培哚普利及美托洛尔对中心动脉压的作用

目的 比较培哚普利和美托洛尔对轻中度高血压病患者中心动脉压与肱动脉压的影响.方法 在冠状动脉造影结束后,分别同步测量145例高血压病或(和)冠心病患者升主动脉根部(直接测量法)和肱动脉(袖带加压法)的血压,其中单药降压治疗二周以上的轻中度高血压病患者分为培哚普利组(4 mg/d,62例)、美托洛尔组(25 mg/d,39例).结果 升主动脉收缩压高于袖带加压法测量的肱动脉收缩压9.6 mm Hg(P＜0.01),升主动脉舒张压低于袖带加压法肱动脉舒张压2.0 mm Hg(P＜0.01),升主动脉脉压较肱动脉脉压大11.6 mm Hg(P＜0.01).虽然培哚普利组和美托洛尔组袖带加压法测得的肱动脉压相同,但是培哚普利组的升主动脉收缩压低于美托洛尔组(P＜0.05).结论 升主动脉压与袖带加压法测得的肱动脉压差异有非常显著意义.虽然培哚普利和美托洛尔降低肱动脉压效果相似,但培哚普利降低升主动脉收缩压较美托洛尔更显著.     

冠心病患者经导管测量中心动脉血压与经袖带测量肱动脉血压的比较研究

目的研究经导管测量主动脉根部血压(中心动脉压)与经袖带测量肱动脉血压间的差异。方法采用介入方法分别记录主动脉根部中心动脉收缩压、舒张压。同步经袖带测量左臂肱动脉无创血压两次,取其平均值,分别记录收缩压、舒张压,然后进行对比分析。结果中心动脉收缩压与肱动脉收缩压差异无显著性,P=0.908。中心动脉舒张压较肱动脉舒张压低7.85mmHg(P<0.001),舒张压净差异变化值在65岁以上组较65岁以下组更为明显(P<0.01)。结论袖带肱动脉收缩压能准确反应中心动脉收缩压变化,袖带肱动脉舒张压较中心动脉舒张压高,差异随年龄增加而加大。     

非洛地平缓释片与美托洛尔缓释片对原发性高血压患者中心动脉压影响的对比研究

目的 比较两种降压方案对原发性高血压患者外周肱动脉压及中心动脉压的影响.方法 357例原发性高血压患者随机分为两组,分别给予非洛地平缓释片及培哚普利或美托洛尔缓释片及氢氯噻嗪两种不同降压方案,于治疗前及血压达标后3个月时(非糖尿病患者血压<140/90 mmHg,糖尿病患者血压<130/80 mmHg)分别测量患者肱动脉压及应用桡动脉脉搏波分析仪获得中心动脉压.结果 治疗后两组药物对患者外周肱动脉压的影响无明显不同(P>0.05);但非洛地平缓释片组较美托洛尔缓释片组中心动脉收缩压进一步下降4.5 mmHg(P<0.05).结论 虽然两种降压方案对外周肱动脉压影响相似,但非洛地平缓释片组降低中心动脉收缩压较美托洛尔缓释片组更显著.     

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。     

四逆汤对腹主动脉缩窄大鼠血压和压力反射敏感性的影响

目的研究四逆汤方对腹主动脉缩窄大鼠血压和压力反射敏感性(BRS)的影响。方法采用腹主动脉缩窄法制备高血压大鼠模型50只,造模成功后随机分为模型组(M组)、假手术组(B组)、四逆汤组(S组)、四逆汤+培哚普利组(SP组)、培哚普利组(P组)共5组,每组10只。术后4周开始灌胃,以假手术组为空白对照组,培哚普利组为阳性药物对照组,药物干预8周。用尾动脉仪连续动态测量大鼠左前肢血压。干预后8周通过股动脉插管,股静脉注射苯肾上腺素观察大鼠BRS、血压变化。结果造模后4周,与假手术组相比,各组收缩压均显著增高(P0.001)、舒张压增高不明显(P0.05),其中四逆汤组、四逆汤+培哚普利组舒张压增高(P0.05)。药物干预后4周,与模型组相比,四逆汤组、四逆汤+培哚普利组、培哚普利组收缩压均明显降低(P0.001),舒张压虽无明显降低,但与造模后血压相比有所下降(P0.05)。药物干预后8周,与前一时间点血压相比,各组血压均无进一步降低(P0.05)。药物干预后,与模型组相比,四逆汤组、四逆汤+培哚普利组、培哚普利组BRS明显上升(P0.001)。结论四逆汤可改善腹主动脉缩窄大鼠的血压,可增加腹主动脉缩窄大鼠压力反射敏感性。     

