动态观察臂踝动脉脉搏波传导速度变化来预测青年人血压的改变

目的观察臂踝动脉脉搏波传导速度(baPWV)对青年人血压进展的影响。方法以2010-2013年(第1次)健康体检且同期参加baPWV检测的指标作为基数,于2014-2015(第2次)健康体检指标作为随访资料,进行对照研究,应用多元线性回归分析及多元Logistic回归分析baPWV与青年人血压进展的相关性。结果①符合入选标准的研究对象共2784例,年龄(38.1±5.1)岁,其中男性2208例(79.3%)。②在多元线性回归分析中,校正其他混杂因素后,baPWV水平不仅与基线及随访血压值呈正相关,而且与它们的差值(Δ收缩压、Δ舒张压)呈线性关系。基线baPWV每增加1.0 m/s,基线收缩压和舒张压分别增加2.01和1.22 mm Hg;随访收缩压和舒张压分别增加1.79和0.86 mm Hg;Δ收缩压和Δ舒张压分别增加0.58和0.26 mm Hg。③在多因素Logistic回归分析中,校正其他混杂因素后,动脉硬化人群新发高血压的风险是非动脉硬化人群的1.29倍(95%CI 1.17～1.39);基线baPWV每增加1个标准差,新发高血压的风险增加至1.76倍(OR=1.76,95%CI 1.53～2.03)。结论动态观察baPWV变化可以反映血压变化及动脉硬化的进展。     

老年单纯收缩期高血压患者动态血压参数对脑白质病变的影响

目的探讨老年单纯收缩期高血压(ISH)患者24h动态血压参数对脑白质病变(WML)的影响。方法选择老年ISH患者96例,根据WML评分标准分为无-轻度WML组49例和中-重度WML组47例,比较2组患者一般情况及动态血压参数。结果中-重度WML组24h收缩压、昼间收缩压、夜间收缩压、昼间收缩压变异系数、夜间收缩压变异系数、非杓型、反杓型比例明显升高,而24h舒张压、昼间舒张压、夜间舒张压及杓型比例明显降低(P<0.05)。多因素logistic回归分析显示,24h收缩压(OR=2.89,95%CI:1.14~5.89,P=0.016)、昼间收缩压变异系数(OR=1.75,95%CI:1.30~3.42,P=0.005)、夜间收缩压变异系数(OR=1.46,95%CI:0.99~1.55,P=0.001)及年龄(OR=1.13,95%CI:0.82~1.57,P=0.021)是WML的独立危险因素。结论老年ISH患者24h收缩压、昼间收缩压变异系数、夜间收缩压变异系数是WML的独立危险因素,高收缩压、低舒张压、高收缩压变异系数及异常的血压节律对WML的发生、发展有不良影响。     

维持性血液透析患者脑梗死发生率及危险因素研究

目的了解维持性血液透析(MHD)患者中脑梗死的发生率及其相关危险因素。方法选择2011年1月1日~2016年6月31日在我院行MHD的尿毒症患者327例,将发生急性脑梗死的34例患者作为脑梗死组,未发生脑梗死的293例患者作为非脑梗死组。回顾性分析MHD患者的临床资料,并进行单因素及多因素logistic回归分析。结果 327例MHD患者中,脑梗死发生率为10.4%。脑梗死组糖尿病(58.8%vs 38.6%)和冠心病(29.4%vs 8.5%)比例、透析前收缩压[(160.38±23.50)mm Hg(1 mm Hg=0.133kPa)vs(136.81±21.05)mm Hg]、舒张压[(91.76±13.74)mm Hg vs(78.90±13.19)mm Hg]和白蛋白水平[(39.75±5.47)g/L vs(37.88±5.10)g/L]明显高于非脑梗死组(P0.05,P0.01)。logistic回归分析显示,糖尿病(OR=3.420,95%CI:1.355~8.632)、冠心病(OR=7.860,95%CI:2.753~22.437)、透析前收缩压(OR=1.029,95%CI:1.004~1.055)、透析前舒张压(OR=1.059,95%CI:1.015~1.106)是发生脑梗死的影响因素。结论糖尿病、冠心病、透析前收缩压及舒张压是MHD患者发生脑梗死的危险因素。     

