北京住院高血压患者心脏结构功能及治疗达标情况的分析

目的回顾性分析北京市三级医院住院的高血压患者的心脏结构功能改变的相关因素,为临床治疗提供依据。方法采用回顾性调查的方法,通过超声诊断技术分析高血压患者的心脏结构及功能的参数,并对患者的年龄、血压水平、合并的危险因素及疾病、降压药物使用情况进行相关分析。结果共分析住院的原发性高血压患者5106例,平均年龄63．78岁,平均血压145．97／84．23mmHg（1mmHg=0．133kPa）。75．5％的患者至少合并一种心血管危险因素,随着血压水平的升高,合并左心室肥厚的患者比例明显增高。有近30％的患者合并不同程度的心功能不全。调查中发现,左房扩大和左心室舒张功能不全是高血压患者最常见的心脏损害。多因素分析显示,较高的收缩压、舒张压、血肌酐水平、老年和低高密度脂蛋白胆固醇是高血压合并左心室肥厚的危险因素。所有患者血压达标率（血压〈140／90mmHg）为32．1％,单药治疗达标率为38．1％。钙拮抗剂和利尿剂是使用最多的两类降压药。结论要重视血压的治疗达标和多重危险因素共同干预以延缓或逆转高血压心脏损害的发生发展,原发性高血压的防治仍任重而道远。     

Impact of age on left ventricular hypertrophy regression during antihypertensive treatment with losartan or atenolol (the LIFE study)

To assess the influence of age on changes in left ventricular (LV) mass and geometry during antihypertensive treatment, we related age to clinical and echocardiographic findings before and after 4 years of antihypertensive treatment in a subset of 560 hypertensive patients without known concurrent disease in the Losartan Intervention For Endpoint reduction in hypertension (LIFE) study, which randomized patients to blinded losartan- or atenolol-based treatment. Patients >/=65 years (older group) included more women and patients with isolated systolic hypertension or albuminuria (all P<0.05). Compared to patients <65 years, older patients had higher pulse pressure, LV mass, and prevalence of concentric hypertrophy at baseline (78 vs 69 mmHg, 234 vs 224 g, and 28 vs 16%, respectively, all P<0.01), while the mean blood pressure did not differ. Over 4 years, reductions in LV mass and the mean blood pressure were similar in both groups, but older patients more often had residual hypertrophy (31 vs 15%, P<0.001) with a preponderance of eccentric geometry. In multivariate analysis of 4-year change in LV mass controlling for baseline mass, larger hypertrophy reduction was associated with losartan treatment, while age, gender, body mass index, and 4-year change in pulse pressure and albuminuria did not enter (Multiple R (2)=0.40, P<0.001). Thus, in up-to-80-year-old hypertensive patients with left ventricular hypertrophy, age did not significantly attenuate hypertrophy reduction during antihypertensive treatment, although residual hypertrophy was more prevalent in older patients as a consequence of higher initial LV mass.     

Persistent remodeling of resistance arteries in type 2 diabetic patients on antihypertensive treatment

We hypothesized that resistance arteries from diabetic patients with controlled hypertension have less remodeling than vessels from untreated hypertensive subjects. Eight normotensive subjects (aged 44+/-3 years, 3 men; values are mean+/-SEM), 19 untreated hypertensive subjects (46+/-2 years, 9 men), and 23 hypertensive subjects with type 2 diabetes mellitus under antihypertensive treatment (58+/-1 years, 15 men) were studied. Resistance arteries dissected from gluteal subcutaneous tissue were assessed on a pressurized myograph. Most diabetic patients (70%) were being treated with angiotensin-converting enzyme inhibitors. Although systolic blood pressure was still above the normotensive range in these patients (144+/-2 versus 150+/-3 mm Hg in hypertensive and 114+/-4 mm Hg in normotensive subjects), diastolic blood pressure was well controlled (83+/-2 mm Hg) and significantly lower compared with that in untreated hypertensives (100+/-1 mm Hg; P<0.001) but higher than in normotensives (76+/-3 mm Hg; P<0.05). Thus, pulse pressure was higher in diabetic patients (P<0.05). The media-to-lumen ratio of resistance arteries was greater in hypertensives (0.083+/-0.002) compared with normotensive controls (0.059+/-0.003; P<0.05) and was even higher in diabetic hypertensive subjects (0.105+/-0.004; P<0.001 versus normotensive controls). The medial cross-sectional area was greater in diabetic and hypertensive patients compared with normotensive controls (P<0.001). Acetylcholine-induced relaxation was impaired in vessels from hypertensive patients and from patients with both diabetes mellitus and hypertension (P<0.05 versus normotensive controls), whereas endothelium-independent vasorelaxation was similar in all groups. Despite effective antihypertensive treatment, resistance arteries from hypertensive diabetic patients showed marked remodeling, greater than that of vessels from untreated, nondiabetic, hypertensive subjects, in agreement with the high cardiovascular risk of subjects suffering from both diabetes and hypertension.     

