Background Subclinical organ damage in hypertension leads to increase of cardiovascular risk. The aim of the study was to analyse the relationship between family history of hypertension and parameters of structure and function of the left ventricle and large arteries in adult offspring.
Material and methods We recruited 80 families (290 subjects). Based on BP in parents we classified the group of offspring as offspring of normotensive parents (OFF/NORM, n = 34, mean age 26.55 ± 8.02 years) and offspring of hypertensive parents (OFF/HT, n = 81, mean age 29.15 ± 6.37). Conventional blood pressure measurements and ambulatory blood pressure monitoring (ABPM), echocardiographic evaluation of left ventricle structure and function and assessment of carotid intima–media thickness were performed. Arterial stiffness was determined from pulse wave analysis (SphygmoCor).
Results OFF/HT had higher diastolic blood pressure from conventional measurements (74.65 ± 7.15 mm Hg v. 71.11 ± ± 7.37 mm Hg, p = 0.021) and from 24 h ABPM (67.02 ± ± 5.97 mm Hg v. 70.25 ± 5.84 mm Hg, p = 0.08). OFF/HT had significantly longer isovolumetric relaxation time (96.09 ± 16.12 ms v. 86.7 ± 12.9 ms, p = 0.003). Tendency to lower E/A ratio was observed (1.82 ± 0.45 m/s v. 1.61 ± 0.41 m/s, p = 0.014). There were no differences among the groups in peripheral and central pulse pressure, but peripheral and central augmentation indexes were significantly higher in OFF/HT (57.06 ± 15.95 v. 46.6 ± 17.47, p = 0.002 and 103.05 ± 14.92 v. 111.99 ± ± 17.18, p = 0.009 respectively). The tendency to higher pulse wave velocities was observed (6.6 ± 0.98 v. 6.05 ± ± 1.02 m/s, p = 0.007, after adjustments p = 0.058).
Conclusions Normotensive adult offspring of hypertensive parents have higher diastolic blood pressure from conventional measurements as well as from ABPM, longer IVRT and higher peripheral and central augmentation indexes than normotensive adult offspring of normotensive parents. These abnormalities may indicate the potential role of hereditary factors in the development of diastolic dysfunction and large artery dysfunction in hypertension.