高龄老年人血压变异性与踝臂指数关系探讨

目的评价高龄老年人群血压变异性(BPV)与踝臂指数(ABI)的关系。方法入选年龄≥80岁高龄老人111例,按照ABI分为异常ABI组(ABI≤0.9或ABI>1.3)56例和正常ABI组(ABI>0.9)55例,比较2组24h动态血压参数和BPV参数;另根据血压将患者分为高血压组48例和非高血压组63例,观察2组BPV及ABI差异。logistic回归分析ABI独立危险因素。结果异常ABI组较正常ABI组24h舒张压、昼间舒张压和夜间舒张压明显降低(P<0.05),24h收缩压变异性[(12.80±2.66)mm Hg(1mm Hg=0.133kPa)vs(14.14±3.64)mm Hg]明显降低、夜间收缩压变异性[(11.99±4.19)mm Hg vs(9.97±4.05)mm Hg]明显增高(P<0.05)。高血压组24h收缩压变异性[(14.87±3.91)mm Hg vs(13.20±3.41)mm Hg]、夜间收缩压变异性[(12.27±5.50)mm Hg vs(10.33±3.93)mm Hg]明显增高,ABI[(0.98±0.21)vs(1.07±0.20)]明显降低(P<0.05)。logistic回归分析提示,夜间舒张压和夜间收缩压变异性为ABI的独立危险因素(P<0.05)。结论高龄老年人群24h舒张压、昼间及夜间舒张压、24h收缩压变异性、夜间收缩压变异性可能是异常ABI的危险因素。     

老年原发性高血压患者血压变异性对新发心房颤动的影响

目的探讨老年原发性高血压患者血压变异性对新发心房颤动(房颤)的影响。方法回顾性研究2010年1月~2011年12月在我院住院治疗不伴房颤的老年原发性高血压患者683例,根据随访期间是否新发房颤分为房颤组69例及非房颤组614例。记录基线特征、超声心动图参数。进行动态血压监测,按收缩压变异性中位数9.89mm Hg(1mm Hg=0.133kPa)将入选患者分为高变异性342例和低变异性341例。应用Cox回归方程分析血压变异性对新发房颤的影响。结果房颤组24h收缩压变异性明显高于非房颤组[(11.13±3.50)mm Hg vs(10.21±3.41)mm Hg,P=0.034],24h舒张压明显低于非房颤组[(67.19±8.16)mm Hg vs(69.33±8.39)mm Hg,P=0.045]。多因素Cox回归分析显示,24h收缩压变异性、脑出血及心脏永久性起搏器置入是老年原发性高血压患者新发房颤的独立危险因素(HR=1.949,95%CI:1.175~3.233,P=0.010;HR=2.983,95%CI:1.075~8.277,P=0.036;HR=2.567,95%CI:1.370~4.810,P=0.003)。结论收缩压变异性升高是老年原发性高血压患者新发房颤的独立危险因素。     

首次腔隙性脑梗死患者扩张的血管周围间隙与动态血压变异性分析

目的探讨首次腔隙性脑梗死患者扩张的血管周围间隙(EVRS)与动态血压变异性(BPV)的关系。方法入选符合标准的腔隙性脑梗死患者118例,均行头颅MRI和24h动态血压监测。利用4分半定量评分系统按EVRS是否2分分为2组,基底节平面:重度组44例,轻度组74例;半卵圆中心平面:重度组54例及轻度组64例。患者完成24h动态血压监测,比较各组动态血压相关参数,进行多因素logistic分析。结果在基底节平面,2组年龄、男性、高血压、冠心病、糖尿病、24h收缩压、昼间收缩压、昼间收缩压标准差、昼间收缩压变异系数和夜间舒张压变异系数有显著差异(P0.05);在半卵圆中心平面,2组年龄、高血压、24h收缩压和夜间收缩压标准差有显著差异(P0.05)。多因素logistic回归分析,基底节平面,年龄(OR=1.16,95%CI:1.01~1.22,P=0.02)、昼间收缩压变异系数(OR=1.62,95%CI:1.47~3.68,P=0.03)、夜间舒张压变异系数(OR=1.32,95%CI:1.12~2.43,P=0.04)是发生重度EVRS的独立危险因素。半卵圆中心平面,BPV与EVRS无相关性。结论首次腔隙性脑梗死患者BPV与基底节平面EVRS密切相关,基底节平面EVRS是高血压相关脑损害的独特表现。     

