Acute effects of cigarette smoking on arterial stiffness and blood pressure in male smokers with hypertension

BACKGROUND: Although the acute increase of arterial stiffness and blood pressure (BP) after cigarette smoking in healthy smokers is considered a possible mechanism of increased cardiovascular risk, the acute effect of smoking on arterial stiffness in hypertensive smokers is unknown. We investigated the acute effects of cigarette smoking on arterial stiffness and BP in hypertensive male smokers. METHODS: Heart rate (HR), brachial and ankle BP, and pulse-wave velocity (PWV) were measured in 22 hypertensive male smokers (HTs) and in 30 normotensive male smokers (NTs) before and 5, 10, and 15 min after smoking one cigarette (nicotine content, 0.9 mg). RESULTS: Smoking induced acute increases of HR, brachial BP, and heart-femoral PWV (hfPWV) in NTs and HTs (P < .05). Ankle systolic BP and femoral-ankle PWV were acutely increased in HTs (P < .05), but not in NTs. In HTs, brachial systolic BP and hfPWV at 15 min were higher than at baseline (P < .05). An acute increase of hfPWV in the HTs was significant (P = .025) after adjustment for total cholesterol, time-dependent HR, and brachial mean arterial pressure, but acute changes of other PWVs lost statistical significance. CONCLUSIONS: Cigarette smoking acutely increases aortic stiffness and BP in male smokers with hypertension, and the effects persist longer than in male smokers without hypertension.     

Significant association of C-reactive protein with arterial stiffness in treated non-diabetic hypertensive patients

C-reactive protein (CRP) has been known to be associated with vascular inflammation and hypertension. Pulse wave velocity (PWV) increases according to the degree of the arterial stiffness in hypertension patients. Therefore, PWV may be correlated with CRP levels in treated hypertensive patients, irrespective of medication. We sought to determine whether there is a correlation between hsCRP and arterial stiffness in non-diabetic treated hypertensive patients, independent of cardiovascular risk factor. This study consisted of 424 non-diabetic patients at least 45-years-old who were being treated for hypertension. At the time of enrollment, the patients underwent a baseline laboratory assessment of C-reactive protein levels and pulse wave velocity (PWV). Heart to femoral PWV (hfPWV) and brachial to ankle PWV (baPWV) were used as a marker of arterial stiffness. Subjects were categorized according to tertiles of hsCRP level [Group 1: first tertile (0.20-0.46 mg/L), Group 2: second tertile (0.47-1.15 mg/L), Group 3: third tertile (1.17-9.71 mg/L)]. Group 1 consisted of 141 patients (mean age 58+/-8 years), Group 2 had 142 patients (mean age 60+/-9 years) and Group 3 had 141 patients (mean age 61+/-8 years). The hfPWV and baPWV increased significantly along with the hsCRP level. Group 1, Group 2 and Group 3 demonstrated hfPWV and baPWV of 965+/-199 and 1438+/-246, 975+/-174 and 1487+/-258 and 1043+/-215 and 1566+/-252 cm/s, respectively (p<0.01). The hfPWV also showed a strong correlation with baPWV (r=0.698, p<0.001). The hsCRP level was independently associated with arterial stiffness (hfPWV: R(2)=0.273, p<0.001; baPWV: R(2)=0.284, p=0.001) after controlling for age, body mass index, systolic blood pressure (BP), heart rate, gender, HDL-cholesterol, triglyceride, glucose level and medications. In conclusion, hsCRP was associated with arterial stiffness, independent of age, systolic BP, gender, heart rate, glucose, lipid profiles and medications in treated hypertension. Therefore, hsCRP could be a useful marker of arterial stiffness in treated hypertension patients and a possible target for arterial inflammation in hypertension.     

