De-stiffening drug therapy and blood pressure control

In hypertensive subjects, cardiovascular risk reduction is critically related to the decrease of systolic blood pressure (SBP). De-stiffening therapy means that, in a controlled therapeutic trial of long duration, a selective reduction of SBP has been obtained in the studied group by comparison with the control group, and that this SBP reduction is due to a decrease of either arterial stiffness, or wave reflections, or both. Central SBP reduction and cardiovascular remodeling are specifically involved. Most protocols require the presence of an angiotensin II blocker, potentially associated with a diuretic compound and/or a calcium-channel blocker. Cardiovascular outcomes are significantly reduced by comparison with the control group, particularly when this latter group involves administration of a beta-blocking agent

Should diastolic and systolic blood pressure be considered for cardiovascular risk evaluation: a study in middle-aged men and women

AbstractOBJECTIVESThe goal of this study was to evaluate the role of diastolic blood pressure (DBP) in cardiovascular mortality for different systolic blood pressure (SBP) levels in middle-aged men and women.BACKGROUNDIn middle-aged subjects it is unclear whether DBP, in addition to SBP, should be considered for risk evaluation.METHODSSubjects (77,023 men; 48,480 women) aged 40 to 70 years old, had no major cardiovascular disease, no antihypertensive treatment and were examined at the Centre d’Investigations Préventives et Cliniques between 1972 and 1988. Mortality was assessed for an 8- to 12-year period.RESULTSIn both genders, cardiovascular mortality increased with the SBP level. In men and women with normal SBP levels, DBP did not influence cardiovascular mortality after adjustment for age and SBP. In men with systolic hypertension, a U-shaped curve relationship between cardiovascular mortality and DBP was observed, with the lowest mortality rates in the group with DBP 90 to 99 mm Hg. Compared with this group, age- and SBP-adjusted cardiovascular mortality was higher by 73% (p < 0.02) in the group with DBP <90 mm Hg and by 65% (p < 0.001) in the group with DBP ≥110 mm Hg. In women with systolic hypertension, however, DBP was positively correlated with cardiovascular mortality.CONCLUSIONSIn middle-aged subjects, classification of cardiovascular risk according to DBP levels should take into account gender, especially when SBP levels are elevated. Men with systolic hypertension are at higher risk when their DBP is “normal” than when they present a mild to moderate increase in DBP. In women of the same age, however, systolic-diastolic hypertension represents a higher risk than isolated systolic hypertension

Sex Difference in Cardiovascular Risk Role of Pulse Pressure Amplification

ObjectivesThe study was to explore whether the brachial/carotid pulse pressure (B/C-PP) ratio selectively predicts the sex difference in age-related cardiovascular (CV) death.BackgroundHypertension and CV complications are more severe in men and post-menopausal women than in pre-menopausal women. C-PP is lower than B-PP, and the B/C-PP ratio is a physiological marker of PP amplification between B and C arteries that tends toward 1.0 with age.MethodsThe study involved 72,437 men (ages 41.0 ± 11.1 years) and 52,714 women (39.5 ± 11.6 years). C-PP was calculated for each sex by a multiple regression analysis including B-PP, age, height and risk factors, and a method validated beforehand in a subgroup of 834 subjects. During the 12 years of follow-up, 3,028 men and 969 women died.ResultsIn the total population, the adjusted hazard ratios (HR) (95% confidence interval [CI]) of B/C-PP ratio were: 1) for all-cause mortality: men, HR: 1.51 (95% CI: 1.47 to 1.56), women; HR: 2.46 (95% CI: 2.27 to 2.67) (p < 0.0001); and 2) for CV mortality: men, HR 1.81 (95% CI: 1.70 to 1.93); women, HR: 4.46 (95% CI: 3.66 to 5.45) (p < 0.0001). The B/C-PP impact on mortality did not significantly increase from younger men to those ≥55 years of age, from: HR: 1.44 (95% CI: 1.31 to 1.58) to HR 1.65 (95% CI: 1.48 to 1.84), but increased significantly with age in women: HR: 3.19 (95% CI: 2.08 to 4.89) versus HR: 5.60 (95% CI: 4.17 to 7.50) (p < 0.01). Thus, the mortality impact of B/C-PP ratio was 3-fold higher in women than in men ≥55 years old.ConclusionsPP amplification is highly predictive of differences in CV risk between men and women. In post-menopausal women, the attenuation of PP amplification, mainly related to increased aortic stiffness, contributes to the significant increase in CV risk

