OBJECTIVE: To examine the influence of genetic susceptibility to essential hypertension (EH) and the genetic susceptibility to premature myocardial infarction (MI) on longitudinal development of systolic blood pressure (SBP) and left ventricular mass (LVM) in youth. METHODS: Individual SBP and LVM growth curves across age were created for a sample of 745 subjects (age range: 4.9-27.5 years) and a sample of 687 subjects (age range: 8.2-27.5 years), respectively. Each sample had an approximately equal proportion of African American and European American males and females, with annual assessments over a 10-year period. Family history (FH) of EH and FH of premature MI were used as measures of genetic susceptibility to EH and to premature MI, respectively. Positive FH (FH(+)) of EH and of premature MI were defined, respectively, as verified EH in 1 or both biological parents, and verified MI in any biological parent or grandparent before 55 years of age. RESULTS: Subjects with an FH(+) of EH had higher SBP levels and stronger increases in SBP over time than subjects with a negative FH (FH(-)) of EH. Subjects with an FH(+) of EH also showed higher LVM levels than subjects with an FH(-) of EH. In addition, the effect of an FH(+) of EH on LVM was stronger in females than males. The effects of FH of EH on SBP and LVM could not be explained by differences in socioeconomic status, but the effect on LVM was no longer significant after adjustment for BMI. FH of MI had no significant effects on SBP or LVM. CONCLUSIONS: Effects of genetic susceptibility to EH on SBP and LVM trajectories were observed in childhood, whereas no such effects were found for FH of MI. Genetic markers of EH may improve the understanding of individual differences in susceptibility to develop hypertension and LV hypertrophy.
OBJECTIVE: To examine the influence of genetic susceptibility to essential hypertension (EH) and the genetic susceptibility to premature myocardial infarction (MI) on longitudinal development of systolic blood pressure (SBP) and left ventricular mass (LVM) in youth. METHODS: Individual SBP and LVM growth curves across age were created for a sample of 745 subjects (age range: 4.9-27.5 years) and a sample of 687 subjects (age range: 8.2-27.5 years), respectively. Each sample had an approximately equal proportion of African American and European American males and females, with annual assessments over a 10-year period. Family history (FH) of EH and FH of premature MI were used as measures of genetic susceptibility to EH and to premature MI, respectively. Positive FH (FH(+)) of EH and of premature MI were defined, respectively, as verified EH in 1 or both biological parents, and verified MI in any biological parent or grandparent before 55 years of age. RESULTS: Subjects with an FH(+) of EH had higher SBP levels and stronger increases in SBP over time than subjects with a negative FH (FH(-)) of EH. Subjects with an FH(+) of EH also showed higher LVM levels than subjects with an FH(-) of EH. In addition, the effect of an FH(+) of EH on LVM was stronger in females than males. The effects of FH of EH on SBP and LVM could not be explained by differences in socioeconomic status, but the effect on LVM was no longer significant after adjustment for BMI. FH of MI had no significant effects on SBP or LVM. CONCLUSIONS: Effects of genetic susceptibility to EH on SBP and LVM trajectories were observed in childhood, whereas no such effects were found for FH of MI. Genetic markers of EH may improve the understanding of individual differences in susceptibility to develop hypertension and LV hypertrophy.
Authors: Zhibin Li; Harold Snieder; Shaoyong Su; Gregory A Harshfield; Frank A Treiber; Xiaoling Wang Journal: J Hypertens Date: 2010-04 Impact factor: 4.844