中心动脉压与肱动脉压关系的探讨

目的研究中心动脉压与外周动脉压之间的关系及影响因素。方法 100例进行冠状动脉造影检查的患者,术中使用动脉导管直接测压法测量中心动脉压及肱动脉压,分析二者之间关系及年龄和高血压对中心动脉压与肱动脉压问的相关性的影响。结果 100例患者肱动脉收缩压显著高于升主动脉收缩压[(132±22)mmHg比(128±21)mm Hg,P=0.0001],肱动脉舒张压与升主动脉舒张压差异无统计学意义[(66±11)mm Hg比(67±11)mm Hg,P0.05],在老年组、非老年组及各年龄组肱动脉脉压均高于升主动脉脉压(P=0.0001);老年组的升主动脉及肱动脉脉压显著高于非老年组[(72±17)mm Hg比(52±14)mm Hg,(77±18)mm Hg比(57±15)mm Hg,P=0.0001],随着年龄的增长中心动脉脉压及肱动脉脉压均有增高的趋势,但差异无统计学意义(P0.05);高血压患者中心动脉及肱动脉脉压均显著高于非高血压患者[(65±20)mm Hg比(53±14)mm Hg,P=0.004;(69±20)mm Hg比(59±13)mm Hg,P=0.013],但是中心动脉舒张压在高血压与非高血压患者间差异无统计学意义[(68±11)mm Hg比(64±11)mm Hg,P=0.132]。结论外周动脉收缩压及脉压均高于中心动脉,与年龄及是否伴高血压无关;老年组中心动脉及外周动脉脉压均显著高于非老年组;高血压患者外周动脉及中心动脉脉压高于非高血压患者,但两者中心动脉舒张压差异无统计学意义。     

中心动脉压、血尿酸浓度与冠心病的相关性

目的探讨中心动脉压、血尿酸与冠心病的相关性。方法随机选择我院2006年7月至2008年6月96例冠状动脉造影确诊为冠心病患者,冠状动脉造影结束后,同步测量升主动脉根部(直接测量法)和肱动脉(袖带加压法)的血压,其中合并高血压组53例,非高血压组43例;采用酶法测定血尿酸浓度。结果冠心病合并高血压组血尿酸浓度[(380±87)μmoL/L]高于非高血压组[(332±90)μmol/L,P0.05],其他因素差异无统计学意义(P0.05)。相关分析显示,血尿酸浓度与中心动脉收缩压(CSP)及脉压显著呈正相关(r=0.411、0.364,P0.01);与中心动脉舒张压(CDP)及肱动脉收缩压(BSP)亦呈正相关(r=0.273、0.256,P0.05)。冠状动脉病变程度与高尿酸血症发生率呈正相关(21.3%比49.0%,P0.01)。Logistic回归分析显示年龄、中心动脉脉压、血尿酸浓度(OR=1.091、1.059、1.010,P0.05)是冠状动脉病变程度的危险因素。结论中心动脉压、血尿酸升高与冠心病的发生率及病变程度关系密切,中心动脉压较肱动脉压与血尿酸水平具有更显著的相关性。     