In-treatment resolution or absence of electrocardiographic left ventricular hypertrophy is associated with decreased incidence of new-onset diabetes mellitus in hypertensive patients: the Losartan Intervention for Endpoint Reduction in Hypertension (LIFE) Study

Treatment of hypertensive patients with electrocardiographic left ventricular hypertrophy with losartan-based therapy is associated with lower incidence of diabetes mellitus and greater regression of hypertrophy than atenolol-based therapy. However, whether in-treatment resolution or continued absence of electrocardiographic hypertrophy is independently associated with decreased incidence of diabetes is unclear. Electrocardiographic hypertrophy was evaluated over time in 7998 hypertensive patients without diabetes at baseline in the Losartan Intervention For Endpoint reduction in hypertension (LIFE) study who were treated with losartan- or atenolol-based regimens and followed with serial electrocardiograms and blood pressure determinations. Electrocardiographic hypertrophy was defined using gender-adjusted Cornell voltage-duration product criteria >2440 mm.ms. During mean follow-up of 4.6+/-1.2 years, diabetes developed in 562 patients (7.0%). In a Cox model adjusting for treatment assignment, in-treatment resolution or continued absence of Cornell product hypertrophy was associated with a 38% lower risk of new diabetes (HR 0.62, 95% CI 0.50 to 0.78). After adjusting for the association of new diabetes with prior antihypertensive treatment, baseline glucose, and Framingham risk score, baseline and in-treatment systolic and diastolic pressure, HDL, uric acid, and body mass index, and the decreased incidence associated with losartan-based therapy, in-treatment continued absence, or resolution of Cornell product hypertrophy remained associated with a 26% lower risk of new diabetes (HR 0.74, 95% CI 0.58 to 0.93). Thus, compared with presence of hypertrophy by Cornell product criteria during antihypertensive treatment, resolution or continued absence of Cornell product hypertrophy is associated with a lower incidence of diabetes, even after adjusting for the impact of treatment with losartan and other risk factors for diabetes.     

The clinical performance of nicardipine in elderly hypertensive patients with concomitant diseases

The efficacy and tolerance of nicardipine were evaluated in 2184 ambulatory hypertensive patients with or without concomitant diseases in a 24-week Italian multicenter study. Of the total patient group 1083 had one or more concomitant diseases (diabetes mellitus, coronary heart disease, cardiac failure, mild renal failure, chronic cerebrovascular disease, obstructive lung disease, and peripheral vascular disease); of these patients, 419 were aged over 65 years. Patients were seen on an outpatient basis and after a 2- to 4-week washout period were admitted to the study. The initial nicardipine dose of 20 mg three times a day was titrated in subsequent weeks; thereafter a second antihypertensive drug was added if seated diastolic blood pressure was not reduced below 90 mm Hg. The nicardipine-based therapy significantly lowered seated blood pressure in the whole population (mean 185/102 to 152/86 mm Hg) without clinically and statistically significant differences between the patient subgroups with concomitant diseases. There were no changes in either symptoms, or biochemical and instrumental tests of the concomitant diseases. The incidence of side effects was low; in particular, there was no orthostatic hypotension. Nicardipine-based treatment is therefore effective, safe, and well tolerated in elderly hypertensive patients with concomitant disease.     