高龄高血压患者动态脉压和血脂与左心室肥厚的关系

目的探讨高龄高血压患者动态脉压(APP)和血脂与左心室肥厚(LVH)的相关性。方法入选年龄≥80岁的高血压患者110例,进行24 h动态血压监测、超声心动图检查及血脂检测。根据APP分为高脉压组(≥60mm Hg,1 mm Hg=0.133 kPa)74例和低脉压组(<60 mm Hg)36例,以左心室重量指数(LVMI)作为LVH的诊断标准,又分为LVH组50例和非LVH组60例。并进行相关分析和logistic回归分析。结果与低脉压组比较,高脉压组LVMI、LVH的发生率及各收缩压参数明显升高(P<0.05)。LVH组24 h收缩压、昼间收缩压、APP、脉压指数明显高于非LVH组(P<0.05),2组舒张压差异无统计学意义(P>0.05)。LVMI与APP、脉压指数、24 h收缩压、昼间收缩压、夜间收缩压呈正相关,与HDL-C呈负相关(P<0.05),与所有舒张压参数均无相关性(P>0.05)。APP是LVH的独立危险因素(OR=1.057,95%CI:1.018～1.096,P=0.003)。结论在高龄高血压患者中,APP与LVMI密切相关,是LVH的独立危险因素;HDL-C与LVMI密切相关。     

老年原发性高血压患者血压晨峰与左心室肥厚的关系

目的探讨老年原发性高血压患者血压晨峰与左心室肥厚的关系。方法选择老年原发性高血压患者80例,根据24 h动态血压监测分为2组:血压晨峰值≥55 mm Hg(1 mm Hg=0.133 kPa)为晨峰组,血压晨峰值<55mm Hg为非晨峰组,每组40例,均常规行超声心动图检查,计算左心室重量指数(LVMI)。结果晨峰组24h、昼间、夜间收缩压及血压晨峰均明显高于非晨峰组(P<0.05),晨峰组LVMI明显高于非晨峰组;左心室肥厚比例明显高于非晨峰组(P<0.05)。结论老年原发性高血压患者血压晨峰与左心室肥厚密切相关。     

老年住院患者衰弱指数与血压水平的关系

目的探讨老年住院患者衰弱指数的分布情况及其与血压水平的相关性。方法选择老年住院患者105例,依据衰弱指数评估量表分为衰弱组20例(0.45≤衰弱指数1)、衰弱前期组40例(0.20衰弱指数0.45)及非衰弱组45例(0衰弱指数≤0.20),同时收集人口学资料、24h平均收缩压、24h平均舒张压、昼间平均收缩压、昼间平均舒张压、夜间平均收缩压、夜间平均舒张压、降压药物数量及慢病情况。结果衰弱组24h平均收缩压明显低于非衰弱组和衰弱前期组[(115.95±12.26)mm Hg vs(124.74±12.96)mm Hg,(124.76±12.19)mm Hg(1mm Hg=0.133kPa),P0.05],昼间平均收缩压明显低于非衰弱组[(116.63±12.08)mm Hg vs(126.10±14.17)mm Hg,P0.05]。衰弱前期组平均降压药物数量明显高于非衰弱组[(2.13±0.99)种vs(1.42±1.10)种,P0.05]。衰弱指数与年龄、降压药物数量、脑卒中、恶性肿瘤、关节炎、慢性肾脏病、共病数量呈正相关,与24h平均收缩压、24h平均舒张压、昼间平均收缩压、昼间平均舒张压、夜间平均收缩压呈负相关(P0.05,P0.01)。结论老年住院患者中,衰弱发生率随增龄而增加;衰弱患者应适当减少降压药物数量,避免血压过低。     

老年心力衰竭患者出院时血压水平与预后的关系

目的探讨老年慢性心力衰竭(CHF)患者出院时血压水平与长期预后的关系。方法入选2010年1月~2011年12月上海市松江区中心医院心内科出院的LVEF<50%的老年CHF患者116例,随访期以心源性死亡33例作为事件组,另外83例作为非事件组。记录入院时和出院时的血压及常规检查参数,按照心力衰竭指南治疗,并进行3年随访。终点事件为心源性死亡。进行单因素Cox和多因素Cox分析。结果与非事件组比较,事件组患者出院时收缩压和舒张压降低[(108.7±10.5)/(68.5±8.4)mm Hg vs(130.3±14.2)/(74.4±10.2)mm Hg,1mm Hg=0.133kPa,P<0.01];脉压降低[(40.2±10.4)mm Hg vs(55.8±13.8)mm Hg,P<0.01]。单因素Cox分析显示,出院时收缩压<100mm Hg、脉压<45mm Hg是心源性死亡的危险因素;多因素Cox风险比例模型分析显示,出院时收缩压<100mm Hg(RR=0.918,95%CI:0.859~0.981)和N末端钠尿肽前体升高(RR=6.148,95%CI:1.841~20.532)是影响心源性死亡事件发生的主要危险因素。结论出院时收缩压<100mm Hg是老年CHF患者死亡终点的独立预测指标。     