Utility of automated brachial ankle pulse wave velocity measurements in hypertensive patients

BACKGROUND: We examined whether pulse wave velocity (PWV), determined by brachial ankle arterial pressure wave measurements, using a newly developed, fully automated device could be a surrogate measure for carotid femoral PWV. METHODS & RESULTS: This device (AT-form PWV/ABI, Nippon Colin, Komaki, Japan) can simultaneously monitor bilateral brachial and ankle pressure wave forms using the volume plethysmographic method, with two optional tonometry sensors for carotid and femoral arterial wave measurements. We examined the right brachial-right ankle PWV and left carotid-left femoral PWV in 89 normotensive and untreated hypertensive patients. The brachial ankle PWV correlated well with carotid femoral PWV (r = 0.755, P <.00001). The Bland-Altman plots of the two variables, however, showed a significant difference exists between the two techniques over the range of measurement. The within-observer and between-observer coefficients of variation of the brachial ankle PWV were 6.5% +/- 4.1% and 3.6% +/- 3.9%, respectively. To determine the factors affecting brachial ankle PWV, we studied treated and untreated hypertensive patients with World Health Organization stage I (n = 146), stage II (n = 74), or stage III (n = 54). In multiple regression analysis, age, brachial ankle PWV, and the presence of diabetes were significant predictors of the severity of hypertensive organ damage. Age, systolic blood pressure, and the stage of hypertensive organ damage were major determinants of brachial ankle PWV. CONCLUSIONS: Although the brachial ankle PWV does not agree with the carotid femoral PWV, this parameter may yet become a new, useful measure for arterial stiffness. Further longitudinal studies are necessary to confirm the clinical significance of the brachial ankle PWV.     

Arterial stiffness and central hemodynamics in treated hypertensive subjects according to brachial blood pressure classification

BACKGROUND: International recommendations have classified brachial blood pressure (BP) in subgroups enabling better cardiovascular risk stratification. Central BP is an independent predictor of cardiovascular risk, differing from brachial BP through the predominant influence of arterial stiffness and wave reflections. Central BP has never been studied in relation to international guidelines for brachial BP classification. METHODS: In 580 chronically treated hypertensive subjects we measured: carotid-femoral pulse wave velocity (PWV), carotid artery augmentation index (AI) and carotid blood pressures, using applanation tonometry and pulse wave analysis, and using brachial BP for carotid pressure wave calibration. RESULTS: For each given brachial value, carotid systolic blood pressure (SBP) and PP were significantly lower than the corresponding brachial SBP and PP. This pressure amplification was significantly lower in the 'optimal' and 'normal' BP ranges (6.8-7.4 mmHg) than in the higher BP ranges (10.1-11.3 mmHg), mainly depending on heart rate (HR) and PWV levels. PWV gradually increased as a function of brachial BP classification and was a significant predictor of this classification independently of age, drug treatment, atherosclerotic lesions and even mean BP. Finally, PWV was a highly sensitive marker of the effective BP control throughout all decades of age. CONCLUSION: Under chronic antihypertensive therapy, central BP does not strictly parallel the corresponding brachial BP classification, depending on differences in aortic stiffness and HR. Whether aortic PWV might predict the brachial BP classification and/or the presence of effective BP control, as suggested in this study, needs further confirmation.     