Salt intake, hypertension and diabetes mellitus

Diabetes mellitus affects approximately 135 million people in the world. Diabetes and hypertension are both relatively common diseases in westernised countries. Both entities increase with age. Essential hypertension accounts for the majority of hypertension in people with type 2 diabetes, who constitute more than 90% of those with a dual diagnosis of diabetes and hypertension. The benefit conferred per mm Hg blood pressure reduction appears to be greater in persons with type 2 diabetes than in those with hypertension and non-coexistent diabetes mellitus. Similar to a subset of patients with essential hypertension, type 2 diabetic patients manifest dietary NaCl-induced exacerbation of hypertension. Recent guidelines have emphasised that the target blood pressure levels for patients with diabetes should be lower than in other hypertensive groups. An increased total body sodium and enhanced vascular reactivity are found in people with diabetes and most type 2 diabetic patients are salt sensitive. Type 2 diabetes with hypertension is associated with reduced renal plasma flow when dietary salt intake is high. Experimental, observational and interventional evidence support the benefits of sodium restriction in hypertensives. However, the full effects of sodium restriction are usually not obvious for at least 5 weeks. Other favourable effects of moderate reduction in sodium intake are a regress left ventricular hypertrophy, decrease in diuretic-induced potassium wastage, reduction in proteinuria, protection against stroke and from osteoporosis and renal stones, and enhancement of the antihypertensive effect of the antihypertensive agents.     

Essential hypertension

Essential hypertension can be defined as a rise in blood pressure of unknown cause that increases risk for cerebral, cardiac, and renal events. In industrialised countries, the risk of becoming hypertensive (blood pressure >140/90 mm Hg) during a lifetime exceeds 90%. Essential hypertension usually clusters with other cardiovascular risk factors such as ageing, being overweight, insulin resistance, diabetes, and hyperlipidaemia. Subtle target-organ damage such as left-ventricular hypertrophy, microalbuminuria, and cognitive dysfunction takes place early in the course of hypertensive cardiovascular disease, although catastrophic events such as stroke, heart attack, renal failure, and dementia usually happen after long periods of uncontrolled hypertension only. All antihypertensive drugs lower blood pressure (by definition) and this decline is the best determinant of cardiovascular risk reduction. However, differences between drugs exist with respect to reduction of target-organ disease and prevention of major cardiovascular events. Most hypertensive patients need two or more drugs for blood-pressure control and concomitant statin treatment for risk factor reduction. Despite the availability of effective and safe antihypertensive drugs, hypertension and its concomitant risk factors remain uncontrolled in most patients.     

Effect of blood pressure reduction on abnormal left atrial appendage function in untreated systemic hypertensive patients with sinus rhythm

To investigate whether reduction in blood pressure has a beneficial effect on left atrial appendage (LAA) function, the authors evaluated 24 untreated systemic hypertensive patients with normal left ventricular systolic function in sinus rhythm at baseline and at 3 months after initiation of antihypertensive therapy. They performed transthoracic and transesophageal echocardiographic examinations in hypertensive patients before and after treatment of hypertension. Three of the 24 patients had blood pressure that failed to respond to the regimen of antihypertensive therapy and were removed from the analysis. Of the remaining 21 patients, mean systolic and diastolic blood pressures at baseline were 170 +/- 18 and 104 +/- 6 mm Hg, respectively, and fell significantly at 3 months to 141 +/- 10 and 90 +/- 5 mm Hg, respectively, (p<0.001) after initiation of antihypertensive therapy. There was no significant change in heart rate with treatment (baseline 81 +/- 8 and at 3 months 84 +/- 9 beats/min). There was no significant change in left ventricular end-diastolic diameter, left ventricular ejection fraction, left ventricular wall thickness, or left atrial diameter from baseline (49 +/- 4 mm, 58 +/- 5%, 12 +/- 1 mm, and 41 +/- 4 mm, respectively) at 3 months (48 +/- 5 mm, 59 +/- 4%, 12 +/- 1 mm, and 40 +/- 3 mm). The treatment caused a significant reduction in maximal LAA areas (6.3 +/- 1.3 cm2 at baseline, 4.6 +/- 0.7 cm2 at 3 months, p<0.001), with a concomitant increase in LAA emptying velocity (44 +/- 7 cm/sec at baseline, 60 +/- 9 cm/sec at 3 months, p<0.001). In conclusion, these findings suggest that reduction in blood pressure with antihypertensive therapy could improve LAA function in hypertensive patients with normal left ventricular systolic function in sinus rhythm.     

