BackgroundThe mechanisms underlying the possible contribution of chronic inflammation to the development of hypertension remain unclear. We examined the longitudinal association of inflammation with the progression of vascular and/or renal abnormalities in the development of hypertension.Methods and ResultsIn 3274 middle‐aged Japanese men without hypertension at the study baseline, brachial‐ankle pulse wave velocity, blood pressure, estimated glomerular filtration rate, and serum CRP (C reactive protein) levels were measured annually during a 9‐year period. During this study period, 474 participants (14.5%) developed hypertension. Analysis of the repeated‐measures data revealed that sustained elevation of serum CRP levels was associated with a longitudinal increase of the brachial‐ankle pulse wave velocity. A linear mixed model analysis revealed that higher log‐transformed serum CRP values (log CRP) at each measurement were associated with a higher annual increase of the brachial‐ankle pulse wave velocity (estimate=32.553±11.635 cm/s per log CRP, P=0.018), and that higher values of the brachial‐ankle pulse wave velocity at each measurement were associated with a higher annual elevation of blood pressure (estimate=0.025±0.002 mm Hg per log CRP, P<0.001).ConclusionsIn middle‐aged Japanese men without hypertension at study baseline, long‐term active inflammation appears to be associated with a longitudinal increase of arterial stiffness. In turn, this longitudinal increase of arterial stiffness appears to be associated with longitudinal elevation of blood pressure to the hypertensive range. Thus, systemic inflammation may play a role in the pathogenesis of hypertension by the progression of arterial stiffness.

In patients with cardiovascular diseases or cardiovascular risk factors, the new simple markers and the commonly used markers are not interchangeable for assessing vascular damage and/or cardiovascular risk. Further study is proposed to examine whether AVI is higher in subjects with cardiovascular disease than in those without a history of cardiovascular disease. Similar to the case for the commonly used markers, age and the blood pressure significantly influenced both the new markers; therefore, age and the blood pressure need to be taken into account while interpreting the changes in these new simple markers.

BackgroundWe conducted analyses of repeated‐measures data to examine whether pressure wave reflection acts additively or synergistically with arterial stiffness in the pathogenesis of hypertension.Methods and ResultsIn 3172 middle‐aged (42±9 years) healthy Japanese men without hypertension at the study baseline, systolic and diastolic blood pressures, brachial–ankle pulse wave velocity, and radial augmentation index were measured annually during a 9‐year study period. Of these, 474 participants (15%) developed hypertension by the end of the study period. Binary logistic regression analysis demonstrated significant individual odds ratios for both baseline brachial–ankle pulse wave velocity and radial augmentation index for the development of hypertension. The rate of onset of hypertension during the study period was highest in the participant group with high values for both brachial–ankle pulse wave velocity and radial augmentation index at study baseline (262 of 965 participants: 27%). The generalized estimating equation analysis revealed that both radial augmentation index (estimate=0.06, SE=0.03, P=0.05) and brachial–ankle pulse wave velocity (estimate=0.07×10−1, SE=0.02×10−1, P<0.01) showed significant longitudinal association with new onset of hypertension, with no significant interaction.ConclusionsIn Japanese men, abnormal wave reflection and increased arterial stiffness may be additively associated with the risk of new onset of hypertension. Abnormal wave reflection and elevated central blood pressure may be longitudinally associated with increase in arterial stiffness, and this longitudinal association may be a mechanism underlying the additive effect of these 2 variables on the risk of new onset of hypertension.

Liver dysfunction is one of the most recognized complications in patients with acute heart failure (HF) and therefore a liver function score may be useful for risk-stratification in those patients. Recently, the albuminbilirubin (ALBI) score was developed as a new model to assess liver function in liver disease. We explored the association between the ALBI score at admission and in-hospital mortality in patients with acute HF.We enrolled 262 patients (median age, 86 years, 137 males) who were admitted to our hospital for treatment of acute HF. The following data were recorded: vital signs, laboratory data including B-type natriuretic peptide (BNP) level, echocardiographic data at admission, demographic and clinical characteristics, and treatment and prognostic information. The Get With the Guidelines-Heart Failure (GWTG-HF) risk score was calculated as an established risk model for each patient. The primary outcome was all-cause in-hospital mortality.During hospitalization, 37 patients (14.1%) died. The in-hospital mortality rate was significantly higher in patients with ALBI scores > 2.25 compared with patients with ALBI scores ! 2.25 (21.1% versus 4.5%, respectively; P = 0.0001). Multivariate analysis revealed that the GWTG-HF score (odds ratio [OR] 1.16, 95% confidence interval [CI] 1.08-1.25, P < 0.0001), BNP level (OR 1.0007, 95% CI 1.0003-1.001, P = 0.0003) and ALBI score (OR 6.0, 95% CI 1.8-19.6, P = 0.0017) were independently associated with in-hospital mortality.Our results indicated that the ALBI score was independently associated with in-hospital mortality in patients hospitalized for acute HF.

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The causes of frequent abnormal phenotypes and low success rate in mammalian cloning are poorly understood. Although epigenetic aberration is suspected to be a cause, its connection to the phenotypes has yet to be investigated. To measure the level of reprogramming of an epigenetic mark, acetylation at lysine 9 of histone H3 (H3K9Ac), in cloned mice, we examined its conservation between two cloned mice derived from distinct cell nuclei and their natural donors by utilizing whole-genome tiling arrays and quantitative PCR. Pairwise comparison of the H3K9Ac enrichment profile between the four mice revealed that H3K9Ac is less conserved in intergenic regions than in promoter regions of protein-coding genes. Intriguingly, the variation of H3K9Ac enrichment in intergenic regions is the most prominent in comparison of the two clones, possibly reflecting an additive effect of aberrant reprogramming of this epigenetic information occurring specifically in each of the two clones.

Objectives: The present prospective observational study was conducted to examine the age-related annual changes of the ankle-brachial pressure index (ABI) and their association with the longitudinal changes of the brachial-ankle pulse wave velocity (baPWV), a marker of arterial stiffness, and the radial augmentation index (rAI), a marker of the pressure wave reflection in middle-aged Japanese men. Methods and Results: In 4264 men (42 ± 9 years old) of a Japanese construction company, the ABI, baPWV and rAI were measured annually over a 9-year observation period. During the study period, ABI (from 1.10 ± 0.07 to 1.13 ± 0.07), baPWV (from 1295 ± 194 to 1344 ± 217 cm/sec) and rAI (from 69 ± 13 to 72 ± 13 %) were increased significantly (p<0.01). Mixed model linear regression analysis of the repeated-measures data revealed that the annual increase of the ABI was lower in men aged over 50 years of age (n = 1237: 0.28 ± 0.06) than in those aged under 50 years of age (n = 3027: 0.50 ± 0.04) (p < 0.01). Furthermore, while increased baPWV (estimate = 0.017, p < 0.05) and increased rAI (estimate 0.254, p < 0.05) were significantly related to the annual increase of the ABI in men aged <50 years (p < 0.01), no such association was observed in men aged > 50 years. Conclusion: In middle-aged Japanese men, the ABI increases with age until the age of 50 years, and increased arterial stiffness and increased pressure wave reflection may contribute to this annual increase. In men aged > 50 years, the annual increase of the ABI was attenuated, which could be related, at least in part, to the attenuation of the increase of the pressure wave reflection and also attenuation of the effect of increased arterial stiffness on the hydrostatic pressure in the arteries with age. These findings may suggest the usefulness of ABI measurement as a screening tool for peripheral arterial disease in men over 50 years old.