We analyzed outcome in 4005 treated hypertensive patients (22% obesity, 8% diabetes and 21% current smoking habit) with target attended office SBP less than 140 mmHg, in relation to quintiles of DBP, cardiovascular risk profile and target organ damage (LV hypertrophy, carotid plaque and left atrial dilatation).
However, the diagnostic accuracy of logistic regression models that included brachial or central hemodynamic parameters was similar for LVH [area under curve (AUC) for SBP: 0.74 versus 0.76, P = 0.16; AUC for PP: 0.75 versus 0.73, P = 0.35] and IMT (AUC for SBP: 0.61 versus 0.61, P = 0.67; AUC for PP: 0.63 versus 0.61, P = 0.29).
Regression analyses revealed associations between ECG-LVH and NT-proBNP, QTc prolongation, ischemic events, and SBP, in the African high γ-GT group exclusively.
Higher ΔSBP was significantly associated with higher incidence of LVH (P < 0.001): 12.8, 27.1, and 58.3% in the lowest, middle, and highest tertiles, respectively.
With stepwise adjusted for potential covariates including age, male gender, fasting plasma glucose, presence of current cigarette smoking, dyslipidemia, statins and SBP, increased cf-PWV remained independently associated with left ventricular hypertrophy and albuminuria, with an increased odds of 41 % and 24 % (<i>p</i> < 0.05), respectively.
In contrast, collegiate participants demonstrated a higher burden of concentric LV hypertrophy (21/87, 24% vs 7/61, 11%, P = 0.026) with concomitant reductions in diastolic tissue velocities (ΔE': -2.0 ± 2.7 cm·s, P < 0.001) and increased arterial stiffness (ΔPWV: Δ0.2 ± 0.6 m·s, P = 0.003), changes that were influenced by linemen who had the highest post-season weight (124 ± 10 kg) and systolic blood pressure ([SBP], 138.8 ± 11 mm Hg).
Variables such as age, female sex, baseline SBP, as well as delta follow-up-baseline SBP, BMI, metabolic syndrome and use of antihypertensive drugs were independently related either to new-onset or to persistent LVH.