Long-term effects of statins on arterial pressure and stiffness of hypertensives

Although lowering blood pressure (BP) reduces aortic stiffness, achieving the recommended BP goal can be difficult. Recent studies have shown that short-term use of statins can reduce BP significantly. To determine the long-term effects of statins on BP and aortic stiffness, a single-blind randomized prospective study was performed on 85 hyperlipidaemic hypertensive patients whose BP was insufficiently controlled by antihypertensive therapy. Every 3 months, aortic stiffness was assessed by measuring pulse wave velocity (PWV). Patients were randomly allocated to groups treated with pravastatin, simvastatin, fluvastatin, or a nonstatin antihyperlipidaemic drug. No significant differences in patient characteristics, kinds of antihypertensive drugs, BP, ankle brachial index, PWV, or serum lipid, creatinine, or C-reactive protein levels were found between the four groups at the start of the study. During the 12-month treatment period, PWV did not change in the pravastatin group or nonstatin group, but it was transiently reduced in the simvastatin group and significantly decreased in the fluvastatin group, even though the doses of the statins used in this study were lower than the usually prescribed dose. All four antihyperlipidaemic drugs significantly decreased serum cholesterol levels without affecting BP, ankle brachial index, or serum triglyceride levels. The C-reactive protein serum levels decreased significantly in the three statin groups but not in the nonstatin group. These results suggest that long-term use of fluvastatin by hyperlipidaemic hypertensive patients is associated with a significant reduction in aortic stiffness without any effect on BP.     

测量踝部动脉血压与肱动脉血压、主动脉内血压的对比研究

目的　探讨下肢血压测量方法。方法　对高血压病组及非高血压病组共 10 7例病人采取将袖带缠于小腿下端监听足背动脉血压 ,并与肱动脉血压、主动脉内血压进行对比研究。结果　两组踝部动脉血压与肱动脉血压呈显著正相关 (P <0 0 0 1) ,两组四肢血压与主动脉内血压相关性检验 ,除高血压组踝部动脉舒张压外均有显著相关性 (P <0 0 5 )。踝部动脉收缩压和舒张压平均比肱动脉分别高 10和 5mmHg;肱动脉收缩压低于主动脉内收缩压 5mmHg ,舒张压约高于主动脉内舒张压 5～ 6mmHg ;踝部动脉收缩压高于主动脉内收缩压 6mmHg ,舒张压约高于主动脉内舒张压 10mmHg。结论　测量踝部动脉血压的方法是可信的 ,但高血压组的踝部动脉舒张压与主动脉内舒张压相关性较差。     

The association between the renin-angiotensin-aldosterone system and arterial stiffness in young healthy subjects

Aldosterone might affect arterial stiffening, in both the short- and long-term. We investigated a possible association between excess aldosterone, reflected by an increased aldosterone : renin ratio (ARR) and pulse wave velocity (PWV) in young healthy adults. In a single-centre study, 60 subjects were evaluated for lipid profile, glucose, hs-CRP, renin and aldosterone. PWV was performed as a simple non-invasive recording and computer analysis of the two artery sites pressure waveform using SphygmoCor (version 7.1, AtCor Medical, Sydney, Australia). The ARR was significantly, positively associated with PWV: r = 0.298, P = 0.02. ARR was not associated with anthropometric variables, blood pressure (BP), metabolic and inflammatory parameters. In conclusion, the ARR was significantly associated with PWV and may exhibit direct effects of aldosterone on the vascular wall, which are not related to changes in conventional cardiovascular risk factors.     

Aldosterone synthase gene polymorphism, stroke volume and age-related changes in aortic pulse wave velocity in subjects with hypertension

PURPOSE: In rats, chronic aldosterone administration with high diet intake increases aortic stiffness independent of mechanical stress. In hypertensive humans, enhanced plasma aldosterone and arterial stiffness are positively associated. Whether the aldosterone synthase gene polymorphism (ASGP) CYP11B2 influences the age-related changes in blood pressure (BP) and arterial stiffness in hypertensive subjects has never been investigated. METHODS: In 425 untreated hypertensive men and women, ASGP was evaluated together with aortic pulse wave velocity (PWV). In 191 of these subjects, cardiac haemodynamics were measured using echo-Doppler techniques. RESULTS: In the overall population, independently of sex, the TC and CC genotypes of ASPG had significantly higher heart rate (HR) (P < 0.05) and lower stroke index (P < 0.01) than the TT genotype, but did not affect BP. In men, the adjusted slopes of the curves relating age to PWV and HR were significantly steeper (P = 0.04; P = 0.002) for the TC and CC than for the TT genotype. Such gene-related differences were not observed for the age-systolic BP relationship. CONCLUSION: In hypertensive subjects, the TC and CC genotypes of ASGP involve, by comparison with the TT genotype, significantly higher HR and reduced stroke index. In men with the C allele, the reduced stroke index (cardiac effect) compensates for the steep increase of PWV with age (arterial effect), thus modulating the cardiovascular phenotype and explaining the lack of increased incidence of systolic hypertension. The results are consistent with a local role of endogenous aldosterone on both heart and vessels.     