用导管法评定硝酸酯类药物对中心动脉压的影响

目的了解硝酸酯类药物对中心动脉压的影响.方法52例行左心导管术患者,平均年龄(53.3±10.8)岁.其中冠心病32例,合并高血压和(或)糖尿病18例;原发性高血压6例;其它14例.晨起停服心血管药物,在冠状动脉造影或射频导管消融术(左心室旁道)后,用导管直接测定升主动脉压,并记录血压波形;同时用袖带汞柱血压计测定右臂肱动脉压,连续测定2次,取均值.其中33例舌下含化硝酸异山梨酯10 mg;19例舌下含化硝酸异山梨酯5 mg后10分重复上述操作.结果舌下含化硝酸异山梨酯10 mg或5 mg后升主动脉收缩压下降均较肱动脉明显,而舒张压变化不大.用药前后升主动脉收缩压差值与升主动脉脉压虽无显著相关,但相关系数为0.2026.结论硝酸酯类药物有降低动脉收缩压的作用,且降低中心动脉收缩压的作用明显大于肱动脉收缩压.     

螺内酯对继发性高血压大鼠肾脏的保护作用

目的 观察螺内酯对高血压大鼠肾动脉重构的影响.方法 在48只雄性Wistar大鼠中,随机选出36只,以腹主动脉缩窄法制备高血压模型,再随机分为3个亚组:高血压模型组(模型组,自来水灌胃 饮用1%盐水),高血压培哚普利组[培哚普利组,培哚普利2 mg/(kg·d)灌胃 饮用1%盐水],高血压螺内酯组[螺内酯组,螺内酯20 mg/(kg·d)灌胃 饮用1%盐水];其余12只进入假手术对照组(假手术组,只分离腹主动脉但不结扎,自来水灌胃 饮用自来水).8周后超声检测肾动脉及肾内动脉收缩期和舒张期阻力指数(RI)和血流速度并比较各组的差异;12周后颈动脉插管法测量血压及病理学方法测定肾内动脉的血管重构指标.结果 培哚普利和螺内酯均能降低高血压大鼠收缩压及舒张压(P＜0.01),均使高血压大鼠的肾动脉RI、肾内动脉RI、血管内膜中膜厚度与管腔内腔的比值(M/L)及肾动脉内中膜纤维化程度明显下降(P＜0.01～0.05),螺内酯上述作用比培哚普利更明显,螺内酯还能使高血压大鼠内中膜厚度显著降低(P＜0.01);虽然培哚普利和螺内酯均能使高血压大鼠肾动脉及肾内动脉舒张末期血流速度及肾内动脉面积增加(P＜0.01～0.05),螺内酯能更进一步降低肾动脉RI、M/L和内中膜纤维化比率(P＜0.01～0.05).结论 培哚普利和螺内酯均能降低高血压大鼠血压,改善动脉重塑,在改善动脉重塑方面螺内酯效果比培哚普利更明显.     

平板运动前后无创中心动脉压与外周动脉压的比较

动脉压(CAP)指升主动脉根部的收缩压、舒张压、脉压。过去受测量仪器的限制,临床高血压管理的血压及脉压测量均采用外周动脉压即肱动脉血压替代中心动脉压。这是假设肱动脉压与中心动脉压相同。事实上外周动脉压不能完全替代中心动脉压,更不能等同于中心动脉压用以评价高血压药物的     

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 v -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 v -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 v -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 v 0.59) and the smoothness index (1.45 v 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 atenolol.     

Mechanism(s) of selective systolic blood pressure reduction after a low-dose combination of perindopril/indapamide in hypertensive subjects: comparison with atenolol

OBJECTIVES: The goal of this study was to determine if a low-dose combination of the angiotensin-converting enzyme inhibitor perindopril (Per) and the diuretic indapamide (Ind) reduces central (thoracic aorta, carotid artery) as well as brachial systolic blood pressure (SBP) more than the beta-blocker atenolol and to determine the hemodynamic factors influencing independently brachial and central SBP: pulse wave velocity (PWV) and pattern of wave reflections. BACKGROUND: In high cardiovascular risk populations, angiotensin blockade improves survival without affecting brachial SBP and diastolic blood pressure (DBP). Whether central SBP, which is physiologically lower than brachial SBP, is significantly reduced has never been investigated. METHODS: This study was a double-blind randomized trial for one year in patients with essential hypertension. RESULTS: For a similar DBP reduction, Per/Ind decreased SBP significantly more than atenolol, with a more pronounced reduction for central than for brachial SBP. After one year, the difference between brachial and central SBP was maintained by Per/Ind (8.28 +/- 1.53 mm Hg) and significantly attenuated by atenolol (0.29 +/- 1.61 mm Hg). Under atenolol, the principal factor modulating SBP reduction was mean blood pressure. Under Per/Ind, this parameter played a minor role, and the central SBP reduction implied a major role for disturbed PWV and wave reflections. CONCLUSIONS: Under Per/Ind, but not atenolol, normalization of brachial SBP is achieved with a significantly greater reduction of central SBP. This hemodynamic profile reflects changes of wave reflections issued from distal arterial and arteriolar territory, where Per/Ind, but not atenolol, is known to improve vessel wall structure.     