Regression of left ventricular mass is accompanied by improvement in rapid left ventricular filling following antihypertensive therapy with metoprolol

Left ventricular hypertrophy is associated with abnormal left ventricular diastolic filling in patients with hypertension. To assess the effects of antihypertensive therapy on the heart in nine previously untreated patients with echocardiographically-detected left ventricular hypertrophy, left ventricular mass and rapid left ventricular filling rate were compared before and after 6 months of treatment with metoprolol monotherapy. Metoprolol was given in doses of 100 to 400 mg/day (average dose, 167 mg/day in two divided doses) and significantly reduced both casual, office blood pressure (150/101 to 130/86 mm Hg, p less than 0.01) and 24-hour ambulatory blood pressure (139/91 to 126/79 mm Hg, p less than 0.05 for systolic, p less than 0.01 for diastolic). Following treatment with metoprolol, left ventricular mass index decreased from 135 +/- 20 to 120 +/- 13 gm/m2 (p less than 0.05), while rapid left ventricular filling rate increased from 1.89 +/- 0.24 to 2.09 +/- 0.27 end-diastolic volumes/sec (p less than 0.01). The reduction in left ventricular mass index was secondary to decreased posterior and septal wall thicknesses (13% and 11%, respectively, p less than 0.05 for both), as there were no changes in the left ventricular internal dimensions. Neither resting nor exercise left ventricular ejection fraction changed on metoprolol therapy compared to the baseline values. These data demonstrate that regression of left ventricular hypertrophy in never-previously-treated hypertensive patients is accompanied by improved diastolic performance following beta-adrenergic blocker monotherapy.     

Is there a relationship between ambulatory intra-arterial blood pressure and left ventricular function?

The relationship between ambulatory intra-arterial blood pressure and left ventricular ejection fraction was examined in a group of 23 untreated hypertensive subjects who underwent concurrent radionuclide ventriculography. All patients had a normal ejection fraction at rest (range, 50-80%), and no significant correlation was found between blood pressure and resting ejection fraction. Sixty-one percent of patients failed to increase their ejection fraction by 5% on exercise; the mean daytime systolic pressure (168 +/- 15 mm Hg) was lower in this group than in those who had a normal exercise response (188 +/- 17 mm Hg; p less than 0.005). Thirty percent of patients had left ventricular hypertrophy based on electrocardiographic criteria; this group had a higher mean blood pressure (189 +/- 20 mm Hg) than the remainder (170 +/- 15 mm Hg; p less than 0.05). A closer correlation was demonstrated between blood pressure and ejection fraction response to exercise in the group with left ventricular hypertrophy (r = 0.8) than in the group without hypertrophy (r = 0.3). These results failed to demonstrate a linear relationship between blood pressure and ejection fraction. However, a relationship between the height of blood pressure and the development of left ventricular hypertrophy was shown, and myocardial response to exercise was increased in patients with left ventricular hypertrophy.     

Impaired left ventricular functional reserve in hypertensive patients with left ventricular hypertrophy

