-SD (20.2mmHg) increment in SBP (HR=1.33, 95% CI=1.18, 1.51). In European Americans across the entire follow-up period, the HR for a one-SD increment in GrimAge (6.13 years) was 1.22 (95% CI=1.06, 1.41), smaller than that for a one-SD (5.50 years) increment in age (HR=1.93, 95% CI=1.63, 2.29) and larger than that for a one-SD (17.9 mmHG) increment in SBP (HR=1.13, 95% CI=0.98, 1.30). In African Americans with follow-up restricted to the first 10 years, adding GrimAge to PCE variables increased AUC by 0.019 (95% CI=0.003, 0.035) and the IDI was 0.010 (95% CI=0.002, 0.019). In European Americans, adding GrimAge did not change AUC appreciably (0.004, 95% CI=-0.006, 0.014) and the IDI was 0.002 (95% CI=0.000, 0.005). Conclusion: ECs are positively associated with HF in African American and European American participants independent of traditional CVD risk factors. GrimAge modestly improved heart failure risk prediction in African Americans. HF-specific DNAm-based measures should be developed and evaluated for improvement in risk prediction.

GENETIC SUSCEPTIBILITY, ELEVATED BLOOD PRESSURE AND RISK OF ATRIAL FIBRILLATION

Objective: Whether elevated blood pressure (BP) is a modifiable risk factor for atrial fibrillation (AF) is not established. We tested (1) whether the association between BP and risk of AF is causal, (2) whether it varies according to individual's genetic susceptibility for AF, and (3) the extent to which specific BP-lowering drugs are expected to reduce this risk. Design and method: First, causality of association was assessed through two-sample Mendelian Randomization (MR), using data from two independent genome-wide association studies that included a total of one million European population. Second, UK Biobank individual participant data of 329 237 participants at baseline was used to study the effect of BP on AF according to genetic susceptibility of developing AF. Third, a possible treatment effect with BP-lowering drug classes on AF risk was predicted through genetic variants in druggable genes that code proteins related to the function of each drug class. Estimated drug effects were compared with effects on incident coronary artery disease, for which direct trial evidence exists. Results: The two-sample MR analysis indicated that on average each 10-mmHg increment in systolic BP increased the risk of AF (odds ratio [OR]: 1.23 [1.11 to 1.36]). This association was replicated in the UK biobank using individual participant data. However, in a further genetic risk-stratified analysis, there was evidence for a linear gradient in the relative effects of systolic BP on AF; while there was no conclusive evidence of an effect in those with low genetic risk, a strong effect was observed among those with high genetic susceptibility for AF (Figure). The indirect comparison of predicted treatment effects using genetic proxies for three main drug classes (angiotensin converting enzyme inhibitors, beta-blockers and calcium channel blockers) suggested similar average effects for prevention of atrial fibrillation and coronary heart disease. Conclusions: The association between elevated BP and higher risk of AF is likely to be causal, suggesting that BP-lowering treatment may be effective in AF prevention. However, average effects masked clinically important variations, with a more pronounced effect in individuals with high genetic susceptibility.

Secular Trends in Blood Pressure in Chinese Children and Adolescents Born 1981-2000: The Impact of Changing Growth Trajectories