肱动脉袖带血压与中心动脉血压差异的分析

目的：比较肱动脉袖带血压与中心动脉血压的差异性,并探讨两者间差异的可能影响因素及机制。方法：选择住院行诊断性冠脉造影患者128例,平均（60．87±9．36）．岁。术前测量脉搏波传导速度（PWV）,容量顺应性（C1）,振荡顺应性（C2）,术中记录升主动脉压力（中心动脉血压,CAP）,并同步测量肱动脉袖带血压。结果：（1）根据中心动脉与肱动脉袖带收缩压（SBP）差异程度分为3组：相符组（两者相差≤4mmHg）21例（16．40％）,高估组（后者高于前者,差值〉4mmHg）14例（10．94％）,低估组（后者低于前者,差值〉4mmHg）93例（72．66％）;（2）低估组人群传统心血管危险因素多,多为老年,高血压、冠心病较多（P〈0．05）;（3）低估组PWV明显增快（P〈0．05）;（4）低估组C2明显降低（P〈0．05）。结论：中老年人肱动脉袖带血压大多数低于中心动脉压,中心动脉硬化可能与之有关。     

Central hemodynamics of hypertensive disorders in pregnancy

BACKGROUND: Preeclampsia is characterized by an increase in peripheral vasoconstriction. Studies of central hemodynamics are limited. Noninvasive evaluation of aortic stiffness and pressure waveform is possible by applanation tonometry. We determined pulse wave velocity (PWV), augmentation index (AI), subendocardial viability ratio (SEVR), and the central to brachial pressure amplification in normotensive, hypertensive, and preeclamptic pregnancies. METHODS: In 51 normotensive, 38 hypertensive, and 33 preeclamptic pregnancies we measured carotid-femoral PWV. The AI, SEVR, and central pressures were determined by analysis of the aortic pressure waveform derived from the radial artery. Measurements were performed in lateral position after 10 min of rest. Linear regression models and ANOVA multiple comparisons were used for statistical analyses. RESULTS: There were no differences in age or other baseline characteristics. The mean PWV for the normotensive, hypertensive, and preeclamptic groups was 5.1 m/sec (SD 0.6), 6.2 m/sec (SD 1.0), and 7.0 m/sec (SD 1.3), respectively. The AI was 6.7% (SD 14.0), 17.7% (SD 15.9), and 31.1% (SD 12.4), respectively. The SEVR was 1.38 (SD 0.2), 1.50 (0.2), and 1.48 (0.3), respectively. Central to brachial pressure amplification was 1.6 (SD 0.2), 1.4 (SD 0.2), and 1.3 (SD 0.2), respectively. After adjustment for blood pressure, no significant differences remained between the groups. CONCLUSIONS: In hypertensive and preeclamptic pregnancies, aortic stiffness and augmentation are significantly higher as compared to normotensive pregnancy. Amplification of central pulse pressure is significantly lower in hypertensive and preeclamptic pregnancies, resulting in relatively higher central pressure. Nevertheless, the supply and demand ratio of the heart is not impaired in hypertensive and preeclamptic pregnancies.     

Higher plasma homocysteine concentration is associated with more advanced systemic arterial stiffness and greater blood pressure response to stress in hypertensive patients.

