OBJECTIVE: We aimed to assess whether apolipoprotein (apo) A-I levels that generated type-2 diabetes and coronary disease among Turks contribute to prehypertension and hypertension. METHODS: A population-based sample of 2207 adults (mean age 53±11 years) was studied prospectively over a 6.5 years' follow-up. Individuals with hypertension and/or prehypertension were excluded at baseline. RESULTS: At baseline, levels of apoA-I increased in each sex, from the normotensive to prehypertensive and hypertensive group (by mean 7.6 mg/dL, p<0.001) concomitantly with age, waist circumference, fasting triglycerides, apoB, C-reactive protein (CRP) and homeostasis model assessment. In logistic regression models, adjusted for confounders comprising waist circumference or triglycerides, prehypertension was predicted independently by apoA-I at RRs of 1.23 (95%CI 0.97; 1.52)] or 1.32 (95%CI 1.04; 1.74), respectively. Despite showing a positive association, apoA-I did not independently predict in similar models the development of hypertension; the determinants were rather waist circumference, or fasting triglycerides or CRP [RR 1.16 (95%CI 1.05; 1.28)] and, in women, diabetes. In a linear regression analysis for circulating apoA-I including 10 variables, apoB and in men systolic blood pressure were positively associated. CONCLUSION: In contributing to prehypertension, the pro-inflammatory apoA-I, mediated by apoB, is independent of triglyceridemia. Other inflammatory processes conjointly are likely mechanistically involved in the development of hypertension in a population with prevalent metabolic syndrome.
OBJECTIVE: We aimed to assess whether apolipoprotein (apo) A-I levels that generated type-2 diabetes and coronary disease among Turks contribute to prehypertension and hypertension. METHODS: A population-based sample of 2207 adults (mean age 53±11 years) was studied prospectively over a 6.5 years' follow-up. Individuals with hypertension and/or prehypertension were excluded at baseline. RESULTS: At baseline, levels of apoA-I increased in each sex, from the normotensive to prehypertensive and hypertensive group (by mean 7.6 mg/dL, p<0.001) concomitantly with age, waist circumference, fasting triglycerides, apoB, C-reactive protein (CRP) and homeostasis model assessment. In logistic regression models, adjusted for confounders comprising waist circumference or triglycerides, prehypertension was predicted independently by apoA-I at RRs of 1.23 (95%CI 0.97; 1.52)] or 1.32 (95%CI 1.04; 1.74), respectively. Despite showing a positive association, apoA-I did not independently predict in similar models the development of hypertension; the determinants were rather waist circumference, or fasting triglycerides or CRP [RR 1.16 (95%CI 1.05; 1.28)] and, in women, diabetes. In a linear regression analysis for circulating apoA-I including 10 variables, apoB and in men systolic blood pressure were positively associated. CONCLUSION: In contributing to prehypertension, the pro-inflammatory apoA-I, mediated by apoB, is independent of triglyceridemia. Other inflammatory processes conjointly are likely mechanistically involved in the development of hypertension in a population with prevalent metabolic syndrome.
Authors: Norbaiyah Mohamed Bakrim; Aida Nur Sharini Mohd Shah; Norlelawati A Talib; Jamalludin Ab Rahman; Aszrin Abdullah Journal: Malays J Med Sci Date: 2020-04-30