老年男性原发性高血压患者动态血压及血压变异性与踝臂指数的关系探讨

目的评价老年男性原发性高血压患者动态血压及血压变异性(BPV)与踝臂指数(ABI)的关系。方法入选老年男性原发性高血压患者160例,按照ABI分为正常ABI组(ABI>0.90)104例和低ABI组(ABI≤0.90)56例,比较并分析其24 h动态血压参数和BPV参数。结果低ABI组较正常ABI组24 h平均脉压[(62.4±13.8)mm Hg比(53.0±13.0)mm Hg]、日间平均脉压[(67.3±17.0)mm Hg比(55.4±20.0)mm Hg]和夜间平均脉压[(63.0±16.0)mm Hg比(52.9±13.6)mm Hg]均高(P<0.01),同时夜间收缩压最大值[(146.5±17.4)mm Hg比(135.5±17.1)mm Hg]、夜间收缩压标准差[(12.4±4.0)mm Hg比(10.1±4.2)mm Hg]均大(P<0.05)。结论老年男性原发性高血压患者夜间收缩压最大值、夜间收缩压标准差、日间平均脉压、夜间平均脉压和24 h平均脉压升高可能是低ABI的危险因素。     

动脉粥样硬化性肾动脉狭窄患者24小时动态血压特征及靶器官损害相关研究

目的探讨动脉粥样硬化性肾动脉狭窄(ARAS)患者24 h动态血压、昼夜节律变化特征及靶器官损害。方法选择2014年1月~2018年12月在上海交通大学医学院附属瑞金医院高血压科连续住院的ARAS患者121例(ARAS组),另选择同期年龄、性别、体质量指数和高血压病程等匹配的原发性高血压(EH)患者418例(EH组),观察并比较2组诊室及24 h动态血压及靶器官损害的差异。结果与EH组比较,ARAS组诊室收缩压[(155±23)mm Hg(1mm Hg=0.133k Pa)vs(145±22)mm Hg,P<0.01]、诊室脉压[(75±20)mm Hg vs(65±18)mm Hg,P<0.01]、24h收缩压[(143±19)mm Hg vs(130±16)mm Hg,P<0.01]、昼间收缩压[(145±18)mm Hg vs(133±16)mm Hg,P<0.01]、夜间收缩压[(138±21)mm Hg vs(123±18)mm Hg,P<0.01]、夜间舒张压[(75±12)mm Hg vs(73±10)mm Hg,P<0.05]明显升高,差异有统计学意义。与EH组比较,ARAS组杓型血压比例明显降低,反杓型血压比例明显升高(P<0.05)。校正相关因素后,与EH组比较,ARAS组颈动脉内膜中层厚度、左心室质量指数及血浆N末端B型钠尿肽前体水平明显升高,差异有统计学意义(P<0.01)。结论ARAS患者收缩压及夜间血压较高,更多表现为反杓型血压。有独立于血压及肾功能水平更严重的靶器官损害。     

