Abstract
BACKGROUND: Ambulatory blood pressure monitoring can sensitively and objectively reflect blood pressure level, which is closely related to target organ damage and disease prognosis. In hypertension, vascular endothelial damage is the most common lesion to target organs. There is little known about how ambulatory pulse pressure correlates to large artery elasticity and vascular endothelial function.
OBJECTIVE: To investigate changes of large artery elasticity and of vascular endothelial function in patients with primary hypertension using an automatic pulse wave velocity determinator and ultrasound techniques, and to analyze the correlation of ambulatory pulse pressure to large artery elasticity and vascular endothelial function.
DESIGN: A non-randomized concurrent control clinical observation.
SETTING: Diagnosis and Treatment Center for Coronary Heart Disease, the 305 Hospital of Chinese PLA.
PARTICIPANTS: A total of 156 inpatients and/or outpatients, who were recently confirmed with primary hypertension, were recruited for this study between June 2005 and April 2007. Patients consisted of 114 males and 42 females. All patients averaged 56 ± 4 years of age (range: 40-75). Inclusive criteria: Corresponding to diagnostic standards for preventing and treating hypertension instituted in 2004 by Chinese scholars. Confirmed as primary hypertension within 1 month. Not receiving any blood pressure lowering, hypolipidemic or nitrate-like drug treatments. Written informed consents for laboratory measurements were obtained from all subjects. The study was approved by the hospital's Ethics Committee.
METHODS: According to the mean pulse pressure over 24 hours, all patients were assigned into 3 groups: Group A (mean pulse pressure < 40 mm Hg, n=92), group B (40 mm Hg ≤ mean pulse pressure < 60 mm Hg, n=39) and group C (mean pulse pressure > 60 mm Hg, n=25). In each group, daytime pulse pressure and night-time pulse pressure, as well as 24-hour mean pulse pressure were measured using a non-invasive portable ambulatory blood pressure monitor (ABPM-04, Meditech Inc, USA). Carotid-femoral and carotid-radial arterial pulse wave velocities were measured using an automatic pulse wave velocity determinator to evaluate large artery dilation. Blood flow mediated and nitroglycerin-dependent dilatation of the brachial artery was determined using a high-resolution ultrasound technique to evaluate vascular endothelial function.
MAIN OUTCOME MEASURES: Correlations of ambulatory pulse pressure to large artery dilation and arterial endothelial function.
RESULTS: All 156 patients were included in the final analysis. Correlation of ambulatory pulse pressure to large artery dilation: Carotid-femoral arterial pulse wave velocity was significantly positively correlated to daytime pulse pressure, night-time pulse pressure and 24-hour mean pulse pressure, with coefficient of partial correlation being 0.310, 0.281 and 0.303, respectively, P < 0.01). There were no significant correlations of carotid-radial arterial pulse wave velocity to daytime pulse pressure, night-time pulse pressure or 24-hour pulse pressure (P > 0.05). Correlation of ambulatory pulse pressure to arterial endothelial function: There was a linear relationship between ambulatory pulse pressure and blood flow-mediated blood vessel dilatation values. Linear correlation analysis was performed, taking ambulatory pulse pressure as an independent variable, and endothelial-dependent dilatation as a dependent variable. Results demonstrated that blood flow-mediated blood vessel dilatation was significantly negatively correlated to daytime pulse pressure, night-time pulse pressure and 24- hour mean pulse pressure (r = -0.684, -0.597, -0.668, P < 0.01). There was no correlation of ambulatory pulse pressure to non-endothelial-dependent blood vessel dilatation.
CONCLUSION: Ambulatory pulse pressure increase is closely related to large artery elasticity decrease and injury to endothelial function in patients with primary hypertension.

