Participants in the bottom 30% (ie, SBP decreased on standing) were significantly older, had a greater prevalence of hypertension and peripheral vascular disease, had higher values of SBP, and had more cigarette-years of smoking.
Multivariable logistic models showed that the two polymorphisms were significantly associated with severe hypertension (SBP > or = 160 mm Hg or DBP > or = 100 mm Hg regardless of medication use), with an OR of 0.6(95% confidence interval [CI]: 0.4-0.98) for S482S vs. G482G and an OR of 1.9(95% CI: 1.2-3.0) for +2962G/G vs. +2962A/A, but not with regular hypertension (SBP > or = 140 mm Hg or DBP > or = 90 mm Hg or current use of antihypertensive medications), with an OR of 0.9(95% CI: 0.7-1.2) for S482S vs. G482G and an OR of 0.9(95% CI: 0.7-1.4) for +2962G/G vs. +2962A/A.
We conducted GWAS for three BP traits [systolic and diastolic blood pressure (SBP and DBP); hypertension (HYP)] in the Kooperative Gesundheitsforschung in der Region Augsburg (KORA) S3 cohort (n = 1644) recruited from general population in Southern Germany.
The genetic risk score, calculated as the sum of BP-increasing alleles of FGF5-rs16998073, CYP17A1-rs11191548, CYP17A1-rs1004467 and MTHFR-rs17367504, was significantly associated with increased SBP (1.16 mmHg/allele, P = 9.01E-5), DBP (0.51 mmHg/allele, P = 4.40E-4) and hypertension risk (OR = 1.22/allele, P = 2.74E-7).
We observed that the non-coding SNP rs2289277 was associated with TSLP mRNA abundance (P=0.04), as well as with SBP [systolic BP (blood pressure)] (P=0.004) and DBP (diastolic BP) (P=0.0003) in men when adjusting for age, waist circumference, smoking and medication treating hypertension.
In contrast, in inactive group, two polymorphisms and genetic risk score were significantly associated with SBP (rs17249754: β = 1.26, 95% confidence interval (CI) 0.61-1.90, p < 0.001; rs1004467: β = 0.68, 95%CI 0.03-1.32, p = 0.039; genetic risk score: β = 1.54, 95%CI 0.74-2.33, p < 0.001); three polymorphisms and genetic risk score were significantly associated with hypertension (rs17249754: odds ratio (OR) = 1.27, 95%CI 1.08-1.49, p = 0.004; rs1378942: OR = 1.25, 95%CI 1.00-1.57, p = 0.050 (marginally significant); rs16998073: OR = 1.17, 95%CI 1.01-1.37, p = 0.044; genetic risk score: OR = 1.38, 95%CI 1.13-1.68, p = 0.001).
In the normal weight group, we did not observe any significant association of 6 SNPs and the genetic risk score (GRS) with SBP/DBP and hypertension (all P > 0.05).
When stratified by the hypertension medication status, interaction effect was found only in individuals taking medication (P-interaction = 0.004 for SBP and 0.001 for DBP).
This exploratory study reports two plausible loci associated with SBP response to hydrochlorothiazide: TET2, an aldosterone-responsive mediator of αENaC gene transcription; and CSMD1, previously described as associated with hypertension in a case-control study.
Pre- and undiagnosed-hypertension was defined as systolic blood pressure/ diastolic blood pressure (SBP/DBP) of 120-139/80-89 mm Hg and SBP⩾140 mm Hg and/or DBP⩾90 mm Hg, respectively, in participants without a history of hypertension and use of antihypertensive medication.
Our results showed a difference of 5 mm Hg in SBP among sustained hypertensive patients, as recommended by the Japanese Society of Hypertension Guidelines for the Management of Hypertension; however, in other hypertensive patient types, the differences in SBP and DBP between office and home measurements differed by >5 mm Hg.
In the multivariate model, initial SBP and DBP levels had the strongest influence on the development of future hypertension (7% increase in men and 5% in women per mmHg SBP).
The costs of drug treatment for hypertension were calculated and general estimation, whereas effectiveness was measured as a reduction in SBP and DBP at the end of a 24-week study period.
Orthostatic hypotension-related hospitalizations were predicted by age [per 1-year increase, hazard ratio 1.14, 95% confidence interval (CI): 1.12-1.16], smoking (hazard ratio 1.35, 95% CI: 1.12-1.64), diabetes (hazard ratio 1.50, 95% CI: 1.00-2.25), baseline orthostatic hypotension (hazard ratio 1.45, 95% CI: 1.05-1.98), in particular, by SBP fall at least 30 mmHg (hazard ratio 3.93, 95% CI: 2.14-7.23), whereas syncope hospitalizations by age (per 1-year increase, hazard ratio 1.09, 95% CI: 1.07-1.11), smoking (hazard ratio 1.27, 95% CI: 1.08-1.49), and hypertension (hazard ratio 1.42, 95% CI: 1.20-1.69).
According to three independent measurements of SBP in 1987, 1989, and 1992, cases of the same age and sex with continuous SBP at least 75 percentile were classified as the high-blood pressure (BP) group, whereas those with SBP less than 50 percentile were classified as the normal-BP group.
Adjusted multiple linear regression models elicited positive associations of age (βa = 0.152, p = 0.001) and duration of hypertension (βa = 0.132, p = 0.003) with achieved level of SBP as well as BMI (βa = 0.135, p = 0.002) with DBP.
Those who converted to normotension were younger, less obese, and had significantly lower baseline SBP, fasting glucose, cholesterol levels, and homeostasis model assessment insulin resistance compared with study participants who continued to have prehypertension or progressed to hypertension.
Distinguishing trajectories allows identification of subgroups at risk of hypertension and cardiovascular disease later in life and in addition can inform the design of targeted interventions to attenuate high SBP and DBP trajectories over time and maintain normal trajectories.
MRI-derived subclinical HFF is associated with SBP and DBP as well as with hypertension in participants from the general population without history of cardiovascular disease.
Reclassification from normal SBP to hypertension was greatest with Canadian Hypertension Education Program guidelines (3% younger, 12% older individuals) and reclassification from hypertension to normal SBP was greatest with National Institute for Health and Care Excellence guidelines (70% younger, 44% older individuals).
In Native Americans, L' carriers had lower SBP (-6.05mm Hg, 95% CI=-9.59 to -2.51) and lower odds of hypertension (OR = 0.34, 95% CI=0.13-0.89) than those with the S'S' genotype.
After 1 month, superior SBP (-3.1 mmHg, P = 0.02) and DBP (-2.8 mmHg, P < 0.001) reductions were observed with perindopril/indapamide/amlodipine, which were even more pronounced after excluding white-coat effect in the sustained hypertension population (-5.3/-3.7 mmHg).
In this cross-sectional study, 200 outpatients (161 women, 39 men) with essential HTN (systolic blood pressure [SBP] ≥ 140 mmHg and diastolic blood pressure [DBP] ≥ 90 mmHg) were recruited from August to November 2012.