动态血压均值及脉压在评估原发性高血压早期肾损害中的临床研究

目的探讨动态血压均值及动态脉压与微量蛋白尿的关系,以期为动态血压监测(ABPM)应用于早期诊断和评价高血压性肾损害提供科学依据。方法将原发性高血压患者125例按动态脉压(24 h PP)≤40 mm Hg(1mm Hg=0.133 kPa)、41～55 mm Hg、56～70 mm Hg、>70 mm Hg分为Ⅰ、Ⅱ、Ⅲ、Ⅳ组,测量24 h 平均收缩压(24h SBP)、24 h 平均舒张压(24 h DBP)、24 h PP、尿微量白蛋白(mA1b)及尿 N-乙酰-β-D-氨基葡萄糖苷酶(NAG),比较各组的尿 mA1b、NAG 检测值及其阳性率,进行24 h SBP、24 h DBP、24 h PP 与尿 mA1b、NAG 的相关回归分析。结果 (1)Ⅰ组与Ⅱ组之间,尿 mA1b、NAG 及微量蛋白尿阳性率差异无统计学意义(P>0.05),Ⅱ组、Ⅲ组与Ⅳ组随24 h PP 的增高,尿 mA1b、NAG 及微量蛋白尿阳性率均依次明显增高,各组间差异有统计学意义(P<0.05);(2)24 h PP、24 h SBP 与尿 mA1b、NAG 呈正相关(r=0.79、0.78、0.78、0.76,P<0.05),24 h DBP 与mA1b、NAG 呈负相关(r=0.64、-0.65,P<0.05);建立多元回归方程得出高血压早期肾损害时对应的24 hSBP、24 h DBP 及24 h PP 值分别为150 mm Hg、91 mm Hg、58 mm Hg。结论动态血压均值及动态脉压可为原发性高血压患者早期肾损害的检测评价指标,24 h SBP 高于150 mm Hg、24 h PP 高于58 mm Hg,24 h DBP 过度下降的患者为高血压性肾损害高危患者。     

Effect of different antihypertensive drug classes on central aortic pressure

Central aortic systolic blood pressure (BP) is an important determinant of cardiac workload and cardiac hypertrophy. The relationship of central aortic systolic BP and brachial BP varies depending on the stiffness of blood vessels. It is not certain whether the different drug classes affect the brachial and aortic systolic BP in a similar manner.In a double-blind crossover study, we measured the effects of the four major drug classes compared with placebo on central aortic pressure. Central aortic pressure and various indices were determined using the Sphygmo Cor apparatus. The study was undertaken in patients aged 65 to 85 years with systolic BP >150 mm Hg at study entry. Results are reported for 32 patients who had satisfactory applanation tonometry in all five periods.Calcium channel blockers and diuretics caused a greater fall in brachial artery systolic BP than angiotensin-converting enzyme (ACE) inhibitors or beta-blocking drugs. On placebo, central aorta augmentation pressure and index were 23 mm Hg and 33.3%; on ACE inhibitors the values were 18 mm Hg and 30%; on beta-blockers, 26 mm Hg and 38.5%; on calcium channel blockers, 16 mm Hg and 28%; and on diuretics, 17 mm Hg and 28.8%. The augmentation pressure on beta-blocking drugs was greater than on the other three drug classes (P <.05), and augmentation pressures on ACE inhibitors, calcium channel blockers, and diuretics were less than on placebo (P <.05). The lowest central aortic pressures were achieved with calcium blocking drugs and diuretics.Therapy based on brachial artery recordings may thus overestimate the effect of beta-blocking drugs on central aortic systolic BP and underestimate the effectiveness of ACE inhibitors and calcium blocking drugs. The clinical importance of this discrepancy needs to be evaluated.     

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 hypertrophy.     

Validation of a generalized transfer function to noninvasively derive central blood pressure during exercise