INTRODUCTION

At present, people have been used to paying much attention to causal blood pressure. However, they study a little about ambulatory blood pressure. Ambulatory blood pressure monitoring can sensitively and objectively reflect blood pressure level, which is closely related to target organ damage and its prognosis. Ambulatory blood pressure is a potent predictor of total cardiovascular risk [1]. Pulse wave velocity determination and high-resolution ultrasound are the common noninvasive methods respectively for evaluating large artery elasticity [2] and vascular endothelial function. The present study aimed to evaluate the changes of large artery elasticity and vascular endothelial function in hypertension using an automatic pulse wave velocity determinator and high-resolution ultrasound technique. Investigating the correlations of ambulatory pulse pressure to large artery elasticity and vascular endothelial functions is significant for identifying the role of pulse pressure in patients with primary hypertension.

SUBJECTS AND METHODS

Subjects
A total of 156 inpatients and/or outpatients, who suffered from primary hypertension, and which were confirmed in recent time, were admitted to the Diagnosis and Treatment Center for Coronary Heart Disease, the 305 Hospital of Chinese PLA between June 2005 and April 2007 and recruited for this study.
The included patients consisted of 114 males and 42 females. All patients averaged (56±4) years of age (range:40-75). Inclusive criteria: ①corresponding to diagnostic standards for preventing and treating hypertension determined in 2004 by Chinese scholars; ② Diagnosed as primary hypertension in the past 1 month; ③ Not receiving any hypolipidemic, blood lipid lowering or nitrate-like drug treatment; ④Written informed consents for determination were obtained from all subjects. Exclusion criteria: ① Complicated by coronary heart disease, diabetes mellitus, valvular heart disease, cardiomyopathy or tachyar rhythmia; ② Complicated by familial hypercholesterolemia, insulin-dependent diabetes or other hereditary matabolic diseases; ③Had the previous history of hepatic and renal inadequacy; ④ Complicated by infection, rheumatic disease, contagious disease or malignant tumor. The study was approved by the Hospital's Ethics Committee.

Methods
According to the mean pulse pressure during the 24 hours, all patients were assigned into 3 groups: group A [mean pulse pressure < 40 mm Hg, n=92. averaged (50±5) years of age], group B [40 mm Hg ≤ mean pulse pressure < 60 mm Hg, n=39, averaged (57±6) years of age] and group C [mean pulse pressure ≥ 60 mm Hg, n=25, averaged (62±6) years of age].

Ambulatory blood pressure monitoring
Ambulatory blood pressure monitoring was performed from 8:00-9:00 on a morning to 8:00-9:00 on the next morning using a noninvasive portable ambulatory blood pressure monitor (ABPM-04, Meditech Inc, USA). Sampling was conducted once every 15 minutes in the daytime (6:00-22:00) and every 30 minutes in the nighttime (22:00-6:00 on the next morning). The patients were asked to maintain their daily life and working. When monitoring time was > 24 hours and valid reading was > 80%, data could be considered meaningful. By statistical analysis, mean pulse pressure, daytime mean pulse pressure, nighttime mean pulse pressure, systolic pressure, diastolic pressure and heart rate were obtained.