老年原发性高血压患者晨峰与脉搏波传导速度相关性研究

目的探讨老年高血压患者血压晨峰与颈桡动脉脉搏波传导速度(crPWV)的相关性。方法选择老年原发性高血压患者159例,根据24 h动态血压结果,将患者分为晨峰组(95例)和非晨峰组(64例)。2组行crPWV检测,并测血生化。结果晨峰组crPWV明显高于非晨峰组[(11.5±1.7)m/s vs(9.1±1.6)m/s,P<0.01]。crPWV与血压晨峰(r=0.787.P<0.01)、24 h收缩压(r=0.649,P<0.01)、年龄(r=0.437,P<0.01)、空腹血糖(r=0.293,P<0.05)及LDL-c(r=0.354,P<0.05)呈正相关;以crPWV为应变量,年龄、高血压病程、体重指数、空腹血糖、24 h收缩压及舒张压、LDL-C、TC、TG、HDL-C、血压晨峰为自变量,进行多元线性逐步回归分析,血压晨峰、24 h收缩压、年龄为crPWV独立影响因素。结论血压晨峰与动脉粥样硬化密切相关。     

奥美沙坦酯与缬沙坦对原发性高血压患者血压晨峰的影响

目的比较奥美沙坦酯和缬沙坦治疗高血压患者血压晨峰的疗效。方法选择我院76例原发性高血压患者随机分为2组,分别接受奥美沙坦酯20-40mg／d或缬沙坦80-160mg／d治疗,共8周,观察服药前及服药后清晨血压变化。结果奥美沙坦酯组和缬沙坦组治疗后晨峰血压均有明显下降,与治疗前比较差异有统计学意义（P〈0．05）。奥美沙坦酯组和缬沙坦组晨峰血压下降的幅度分别为：／kSBP（10．22±0．35）mmHg、（5．63±0．21）mmHg;△DBP（7．71±0．29）mmHg、（3．55±0．14）mmHg,奥美沙坦酯组血压晨峰下降幅度高于缬沙坦组,差异有统计学意义（P〈0．05）。结论奥美沙坦酯和缬沙坦均可以有效地控制原发性高血压患者血压晨蜂现象,奥美沙坦酯优于缬沙坦。     

Morning blood pressure surge and hypertensive cerebrovascular disease: role of the alpha adrenergic sympathetic nervous system

BACKGROUND: The morning surge of blood pressure (BP) is associated with alpha-adrenergic activity. We studied the association between the alpha-adrenergic morning surge in BP and silent cerebrovascular disease in elderly patients with hypertension. METHODS: We conducted ambulatory BP monitoring three times (twice at baseline and after nighttime dosing of the alpha1-blocker doxazosin) in 98 elderly hypertensive patients in whom the presence of silent cerebral infarcts (SCI) was assessed by brain magnetic resonance imaging. The morning BP surge (MBPS) was calculated as the mean systolic BP during the 2 h after waking minus the mean systolic BP during 1 h that included the lowest sleep BP. The alpha-adrenergic MBPS was calculated as the reduction of MBPS by doxazosin. RESULTS: The prevalence of multiple SCI was higher in the Surge group (top quartile: MBPS > or = 45 mm Hg, n = 24) than in the Nonsurge group (MBPS < 45 mm Hg, n = 74) (54% v 31%, P = .04), and in the higher alpha-adrenergic surge group (top quartile: alpha-adrenergic MBPS > or = 28 mm Hg, n = 25) than in the lower alpha-adrenergic surge group (< 28 mm Hg, n = 73) (68% v 26%, P < .0001). In the Surge group, subjects with higher alpha-adrenergic surge (n = 17) had a markedly higher frequency of multiple SCI, whereas none in the lower alpha-adrenergic surge group had multiple SCI (n = 7) (77% v 0%, P = .001). The alpha-adrenergic MBPS was closely associated with multiple SCI (10 mm Hg increase: OR = 1.96, P = .006), independently of age, MBPS, 24-h systolic BP, and other confounding factors. CONCLUSION: The morning BP surge, particularly that dependent on alpha-adrenergic activity, is closely associated with advanced silent hypertensive cerebrovascular disease in elderly individuals.     