Background: Globally, 80% of cardiovascular disease (CVD) deaths occur in low-/middle-income countries. High blood pressure (BP) is a major risk factor for CVD and has its origins in early-life. Childhood development of BP provides important information about the development of CVD risk. This study investigated how age trajectories of BP, from child to late adolescence, have changed in recent decades in China, and the mediating roles of physical growth. Methods: We used longitudinal data on 5,118 children with physical measurements between 7-18y from the China Health and Nutrition Survey 1991-2015. We applied fractional polynomial models with random effects to estimate mean trajectories of BP, BMI and height for cohorts born in 1981-85, 1986-90, 1991-95, and 1996-2000. Models for BP trajectories were also adjusted for BMI and/or height growth to assess their impact on BP trends. Results: BP trajectories (7-18y) shifted upwards with successive cohort. Compared to the earliest cohort, mean BP was higher in the latest cohort throughout childhood to late-adolescence. The increment in systolic BP was 3.8mmHg [95% CI: 2.5-5.1] in boys and 3.9mmHg [2.6-5.3] in girls at 9y, narrowed slightly during adolescence, remained at 2.8mmHg [0.7-4.9] and 2.3mmHg [0.3-4.3] respectively at 17y. Diastolic BP had similar increments to systolic BP in childhood and adolescence, but little increment in late-adolescence in girls. BMI and height trajectories also shifted upwards. The overall increment (in z-scores) was greater for height (0.55 [0.47-0.63]) than BMI (0.28 [0.20-0.35]). When adjusting for physical growth, the increment in systolic BP trajectories reduced but remained in childhood (p<0.05). The reduction was greater with adjustment for height than for BMI and the pattern was more evident in boys. Conclusions: The upward trends in BP trajectories over time among Chinese youths was largely (not entirely) explained by the increasing trends in physical growth, especially in height. The increment in BP remained in childhood after adjusting for growth, suggesting that other early-life factors might also contribute to the BP trends in Chinese children. How changes in BP within a short time frame will affect future CVD in the long term is unclear, particularly in the developing world. Funding Statement: This work was supported by the UCL Overseas Research Scholarship and China Scholarship Council to MG, https://www.csc.edu.cn/. Declaration of Interests: None declared. Ethics Approval Statement: The University of North Carolina and the Chinese Centre for Disease Control and Prevention reviewed and approved the data collection procedures.

Discrepant acute effect of saline loading on blood pressure, urinary sodium and potassium according to salt intake level: EpiSS study.

Acute dietary salt intake may cause an elevation in blood pressure (BP). The study aimed to assess the acute effect of saline loading on BP in subjects with different levels of salt intake. This study is based on the baseline survey of systemic epidemiology of salt sensitivity study. The sodium excretion in the 24‐hour urine was calculated for estimating the level of salt intake. Subjects were performed an acute oral saline loading test (1 L), and data of 2019 participants were included for analyses. Multivariate linear regression and stratified analyses were performed to identify associations between 24‐hour urinary sodium (24hUNa) with BP changes. Due to saline loading, systolic BP (SBP), pulse pressure, and urinary sodium concentration were significantly increased, while diastolic BP, heart rate, and urinary potassium concentration were significantly decreased. The SBP increments were more significant in subjects with lower salt intake, normotensives, elders, males, smokers, and drinkers. There was a significant linear negative dose‐response association between SBP increment with 24hUNa (β = −0.901, 95% CI: −1.253, −0.548), especially in lower salt intake individuals (β = −1.297, 95% CI: −2.338, −0.205) and hypertensive patients (β = −1.502, 95% CI: −2.037, −0.967). After excluding patients who received antidiabetic or antihypertensive medicines, the effects of negative associations weakened but remained significantly. In conclusion, acute salt loading leads to an increment in SBP, and the increased SBP was negatively related with 24hUNa. This study indicated avoiding acute salt loading was important for escaping acute BP changes, especially in lower salt intake populations.

Genetic susceptibility, elevated blood pressure and risk of atrial fibrillation

Abstract Background Whether elevated blood pressure (BP) is a modifiable risk factor for atrial fibrillation (AF) is not established. Purpose We tested (1) whether the association between BP and risk of AF is causal, (2) whether it varies according to individual's genetic susceptibility for AF, and (3) the extent to which specific BP-lowering drugs are expected to reduce this risk. Methods First, causality of association was assessed through two-sample Mendelian Randomization (MR), using data from two independent genome-wide association studies that included a total of one million European population. Second, UK Biobank individual participant data of 329,237 participants at baseline was used to study the effect of BP on AF according to genetic susceptibility of developing AF. Third, a possible treatment effect with BP-lowering drug classes on AF risk was predicted through genetic variants in druggable genes that code proteins related to the function of each drug class. Estimated drug effects were compared with effects on incident coronary heart disease, for which direct trial evidence exists. Results The two-sample MR analysis indicated that on average each 10-mm Hg increment in systolic BP increased the risk of AF (odds ratio [OR]: 1.23 [1.11 to 1.36]). This association was replicated in the UK biobank using individual participant data. However, in a further genetic risk-stratified analysis, there was evidence for a linear gradient in the relative effects of systolic BP on AF; while there was no conclusive evidence of an effect in those with low genetic risk, a strong effect was observed among those with high genetic susceptibility for AF (Figure). The indirect comparison of predicted treatment effects using genetic proxies for three main drug classes (angiotensin-converting enzyme inhibitors, beta-blockers and calcium channel blockers) suggested similar average effects for prevention of atrial fibrillation and coronary heart disease. Conclusions The association between elevated BP and higher risk of AF is likely to be causal, suggesting that BP-lowering treatment may be effective in AF prevention. However, average effects masked clinically important variations, with a more pronounced effect in individuals with high genetic susceptibility. Figure 1 Funding Acknowledgement Type of funding source: Foundation. Main funding source(s): British Heart Foundation