Cardiac and arterial interactions in end-stage renal disease

Cardiac and arterial interactions in end-stage renal disease. Although cardiac hypertrophy is a frequent complication of end-stage renal disease (ESRD), relatively little is known about large arterial geometry and function in vivo in these patients, and the relationship between arterial changes and cardiac hypertrophy is unknown. Common carotid artery (CCA) intima-media thickness and internal diameter and left ventricular geometry and function were determined by ultrasound imaging in 70 uncomplicated ESRD patients and in 50 age-, sex-, and blood pressure-matched controls. Arterial distensibility and compliance were determined from simultaneously recorded CCA diameter and stroke changes in diameter and CCA pressure waveforms, obtained by applanation tonometry, and also by the measurement of carotid-femoral pulse wave velocity. Compared with control subjects, ESRD patients had greater left ventricular diameter (P < 0.01), wall thicknesses and mass (P < 0.001), increased CCA diameter (6.25 ± 0.87 vs. 5.55 ± 0.65 mm; P < 0.001), larger CCA intima-media thickness (777 ± 115 vs. 678 ± 105 µ m; P < 0.001) and intima-media cross-sectional area (17.5 ± 4.5 vs. 13.4 ± 3.3mm2; P < 0.001). In uremic patients, arterial hypertrophy was associated with decreased CCA distensibility (17.8 ± 8.8 vs. 24.0 ± 12.7kPa−1 · 10−3; P < 0.001) and compliance (5.15 ± 2 vs. 6.0 ± 2.5m2 · kPa−1 · 10−7; P < 0.05), accelerated carotid-femoral pulse wave velocity (1055 ± 290 vs. 957 ± 180 cm/seconds; P < 0.001), early return and increased effect of arterial wave reflections (20.5 ± 15.4 vs. 9.2 ± 18.4%; P < 0.001). The latter phenomenons were responsible for increased pulsatile pressure load in CCA (58.3 ± 21 vs. 48 ± 17mm Hg; P < 0.01) and were associated with a decreased subendocardial viability index (157 ± 31 vs. 173 ± 30%; P < 0.001). The CCA diameter was correlated with the left ventricular diameter (P < 0.01), and a significant correlations existed between CCA wall thickness or CCA intima-media cross-sectional area and left ventricular wall thicknesses and/or left ventricular mass (P < 0.01). In multivariate analysis, these relationships were independent regarding age, sex, blood pressure and body surface area. The present study documents parallel cardiac and vascular adaptation in ESRD, and demonstrates the potential contribution of structural and functional large artery alterations to the pathogenesis of left ventricular hypertrophy and functional alterations

Twenty-four-hour ambulatory blood pressure monitoring efficacy of perindopril/indapamide first-line combination in hypertensive patients: the REASON study

Background: Circadian blood pressure (BP) measurements provide more information on hypertensive complications than office BP measurements. The purpose of this study was to analyze the efficacy of the first-line combination of perindopril 2 mg plus indapamide 0.625 mg versus atenolol 50 mg on BP parameters and variability over 24 h in patients with hypertension. Methods: A double-blind, randomized, controlled, 12-month study comparing perindopril/indapamide and atenolol was performed in 201 patients (age 55.0 years) with uncomplicated sustained essential hypertension. Ambulatory BP measurements (ABPM) were done every 15 min over 24 h. Results: After 1 year of treatment, the decrease in systolic BP was significantly greater for perindopril/indapamide than for atenolol during the entire 24-h period (-13.8 ν −9.2 mm Hg), the daytime and the nighttime periods (P < .01). Diastolic blood pressure (DBP) variations were comparable for the two groups (−7.2 ν −8.3 mm Hg, NS). Pulse pressure (PP) reduction was also significantly greater for perindopril/indapamide than for atenolol (for the whole 24 h, −6.6 ν −0.9 mm Hg, P < .001). The through to peak (T/P) BP ratio and the smoothness index were comparable in the two groups for DBP. For systolic blood pressure (SBP), higher values of the T/P ratio (0.80 ν 0.59) and the smoothness index (1.45 ν 0.98; P < .02) were achieved for the perindopril/indapamide combination than for atenolol. Conclusions: The perindopril/indapamide first-line combination decreased SBP and PP more effectively than atenolol. Moreover, the BP control effect was smooth and consistent throughout the 24-h dosing interval and BP reduction variability was lower than the one induced by atenolo

