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Background: Two-dimensional speckle tracking echocardiography (2D-STE) is a novel technology that directly measures regional left ventricular (LV) wall contraction. This study aimed to directly measure inner-layer thickening (radial strain) of the LV using 2D-STE, and to examine the relationship between radial strain and the degree of hypertrophy., Methods: The study enrolled 63 untreated hypertensive patients with normal geometry (N group, n=32) or concentric hypertrophy (CH group, n=31), classified according to LV mass index (LVMI) and relative wall thickness (RWT). Thirty normotensive subjects (C group, n=30) served as controls. Radial strain (ɛ) in the inner half (ɛi) and all layers of the LV wall (ɛa) were calculated from the LV short-axis view by 2D-STE., Results: LV ejection fraction did not differ significantly among the groups. However, ɛi and ɛa were significantly lower in the CH group compared with the C and N groups (p<0.01). A ratio of ɛi to ɛa was significantly lower in the CH group compared with the C and N groups (p<0.01). A multivariate regression model that included midwall fractional shortening, E/e', LVMI, RWT, and LV ejection fraction showed that LVMI (p=0.002) and RWT (p=0.014) were independent predictors (R(2)=0.59) of ɛi., Conclusion: Radial strain in the inner half layer of the LV wall decreases in parallel with the degrees of LV concentricity and hypertrophy in hypertensive patients. Radial strain in the inner half layer may identify subtle systolic dysfunction even in hypertensive patients with preserved LV chamber function., (Copyright © 2011 Japanese College of Cardiology. Published by Elsevier Ltd. All rights reserved.)

Background: The aim of this study was to investigate the differences in left ventricular (LV) twisting behavior between patients with hypertrophic cardiomyopathy (HCM) and hypertensive heart disease (HHD)., Methods: Forty-four patients with HCM (mean age, 63±15 years), 35 patients with HHD (mean age, 63±13 years) and 20 age and sex-matched control subjects were evaluated. After a standard echocardiographic examination, LV twist and twisting velocity profiles from apical and basal short-axis images were analyzed using two-dimensional speckle tracking imaging., Results: LV diastolic and systolic dimensions, and ejection fraction were not significantly different among the groups. LV mass index and early diastolic mitral annular velocity were not significantly different between the HCM and HHD groups. The peak torsion in the HCM and HHD groups was significantly greater than that in the control group. The peak untwisting velocity in the HCM group was comparable with that in the control group. However, when the peak untwisting velocity was corrected by peak torsion, this ratio was significantly decreased in the HCM group compared with the values in the HHD and control groups. The time to peak untwisting velocity in the HCM group was significantly longer than the values in the HHD and control groups., Conclusions: These results suggest that enhanced peak torsion in HCM may improve untwisting behavior, but this mechanism fails to fully compensate for impaired untwisting behavior compared with HHD., (Copyright © 2010 Elsevier Ireland Ltd. All rights reserved.)

Background: The present study examined the inhibitory action of temporary treatment with an angiotensin type 1 (AT(1)) receptor blocker (ARB) on vascular remodeling using hypertensive mice with overexpression of the human renin (hRN) and angiotensinogen (hANG) genes., Methods: hRN/hANG transgenic mice (hRN/hANG-Tg) were treated with an ARB, valsartan, from 4 weeks of age. In some mice, valsartan treatment was stopped at 8 weeks of age (temporary treatment). Inflammatory vascular injury was induced by polyethylene-cuff placement around the femoral artery at the age of 10 weeks., Results: Compared with wild-type (WT) mice, hRN/hANG-Tg showed higher blood pressure (BP) and enhancement of oxidative stress and medial thickening even before cuff placement. Inflammatory vascular remodeling and oxidative stress after cuff placement were further enhanced in hRN/hANG-Tg. Temporary treatment with valsartan continuously lowered BP even after cessation of administration, and inhibited these changes. In contrast, administration of hydralazine lowered BP to a similar level to that with valsartan, but did not inhibit medial thickening and inflammatory vascular remodeling. In contrast to the valsartan treatment, BP immediately increased to the untreated level after cessation of hydralazine., Conclusions: These results indicate that temporary ARB treatment leads to prolonged effect of BP lowering and prevents vascular remodeling in hypertensive mice induced by activation of the human renin-angiotensin system. The inhibitory action of valsartan is not due to the BP lowering but is at least in part due to a decrease in oxidative stress and inflammation.