Large artery elasticity determination
Pulse wave velocity could exactly reflect large artery dilatation change [2]. Carotid-femoral and carotid-radial arterial pulse wave velocities were determined using an automatic pulse wave velocity determinator (Complior, France) to evaluate large artery elasticity and other indices. The patients were asked to lie in a supine position. The patients' right carotid artery and femoral artery were selected for measuring sites. A pressure receptor was separately positioned on the places where carotid and femoral pulses were the most noticeable. The data of body surface distance between the two measurement sites were input into the computer. When the waveshapes revealed on the screen were stable, and the determined real-time variance rate was < 5.0%, data were collected by pressing the "OK" key. A total of 16 pulse wave velocity readings were recorded in succession. The 3 largest ones and 3 smallest ones were rejected. The mean pulse pressure of the remaining 10 readings was calculated.
Evaluation of arterial endothelial function by high- resolution ultrasound technique
According to the method introduced by Celemaijer et al, the subjects were asked to lie in prostrate position for over 15 minutes in a quiet lightproof room. A set of medical ultrasonic diagnostic equipment was used for the examination. Firstly, it was positioned at 2-5 cm above right cubital fossa to reveal the long-axis image of brachial artery and lock it; At the mean time, it also determined the ventricular end-diastolic and end-systolic basic internal diameter of brachial artery. The mean ventricular end-diastolic and end-systolic basic internal diameter of brachial artery was respectively calculated after 3 cardiac cycles. The detected region was marked on the skin to avoid repeated manipulation. A cuff sphygmomanometer was tied to the forearm of right upper extremity. It was pressurized to 300 mm Hg, maintained for 4 minutes, and then rapidly deflated. Internal diameter of brachial artery was determined at the original site by high-resolution ultrasound technique within 90 seconds. After 15-minute rest, when the internal diameter of brachial artery recovered to basic status, 0.5 mg nitroglycerin was sublingually administrated. Five minutes later, the internal diameter of brachial artery was determined for the third time. The last two measurement values of diastolic internal diameters of brachial artery were recorded and respectively subtracted the basic internal diameter at resting. Results were expressed as percentage. Following pressurization and deflation, the widening of internal diameter of brachial artery was blood flow-mediated endothelial dependent dilatation, while after sublingual administration of nitroglycerin, the widening of internal diameter of brachial artery was non-endothelial-dependent blood vessel dilation.

Statistical analysis
Statistical analysis was performed by the first and third authors with SPSS 10.0 software. Test of normality showed that main outcome measures accorded with normal distribution. Measurement data were expressed as Mean ± SD. Analysis of variance was used for comparing the means among groups, LSD test for comparing the means between two groups, Chi-square test for comparing enumeration data, and partial correlation analysis and linear correlation analysis for factor-factor correlation. A level of P < 0.05 was considered significant.

RESULTS

Quantitative analysis of participants
All 156 participants were included in the final analysis.

General condition of patients and comparisons of large artery dilatation and vascular endothelial function
There were no significant differences in gender constituent ratio, body mass index, waist circumference / hip circumference, fasting blood glucose level, and blood lipid level among the three groups (P > 0.05). No significant difference in carotid-radial arterial pulse wave velocity was found among the three groups (P > 0.05). There were significant differences in age, systolic blood pressure and diastolic blood pressure among the three groups (P < 0.05). Carotid-femoral arterial pulse wave velocity increased with ambulatory pulse pressure increasing (P < 0.05). Carotid-femoral arterial pulse wave velocity was significantly larger in the group B than in the group A (P < 0.05). It was significantly larger in the group C than in the group A and in the group B (P < 0.001). There was no significant difference in non-endothelial-dependent blood vessel dilation among the three groups (P = 0.328). Endothelial-dependent blood vessel dilation attenuated with ambulatory pulse pressure increasing. Endothelial-dependent blood vessel dilation was significantly lower in the group B than in the group A (P = 0.039). And it was significantly lower in the group C than in the group A and in the group B (both P < 0.01) (Table 1).

Correlation of ambulatory pulse pressure to large artery dilation
Partial correlation analysis was performed for controlling age and heart rate. Results demonstrated that carotid-femoral arterial pulse wave velocity was significantly positively correlated to daytime pulse pressure, nighttime pulse pressure and mean pulse pressure, with coefficient of partial correlation being 0.310, 0.281 and 0.303, respectively (all P < 0.001). However, there were no significant correlations of carotid-radial arterial pulse wave velocity to daytime pulse pressure, nighttime pulse pressure and mean pulse pressure (all P > 0.05).
Correlation of ambulatory pulse pressure to endothelial function
From the scatterplot of ambulatory pulse pressure and endothelial-dependent blood vessel dilation, it was known that there was a linear relationship between ambulatory pulse pressure and endothelial-dependent blood vessel dilatation values. Linear correlation analysis was performed taking ambulatory pulse pressure as an independent variable and endothelial-dependent blood vessel dilatation as a dependent variable. Analysis results showed that endothelial-dependent blood vessel dilatation was significantly negatively correlated to daytime pulse pressure (r =-0.684, P < 0.01), nighttime pulse pressure (r = -0.597, P < 0.01) and 24-mean pulse pressure (r = -0.668, P < 0.01). There was no correlation between ambulatory pulse pressure and non-endothelial-dependent blood vessel dilation.

