Rate Of Increase In Systolic Blood Pressure Research Articles

Metabolic dysfunction-associated fatty liver disease is associated with an increase in systolic blood pressure over time: linear mixed-effects model analyses.

Metabolic dysfunction-associated fatty liver disease (MAFLD), a new feature of fatty liver (FL) disease that is defined as FL with overweight/obesity, type 2 diabetes mellitus or metabolic dysregulation, has been reported to be associated with the development of diabetes mellitus, chronic kidney disease and cardiovascular disease. However, the association between MAFLD and hypertension remains unclear. We investigated the association between MAFLD and systolic blood pressure (SBP) over a 10-year period in 28,990 Japanese subjects who received annual health examinations. After exclusion of subjects without data for SBP and abdominal ultrasonography at baseline, a total of 17,021 subjects (men/women: 10,973/6048; mean age: 49 years) were recruited. Linear mixed-effects model analyses using diagnoses of FL, nonalcoholic fatty liver disease (NAFLD) or MAFLD and age, sex, SBP, use of anti-hypertensive drugs, levels of uric acid and estimated glomerular filtration rate, family history of hypertension and habits of current smoking and alcohol drinking at baseline as well as the duration of the observation period and the interaction between each covariate and the duration of the observation period showed that the significant association of change in SBP over time with diagnosis of MAFLD (estimate: 0.223 mmHg/year, P < 0.001) was greater than that with diagnoses of FL (estimate: 0.196 mmHg/year, P < 0.001) and NAFLD (estimate: 0.203 mmHg/year, P < 0.001). Furthermore, the rate of increase in SBP over time was higher in subjects with MAFLD than in subjects without FL and subjects with FL who had no MAFLD. In conclusion, MAFLD is significantly associated with an increase in SBP over time. The presence of metabolic dysfunction-associated fatty liver disease (MAFLD) is significantly associated with an increase in systolic blood pressure over time.

Puberty Timing and Sex-Specific Trajectories of Systolic Blood Pressure: a Prospective Cohort Study.

Background:Sex differences in systolic blood pressure (SBP) emerge during adolescence but the role of puberty is not well understood. We examined sex-specific changes in SBP preceding and following puberty and examined the impact of puberty timing on SBP trajectories in females and males.Methods:Trajectories of SBP before and after puberty and by timing of puberty in females and males in a contemporary birth cohort study were analyzed. Repeated measures of height from age 5 to 20 years were used to identify puberty timing (age at peak height velocity). SBP was measured on ten occasions from 3 to 24 years (N participants, 4062; repeated SBP measures, 29 172). Analyses were performed using linear spline multilevel models based on time before and after puberty and were adjusted for parental factors and early childhood factors.Results:Mean age at peak height velocity was 11.7 years (SD, 0.8) for females and 13.6 years (SD, 0.9) for males. Males had faster rates of increase in SBP before puberty leading to 10.19 mm Hg (95% CI, 6.80–13.57) higher mean SBP at puberty which remained similar at 24 years (mean difference, 11.43 mm Hg [95% CI, 7.22–15.63]). Puberty timing was associated with small transient differences in SBP trajectories postpuberty in both sexes and small differences at 24 years in females only.Conclusions:A large proportion of the higher SBP observed in males compared with females in early adulthood is accrued before puberty. Interventions targeting puberty timing are unlikely to influence SBP in early adulthood.

Urinary Heavy Metals and Longitudinal Changes in Blood Pressure in Midlife Women: The Study of Women's Health Across the Nation.

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Hypertension and aging in rural Haiti: results from a preliminary survey.