Hyperhomocysteinemia has been reported to be associated with both vascular structure alteration and increased cardiovascular risk. This study examined whether hyperhomocysteinemia causes increased systemic arterial stiffness, thereby enhancing blood pressure response to stress in hypertensive patients. In 50 treated hypertensive patients, we studied brachial-ankle pulse wave velocity (PWV), a new measure for arterial stiffness, blood pressure response to stress, and blood pressure recovery after stress. Autonomic nervous activities were examined by spectral analysis of blood pressure and RR interval variabilities. Total plasma homocysteine and neurohumoral parameters were determined from fasting blood. Brachial-ankle PWV correlated with age (r=0.64, p<0.001), plasma homocysteine concentration (r=0.35, p<0.05), and systolic blood pressure (SBP) (r=0.62, p<0.001). Higher plasma homocysteine concentration was independently associated with greater brachial-ankle PWV (beta=0.388, p=0.01). We classified the subjects into high homocysteine (7.3 nmol/ml or over) and low homocysteine (7.2 nmol/ml or below) groups. Baseline SBP, plasma renin activity, aldosterone, and norepinephrine concentrations were similar between the two groups. However, the SBP values during stress and the recovery periods were higher in the high homocysteine group than the low homocysteine group even after adjusting for sex and age. The behavior of sympathetic vasomotor activity did not differ between the two groups. These data suggest that higher plasma homocysteine concentration is associated with increased systemic arterial stiffness, which may enhance blood pressure reactivity to stress in hypertensive patients.     

Aldosterone-to-renin ratio, arterial stiffness, and the response to aldosterone antagonism in essential hypertension

BACKGROUND: Some 10% to 15% of hypertensive patients have hyperaldosteronism, an increased ambulant aldosterone-to-renin ratio. As aldosterone reduces arterial compliance, we examined the relationship between aldosterone-to-renin ratio, aortic blood pressure (BP), arterial stiffness, and the effect of spironolactone in a hypertensive population. METHODS: In 24 untreated patients (mean age 51 +/- 2 years, 10 women), we assessed arterial stiffness by augmentation index-height of the late systolic peak in the aorta, pulse pressure (Sphygmocor), and aortic pulse wave velocity (Complior). RESULTS: There were significant positive correlations between the aldosterone-to-renin ratio and aortic systolic pressure, aortic pulse pressure, and augmentation index and negative correlations with pulse pressure amplification, but none with brachial BP or pulse wave velocity. After randomization in a cross-over design to 50 mg of spironolactone or 2.5 mg of bendroflumetazide for 4 weeks with washout period of 1 month, both drugs significantly reduced brachial BP, but only spironolactone reduced (P < .001) pulse wave velocity and augmentation index, which remained significant when corrected for its greater reduction in mean BP. There were significant (P < .001) positive correlations between the ratio and decrease in aortic systolic (r = 0.78), mean (r = 0.75), diastolic BP (r = 0.66), aortic pulse pressure (r = 0.69, augmentation index (r = 0.64) and with, brachial systolic pressure (r = 0.66), brachial pulse pressure (r = 0.44, P < .05) and pulse pressure amplification (r = 0.46, P < .05). Such relationships were not found with pulse wave velocity. CONCLUSIONS: The aldosterone-to-renin ratio may have an important role in determining arterial stiffness, particularly wave reflection and aortic systolic pressure and is of predictive value for the responsiveness to spironolactone. Aldosterone antagonism has BP-independent effects on arterial stiffness.     

高甘油三酯血症患者动脉僵硬度与超敏C反应蛋白的相关性研究

目的探讨高甘油三酯血症患者动脉僵硬度与超敏C反应蛋白（hsCRP）的关系。方法以脉搏波速度（PWV）水平作为动脉僵硬度的评价手段。112名高甘油三酯血症患者根据动脉硬化的程度分为低PwV组和高PWV组，分别测定肱踝脉搏波传导速度（ba—PWV）和hsCRP，并收集相关临床资料。结果高PwV组log hsCRP水平显著高于低PWV组（P〈0．05）。偏相关分析显示在校正年龄、性别、吸烟史、合并用药情况、冠心病、高血压、血脂谱、空腹血糖、胰岛素抵抗指数后ba—PWV和log hsCRP正相关（r=0．261，P=0．039）。多元回归分析显示年龄（P〈0．01）、收缩压（P〈0．05）及log hsCRP（P〈0．05）与ba—PWV相关。结论高甘油三酯血症患者中hsCRP与ba—PwV水平相关，提示动脉僵硬度可能与全身的炎症状态相关。     