DISCUSSION

Studies have demonstrated for no matter single measurement by mercurial sphygmomanometer or ambulatory blood pressure monitoring, pulse pressure is an independent predictor of total cardiovascular risk [3]. Franklin et al summed up 1924 cases. All the cases were aged 50-79 years and had not suffered from coronary heart disease or received anti-hypertension drugs. Univariate analysis results of 20-year follow-ups demonstrated systolic blood pressure, diastolic blood pressure and pulse pressure all were positively correlated to coronary heart disease risk. Among them, pulse pressure was mostly correlated to coronary heart disease risk. When blood pressure was increased by 10 mm Hg, the correlation coefficient between pulse pressure, systolic blood pressure and mean blood pressure, and coronary heart disease risk was 1.23 (P < 0.01), 1 .16(P < 0.001) and 1.14(P < 0.005), respectively. Diastolic blood pressure was negatively correlated to coronary heart disease risk, with the relative correlation coefficient of 0.86[4]. Vaccarino et al studied the pulse pressure change in 2152 cases, who were more than 65 years old and had no coronary heart disease or heart failure, and conducted 10-year follow-up. Study findings demonstrated that when pulse pressure increased by 10 mm Hg, coronary heart disease risk increased by 12%, congestive heart failure risk increased by 14%, and overall case-fatality rate increased by 6%. It indicated that increased pulse pressure is a potent predictor of cardiovascular disease risk [5]. It is thus inferred that among aging population, coronary heart disease risk increased with diastolic blood pressure attenuating, indicating that increased pulse pressure leads to coronary heart disease risk increases. By analyzing the study results in Framingham Study and MRC Trial（Medical Research Council trial of treatment of hypertension in older adults）, Millar and Franklin et al found that among population of hypertension, pulse pressure than systolic blood pressure had better predicting value for myocardial infarction. Moreover, the predicting value of pulse pressure is similar to the best linear combination of systolic blood pressure and diastolic blood pressure. It indicates that pulse pressure is indeed associated with myocardial infarction, and the false positive statistical outcomes resulted from the close association of pulse pressure and systolic blood pressure is not the real reason [6-7]. Benetos et al found that among the population with normal blood pressure, pulse pressure was independently correlated to cardiovascular risk, and the correlation of pulse pressure to death of coronary heart disease was even stronger compared to hypertension population [8-9]. Study findings [10] demonstrated that different kinds of blood pressure-lowering drugs had different impacts on central arterial pressure and pulse pressure, and were closely related to cardiovascular risk in the future time. Compared to other independent risk factors of cardiovascular disease (blood lipid, blood glucose, serum creatinine, body mass index), pulse pressure is a best index for predicting cardiovascular events. Pulse pressure is also an index for evaluating coronary heart disease risk degree and prognosis after interventional therapy [11]. It is thus seen that pulse pressure is independent from other indices of blood pressure, and can reflect arteriosclerosis degree and predict cardiovascular events.
Firstly, vascular wall injury caused by hypertension mainly involves elastorrhexis, collagen fiber increase, smooth muscle hypertrophy, and calcium content deposition. The thinning and fragmentation of elastic fibers and collagen increase may be the main reason of arteriosclerosis. The increase of pulse pressure plays a "hammer striking" effect on large artery vessel. It increases the pressure to vascular wall, causes vascular wall elastic component easily fatigued and fragmented, seriously damage vascular wall, promote artherosclerosis, and cause target organ injury. The increase of pulse pressure inevitably speeds up arterial hardening process. Secondly, pulse pressure widening can promote the pachynsis and/or hyperplasy of arterial wall smooth muscle. Arterial media mainly consisted of vascular smooth cell mass. Vascular smooth