Hypertension has long been recognized as a major risk factor of several cardiovascular diseases. It is well known that the renin-angiotensin system(RAS) is involved in the pathogenesis of both hypertension and hypertensive end-organ damage. Untreated hypertension is self-accelerating condition through RAS stimulation. Activation of RAS contributes to the transition from borderline hypertension to established hypertension. Recently, "the Seventh Report of Joint National Committee on Prevention, Detection, Evaluation and Treatment of High Blood Pressure (JNC 7)" proposed a new classification of borderline blood pressure levels, as "prehypertension". The therapeutic focus has begun to shift from the therapy of established hypertension to the prevention of hypertension. This review addressed the relationship between hypertension, prehypertension and the role of RAS.

Background: It was recently suggested that insulin resistance is significantly correlated with activation of the cardiac sympathetic nervous system in patients with essential hypertension., Objectives: To examine the effects of troglitazone, an agent used to treat insulin resistance, on cardiac sympathetic nervous dysfunction and insulin resistance in patients with essential hypertension., Methods: The study participants included 34 patients (14 men, 20 women) with mild essential hypertension and 17 normal controls (group C, seven men). The patients were randomly divided into two groups, one treated with 400 mg troglitazone and antihypertensive drugs (group T, n = 17) and the other treated with antihypertensive drugs only (group N, n = 17). We evaluated insulin resistance and cardiac sympathetic nervous function before and after 6 months of treatment. Insulin resistance was evaluated using steady-state plasma glucose (SSPG; mg/dl) concentrations and cardiac sympathetic nervous function was evaluated using the heart-to-mediastinum ratio (H : M) and mean washout rate measured by 123I-meta-iodobenzylguanidine (MIBG) cardiac imaging., Results: There were significant differences in SSPG (P < 0.01), early (P < 0.05) and delayed (P < 0.05) phases of H : M and washout rate (P < 0.05) between the hypertensive patients and group C. The SSPG concentration was significantly improved after treatment only in group T, from 153.3 to 123.7 mg/dl (P < 0.01). The early and delayed phases of H : M and washout rate also were significantly improved (P < 0.05) (from 2.59 to 2.63, from 2.12 to 2.27 and from 18.1 to 13.7%, respectively) in only group T.The change in SSPG was significantly correlated with the changes in H : M and washout rate (r = -0.639 and 0.577, respectively)., Conclusion: Troglitazone had a beneficial effect on cardiac sympathetic nervous function through a decrease in insulin resistance in patients with essential hypertension.

BackgroundThe present study examined the inhibitory action of temporary treatment with an angiotensin type 1 (AT1) receptor blocker (ARB) on vascular remodeling using hypertensive mice with overexpression of the human renin (hRN) and angiotensinogen (hANG) genes.MethodshRN/hANG transgenic mice (hRN/hANG-Tg) were treated with an ARB, valsartan, from 4 weeks of age. In some mice, valsartan treatment was stopped at 8 weeks of age (temporary treatment). Inflammatory vascular injury was induced by polyethylene-cuff placement around the femoral artery at the age of 10 weeks.ResultsCompared with wild-type (WT) mice, hRN/hANG-Tg showed higher blood pressure (BP) and enhancement of oxidative stress and medial thickening even before cuff placement. Inflammatory vascular remodeling and oxidative stress after cuff placement were further enhanced in hRN/hANG-Tg. Temporary treatment with valsartan continuously lowered BP even after cessation of administration, and inhibited these changes. In contrast, administration of hydralazine lowered BP to a similar level to that with valsartan, but did not inhibit medial thickening and inflammatory vascular remodeling. In contrast to the valsartan treatment, BP immediately increased to the untreated level after cessation of hydralazine.ConclusionsThese results indicate that temporary ARB treatment leads to prolonged effect of BP lowering and prevents vascular remodeling in hypertensive mice induced by activation of the human renin-angiotensin system. The inhibitory action of valsartan is not due to the BP lowering but is at least in part due to a decrease in oxidative stress and inflammation.American Journal of Hypertension (2011). doi:10.1038/ajh.2011.6 [ABSTRACT FROM AUTHOR]