Matrix metalloproteinase-9 polymorphism contributes to blood pressure and arterial stiffness in essential hypertension

Arterial stiffness is an independent predictor of cardiovascular events in a hypertensive population. Serum levels of matrix metalloproteinase (MMP)-9 are associated with arterial stiffness and predict cardiovascular risk. We investigated the role of MMP-9 polymorphism -1562C>T on blood pressure (BP) and arterial stiffness in a newly diagnosed hypertensive population. Untreated hypertensive patients (n=215, mean age 46+/-13 years) were studied. Supine BP, carotid-femoral pulse wave velocity (PWV) and augmentation index were assessed. Serum biochemistry and plasma MMP-9 concentrations were measured and genotyping performed following extraction of genomic DNA. BP, aortic PWV and serum MMP-9 levels were significantly higher in T-allele carriers of the -1562C>T polymorphism with a significant gene-dose effect (P<0.0001). In a stepwise regression model adjusting for known or likely determinants, the 1562C>T polymorphism emerged as an independent predictor of systolic BP (R(2)=0.25, P<0.0001), diastolic BP (R(2)=0.16, P<0.0001) and PWV (R(2)=0.47,P<0.0001). This is the first study to show the effect of MMP-9 polymorphism on BP and aortic stiffness in a hypertensive population. These results suggest that hypertensive patients carrying the T allele may be at increased risk of cardiovascular events.     

Relationship between hyperinsulinemia and pulse wave velocity in moderately hyperglycemic patients

AIM: Arterial stiffness assessed by pulse wave velocity (PWV) reflects early stage arteriosclerosis. The influence of hyperinsulinemia on peripheral vascular disease (PVD) is still unknown. We determined the influences of hyperinsulinemia on PVD assessed by PWV in moderately hyperglycemic patients. METHODS: Thirty-six moderately hyperglycemic, outcoming patients were recruited in this study. All subjects were divided into two groups by fasting immunoreactive insulin (F-IRI) concentrations; group A; F-IRI> or =5 microU/ml, group B; F-IRI<5 microU/ml. Both hbPWV (from heart to brachial artery) and baPWV (brachial to artery to ankle) were evaluated by using Form PWV/ABI, in addition to ankle-brachial pressure index (ABPI). RESULTS: In group A, both hbPWV and baPWV showed significantly higher values than in group B. ABPIs were not different between two groups. Although age, FPG, plasma HbA1c, serum total-cholesterol, HDL-cholesterol concentrations, and systolic and diastolic blood pressure were at same levels in group A as group B, body mass index, HOMA-R, serum triglyceride concentrations were significantly higher in group A, indicating the existence of insulin resistance in group A. CONCLUSION: Hyperinsulinemia may be involved in the development of PVD in moderately hyperglycemic patients.     