muscle is normally in resting state, and little (< 5%) can split and proliferate, but under the hypertension and arteriosclerosis and other pathological conditions, phenotype of vascular smooth muscle will change, presenting pachynsis and/or hyperplasy strengthening, lipid metabolism change, receptor expression change and extracellular matrix deposition increasing. These can lead to vascular pachynsis and/or hyperplasy in hypertension. Data from Table 1 demonstrate that pulse pressure increase was apparently due to systolic blood pressure increase and diastolic blood pressure decrease, but in fact, it was positively correlated to large artery elasticity decrease. Pulse pressure and large artery elasticity interact as both cause and effect, promote and influence each other. The increase of pulse pressure obviously decreases large artery elasticity, increases large artery rigidity, speeds up pulse wave and pressure wave conduction velocities, causes reflected wave superposition in the late systolic period, leads to the second pressure peak wave of systolic period, increases systolic blood pressure, decreases diastolic blood pressure and enlarges pulse pressure [12-13]. In the present study, we found that pulse pressure increase in hypertension population hardly influenced peripheral medium muscle artery elasticity. This may be related to the uneven buffer function changes in different arterial segments [14]. We also found that with aging, pulse pressure presents with an increasing tendency, which is related to the effect of aging and blood pressure on vascular wall structure. It is thus seen that blood pressure and pulse pressure increasing and aging process lead to large artery dilation decrease, which increases blood pressure. Such a vicious circle speeds up vascular damage and causes to the complications of various organs.
Ultrasound technique is currently a noninvasive easy and reliable method for detecting vascular endothelial function in clinical practice. In the target organ damages in hypertension, vascular endothelial damage is a frequently seen manifestation. Of many factors, which influence the secretion of endothelial cells, the most important physiologic adjustment is shear stress and pulsate flow. The increase of pulse pressure speeds up pulse wave velocity, increases vascular shear stress, accelerates pulsate flow, destroys the balance between vascular relaxing factor and shrinkage factor, both of which are released by endothelial cells to maintain angiotasis, and leads to the changes which are characterized by endothelial-dependent relaxation attenuation [15]. The present study findings demonstrated that with pulse pressure increasing, endothelial-dependent blood vessel dilation was noticeably decreased, there was a linear negative correlation between pulse pressure and endothelial-dependent blood vessel dilation (r=-0.668, P < 0.01), however, non- endothelial-dependent blood vessel dilation did not alter with the increase of pulse pressure. It demonstrated that the increase of pulse pressure led to vascular endothelial function damage, but it hardly influenced drug-dependent vascular smooth muscle dilation. It indicates that pulse pressure is closely related to brachial arterial endothelial function in hypertension population, and it can be used as an index for evaluating and predicting arterial endothelial functions in hypertension population.
There exist some limitations for pulse pressure as an evaluation index. Pulse pressure has alterability in the same individual. Blood pressure has large fluctuations in one day, in particular following short-time drug intervention. There is certain casualness when choosing pulse pressure as observation index due to large change of blood pressure. Ambulatory blood pressure monitoring can sensitively and objectively reflect practical blood pressure level, so it can more effectively predict cardiovascular risk. The increase of pulse pressure reflects the changes of vascular structure and function, and manifests the damages of heart and its target organs. Much attention should be paid to pulse pressure in clinical practice. On the basis of effective pressure lowering, application of pressure-lowering drugs may reduce total cardiovascular risk in hypertension population.