Associations of Left Ventricular Structure and Function With Blood Pressure in Heart Failure With Preserved Ejection Fraction: Analysis of the TOPCAT Trial.

BackgroundData on the association of systolic and diastolic blood pressure with the structure and function of failing hearts with preserved ejection fraction (EF) are sparse.Methods and ResultsThis analysis included 935 patients with heart failure (49.4% women; mean age, 69.9 years) with preserved EF (≥45%) enrolled in the TOPCAT (Treatment of Preserved Cardiac Function Heart Failure With an Aldosterone Antagonist) Trial before initiation of randomized therapy. Left ventricular (LV) structure (dimensions, wall thickness, and mass index), diastolic function (left atrial volume index, transmitral blood flow, and mitral annular velocities), and systolic function (EF and longitudinal strain) were assessed echocardiographically. In multivariable‐adjusted analyses, association sizes expressed per 1‐SD (14.8–mm Hg) increment in systolic blood pressure were 0.020 cm (P=0.003) and 0.018 cm (P=0.004) for LV septal and posterior wall thickness, respectively, and 2.42 mg/m2 (P=0.018) for LV mass index. The corresponding associations with diastolic blood pressure were nonsignificant (P≥0.067). In similarly adjusted analyses, the association sizes expressed per 1‐SD (10.7–mm Hg) increment in diastolic blood pressure were −0.15 for E/A (P<0.001), −0.76 for E/e′ (P=0.006), and −0.62% for EF (P=0.024). These findings were consistent, if models including systolic blood pressure were additionally adjusted for diastolic blood pressure and vice versa, albeit that the relation of EF with diastolic blood pressure weakened (−0.54%; P=0.10).ConclusionsIn diastolic heart failure, LV wall thickness and LV mass index increased with higher systolic blood pressure, but not with higher diastolic blood pressure, whereas functional measures reflecting diastolic LV function decreased with higher diastolic blood pressure, independent of systolic blood pressure. These observations highlight the importance of controlling both systolic and diastolic blood pressure as modifiable risk factors to reduce the risk of LV remodeling and diastolic LV dysfunction.

Association of systolic blood pressure with atrial fibrillation among treated hypertensive patients.

Although many studies have suggested the association between elevated blood pressure and atrial fibrillation (AF), how the relationship between systolic blood pressure (SBP) and AF differ by antihypertensive treatment has been unclear. Therefore, this study aimed to explore the relationship between SBP and AF in hypertensive patients with or without antihypertensive treatment. This was a cross-sectional study that enrolled 7,808 hypertensive patients aged ≥18 years old in 2013 in Guangdong, China. AF was screened and diagnosed by rest 12-lead electrocardiogram (ECG) or by self-reported. Patients were categorized into 5 groups according to a 10 mmHg increment in SBP. We then performed logistic regression and restricted cubic spline regression to evaluate the relationship between SBP and AF. Out of 7,808 participants (women 52.9%, mean age 62.3 years), 78 cases of AF were identified. Both univariate and multivariate logistic regression illustrated that SBP associated with a lower chance of AF in all participants when SBP was treated as a continuous variable (P<0.05) or as a categorical variable (P for trend <0.001). Similar trend was found in patients with antihypertensive therapy (P for trend <0.001) but not for those without antihypertensive medications. Our findings suggested that higher SBP is associated with lower likelihood of AF among all hypertensive patients and participants with antihypertensive treatment.