A comparison of atenolol and nebivolol in isolated systolic hypertension

OBJECTIVES: Some beta-blockers are less effective in reducing central blood pressure than other antihypertensive drugs, which may explain the higher rate of events in subjects randomized to atenolol in recent trials. We hypothesized that nebivolol, a mixed beta-blocker/nitro-vasodilator, would be more effective than atenolol in reducing central blood pressure and augmentation index (AIx). The aim of the present study was to test this in a double-blind, randomized, cross-over study, in a cohort of subjects with isolated systolic hypertension. METHODS: Following a 2-week placebo run-in, 16 never-treated hypertensive subjects received atenolol (50 mg), nebivolol (5 mg) and placebo, each for 5 weeks, in a random order. Seated brachial blood pressure and heart rate were measured. Aortic blood pressure, AIx and pulse wave velocity (PWV) were assessed non-invasively. RESULTS: The placebo-corrected fall in brachial pressure was similar between nebivolol and atenolol, as was the reduction in PWV (mean change +/- SEM: -1.0 +/- 0.3 and -1.2 +/- 0.2 m/s; P = 0.2). However, there was less reduction in heart rate (-19 +/- 2 versus -23 +/- 2 beats/min; P < 0.01) and increase in AIx (+6 +/- 1 versus +10 +/- 1%; P = 0.04), following nebivolol. Aortic pulse pressure was significantly lower (50 +/- 2 versus 54 +/- 2 mmHg; P = 0.02) after nebivolol. N-terminal pro-B-type natriuretic peptide (proBNP) rose on both drugs (100 +/- 33 versus 75 +/- 80 pg/ml; P < 0.01 for both, NS for comparison). CONCLUSIONS: Nebivolol and atenolol have similar effects on brachial blood pressure and aortic stiffness. However, nebivolol reduces aortic pulse pressure more than atenolol, which may be related to a less pronounced rise in AIx and bradycardia. Whether this will translate into differences in clinical outcome requires further investigation.     

Microalbuminuria and arterial stiffness in a general population: the Shimanami Health Promoting Program (J-SHIPP) study.

Microalbuminuria is an early marker of renal damage and has been shown to predict future cardiovascular mortality and morbidity in patients with diabetes or hypertension, as well as in subjects in the general population. In this study, we investigated the hypothesis that the presence of microalbuminuria reflects the advancement of arterial stiffness by using a study group of 136 community residents who had no cardiovascular diseases except for hypertension and who were not taking any medications. Urinary albumin concentration was determined by the standard method and corrected by creatinine. Microalbuminuria was defined as a urinary albumin/creatinine ratio of 2.0-30.0 mg/mmol creatinine. Arterial stiffness was evaluated by pulse wave velocity (PWV) determined at three points: from the heart to the carotid artery, to the brachial artery, and to the ankle. Carotid arterial pressure was determined using a tonometric sensor. Carotid ultrasonography was performed to measure carotid intima-media thickness (IMT) and carotid arterial internal dimension. Subjects with microalbuminuria had higher blood pressure and wider pulse pressure not only in the brachial artery but also in the carotid artery. Microalbuminuria was associated with significantly higher PWV compared with that of normoalbuminuric subjects at all sites studied (mean PWV: 821.2+/-137.4 cm/s vs. 933.8+/-137.5 cm/s, p<0.0001). Stepwise regression analysis revealed that the presence of mircroalbuminuria (p=0.047) was a significant independent predictor of PWV in addition to age, sex, and systolic blood pressure. These findings suggest that microalbuminuria is associated with advanced atherosclerosis in the general population. Underlying arterial stiffness may explain the high cardiovascular mortality in subjects with microalbuminuria. Hypertension may be the mechanism linking microalbuminuria and arterial stiffness in the general population.     

History of gestational hypertension is associated with the metabolic syndrome and masked hypertension but not arterial stiffness in women with essential hypertension

The underlying mechanisms of subsequent increased risk of cardiovascular disease with a history of gestational hypertension (GH) are not known. Untreated hypertensive women (n=155, age 43+/-1 years) underwent ambulatory blood pressure (BP) monitoring and assessment of aortic pulse wave velocity (PWV) and augmentation index (AIx). Despite identical clinic BP readings, the group of women with GH (n=54) had higher (P=.002) ambulatory daytime systolic BP levels and a greater number of extreme nocturnal dippers (P=.005) than the group without GH. Women with GH had higher body mass index (P=.003), greater waist circumference (P=.02), higher levels of triglycerides (P=.002), lower levels of high-density lipoprotein cholesterol (P=.004), a higher prevalence of the metabolic syndrome (P<.05) and microalbuminuria (P=.004), higher plasma renin activity (P=.03), and higher aldosterone levels (P=.01). There was no significant difference in PWV and AIx between the 2 groups. The higher prevalence of the metabolic syndrome, microalbuminuria, masked hypertension, and activation of the renin-angiotensin-aldosterone system but not arterial stiffness may explain the subsequent propensity to high BP and cardiovascular disease in women with GH.     