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原发高血压患者动态脉压与大动脉
弹性及血管内皮功能的关系*★

杜大勇1,李运田1,王红宇2,丁 康1,李 艳1
1解放军第三○五医院冠心病诊疗中心， 北京市 100013；2北京大学人民医院心内科, 北京市 100044
杜大勇★,男，1972年生，山西省定襄县人，汉族，1996年山西医科大学毕业，硕士，主治医师，主要从事冠心病基础与临床、冠心病介入治疗的研究。
通讯作者：李运田，解放军第三○五医院冠心病诊疗中心, 北京市100044
全军“十一五”科技攻关项目支助（06G145）*
摘要
背景：动态血压监测能较敏感、客观的反映实际血压水平, 与靶器官损害及预后的关系密切。高血压靶器官损害中以血管内皮损害最常见。动态血压与大动脉弹性及血管内皮功能变化是否有一定相关性？
目的：应用自动脉搏波速度测定仪和超声技术评价原发高血压患者大动脉弹性和内皮功能的变化，分析患者动态脉压与大动脉弹性、内皮功能的关系。
设计：非随机化同期对照临床观察。
单位：解放军第三○五医院冠心病诊疗中心。
对象：选择2005-06/2007-04在解放军第三○五医院冠心病诊疗中心门诊和住院156例新近诊断原发性高血压患者,男114例,女42例，年龄40~75岁，平均(56±4)岁。纳入标准：①符合2004年中国高血压防治指南诊断标准。②近1月内在门诊或住院诊断原发高血压。③未服任何降压、降脂以及硝酸酯类药物治疗。患者均对检测知情同意，实验经过医院伦理委员会批准。
方法：①实验分组：根据24 h平均脉压水平将患者分为3组: 24 h脉压< 40 mm Hg组(n=92), 40 mm Hg≤24 h脉压< 60 mm Hg组(n=39)及24 h脉压≥60 mm Hg组 (n=25)。②项目检测：采用美国Meditech公司ABPM-04无创性携带式动态血压监护仪检测各组患者白昼及夜间脉压及24 h平均脉压；应用自动脉搏波速度测定仪测定颈-股动脉脉搏波速度和颈-桡动脉脉搏波速度评价大动脉扩张性；应用高分辨率血管外超声分别通过对肱动脉进行血流介导的血管扩张和硝酸甘油依赖性的血管扩张测定来评价内皮功能。
主要观察指标：患者动态脉压与大动脉扩张性及动脉内皮功能的相关性。
结果：纳入患者156例均进入结果分析。① 动态脉压与大动脉扩张性的相关分析：颈-桡动脉脉搏波速度与白昼脉压、夜间脉压及24 h平均脉压均呈显著正相关,偏相关系数分别为0.310、0.281和0.303 (P均< 0.01), 颈-桡动脉脉搏波速度与白昼脉压、夜间脉压及24 h平均脉压均无显著相关（P > 0.05）。②动态脉压与动脉内皮功能的相关分析：动态脉压与血流介导的血管扩张两变量在数值上呈直线关系。以动态脉压为自变量,以内皮依赖性血管扩张为因变量进行直线相关分析显示, 血流介导的血管扩张与白昼脉压、夜间脉压及平均脉压呈显著性负相关(r=-0.684，-0.597，-0.668，P < 0.01)。动态脉压与非内皮性依赖性血管扩张无相关性。
结论：动态脉压升高与原发高血压患者大动脉弹性降低和内皮功能受损密切相关。
关键词：高血压; 脉压; 大动脉弹性; 内皮功能；组织构建
中图分类号: R544.1 文献标识码: A 文章编号: 1673-8225(2008)07-01363-05
杜大勇,李运田,王红宇,丁康,李艳. 原发高血压患者动态脉压与大动脉弹性及血管内皮功能的关系[J].中国组织工程研究与临床康复, 2008,12(7):1363-1367
[www.zglckf.com/zglckf/ejournal/upfiles/08-7/7k-1363(ps).pdf]
(Edited by Akman B/Vernaglione L/Song LP/Wang L)