Blood pressure, hypertension and the risk of sudden cardiac death: a systematic review and meta-analysis of cohort studies

Cardiovascular disease is the leading cause of death worldwide, while sudden cardiac death (SCD) accounts for over 60% of all cardiovascular deaths. Elevated blood pressure and hypertension have been associated with increased risk of SCD, but the findings have not been consistent. To clarify whether blood pressure or hypertension is associated with increased risk of SCD and to quantify the size and the shape of any association observed. PubMed and Embase databases were searched for published prospective studies on blood pressure or hypertension and SCD up to 30 April 2018. Summary relative risks (RRs) and 95% confidence intervals (CIs) were calculated using a random effects model. The meta-analysis included 2939 SCDs among 418,235 participants from 18 studies. The summary RRs were 2.10 (95% CI 1.71–2.58, I2 = 56.7%, pheterogeneity = 0.018, n = 10) for prevalent hypertension, 1.28 (95% CI 1.19–1.38, I2 = 45.5%, pheterogeneity = 0.07, n = 10) per 20 mmHg increment in systolic blood pressure (SBP) and 1.09 (95% CI 0.83–1.44, I2 = 83.4%, pheterogeneity = 0.002, n = 3) per 10 mmHg increment in diastolic blood pressure (DBP). A nonlinear relationship was suggested between SBP and SCD. The results persisted in most subgroup and sensitivity analyses. There was no evidence of publication bias. This meta-analysis found an increased risk of SCD with hypertension diagnosis and increasing SBP. Future studies should clarify the association for DBP and the shape of the dose–response relationship between blood pressure and SCD.

Blood pressure-related electrocardiographic findings in healthy young individuals

Purpose: Elevated blood pressure induces electrocardiographic changes and is associated with an increase in cardiovascular disease later in life compared to normal blood pressure levels. The purpose of this study was to evaluate the association between normal to high normal blood pressure values (90–139/50–89 mmHg) and electrocardiographic parameters related to cardiac changes in hypertension in healthy young adults.Methods: Data from 1449 volunteers aged 18–30 years collected at our centre were analyzed. Only subjects considered healthy by a physician after review of collected data with systolic blood pressure values between 90 and 139 mmHg and diastolic blood pressure values between 50 and 89 mmHg were included. Subjects were divided into groups with 10 mmHg systolic blood pressure increment between groups for analysis of electrocardiographic differences. Backward multivariate regression analysis with systolic and diastolic blood pressure as a continuous variable was performed.Results: The mean age was 22.7 ± 3.0 years, 73.7% were male. P-wave area, ventricular activation time, QRS-duration, Sokolow–Lyon voltages, Cornell Product, J-point–T-peak duration corrected for heart rate and maximum T-wave duration were significantly different between systolic blood pressure groups. In the multivariate model with gender, body mass index and cholesterol, ventricular rate (standardized coefficient (SC): +0.182, p < .001), ventricular activation time in lead V6 (SC= +0.065, p = .048), Sokolow–Lyon voltage (SC= +0.135, p < .001), and Cornell product (SC= +0.137, p < .001) were independently associated with systolic blood pressure, while ventricular rate (SC= +0.179, p < .001), P-wave area in lead V1 (SC= +0.079, p = .020), and Cornell product (SC= +0.091, p = .006) were independently associated with diastolic blood pressure.Conclusion: Blood pressure-related electrocardiographic changes were observed incrementally in a healthy young population with blood pressure in the normal range. These changes were an increased ventricular rate, increased atrial surface area, ventricular activation time and increased ventricular hypertrophy indices on a standard 12 lead electrocardiogram.

The long-term effectiveness of metabolic control on cardiovascular disease in patients with diabetes in a real-world health care setting — A prospective diabetes management study

AimsTo determine the incidence rates of cardiovascular disease (CVD) and assess the effect of metabolic risk factor management on the development of CVD in patients with diabetes. MethodsWe studied 733 patients with diabetes without prior CVD in the Shanghai Taopu community health service center. Success in managing CVD risk factors was evaluated as follows: (1) glucose control (haemoglobin A1c [HbA1c] <7.0% in patients aged <65years and <8.0% in patients aged ≥65years), (2) blood pressure control (<140/90mmHg), and (3) lipid control (high-density lipoprotein cholesterol ≥1.0mmol/L in men and ≥1.3mmol/L in women, and triglycerides <1.7mmol/L). ResultsDuring a median 8.0-year follow-up, 206 CVD incident cases were identified. Each 1% increment in HbA1c, 10mmHg increment in systolic blood pressure (SBP), and 1mmol/L increment in triglycerides during follow-up significantly increased the risk of CVD by 17%, 37%, and 14%, respectively. Compared to those who did not, patients who met the blood pressure and glucose control goals during follow-up had a 64% and a 29% decreased risk of CVD, respectively. The multivariable-adjusted hazard ratios of CVD were 1.00, 1.78 (95% confidence interval [CI] 1.10–2.87), and 2.51 (95% CI 1.54–4.07) among patients who attained three, two, and one/none of the CVD factor control goals (HbA1c, blood pressure, and lipid) during follow-up, respectively. ConclusionsAverage levels of HbA1c, SBP, and triglycerides during follow-up were positively associated with the risk of CVD, and treatment targeting multiple factors can significantly reduce CVD risk.