To determine whether patients with hypertension and especially those with left ventricular hypertrophy have subtle changes in cardiac function, we measured the increase in left ventricular ejection fraction and in systolic blood pressure to end-systolic volume index ratio with exercise in 40 hypertensive patients and 16 age-matched normotensive volunteers. Twenty-two hypertensive patients without hypertrophy had normal end-systolic wall stress at rest and exercise responses. In contrast, the 18 patients with echocardiographic criteria for left ventricular hypertrophy demonstrated a significant increase in end-systolic wall stress at rest compared with normal subjects (69 +/- 16 vs. 55 +/- 15 10(3) x dyne/cm2, p less than 0.05) despite having normal resting left ventricular size and ejection fraction. In patients with left ventricular hypertrophy, the increase in ejection fraction with exercise was less than in the normotensive control subjects (7 +/- 7 vs. 12 +/- 8 units, p less than 0.05), and delta systolic blood pressure to end-systolic volume with exercise was reduced (3.3 +/- 3.8 vs. 8.3 +/- 7.7 mm Hg/ml/m2, p less than 0.05). The hypertensive patients with hypertrophy displayed a shift downward and to the right in the relation between systolic blood pressure to end-systolic volume ratio and end-systolic wall stress compared with control subjects and hypertensive patients without left ventricular hypertrophy. Thus, hypertensive patients with left ventricular hypertrophy by echocardiography and normal resting ejection fraction exhibit abnormal ventricular functional responses to exercise. This finding may have implications in identifying patients at higher risk for developing heart failure.     

Beyond the Usual Strategies for Blood Pressure Reduction: Therapeutic Considerations and Combination Therapies

Rapidly accumulating clinical data have repeatedly demonstrated not only the critical importance of even small increases in blood pressure as a pathophysiologic factor in the development of cardiovascular disease, particularly in individuals with diabetes mellitus, but also the therapeutic necessity of more aggressive blood pressure reduction and the achievement of progressively lower blood pressure targets in reducing cardiovascular event rates. JNC VI has defined optimal blood pressure as ≤120/80 mm Hg, and Stage 1 hypertension as ≥140/80 mm Hg. Target blood pressures are now ≤130/80 mm Hg in patients with diabetes and <125/75 mm Hg for patients with hypertensive renal disease with proteinuria of>1 gm/24 hours. Achieving such target pressures is increasingly difficult, particularly in diabetic patients with chronic renal disease, who require complex multidrug antihypertensive regimens. This review attempts to provide some suggestions for constructing such antihypertensive regimens, and provides considerations for the appropriate use of diuretics and the most effective drug combinations. Factors potentially contributing to drug resistant hypertension include such problems as failure to maximize drug dosing, suboptimal diuretic use, noncompliance, and possible confounding effects of such concomitant medications as nonsteroidal and anti-inflammatory drugs or decongestants. The issues underlying drug-resistant hypertension are listed, together with strategies for overcoming this problem.     

Determinants of left ventricular hypertrophy in arterial hypertension

A long term study (2-7 years, mean 3.6 years) monitoring 112 clinical and echocardiographic pattern in 593 hypertensives and 156 normotensives was performed in order to find associations to left ventricular hypertrophy (LVH) developing later. 49% of the hypertensives developed echocardiographic signs of LVH (wall thickness of 12 mm and more), in contrast to 5.1% of normotensive persons. Multivariate analysis revealed the following parameters examined at entry were associated with LVH on follow-up: male sex, prolonged hypertensive history, higher diastolic blood pressure, frequent lipid-metabolism disturbances, uncharacteristic chest pain and less effective antihypertensive treatment. Thus, LVH development can be regarded as a multifactorial process.     

Risk of new-onset diabetes in the Losartan Intervention For Endpoint reduction in hypertension study