Cross-sectional studies in the developed countries document strong relationships among age, systolic blood pressure (SBP) and pulse pressure (PP). There is little information about these trends and their impact in underdeveloped countries with different socioeconomic and lifestyle characteristics. We studied a convenience sample of 572 residents of rural Fontaine, Haiti: 193 males and 379 females (mean, s.d.) age 40.2 (17.1) years and performed intake questionnaires and BP measurements in participants' homes. Income and educational achievement were very low but most-recommended lifestyle factors were very favorable: very high physical activity, low dietary fat, virtually no obesity (body mass index 21.8 (4.9)), and low smoking prevalence. Rough estimates of salt intake were high (~13 g per day) as was the overall prevalence of hypertension: 34.4% (23.4% in males, 40.2% in females). SBP and PP were related closely to age (r2=0.28, P<0.001 and r2=0.22, P<0.001); for each decade of age, SBP increased by 7.6 mm Hg. Diastolic BP peaked in the 6th decade (polynomial r2=0.22, P<0.001) and the nadir of PP occurred in the 3rd decade. We conclude that, despite a favorable profile of lifestyle characteristics and no obesity, the prevalence of hypertension and rate of increase in SBP and PP with age in Haiti are at least as high as those of developed countries.

Midlife blood pressure predicts future diastolic dysfunction independently of blood pressure

ObjectivesHigh blood pressure (BP) is associated with diastolic dysfunction, but the consequence of elevated BP over the adult life course on diastolic function is unknown. We hypothesised that high BP...

Midlife blood pressure change and left ventricular mass and remodelling in older age in the 1946 British Birth Cohort Study.

AimsAntecedent blood pressure (BP) may contribute to cardiovascular disease (CVD) independent of current BP. Blood pressure is associated with left ventricular mass index (LVMI) which independently predicts CVD. We investigated the relationship between midlife BP from age 36 to 64 and LVMI at 60–64 years.Methods and resultsA total of 1653 participants in the British 1946 Birth Cohort underwent BP measurement and echocardiography aged 60–64. Blood pressure had previously been measured at 36, 43, and 53 years. We investigated associations between BP at each age and rate of change in systolic blood pressure (SBP) between 36–43, 43–53, and 53–60/64 years on LVMI at 60–64 years. Blood pressure from 36 years was positively associated with LVMI. Association with SBP at 53 years was independent of SBP at 60–64 years and other potential confounders (fully adjusted β at 53 years = 0.19 g/m2; 95% CI: 0.11, 0.27; P < 0.001). Faster rates of increase in SBP from 43 to 53 years and 53 to 60/64 years were associated with increased LVMI. Similar relationships were seen for diastolic, pulse, and mean pressure. Rate of increase in SBP between 43–53 years was associated with largest change in LVMI (β at 43–53 years = 3.12 g/m2; 95% CI: 1.53, 4.72; P < 0.001). People on antihypertensive medication (43 years onwards) had greater LVMI even after adjustment for current BP (β at 43 years = 12.36 g/m2; 95% CI: 3.19, 21.53; P = 0.008).ConclusionHigher BP in midlife and rapid rise of SBP in 5th decade is associated with higher LVMI in later life, independent of current BP. People with treated hypertension have higher LVMI than untreated individuals, even accounting for their higher BP. Our findings emphasize importance of midlife BP as risk factor for future CVD.

Blood pressure in young adulthood and the risk of type 2 diabetes in middle age.

Hypertension is known to accompany type 2 diabetes in middle age, but it is unknown how early in life blood pressure (BP) begins to rise among individuals who later develop diabetes. The objective of this study was to evaluate elevated BP as a long-term predictor of type 2 diabetes. We conducted a prospective cohort study of 1,152 white male medical students in The Johns Hopkins Precursors Study to longitudinally assess systolic BP (SBP) and diastolic BP (DBP) from young adulthood through middle age in men who went on to develop diabetes. Incident diabetes was identified by self-report through mailed questionnaires verified by medical record review. During a median follow-up of 38 years, 77 cases of incident diabetes occurred. The mean age of diabetes diagnosis was 58 years. As early as age 30 years, mean SBP and DBP were significantly higher in men who developed diabetes during follow-up than in those who remained nondiabetic (SBP 122 vs. 119 mmHg, P = 0.009; DBP 78 vs. 75 mmHg, P = 0.0005). The rate of increase in SBP and DBP over time in men who developed diabetes was greater than the rate of increase in men who did not develop diabetes (SBP 0.49 vs. 0.27 mmHg/year, P < 0.00003; DBP 0.24 vs. 0.17 mmHg/year; P = 0.09). After adjustment for BMI and other risk factors for diabetes, SBP and DBP at age 30 years remained significantly higher in individuals who developed diabetes than in their nondiabetic counterparts; however, the difference in the rate of increase in SBP was no longer significant following multivariate adjustment. BP elevations precede the development of type 2 diabetes in middle age by 20-25 years. Higher BP in the prediabetic state might contribute to the presence of vascular disease at the time of diagnosis of type 2 diabetes.