Hypertension-induced cardiac impairment is reversed by the inhibition of endoplasmic reticulum stress.

Endoplasmic reticulum stress (ERS) has been shown to play a crucial role in the pathogenesis of hypertension. However, the role and mechanisms of ERS on hypertension-induced cardiac functional and morphological changes remain unclear. In this study, the effect of ERS inhibition with tauroursodeoxycholic acid (TUDCA) on hypertension-induced cardiac remodelling was examined. Hypertension was induced by deoxycorticosterone-acetate (DOCA) and salt administration in uni-nephrectomized rats for 12weeks. TUDCA was administered for the last four weeks. Rhythmic activity and contractions of the right atrium and left papillary muscle (LPM) were recorded. In the left ventricle, the expression of various proteins was examined and histopathological evaluation was performed. Hypertension-induced increments in systolic blood pressure and ventricular contractions were reversed by TUDCA. In the hypertensive heart, while expressions of glucose-regulated protein-78 (GRP78), phospho-dsRNA-activated protein kinase-like ER kinase (p-PERK), sarcoplasmic reticulum Ca-ATPase-2 (SERCA2), matrix metalloproteinase-2 (MMP-2) and nuclear NF-κB p65 increased; Bcl-2 (B-cell lymphoma-2) expression decreased and the altered levels of all these markers were restored by TUDCA. In the microscopic examination, TUDCA treatment attenuated hypertension-stimulated cardiac inflammation and fibrosis. These results suggest that ERS inhibition may ameliorate cardiac contractility through improving ERS-associated calcium mishandling, apoptosis, inflammation and fibrosis, thereby offering therapeutic potential in hypertension-induced cardiac dysfunction.

Systolic Blood Pressure and Risk of Valvular Heart Disease

Modifiable risk factors for valvular heart disease remain largely unknown, which limits prevention and treatment. To assess the association between systolic blood pressure (BP) and major valvular heart disease. A UK Biobank population-based cohort of 502 602 men and women aged 40 to 96 years at baseline was evaluated through mendelian randomization using individual participant data. Inclusion criteria were valid genetic data and BP measurements. The participants were recruited between 2006 and 2010; data analysis was performed from June 2018 to January 2019. Systolic BP was measured during clinical assessment and instruments for the genetic effect of high BP were identified from variants that were independently (linkage disequilibrium threshold of r2<0.1) associated with systolic BP with minor allele frequency greater than 0.01. A total of 130 single-nucleotide polymorphisms that have been shown to be associated with systolic BP in a genome-wide association meta-analysis involving 1 million participants of European ancestry were selected. Incident aortic stenosis, aortic regurgitation, and mitral regurgitation, individually and combined. Cases were largely based on hospital records linked to the UK Biobank with International Classification of Diseases and Health Related Problems, Tenth Revision codes. Of the 502 602 individuals screened, 329 237 participants (177 741 [53.99%] women; mean [SD] age, 56.93 [7.99] years) had valid genetic data and BP measurements; of this cohort, 3570 individuals (1.08%) had a diagnosis of valvular heart disease (aortic stenosis, 1491 [0.45%]; aortic regurgitation, 634 [0.19%]; and mitral regurgitation, 1736 [0.53%]). Each genetically associated 20-mm Hg increment in systolic BP was associated with an increased risk of aortic stenosis (odds ratio [OR], 3.26; 95% CI, 1.50-7.10), aortic regurgitation (OR, 2.59; 95% CI, 0.75-8.92), and mitral regurgitation (OR, 2.19; 95% CI, 1.07-4.47), with no evidence for heterogeneity by type of valvular heart disease (P = .90). Sensitivity analyses confirmed the robustness of the association. Lifetime exposure to elevated systolic BP appears to be associated with an increased risk of major valvular heart disease.