A multicenter, 14-week study of telmisartan and ramipril in patients with mild-to-moderate hypertension using ambulatory blood pressure monitoring

BACKGROUND: Blood pressure (BP) has a circadian pattern with a morning surge that is associated with an increased risk of acute coronary and cerebrovascular events. In a prospective, randomized, open-label, blinded-endpoint, parallel-group, multicenter, forced-titration study of telmisartan and ramipril, the efficacy of both drugs on mean ambulatory diastolic BP (DBP) and systolic BP (SBP) during the last 6 h of a 24-h dosing interval was evaluated. METHODS: After screening and a single-blind run-in phase, 812 adults with mild-to-moderate hypertension (defined as a mean seated DBP > or =95 mm Hg and < or =109 mm Hg and a 24-h ABPM mean DBP 7 > or = 85 mm Hg) were randomized to the open-label, 14-week, forced-titration, active-treatment phase as follows: telmisartan 40 mg/80 mg/80 mg (n = 405) or ramipril 2.5 mg/5 mg/10 mg (n = 407), once daily in the morning. The primary efficacy variable was change from baseline in the last 6-h mean DBP and SBP at 8 and 14 weeks as assessed by ambulatory BP monitoring (ABPM). Secondary efficacy variables were changes from baseline in BP control during each of the 24-h periods and in-clinic trough cuff BP. RESULTS: Telmisartan 80 mg was superior to ramipril 5 mg and 10 mg in change from baseline in the last 6-h ABPM mean DBP and SBP at both 8 and 14 weeks (both P < .0001), respectively. At 14 weeks, the adjusted mean change from baseline in DBP for telmisartan 80 mg was -8.8 mm Hg compared with that for ramipril 10 mg of -5.4 mm Hg (P < .0001). For SBP, the adjusted mean change from baseline for telmisartan 80 mg was -12.7 mm Hg compared with that for ramipril 10 mg of -7.9 mm Hg (P < .0001). At 14 weeks, telmisartan 80 mg also yielded superior reductions from baseline in trough cuff BP compared with ramipril 10 mg (DBP: -11.0 mm Hg v -7.8 mm Hg, respectively; SBP: -14.3 mm Hg v -9.1 mm Hg, respectively; both P < .0001). Measures of 24-h BP control favored telmisartan 80 mg versus ramipril 10 mg (P < .0001), as did other secondary ABPM endpoints during the daytime, night-time, and morning periods. Treatment-related adverse events were uncommon; patients treated with ramipril had a higher incidence of cough than those treated with telmisartan (10.1% v 1.5%, respectively). CONCLUSIONS: Telmisartan 80 mg was consistently more effective than ramipril 10 mg in reducing both DBP and SBP during the last 6 h of the dosing interval, a measure of the early morning period when patients are at greatest risk of life-threatening cardiovascular and cerebrovascular events. Telmisartan 80 mg was also more effective than ramipril 10 mg in reducing BP throughout the entire 24-h dosing interval. Both drugs were well tolerated.     

老年轻中度原发性高血压患者家庭自测血压变异与冷加压试验的相关性

目的探讨老年轻中度原发性高血压患者家庭自测血压变异与冷加压试验的相关性。方法于2012年5月~2013年8月自山东省临沂市兰山区高血压社区管理的高血压患者中,筛选老年轻中度原发性高血压患者259例,所有入选受试者均进行7d家庭血压自测,计算后6d连续的收缩压及舒张压变异性相关指标及平均心率;采用冷加压试验以刺激全身交感神经兴奋,并将冷加压试验阳性作为阳性组116例,冷加压试验阴性作为阴性组143例。结果阳性组早间舒张压、收缩压标准差、舒张压标准差、最高收缩压、最高舒张压、早-晚收缩压差、早-晚舒张压差、最高-最低收缩压差、最高-最低舒张压差,平均心率均高于阴性组(P<0.05)。阳性组晚间收缩压、晚间舒张压低于阴性组(P<0.05)。回归分析显示,即刻及60s收缩压变化幅度始终是影响收缩压标准差、舒张压标准差、早-晚收缩压差、早-晚舒张压差、最高-最低收缩压差及最高-最低舒张压差的主要因素。结论老年轻中度原发性高血压患者的家庭自测血压变异与冷加压试验反应相关,冷加压试验反应越强,血压变异越大。     