BackgroundTo explore the metabolic actions of nifedipine on diabetes, we examined glucose intolerance and white adipose tissue changes in type 2 diabetic KK-Ay mice.MethodsMale KK-Ay mice were treated with nifedipine (1.5 mg/kg/day in lab chow) for 5 weeks, which did not affect blood pressure or feeding of KK-Ay mice.ResultsAfter treatment with nifedipine, body weight tended to decrease and the weight of white adipose tissue was reduced. Without food restriction, nifedipine decreased plasma insulin level, while plasma glucose level tended to decrease. In oral glucose tolerance test, nifedipine suppressed the increase in glucose level after a glucose load without affecting plasma insulin concentration. Nifedipine also improved the result of insulin tolerance test. In white adipose tissue, nifedipine increased adipocyte number and the expression of peroxisome proliferator-activated receptor-γ (PPARγ) and adipocyte fatty acid-binding protein related to adipocyte differentiation. In addition, expression of adiponectin, insulin receptor, insulin receptor substrate-1, and glucose transporter type-4 was also increased by nifedipine. Nifedipine also increased the expression of NO synthase in white adipose tissue. Nifedipine did not affect expression of angiotensin II type 1 (AT1) and type 2 (AT2) receptors in white adipose tissue. Such changes in white adipose tissue were apparent in retroperitoneal adipose tissue. Nifedipine did not change the expression of angiotensin receptors, renin receptor, and angiotensinogen in white adipose tissue. Moreover, nifedipine attenuated nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activity and increased superoxide dismutase (SOD) activity in white adipose tissue.ConclusionThese results suggest that nifedipine can enhance insulin sensitivity and reduce white adipose tissue, possibly related to stimulation of adipocyte differentiation.American Journal of Hypertension (2011). doi:10.1038/ajh.2010.198 [ABSTRACT FROM AUTHOR]

BackgroundA combination of different types of antihypertensive drugs is widely used for the treatment of hypertension. We examined the inhibitory effects of a combination of an AT1 receptor blocker (ARB), olmesartan, with various calcium channel blockers (CCBs) on inflammatory vascular remodeling.MethodsInflammatory vascular remodeling was induced by polyethylene-cuff placement around the femoral artery of C57BL/6J mice at 10 weeks of age. Olmesartan (0.5 mg/kg/day) was administered intraperitoneally using an osmotic minipump. CCBs (nifedipine 1.0 mg/kg/day, amlodipine 0.1 mg/kg/day, azelnidipine 0.1 mg/kg/day), and hydrochlorothiazide (HCTZ 0.5 mg/kg/day) were administered orally.ResultsIn the injured artery, superoxide anion production and expression of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase subunits p47phox and Rac-1 were markedly increased, together with expression of monocyte chemotactic protein-1 (MCP-1) and tumor necrosis factor (TNF)-α. Administration of a single drug alone at each concentration did not significantly inhibit these changes in the injured artery. However, a combination of olmesartan with various CCBs inhibited neointimal formation as well as oxidative stress and inflammatory markers in the injured artery. Moreover, among these CCBs, inhibition of these markers by olmesartan with azelnidipine was stronger than that caused by a combination with other CCBs. On the other hand, a combination of subeffective doses of olmesartan and HCTZ did not significantly affect vascular changes after cuff placement.ConclusionsThese results suggest that the combination of ARB with CCB synergistically inhibits vascular remodeling and that the inhibitory actions of ARB on vascular remodeling may vary depending on the combined CCB.American Journal of Hypertension (2009). doi:10.1038/ajh.2008.344American Journal of Hypertension (2009); 22, 2, 145–150. doi:10.1038/ajh.2008.344 [ABSTRACT FROM AUTHOR]