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Although aortic-to-brachial pulse pressure amplification (PPamp) may offer prognostic information beyond brachial blood pressure (BP), this approach is limited in resource-limited settings. We aimed to derive an equation to impute central aortic PP (PPc) from simple clinical measures and assess whether imputed PPamp adds to the ability of brachial BP to predict mortality. METHODS An imputation equation for PPc, incorporating brachial PP, age, mean arterial pressure, and pulse rate, was identified from multivariate modeling of the factors associated with radial applanation tonometry-derived (measured) PPc in 1,179 community participants and validated in a clinical sample of 351 patients. We applied the equation to ambulatory awake BP and pulse rate values in a separate group of 4,796 patients referred for ambulatory monitoring and evaluated the impact on all-cause mortality. RESULTS Imputed PPc values closely approximated measured PPc (r2 = 0.96, mean difference ± (2 × SD) = 1.4 ± 6.2 mm Hg). In adjusted Cox proportional models including adjustments for awake brachial PP during 47,111 person-years of follow-up, where 648 patients died, hazards ratio for all-cause mortality per SD of awake PPamp was 0.79 (95% confidence interval (CI): 0.68-0.93, P < 0.005). The hazards ratio for brachial PP with (1.49, CI = 1.36-1.64, P < 0.0001) or without (1.46, CI = 1.35-1.59, P < 0.0001) PPamp in the model was similar. Awake PPamp also predicted survival independent of awake brachial systolic BP (P < 0.0001). CONCLUSIONS PPc imputed from simple clinical assessments closely approximates measured PPc. PPamp derived from imputed PPc adds to the ability of brachial BP to predict survival. In resource-limited settings, an imputation equation may be employed to approximate aortic BP and enhance risk prediction. [ABSTRACT FROM AUTHOR]

BackgroundExogenous hyperisulinemia causes pregnancy, induced hypertension and intrauterine growth restriction (IUGR) in pregnant rats. Hyperinsulinemia may increase production of endothelin-1 (ET-1), produced by sequential proteolysis of the big endothelin by the endothelin-converting enzyme (ECE)-1, the expression of which is examined here in the placenta, kidney, heart, and liver.MethodsRats were rendered hyperinsulinemic by subcutaneous insulin pellet, mated and followed to the twenty-first day of pregnancy. They were then killed, and their fetuses and placentas were examined.ResultsHyperinsulinemic dams (HD) had higher blood pressure (BP) (130 ± 17 mm Hg in HD vs. 115 ± 16 mm Hg in normal pregnant dams (NPD), P < 0.05), lower placenta weight (0.44 ± 0.08 g in HD vs. 0.47 ± 0.08 NPD, P < 0.05) and lower fetus weight: males 4.9 ± 0.4 g in HD vs. 5.5 ± 0.4 g in NPD, P < 0.0001; females 4.7 ± 0.4 g in HD vs. 5.2 ± 0.4 g in NPD (P < 0.0001). ECE-1 expression as determined by western blot was significantly increased in the placenta and its implantation site, i.e., the mesometrial triangle (MT) of HD by 46 and 48%, respectively. In the kidney and heart of HD ECE-1, protein expression was increased by 230 and 220%, respectively, but its level in the liver was similar in both groups. Immunohistochemical staining revealed ECE-1 expression in endothelial cells and trophoblastic cells of the placenta and MT. Endothelin receptor A (ET-A), a mediator of vasoconstriction by ET-1, was also expressed in the endothelium and in trophoblasts of the placenta and MT. The expression of both ECE-1 and ET-A, as measured by automated image analysis, was generally stronger in placentas of HD.ConclusionsECE-1 and ET-A are expressed in the trophoblastic cells of the placenta and MT. This may affect local endothelin levels, BP and IUGR.American Journal of Hypertension (2012). doi:10.1038/ajh.2011.164 [ABSTRACT FROM AUTHOR]

BackgroundMorning blood pressure surge (MS) is accepted to increase cardiovascular risk, but it is not clear how it should be defined. Because dipping on 24-h ambulatory blood pressure monitoring (ABPM) associates with improved outcome we hypothesized that MS will not predict mortality independent of dipping.MethodsWe investigated a cohort of 2,627 patients referred for ABPM with available values for at least 1-h after awakening, and related them to all-cause mortality.ResultsDuring 22,353 person-years of follow-up, 246 patients died. We used Cox proportional hazards models to explore mortality associated with different definitions of the MS. Only the '1-h' MS (difference between average blood pressure (BP) 1-h before and after awakening) was related to mortality: after multiple adjustments including 24-h systolic BP, those whose '1-h' MS was above median (>12 mm Hg) had mortality hazard ratio (HR) of 0.61, 95% CI: 0.47-0.79, P < 0.001. In predetermined subgroup analyses, nondippers (n = 1,039), had a highly significant MS-related decrease in mortality: HR 0.49, 95% CI: 0.34-0.73, P < 0.001, unlike dippers (n = 1,588), HR = 0.90, 95% CI: 0.60-1.34.ConclusionAmong nondipping subjects referred for ABPM, the MS is associated with decreased mortality.American Journal of Hypertension (2011). doi:10.1038/ajh.2011.58 [ABSTRACT FROM AUTHOR]