Mm Hg Increment In Systolic Blood Pressure Research Articles

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 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.

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.

Elevated blood pressure and risk of mitral regurgitation: A longitudinal cohort study of 5.5 million United Kingdom adults.

BackgroundMitral regurgitation in people without prior cardiac disease is considered a degenerative disease with no established risk factors for its prevention. We aimed to test the hypothesis that elevated systolic blood pressure (SBP) across its usual spectrum is associated with higher risk of mitral regurgitation.Methods and findingsWe used linked electronic health records from the United Kingdom Clinical Practice Research Datalink (CPRD) from 1 January 1990 to 31 December 2015. CPRD covers approximately 7% of the current UK population and is broadly representative of the population by age, sex, and ethnicity. About 5.5 million UK patients with no known cardiovascular or valve disease at baseline were included in this cohort study. We investigated the relationship between blood pressure (BP) and risk of mitral regurgitation using Cox regression models. Our primary exposure variable was SBP and our primary outcome was incident reports of mitral regurgitation, which were identified from hospital discharge reports or primary care records.Of the 5,553,984 patients in the CPRD that met our inclusion criteria, during the 10-year follow-up period, 28,655 (0.52%) were diagnosed with mitral regurgitation and a further 1,262 (0.02%) were diagnosed with mitral stenosis. SBP was continuously related to the risk of mitral regurgitation with no evidence of a nadir down to 115 mmHg (p < 0.001). Each 20 mmHg increment in SBP was associated with a 26% higher risk of mitral regurgitation (hazard ratio [HR] 1.26; CI 1.23, 1.29). The observed association was partially mediated by diseases affecting the left ventricle during follow-up (myocardial infarction [MI], ischaemic heart disease [IHD], cardiomyopathy, and heart failure). However, the percentage of excess risk mediated (PERM) by these proximate causes of secondary mitral regurgitation was only 13% (CI 6.1%, 20%), and accounting for them had little effect on the long-term association between SBP and mitral regurgitation (mediator-adjusted HR 1.22; CI 1.20, 1.25; p < 0.001). Associations were similar for each 10 mmHg increment in diastolic blood pressure (DBP) (p < 0.001) or each 15 mmHg increment in pulse pressure (PP) (p < 0.001). By contrast, there was no association between SBP and risk of mitral stenosis (HR per 20 mmHg higher SBP 1.03; CI 0.93, 1.14; p = 0.58). These analyses are based on routinely collected data from health records which may be sensitive to measurement errors, and the observed associations may not be generalizable to less severe and subclinical cases of mitral regurgitation.ConclusionsLong-term exposure to elevated BP across its whole spectrum is associated with an increased risk of primary and secondary mitral regurgitation. These findings suggest that BP control may be of importance in the prevention of mitral regurgitation.

Comparison of the Sex-Specific Associations Between Systolic Blood Pressure and the Risk of Cardiovascular Disease

Conflicting results have been reported on whether the association between increments in systolic blood pressure (SBP) and cardiovascular disease differs between men and women. We performed a systematic review with meta-analysis to compare reliably sex-specific associations between SBP and cardiovascular risk. PubMed MEDLINE was systematically searched for prospective population-based cohort studies published between January 1, 1966, and March 31, 2012. Studies were selected if they presented sex-specific estimates, with associated variability, of the relative risk for either ischemic heart disease or stroke according to SBP. The data were pooled using random effects models with inverse variance weighting, and estimates of the ratio of the relative risks per 10 mm Hg increment in SBP, comparing women with men, were derived. Data from 124 prospective cohort studies, including information on 1197 472 individuals (44% women) and 26 176 stroke and 24 434 ischemic heart disease events, were included. Overall, there was no evidence to suggest a sex difference in the relationship between SBP and either the risk of stroke (pooled ratio of relative risks, 0.98 [95% confidence interval, 0.96; 1.01]; P=0.13) or ischemic heart disease (pooled ratio of relative risks, 1.00 [95% confidence interval, 0.97; 1.04]; P=0.85). Elevated levels of SBP are a major risk factor for stroke and ischemic heart diseases in both women and men. This study unequivocally demonstrates the broadly similar impact of SBP increments on cardiovascular outcomes in both sexes.

Late afternoon blood pressure increase is associated with diabetic retinopathy in normotensive type 2 diabetes mellitus patients

Aims To identify if the variability of blood pressure (BP) is associated with diabetic retinopathy (DR) in normotensive type 2 DM patients. Methods Sixty-five normotensive type 2 DM patients that had 24-h ambulatory BP monitoring (ABPM) were grouped according any degree of DR. Results Fourteen (21%) patients had DR. Office BP and 24-h BP parameters did not differ between groups. At late afternoon period, patients with DR had higher increment in both systolic (11.3 ± 12.7 mmHg vs. 1.0 ± 11.4 mmHg, P = 0.006) and diastolic (6.7 ± 8.6 mmHg vs. −0.73 ± 10.0 mmHg, P = 0.017) BP levels than those without. Multivariate logistic analyses were performed with DR as a dependent variable. Each 1 mmHg increment in systolic BP at the late afternoon period was associated with a 10.2% increase in DR prevalence [OR 1.102 (CI 95% 1.011–1.202, P = 0.027)], after adjustments for A1C test, DM duration, age, albuminuria and current smoking. Conclusions In conclusion, in normotensive type 2 DM patients, BP increase at late afternoon is associated to DR independently from confounder factors or other ABPM parameters.

Cigarette Smoking, Systolic Blood Pressure, and Cardiovascular Diseases in the Asia-Pacific Region

Smoking and increased levels of blood pressure (BP) substantially increase the risk of cardiovascular diseases (CVD). If these 2 risk factors have a synergistic impact on cardiovascular events, lowering BP and quitting smoking will contribute more to reducing CVD than would be expected from ignoring their interaction. Individual participant data were combined from 41 cohorts, involving 563 144 participants (82% Asian). During a median of 6.8 years follow-up, 4344 coronary heart disease (CHD) and 5906 stroke events were recorded. Repeat measures of systolic blood pressure (SBP) were used to adjust for regression dilution bias. Hazard ratios (HRs) and 95% confidence intervals (CIs) for SBP by cigarette smoking status were estimated from Cox proportional hazard models adjusted for age and stratified by study and sex. Data suggested a log-linear relationship between SBP and all subtypes of CVD. The HRs relating SBP to both CHD and ischemic stroke were broadly similar irrespective of smoking status (P>/=0.1). For hemorrhagic stroke (intracerebral hemorrhage), the HRs (95% CIs) for an additional 10 mm Hg increment in SBP were 1.81 (1.73 to 1.90) for present smokers and 1.66 (1.59 to 1.73) for nonsmokers (P=0.003). For every subtype of cardiovascular events, similar results were found for analyses involving only fatal events. Smoking exacerbated the impact of SBP on the risk of hemorrhagic stroke. Although quitting smoking and lowering BP are both crucial for prevention of CVD, combining the 2 could be expected to have extra beneficial effect on preventing hemorrhagic stroke.