BLOOD PRESSURE AND RISK OF VALVULAR HEART DISEASE

Objective: In the absence of randomized clinical trials (RCTs) of blood pressure (BP) lowering treatment on risk of incident valvular heart disease, we aimed to test the hypothesis that systolic BP is causally associated with the risk of aortic stenosis, aortic regurgitation and mitral regurgitation, using a Mendelian randomisation study design. This gene-based approach takes advantage of the naturally occurring randomized exposure of individuals to genetic variants that are highly associated with lifetime systolic BP. It is similar to random allocation of intervention in RCTs and it can thus overcome the problems of reverse causation and confounding that are typical of non-randomized observational studies. Design and method: 337,335 participants in the UK Biobank study, aged 40 to 96 years, with valid genetic data and blood pressure measurements were included. 130 genetic variants associated with systolic BP in a genome-wide association meta-analysis were used. Instrumental variable analysis was performed using an adjusted two-stage predictor substitution method to assess the effect of systolic BP on incident aortic stenosis, aortic regurgitation and mitral regurgitation, individually and as a composite outcome. Results: Among 3570 (1.08 %) patients with valvular heart disease in the study cohort, 1491 had aortic stenosis, 634 had aortic regurgitation and 1736 had mitral regurgitation. Each genetically-determined 20 mmHg increment in systolic BP almost tripled the odds ratio (OR) of the composite valvular heart disease (OR 2.85; 95% CI 1.72 to 4.72). This association was consistent for individual valvular conditions (p for heterogeneity =0.89), although statistical power was limited for aortic regurgitation when considered individually (aortic stenosis OR 3.26; 95% CI 1.50 to 7.10, aortic regurgitation OR 2.59; 95% CI 0.75 to 8.92, and mitral regurgitation OR 2.19; 95% CI 1.07 to 4.47). Sensitivity analysis confirmed the robustness of the association.Conclusions: The present study showed that lifetime exposure to higher systolic BP substantially and causally increased the risk of major valvular heart disease, with stronger evidence for aortic stenosis in particular, therefore suggesting that BP-lowering treatment may be an effective strategy for prevention of valvular heart disease.

Difference in positive relation between cardio-ankle vascular index (CAVI) and each of four blood pressure indices in real-world Japanese population.

This study aimed to investigate the association of cardio-ankle vascular index (CAVI), an arterial stiffness parameter, with four blood pressure (BP) indices, systolic BP (SBP), diastolic BP (DBP), pulse pressure (PP) and mean BP (MBP), in real-world population including untreated hypertension. We analyzed the cross-sectional data from 23,257 Japanese subjects (12,729 men and 10,528 women, aged 47.1 years) without a past history of cardiovascular disease, stroke, hypertension, diabetes or dyslipidemia. Gender differences in four BP indices were slight, but significant for SBP, DBP and MBP. All four BP indices increased linearly with age. After adjusting for confounders comprising gender, age, HDL-C and BMI identified by multiple regression analysis, CAVI was lower in normotensive subjects compared to hypertensive subjects. Trend test detected an almost linear relation of adjusted CAVI with each of four BP indices even within ideal range. Exceptionally, the increment in adjusted CAVI reached its peak over 140 mm Hg range in SBP. Logistic regression models showed that 1-SD increment in each BP index contributed independently to high CAVI (≥90th percentile), whereas that in PP showed a somewhat lower contribution. Subgroup analyses revealed that older age, dyslipidemia and hypertension were independently associated with relatively small contributions to high CAVI per 1-SD increment in SBP. PP might be less useful to assess arterial stiffness compared to other BP indices. Besides, the contribution of SBP increment to arterial stiffening was relatively large in normotensive, normolipidemic non-elderly subjects, whose individual transition of SBP should be noticed.

Elevated blood pressure and risk of aortic valve disease: a cohort analysis of 5.4 million UK adults.