BACKGROUND: There has been uncertainty about the risk of new-onset diabetes in hypertensive individuals treated with different blood pressure-decreasing drugs. OBJECTIVES: To study this risk in hypertensive individuals who were at risk of developing diabetes mellitus in the Losartan Intervention For Endpoint reduction in hypertension (LIFE) study. METHODS: In the LIFE study, with a double-masked, randomized, parallel-group design, 9193 patients (46% men) with hypertension (mean age 67 years, average pressure 174/98 mmHg after placebo run-in) and electrocardiogram-documented left ventricular hypertrophy were randomly assigned to once-daily losartan- or atenolol-based antihypertensive treatment and followed for at least 4 years (mean 4.8 years). At baseline, 7998 patients did not have diabetes mellitus and were thus at risk of developing this condition during the study. To demonstrate ability to predict new-onset diabetes, we developed a prediction score using the significant variables from multivariate analyses (serum glucose, body mass index, serum high-density lipoprotein cholesterol, systolic blood pressure and history of prior use of antihypertensive drugs). RESULTS: There was a steadily increasing risk of diabetes with increasing level-of-risk score; patients in the highest quartile were at considerably greater risk than those in the three lower ones. Treatment with losartan was associated with lower risk of development of diabetes within each of the four quartiles of the risk score. As previously reported, new-onset diabetes mellitus occurred in 242 patients receiving losartan (13.0 per 1000 person-years) and 320 receiving atenolol (17.5 per 1000 person-years); relative risk 0.75 (95% confidence interval 0.63 to 0.88; P<0.001). CONCLUSIONS: New-onset diabetes could be strongly predicted by a newly developed risk score using baseline serum glucose concentration (non-fasting), body mass index, serum high-density lipoprotein cholesterol concentration, systolic blood pressure and history of prior use of antihypertensive drugs. Independently of these risk factors, fewer hypertensive patients with left ventricular hypertrophy developed diabetes mellitus if they were treated with losartan than if they were treated with atenolol.     

Blood pressure lowering and life expectancy based on a Markov model of cardiovascular events

The life expectancy benefits of antihypertensive treatment, based on both systolic and diastolic blood pressure reduction, was estimated with a cardiovascular disease event Markov model with prospective data from 57 573 men and women. Seven patient states were defined, including (1) no cardiovascular disease, (2) stroke, (3) myocardial infarction, (4) revascularization, (5) history of cardiovascular disease, (6) noncardiovascular disease death, and (7) cardiovascular death. Risk functions were developed from gender-specific multivariate Cox proportional hazards models for primary events and age-, smoking-, and diabetes-adjusted models for secondary events. At baseline we assumed (1) hypothetical pretreatment blood pressures of 160/95 or 150/90 mm Hg; (2) strategies A and B lower blood pressure by 20/13 and 13/8 mm Hg, respectively; and (3) baseline age of 35 years. For subjects initially at 160/95 mm Hg, those with antihypertensive treatment, antihypertensive treatment and diabetes, or antihypertensive treatment, diabetes, and currently smoking had corresponding gains in life expectancy of 2.43, 2.80, and 2.43 years for Strategy A. An initial blood pressure of 150/90 mm Hg resulted in similar gains. Compared with Strategy B, with blood pressure reductions of 13/8 mm Hg, Strategy A provided additional gains in life expectancy of 0.84, 0.99, and 0.87 years for those with antihypertensive treatment, antihypertensive treatment and diabetes, or antihypertensive treatment, diabetes, and currently smoking. The initial blood pressure level did not affect the magnitude of life expectancy gains for equivalent blood pressure reductions. Greater gains in life expectancy among hypertensive and diabetic women suggest that blood pressure lowering may yield greater benefits in selected subgroups.     

Effect of regression of left ventricular hypertrophy from systemic hypertension on systolic function assessed by midwall shortening (HOT echocardiographic study)

Depressed midwall shortening has been shown to be an independent predictor of cardiovascular morbid events in hypertensive patients with left ventricular (LV) hypertrophy despite normal endocardial fractional shortening. The effects of LV mass changes in hypertensive patients on midwall shortening are unclear. To determine the impact of LV hypertrophy regression on LV systolic function assessed at the endocardium and the midwall level, 508 patients (58% men, 57% Caucasians, mean age 60 +/- 7 years) participating in the Hypertension Optimal Treatment study were prospectively studied by serial echocardiography at baseline, year 1, year 2, and at the end of the study. The Hypertension Optimal Treatment study was designed to challenge the existence of the J-curve phenomenon in hypertension. This study enrolled men and women between 50 and 80 years of age with mild to moderate hypertension. Patients were treated with a regimen based on felodipine with the addition of other antihypertensive drug classes as needed to reduce the diastolic blood pressure to a predefined target of < or =80, < or =85, or < or =90 mm Hg. From baseline to year 1, year 2, and end of the study, body mass index was unchanged (30.4, 30.1, 30.2, and 30.5 kg/m(2)); however, diastolic blood pressure was significantly reduced (99, 83, 80, and 80 mm Hg, p <0.0001), as was systolic blood pressure (161, 139, 137, and 134 mm Hg, p <0.0001) and LV mass index (117, 119, 107, and 106 g/m(2), p <0.0001). Over the same period of observation the endocardial fractional shortening did not change significantly (40%, 42%, 43%, and 44%); however, shortening at the midwall level showed improvement (20%, 21%, 22%, and 30%, p <0.001). In conclusion, midwall shortening is a more sensitive index of systolic function in subjects with pressure-overload hypertrophy, and it identifies high-risk patients who may benefit from a more aggressive antihypertensive program. The disparity between midwall and endocardial shortening suggests reduced myofibril function in patients with hypertension-induced hypertrophy.     