Long-term effects of intensive blood-pressure lowering on arterial wallstiffness in hypertensive patients

BackgroundAortic stiffness is assessed by pulse wave velocity (PWV) and predicts the cardiovascular morbidity and mortality of hypertensive patients. To determine the long-term effects of intensive blood pressure (BP) lowering by antihypertensive drug therapy on aortic stiffness assessed by PWV, a single-blind randomized prospective study was performed.MethodsOne hundred forty nondiabetic hypertensive patients (67.6 ± 0.9 years old; systolic/diastolic BP: 177 ± 1/101 ± 1 mm Hg) were assigned to an intensive control group (IC) with a target BP of <130/85 mm Hg (n = 71) or a moderate control group (MC) with a target BP of <140/90 mm Hg (n = 69), and aortic stiffness was assessed every 3 months by measuring aortic PWV with a pulse pressure analyzer.ResultsDuring the 12-month treatment period, BP significantly decreased to 129 ± 1/78 ± 1 mm Hg and 152 ± 2/87 ± 1 mm Hg in the IC and MC, respectively. At the beginning of the study, PWV in the IC and MC was similar, averaging 1779 ± 41 and 1885 ± 50 cm/sec, respectively. By the end of the treatment period, however, PWV had decreased to 1621 ± 34 cm/sec in the IC, but had not changed significantly in the MC. In the IC, the ratio of the change in PWV to the change in BP increased with the duration of BP lowering. Clinical and biological parameters were similar in both groups, except that higher doses of amlodipine were used in the IC.ConclusionsLong-term intensive BP lowering in the hypertensive patients was associated with a significant reduction in aortic stiffness distinct from its acute depressor effect.     

A randomized,double‐blind clinical trial to evaluate the blood pressure lowing effect of low‐sodium salt substitution on middle‐aged and elderly hypertensive patients with different plasma renin concentrations

This study aimed to evaluate the blood pressure (BP) lowing effect of low‐sodium (LS) salt substitution and how the effect influenced by plasma renin concentration (PRC) on middle‐aged and elderly hypertensive patients. Three hundred fifty‐two hypertensives were randomized at a 1:1 ratio into a LS group and a normal salt (NS) group. We compared intergroup changes observed in office blood pressure measurement (OBPM) and home blood pressure measurement (HBPM). Then, all patients in LS group were divided into tertiles according to baseline PRC, aldosterone concentration, and aldosterone/renin ratio (ARR), and changes in OBPM and HBPM were compared across the three tertile subgroups. Follow‐up surveys were completed by 322 patients. The intergroup net reduction in systolic OBPM, systolic HBPM, and diastolic HBPM was −6.6, −4.6, and −2.3 mmHg, respectively (all P < .05), and −1.8 mmHg in diastolic OBPM (P = .068). There was a more significant reduction in OBPM and HBPM among the low baseline PRC subgroup than among the high PRC subgroup. There were no significant differences in the changes in OBPM and HBPM between the three subgroups when grouped according to baseline aldosterone concentration. The reduction in OBPM and HBPM in the high tertile of ARR was larger than that in the low tertile subgroup. LS salt substitution is effective in reducing systolic OBPM, systolic HBPM, and diastolic HBPM in middle‐aged and elderly hypertensive patients. LS salt substitution may offer a non‐pharmaceutical therapy for hypertensive patients. Baseline PRC may be a marker to predict BP response after salt restriction.