AimsTo test two related hypotheses that elevated blood pressure (BP) is a risk factor for aortic valve stenosis (AS) or regurgitation (AR).Methods and resultsIn this cohort study of 5.4 million UK patients with no known cardiovascular disease or aortic valve disease at baseline, we investigated the relationship between BP and risk of incident AS and AR using multivariable-adjusted Cox regression models. Over a median follow-up of 9.2 years, 20 680 patients (0.38%) were diagnosed with AS and 6440 (0.12%) patients with AR. Systolic BP (SBP) was continuously related to the risk of AS and AR with no evidence of a nadir down to 115 mmHg. Each 20 mmHg increment in SBP was associated with a 41% higher risk of AS (hazard ratio 1.41, 95% confidence interval 1.38–1.45) and a 38% higher risk of AR (1.38, 1.31–1.45). Associations were stronger in younger patients but with no strong evidence for interaction by gender or body mass index. Each 10 mmHg increment in diastolic BP was associated with a 24% higher risk of AS (1.24, 1.19–1.29) but not AR (1.04, 0.97–1.11). Each 15 mmHg increment in pulse pressure was associated with a 46% greater risk of AS (1.46, 1.42–1.50) and a 53% higher risk of AR (1.53, 1.45–1.62).ConclusionLong-term exposure to elevated BP across its whole spectrum was associated with increased risk of AS and AR. The possible causal nature of the observed associations warrants further investigation.

Increment in Systolic Blood Pressure During Cold Pressure Test Is Associated with Baseline LF Power in Young Prehypertensive Men

The cold pressor test (CPT) is commonly used as a sympathoexcitatory maneuver to provoke an increment in arterial pressure and heart rate and to measure cardiovascular reactivity to stress. However, use of the CPT as a predictor test of future hypertension is still debatable. We investigated whether exaggerated blood pressure responsiveness to CPT is observed in young prehypertensive men and determined baseline HRV indices and autonomic nervous system contribution into the elevation of blood pressure.CPT was performed in 81 normotensive and 72 prehypertensive men enrolled from V.N. Karazin Kharkiv National University student population. All participants gave written informed consent. After 5 min resting stage subjects placed their right hand into ice‐cold water for 1 minute. ECG was continuously recorded and resting HRV indices were interpreted (CardioLab 2010). Blood pressure was measured at the end of each stage (Nissei WS‐1011). GLM one‐way MANOVA and MANCOVA with height and BMI were used to test for possible effects of prehypertension on heart rate (ΔHR) and blood pressure (ΔSBP and ΔDBP) responses. The stepwise multiple linear regression analysis was carried out to assess the relative importance of baseline LnLF (LnLFrest) and LnHF (LnHFrest) power in HR, SBP, and DBP increments, adjusted also for the presence of prehypertension, BMI, height, and two‐way interactions.In the current study, prehypertensive subjects did not demonstrate higher cardiovascular reactivity to CPT (Table 1). Moreover, normotensives had higher SBP response to CPT (Table 1). When height and BMI were taken into account this difference was even more significant (not shown). Previous studies have yielded inconsistent results with some showing higher and some showing the same and even lower blood pressure reactivity to CPT in prehypertensive subjects or in persons with family history of hypertension.The stepwise multiple regression analysis revealed that ΔSBP in prehypertensives and ΔDBP in all subjects were negatively associated with LnLFrest possibly indicating, according to our hypothesis, activity of the inhibitory interneurons projected to the presympathetic neurons in the rostral ventrolateral medulla. The central inhibition of sympathetic activity reduced the increment of SBP in subjects developing hypertension and controlled increment of DBP in all subjects (Table 2).It was shown that increments in both SBP and DBP were associated with ΔHR only in the prehypertensive subjects and in persons with increased BMI (Table 2). These findings may be partially explained by blunting of baroreceptor reflex sensitivity and/or resetting of the baroreceptor reflex to a higher control point.in prehypertensives and in subjects with increased BMI. The increments in SBP and DBP associated also with ΔHR in subjects with a high level of baseline parasympathetic activity as shown by the positive association between LnHFrest by ΔHR interaction and ΔSBP or ΔDBP (Table 2) possibly because high LnHFrest reduces HR and increases atrioventricular delay which may contribute to a ventricular filling.In conclusion, young prehypertensive subjects demonstrated lower SBP response to CPT than normotensives possibly due to their increment in SBP was associated with resting LnLF power, indicating according to our hypothesis, inhibition of the presympathetic medullary neurons; ΔSBP and ΔDBP were associated with ΔHR only in prehypertensives and in persons with high baseline parasympathetic activity.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.