初始低剂量氨氯地平加替米沙坦或复方阿米洛利联合治疗对高血压患者血压控制率影响的阶段报告

目的 探讨以氨氯地平为基础的联合治疗方案,对高血压患者血压达标及对心血管事件的影响.方法 2007年10月至2008年10月,在全国180家医疗机构,入选50～79岁伴心血管病危险因素的高血压患者13 542例.采用多中心随机开放对照盲终点评估的临床试验方法,患者随机分为低剂量氨氯地平(商品名:安内真2.5 mg/d,苏州东瑞制药有限公司产品)+复方阿米洛利(商品名:安利亚半片/d,苏州东瑞制药有限公司产品)组或氨氯地平+替米沙坦(商品名:安内强40 mg/d,苏州东瑞制药有限公司产品)组,计划治疗随访4年.主要研究终点是心血管病复合事件.结果氨氯地平+复方阿米洛利组(n=6776)和氨氯地平+替米沙坦组(n=6766)患者基线临床特征相似:平均年龄均为(61.5 ±7.7)岁,脑血管病史占19%、冠心病病史占12%,糖尿病占18%,血脂异常占 42%,平均血压水平为157/93 mm Hg(1 mm Hg=0.133 kPa).治疗第8周氨氯地平+复方阿米洛利组与氨氯地平+替米沙坦组血压分别降至(133.0±11.0)/(81.0±7.6)mm Hg与(132.9±11.6)/(80.6± 7.9)mm Hg;血压控制率分别达72.1%和72.6%.结论早期资料分析提示本研究患者多为高危人群,随机分配良好;以氨氯地平为基础的联合降压治疗血压控制率较高.     

Increased stiffness and persistent narrowing of the aorta after successful repair of coarctation of the aorta: relationship to left ventricular mass and blood pressure at rest and with exercise.

Fifteen children and adolescents who had repair of coarctation of the aorta before age 15, who were not hypertensive at rest, and who had resting arm-leg blood pressure gradients of less than 20 mm Hg underwent noninvasive evaluation of left ventricular structure and function, aortic stiffness, and residual coarctation as well as bicycle exercise testing. These results were compared with those in 15 age- and sex-matched control subjects. The mean resting age-related systolic blood pressure percentiles (63% versus 46%), transverse aortic stiffness measured by the elastic modulus (Ep) (42.1 versus 23.2 kPa), stiffness index beta (beta) (3.66 versus 2.17), echocardiographic left ventricular fractional shortening (0.42 versus 0.36), left ventricular mass index (99.3 versus 81.0 gm/m2), maximum exercise right arm systolic blood pressure (173 versus 156 mm Hg), and exercise arm-leg blood pressure gradient (35 versus 6 mm Hg) were significantly increased in the coarctectomy patients compared with controls. Univariate correlations in the coarctectomy group showed significant relationships of residual aortic narrowing with left ventricular mass index (r = 0.68, p less than 0.01) and resting systolic blood pressure percentile for age (r = 0.55, p less than 0.05). Residual aortic narrowing did not significantly correlate with aortic stiffness, resting blood pressure gradient, or exercise blood pressure gradient. Neither left ventricular mass index nor resting systolic blood pressure percentile significantly correlated with age of repair or years after repair. These results demonstrate persistent abnormalities in aortic stiffness and left ventricular mass and function after successful repair of coarctation of the aorta in childhood and adolescence.(ABSTRACT TRUNCATED AT 250 WORDS)     