Exercise brachial blood pressure (BP) predicts mortality, but because of wave reflection, central (ascending aortic) pressure differs from brachial pressure. Exercise central BP may be clinically important, and a noninvasive means to derive it would be useful. The purpose of this study was to test the validity of a noninvasive technique to derive exercise central BP. Ascending aortic pressure waveforms were recorded using a micromanometer-tipped 6F Millar catheter in 30 patients (56+/-9 years; 21 men) undergoing diagnostic coronary angiography. Simultaneous recordings of the derived central pressure waveform were acquired using servocontrolled radial tonometry at rest and during supine cycling. Pulse wave analysis of the direct and derived pressure signals was performed offline (SphygmoCor 7.01). From rest to exercise, mean arterial pressure and heart rate were increased by 20+/-10 mm Hg and 15+/-7 bpm, respectively, and central systolic BP ranged from 77 to 229 mm Hg. There was good agreement and high correlation between invasive and noninvasive techniques with a mean difference (+/-SD) for central systolic BP of -1.3+/-3.2 mm Hg at rest and -4.7+/-3.3 mm Hg at peak exercise (for both r=0.995; P<0.001). Conversely, systolic BP was significantly higher peripherally than centrally at rest (155+/-33 versus 138+/-32 mm Hg; mean difference, -16.3+/-9.4 mm Hg) and during exercise (180+/-34 versus 164+/-33 mm Hg; mean difference, -15.5+/-10.4 mm Hg; for both P<0.001). True myocardial afterload is not reliably estimated by peripheral systolic BP. Radial tonometry and pulse wave analysis is an accurate technique for the noninvasive determination of central BP at rest and during exercise.     

Central hemodynamics and cardiovascular risk in nondippers

J Clin Hypertens (Greenwich). 2011;13:557–562. ©2011 Wiley Periodicals, Inc. Failure of blood pressure (BP) to decline appropriately overnight (nondipping) is associated with increased risk. This may be due to inappropriately raised supine central BP and this study’s first aim was to examine this hypothesis. Secondly, aortic stiffness, central hemodynamics, and left ventricular (LV) mass were measured as other possible mechanisms of higher risk. Brachial and central BP (supine and seated), aortic stiffness, central hemodynamics, and LV dimensions were measured in 95 patients with hypertension (mean age 62±8 standard deviation). Central hemodynamics were recorded by combined radial tonometry and 3‐dimensional echocardiography. Seated brachial and central systolic BP (SBP) were similar between dippers (n=52) and nondippers (n=43). However, nondippers had higher supine brachial (132±14 mm Hg vs 126±11 mm Hg; P=.029) and central (121±15 mm Hg vs 115±11 mm Hg; P=.024) SBP. Aortic stiffness was not different between groups (P=.76), but LV mass index (33.0±6.2 vs 29.4±7.2 g/m^2.7; P=.019), stroke volume index (30.2±6.2 mL/m² vs 27.4±6.0 mL/m²; P=.040), and LV stroke work (3246±815 mm Hg/mL/m² vs 2778±615 mm Hg/mL/m²; P=.005) were all higher in nondippers. Dipper status independently predicted LV mass index (β=3.61; P=.001). Nondippers have higher supine brachial and central SBP, significantly different central hemodynamics, and elevated LV mass index compared with dippers. These cardiovascular anomalies possibly contribute to increased mortality risk.     

Central blood pressure measurement may improve risk stratification

Central systolic blood pressure (SBP) may differ between individuals with similar brachial SBP, which may have implications for risk assessment. This study aimed to determine the variation and potential clinical value of central SBP between patients with similar brachial SBP. Brachial SBP was measured by sphygmomanometer and central SBP by radial tonometry in 675 people (430 men), comprising healthy individuals (n = 222), patients with known or suspected coronary artery disease (n = 229) and diabetes (n = 224). Individuals were stratified by brachial SBP in accordance with European Society of Hypertension guidelines (optimal, normal, high-normal, grades 1, 2 and 3 hypertension). The potential clinical value of central SBP was determined from the percentage of patients re-classified into different brachial SBP groups due to the difference between brachial and aortic SBP (defined as brachial SBP-central SBP). Central SBP increased with each brachial SBP level (optimal to grade 3 hypertension; P < 0.001 for all). However, large variation in brachial-aortic SBP difference occurred within each brachial SBP group (range 2-33 mm Hg), resulting in sizeable overlap of central SBP between brachial SBP groups. For patients with normal brachial SBP, 96% had central SBP within the range of patients with high-normal brachial SBP, as well as 64% within the range of patients with grade 1 hypertension. We conclude that wide variation in brachial-aortic SBP difference occurs between patients with similar brachial SBP. This results in a significant overlap of central SBP scores between brachial SBP risk groups. This is likely to have treatment implications but remains to be tested.