老年高血压患者动态血压负荷和脉搏波传导速度的相关性研究

目的探讨老年高血压患者24 h动态血压负荷与颈桡动脉脉搏波传导速度(crPWV)的相关性。方法选取60～79岁的老年原发性高血压患者187例,对所有入选对象进行24 h动态血压监测,根据获取的24 h动态血压监测参数分为杓型组90例与非杓型组97例,选择同期体检人群82例为正常对照组。所有受试者行24 h动态血压监测,应用脉搏波速度测定仪测定crPWV,并进行分析。结果杓型组及非杓型组24 h、昼间及夜间收缩压、舒张压负荷均显著高于正常对照组(P<0.01)。非杓型组夜间血压负荷较杓型组升高(P<0.05)。杓型组及非杓型组crPWV均较正常对照组升高(P<0.05)。控制性别、年龄因素后,老年高血压患者24 h收缩压、夜间收缩压负荷、昼间舒张压负荷是crPWV影响的主要因素。结论老年高血压患者动态血压负荷升高,大动脉顺应性降低,其中24 h收缩压、夜间收缩压负荷、昼间舒张压负荷是影响大动脉顺应性的主要危险因素。     

老老年人群动态血压参数与动脉僵硬度的相关性

目的探讨老老年人群动态血压参数与动脉僵硬度的相关性。方法筛选年龄≥80岁的老老年人238例,以血压≥160/95 mm Hg(1 mm Hg=0.133 kPa)为标准,分为高血压组(134例)和对照组(104例),并进行臂-踝脉搏传导速度(baPWV)和24 h动态血压监测。用Pearson分析动态血压各参数与动脉僵硬度的相关性。结果高血压组baPWV高于对照组(P<0.05)。高血压组偶测收缩压,24 h、昼间和夜间收缩压、舒张压、脉压,收缩压负荷及舒张压负荷均高于对照组.夜间收缩压下降率、舒张压下降率低于对照组,差异有统计学意义(P<0.05,P<0.01)。baPWV与偶测血压;24 h收缩压、舒张压、脉压;昼间收缩压、舒张压、脉压、心率;夜间收缩压、舒张压、脉压;收缩压负荷、舒张压负荷呈正相关(P<0.05,P<0.01),而与夜间收缩压下降率呈负相关(P<0.01)。结论高血压是老老年人群动脉僵硬度增加的一个重要因素,动脉僵硬度与动态血压、脉压、心率及血压负荷相关。     

Hypertension is associated with a high risk of cancer.

To investigate the possible relationship between hypertension and cancer, a retrospective analysis was carried out using a database including 1225 cases, of which 552 were hypertensives and 673 normotensives. Seventy cases of cancers with different origins were found during a 17-year follow-up. Odds ratio (OR) for occurrence of cancer was calculated. It was shown that an age over 40 years, male sex, alcohol-taking, systolic and diastolic blood pressures (SBP/DBP) were the five risk factors for the occurrence of cancers, while occupation, smoking, body mass index, left ventricular hypertrophy, and antihypertensive medication had no effect on cancer incidence. Hypertensives were at a high risk of overall cancer incidence with OR 2.2 (P < 0.01). After stratification of age, OR for hypertensives aged 40-49 years old with SBP > or =140 mm Hg or DBP > or =90mm Hg was 3.18 and 2.98 (P < 0.01 respectively). The OR of cancer for non-alcohol taking male hypertensives with SBP < or =140 mm Hg or DBP > or =90 mm Hg were 3.6 (95%CI 1.37-9.68, P = 0.003) and 5.67 (95%CI 2.01-16.75, P < 0.001), 7.55 (95%CI 2.10-33.19, P < 0.001) and 7.80 (95%CI 2.14-33.79, P < 0.001) for non-alcohol taking female hypertensives with SBP > or =140 mm Hg or DBP > or =90 mm Hg. After adjustment of age, sex and alcohol taking, the OR of the cancer incidence was 3.45 (95%CI 1.30-9.01, P < 0.01) for male and 5.0 (95%CI 1.56-16.67, P < 0.01) for female hypertensives aged 40-49 years. Multiple logistic regression analysis shows that age over 40 years, male sex, alcohol-taking, and DBP were the four independent risk factors for cancers. It is concluded that hypertension is associated with a high risk of cancer.