The effect of prenatal diet and glucocorticoids on growth and systolic blood pressure in the rat.

Hypertension is a major cardiovascular risk factor for stroke and CHD in Westernized societies (Thom et al. 1992). Whilst many factors contribute towards elevated blood pressure, such as low physical activity, obesity, saturated fat, salt and alcohol intake (Ward, 1993), they only explain a proportion of cardiovascular risk. Since adult systolic blood pressure (SBP) tracks growth from infancy, i.e. SBP increases in proportion to the increase in growth from infancy (Law et al. 1993) and is related to the rate of increase in SBP in childhood (Lever & Harrap, 1992), then factors that influence SBP in early life may determine future cardiovascular risk. Barker and colleagues (Law et al. 1991) have identified a negative relationship between birth weight and SBP in childhood. The relationship remains into adult life and, furthermore, is amplified (Barker et al. 1989). Thus, determinants of intrauterine growth leading to an asymmetric or a proportionately-small baby at term also influence future cardiovascular risk (Barker, 1994). Cross-fostering and sibling studies have clearly shown that the maternal environment, rather than genetic factors, largely accounts for variations in birth weight (Walton & Hammond, 1938; Milner & Gluckman, 1996). Intrauterine growth is primarily substrate driven (Karlberg et al. 1994) and, thus, the supply of substrate may influence the intrauterine growth process. Indeed, low birth weight in man is associated with a reduced maternal intake of protein coupled with a high intake of carbohydrate (Godfrey et al. 1996 and indices of poor maternal nutritional status, such as reduced skinfold thickness (Godfrey et al. 1994) and reduced maternal Fe stores (Godfrey et al. 1991). SBP in childhood and adult life is inversely related to the same indices of poor maternal nutritional status, i.e. maternal anaemia (Law et al. 1991) and reduced maternal skinfold thickness (Godfrey et al. 1994). A low intake of protein coupled with a high intake of carbohydrate during gestation is associated with an elevated SBP in the offspring when measured 40 years later (Campbell et al. 1996). The propensity towards hypertension and thus towards CHD, therefore, is partially determined in utero by nutritional factors. The underlying physiological processes relating maternal nutrition, intrauterine growth patterns and adult hypertension are as yet unknown. Research using animal models has provided some insight into the mechanism of intrauterine programming of adult hypertension. Whilst hypertension can be experimentally produced in animal models through reno-vascular manipulations such as Goldblatts or aortic coarctation (Wilkinson, 1994), or steroid-induced using deoxycorticosterone acetate or dexamethasone (Kenyon & Morton, 1994), these methodologies do not account for an early origin of adult hypertension. Steroid-induced hypertension associated with reduced birth weight can be reproduced, however, by either dexamethasone (Benediktsson et al. 1993; Levitt et al. 1996) or carbenoxolone (Lindsay et al. 1996) injections during pregnancy in the rat. Maternal glucocorticoids (GC) are metabolized by the placental enzyme 1 1 P-hydroxysteroid dehydrogenase type 2 (EC 1.1.1.146; 11-HSD2; Seckl, 1997~). Placental 11HSD2 is inhibited by carbenoxolone and has weak activity towards dexamethasone. Thus, increased fetal exposure to excess maternal GC reduces birth weight and renders the resultant offspring hypertensive. Importantly, hypertension associated with carbenoxolone injections requires a product of the maternal adrenal gland, since carbenoxolone injections to adrenalectomized dams have no effect on birth weight or SBP of the resultant offspring (Lindsay et al. 1996). The activity of placental 11-HSD2 is positively correlated with birth weight in rats (Benediktsson et al. 1993) and man (Stewart et al. 1995), and activity at term predicts birth weight (Benediktsson et al. 1995). Thus, Edwards et al. (1993) contend that placental 1 1-HSD2 has an important role in determining birth weight and, through maternal GC influence, may mediate the fetal origins of