我国部分地区高血压登记调查及治疗达标研究

目的通过对我国不同地区高血压人群的基线资料调查,了解我国高血压患者相关危险因素、靶器官损害及并存疾病（心、脑、糖尿病及。肾病）的发生率以及不同危险分层和不同高血压类型的分布状态,并观察4周、12周经药物治疗后总体人群和不同危险分层及不同高血压类型患者的高血压治疗达标情况。方法前瞻性高血压基线调查,然后由医师根据日常医疗实践常规,自主选用不同药物及剂量进行4周、12周高血压治疗达标观察。共观察26655例。结果26655例患者中相关危险因素中缺乏体力活动、吸烟、体重指数增高、血脂紊乱分别占52．2％、34．4％、31．8％、24．5％;靶器官损害及伴随疾病中微量白蛋白尿、左室肥厚、临床诊断冠心病及糖尿病分别占21．0％、23．6％、20．1％、26．7％;平均收缩压（158±14）mmHg（1mmHg=0．133kPa）,舒张压（94±11）mmHg,其中1、2、3级高血压分别为42．1％、43．2％、15．6％;危险分层中低危、中危、高危及重度高危分别为3．2％、22．2％、21．1％及53．3％;男性平均危险程度高于女性;高血压类型以混合性高血压最多,占77．2％,单纯收缩及舒张性高血压分别为20．4％、2．4％。4周、12周药物治疗达标率分别为50．2％及56．7％。随危险分层增高,达标率依次下降。糖尿病、肾病患者达标率显著低于平均水平。收缩压达标率显著低于舒张压。不论4周或12周,达标患者平均每人用药均在1．5种以上,60％患者需用2种或3种药物才能治疗达标。结论国人高血压合并相关危险因素、靶器官损害及伴同疾病发生率高,除积极降压达标外,加强综合治疗十分重要。在日常医疗模式下,通过加强对患者的登记随访、联合用药及督促指导在毪国宴瑚高向乐榨制率的昂著椹高县切空可行的．     

Doxazosin added to single-drug therapy in hypertensive patients with benign prostatic hypertrophy

The purpose of this study was to evaluate the efficacy and safety of the addition of doxazosin in the treatment of hypertensive patients who are being treated on another antihypertensive drug. The open-labeled, noncomparative, multicenter study was carried out in 2363 male hypertensive outpatients > 40 years of age, under reasonable control with single antihypertensive drug treatment (diastolic blood pressure < 95 mm Hg), and diagnosed with benign prostatic hypertrophy. Doxazosin was started at a dose of 1 mg/day, which was increased at 2-week intervals to 2 mg/day and 4 mg/day. The study lasted 14 weeks. Blood pressure and heart rate were measured at each of the visits. At baseline and after 14 weeks of treatment, prostatism symptoms were quantified with the International Prostate Symptom Score and quality of life was determined with the American Urology Association Committee Guidelines. Adverse effects were recorded. At the fourth visit, when the patients were taking 4 mg of doxazosin, the blood pressure reduction was 10.7 +/- 3/7.1 +/- 7.1 mm Hg. The decrease in diastolic blood pressure was significantly more marked in patients treated with beta blockers than in patients on calcium antagonists or angiotensin-converting enzyme inhibitors. For systolic blood pressure, decreases were larger in patients treated with diuretics than with calcium antagonists or angiotensin-converting enzyme inhibitors. Prostatism symptoms decreased from 15 +/- 5.8 points to 7.9 +/- 4.3 points (p is less than 0.001) and quality of life improved. Tolerability was good, with only a 4.4% cumulative incidence of adverse effects related to doxazosin. The patients who experienced adverse effects were older and their final blood pressures were lower. The results of this open-label study suggest that the addition of doxazosin to another antihypertensive drug in hypertensive patients with benign prostatic hypertrophy is well tolerated and leads to a reduction in prostatic symptoms. The additional beneficial effects on blood pressure suggest that the use of doxazosin may provide a rational approach to this category of patients.(c)2001 Le Jacq Communications, Inc.