Regression of left ventricular mass in hypertensive patients treated with perindopril/indapamide as a first-line combination: The REASON echocardiography study

Background: Increase in left ventricular mass (LVM) may be linked to morbidity and mortality in hypertensive patients. Arterial stiffness, systolic blood pressure (BP), and pulse pressure (PP) seem to be the main determinants of LVM. The perindopril/indapamide combination normalizes systolic BP, PP, and arterial function to a greater extent than atenolol. The aim of this study was to compare the effects of perindopril (2 mg)/indapamide (0.625 mg) first-line combination with atenolol (50 mg) on LVM reduction in hypertensive patients. Methods: Two hundred fourteen patients with essential hypertension participating in the PREterax in Regression of Arterial Stiffness in a ContrOlled Double-BliNd (REASON), randomized, double-blind, parallel-group study, underwent M-mode two-dimensional-guided echocardiography. Results: Perindopril/indapamide and atenolol were both effective at brachial BP reduction during the 12-month period. The systolic BP reduction was significantly greater with perindopril/indapamide than with atenolol (−21.2 v −15.3 mm Hg), whereas the reduction in diastolic BP was similar between treatment groups (−12.1 v −11.3 mm Hg). Reduction in LVM was higher with perindopril/indapamide than with atenolol. The between-group difference was significant for LVM (−13.6 v −4.3 g, P = .027), LVM/body surface area (LVMI1, P = .032), and LVM/body height2.7 (LVMI2, P = .013). The 124 patients with LV hypertrophy at baseline showed greatest LVM regression (LVM: −22.5 v −8.9 g, P = .009; LVMI1, P = .031; LVMI2, P = .028). The reduction in LVM adjusted for brachial systolic BP and heart rate was still significantly greater with perindopril/indapamide than with atenolol. Conclusions: Treatment, based on a first-line perindopril/indapamide combination in hypertensive patients, was more effective than atenolol on regression of echocardiographic indices of LVM and LV hypertroph

Topological Defects in the Random-Field XY Model and the Pinned Vortex Lattice to Vortex Glass Transition in Type-II Superconductors

As a simplified model of randomly pinned vortex lattices or charge-density waves, we study the random-field XY model on square ($d=2$) and simple cubic ($d=3$) lattices. We verify in Monte Carlo simulations, that the average spacing between topological defects (vortices) diverges more strongly than the Imry-Ma pinning length as the random field strength, $H$, is reduced. We suggest that for $d=3$ the simulation data are consistent with a topological phase transition at a nonzero critical field, $H_c$, to a pinned phase that is defect-free at large length-scales. We also discuss the connection between the possible existence of this phase transition in the random-field XY model and the magnetic field driven transition from pinned vortex lattice to vortex glass in weakly disordered type-II superconductors.Comment: LATEX file; 5 Postscript figures are available from [email protected]

Hyper tension, Systolic Blood Pressure, and Large Ar teries Hypertension Pulse pressure Larges arteries Arterial stiffness Wave reflections

The authors of epidemiologic studies have long emphasized the close relationship between high systolic blood pressure (SBP) or diastolic blood pressure (DBP) and the incidence of cardiovascular (CV) disease. 1-3 The hemodynamic characteristics of the disease were attributed to a reduction of the caliber and/or number of small arteries, causing elevated peripheral vascular resistance and secondary adaptive changes of the structure and function of arterioles and the heart. Later, prospective studies on Framingham Heart Study populations 4 redirected attention to SBP as a better guide than DBP to evaluate CV and all-cause mortality. In 1988 and later, A major function of the large arteries is to change the pulsatile pressure and flow coming from the heart into a steady pressure and flow at the periphery, to obtain optimal oxygenation of tissues. 1,2,9,10 This major modification is a consequence of This work was performed with the hel