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06.01 Life-Course of Mean Arterial Pressure and Its Impact on Arterial Stiffness: the Amsterdam Growth and Health Longitudinal Study (Agahls)

Artery Research(2008)

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Model: adjustments Stiff vs. normal CCA Stiff vs. normal CFA β 95% CI β 95% CI 1. time, sex, height, smoking, alcohol, energy intake –376 –724; –27 –500 –839; –161 2. + body fatness (sum of 4 skinfolds) –317 –668; 34 –471 –810; –132 3. + cardiopulmonary fitness (VO 2 max) –172 –510; 166 –386 –712; –60 4. + blood lipids (total-to-HDL cholesterol ratio) –234 –585; 117 –489 –826; –152 5. + resting heart rate –328 –670; 15 –461 –794; –128 6. + systolic blood pressure –350 –709; 8 –482 –828; –136 7. + all variables in models 2 to 6 –145 –490; 201 –422 –750; –93 Purpose To investigate how the development over time (i.e. from adolescence to adulthood) of mean arterial pressure (MAP) impacts on arterial stiffness in adulthood. Methods Longitudinal data on systolic (SP) and diastolic (DP) blood pressure were retrieved from the AGAHLS ( n = 373, 196 women; 8 follow-up measures between the ages of 13 and 36 yrs). MAP was calculated as [(2*DP) + SP]/3. Arterial stiffness (i.e. carotid, brachial and femoral distensibility and compliance coefficients) was assessed by non-invasive ultrasonography when subjects were 36 yrs old; a sex-specific total stiffness score was calculated by averaging the height and local MAP-adjusted z-scores of each of these estimates. Generalized estimating equations were used to compare the mean levels (and the patterns of development) of MAP throughout the 24-yr follow-up period between subjects with ‘stiffer’ (i.e. lowest quartile) vs . ‘normal’ arteries (highest 3 quartiles of the total stiffness score) at the age of 36. Results Compared to subjects with ‘normal’, those with ‘stiffer’ arteries had, on average, 6.36 mmHg (95%CI: 5.04; 7.67) greater levels of MAP throughout the longitudinal period. These differences were already present in adolescence and were further amplified thereafter with subjects with stiffer arteries showing a steeper increase in MAP between adolescence and age 36 (Figure). Adjustments for other risk factors (i.e. smoking behaviour, energy and alcohol intake, physical activity, body fatness, blood lipids and heart rate) only slightly attenuated these differences. Conclusion Blood pressure monitoring should start already in early age in order to avoid/delay arterial stiffening and related cardiovascular complications.
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