无症状人群颅内动脉狭窄的分布特征及危险因素调查

目的：分析中年以上无症状人群脑血管狭窄频率及分布。方法：对无症状人群应用经颅多谱勒超声仪（TCD）检测双侧大脑中动脉（MCA）、前动脉（ACA）、后动脉（PCA）、椎-基底动脉（V-BA）,并统计调查人群的年龄、血压、血糖、血脂、头痛、头晕、吸烟、饮酒等因素,对各因素与血管狭窄的相关性应用统计学方法进行处理。结果：805例中血管狭窄发生率为4.09%。高血压、糖尿病、年龄等因素与血管狭窄有显著相关性（P〈0.01）。性别、头痛、头晕、吸烟、饮酒与颅内血管狭窄之间无统计学意义（P〈0.05）。且有高血压和（或）糖尿病史的无症状人群脑血管狭窄率（10.18%）明显高于无病史者（1.72%）。结论：无症状人群中高血压、糖尿病、年龄因素是脑血管狭窄主要危险因素。     

高血压与血液流变学

血液流变学是研究血液和血管怎样进行功能活动和如何相互作用的科学。血液粘度是血液流变特性的综合指标。决定血液粘度的内在因素有血细胞比容、红细胞聚集性、红细胞变形性和血浆成分。体内血液粘度还受血液流速、血管口径和血管舒缩运动影响。近年研究表明 ,高血压与血液流变特性改变之间的关系密切 ,血液粘度和血管半径是决定外周血管阻力的两大主要因素 ,显然亦是调控血压的重要因素。1　原发性高血压的血液流变特性原发性高血压 (ｅｓｓｅｎｔｉａｌｈｙｐｅｒｔｅｎｓｉｏｎ ,ＥＨＴ)患者血液流变学改变与血压幅度、病程、是否并发靶…     

经颅多普勒超声在高血压人群体检中的应用价值

目的探讨经颅多普勒超声（TCD）在高血压人群体检中的应用价值。方法选取2012年2月至2013年3月期间在健康体检中发现的高血压患者200例作为高血压组,另选同期健康体检且除外高血压病的正常人群150例作为对照组。所有受试人员均采用经颅多普勒超声诊断仪对颈内动脉系统及椎基底动脉系统的血管情况进行探查。比较分析两组受试者TCD检测结果、双侧大脑中动脉（MCA）及基底动脉（BA）各血液运动参数。结果与对照组健康受试者相比,高血压组患者TCD检测结果脑动脉硬化频谱改变比率、血流速度升高比率以及血流速度降低比率均明显提高,正常比率明显下降,差异均具有统计学意义（P〈0.05）。与此同时,与对照组健康受试者相比,高血压组患者双侧MCA及BA血液运动参数平均血流速度、峰值流速及舒张期流速有所降低,而脉动指数和搏动指数有所升高,差异具有统计学意义（P〈0.05）。结论经颅多普勒超声能够确切地反映脑部血流动力学的状况以及基本的病理改变,有助于高血压病情的评估及诊断,为临床治疗合理方案的选择提供了参考。     

50例高血压患者血液流变指标检测分析

临床血液流变学是研究血液流变特性异常在疾病发生、发展及诊治中作用的一门科学,在心脑血管疾病中高血压是主要危险因子之一,其血液流变学的变化有着重要意义。本文对健康体检、正常高值血压（收缩压120～139mmHg／或舒张压80～89mmHg）及高血压组进行了血液流变学检测,为探讨在高血压发生发展中的作用提供实验依据。     

原发性高血压的健康教育指导

原发性高血压是一种以动脉血压升高为特征并伴有动脉、心、脑和肾等器官病理改变的全身性疾病.     

深圳市中高层职业人群腰臀比值、体质指数与高血压危险因素的相关性研究

目的探讨深圳市中高层职业人群腰臀比值、体质指数与肥胖、高脂血症、高血压等危险因素的相关性及流行病学特征.方法对2004年9月～2005年8月深圳市企事业单位中高层职业人群1 515例健康体检者进行身高、体重、腰围、臀围、血压、血脂等检测,并按腰臀比值、体质指数进行分层分析各组与肥胖、高脂血症、高血压等危险因素的相关性及流行病学特征.结果受检者肥胖患病率为27.9%,超重的患病率为21.6%,中心性肥胖患病率为24.8%.高脂血症的患病率为55.3%（男性：63.9%,女性：39.8%）,高血压患病率为10.7%（男性：13.3%,女性：6.1%）.中心性肥胖组（按WHR分型）和外周肥胖组（按BMI分型）的高脂血症、高血压的检出率明显高于正常体型和正常体重组（P＜0.01）.中心性肥胖的高脂血症、高血压患病率的检出率明显高于外周肥胖（P＜0.01）.中心性肥胖与外周肥胖都与高脂血症、高血压的患病率呈正相关（P＜0.01）.结论深圳市中高层职业人群肥胖、高脂血症和高血压的患病率明显增高,尤其是高脂血症值得关注.肥胖、高脂血症是导致高血压的独立危险因素,中心性肥胖比外周型肥胖危险性更大.腰臀比值与体质指数都可作为高血压的危险预测因素,腰臀比值比体质指数特异性更高,两者结合进行可明显提高高血压风险预测的特异性和敏感性.     

成都地区中老年人群体重指数对高血压患病率及血压水平的影响

目的：研究成都地区中老年人群体重指数（BMI）与高血压患病率及血压水平的关系。方法：按照随机抽样的方法抽取样本,对711人（平均年龄为63.28±6.25岁;男性占57.8%）进行了相关调查,调查内容中包括身高、体重、血压及脉搏等。结果：成都地区中老年人群的超重及肥胖所占比重较大（约45%）,按BMI分组（〈18.5 kg/m~2,18.5～23.9 kg/m~2,24～27.9 kg/m~2,≥28.0 kg/m~2）的高血压患病率分别是31.6%,54.8%,64.4%,82.8%,差异有统计学意义。采用logistic回归分析发现在调整年龄、性别、腰围及尿酸等后,BMI对高血压的患病率有独立影响。在整个人群及女性病人中,血压随着BMI的升高而有升高的趋势,差异有统计学意义。结论：成都地区中老年人群超重及肥胖所占比重较大。BMI可以影响高血压的患病率及影响女性病人的血压水平,是高血压的独立危险因素。     

高血压病的诊断与鉴别诊断

血管内血液对于血管壁的侧压力称为血压(blood pressure,BP).高血压是以体循环动脉血压增高为主要表现的临床综合征,可分为原发性及继发性两大类.在绝大多数患者中,高血压的病因不明,称之为原发性高血压或高血压病,占高血压患者中的95%以上;在不足5%患者中,血压升高是某些疾病的一种临床表现,本身有明确而独立的病因,称为继发性高血压.     

高粘血症相关因素探讨

目的 研究高粘血症与性别、年龄、超重、高血压、高血脂、空腹血糖异常的相关性.方法 对760名健康体检者的性别、年龄、血液流变学指标、体质指数、血压、血脂、空腹血糖资料进行统计分析.结果 （1）高粘血症患病率为30.92%,男多于女,差异具有显著的统计学意义（ P＜0.001）;（2）高粘血症的发病率与年龄无相关性（ P＞0.05）.（3）高粘血症人群中超重、高血压、高血脂、空腹血糖异常发生率均明显高于血液流变学指标正常者,差异具有统计学意义（ P＜0.001）.结论 高粘血症的发生是多种代谢因素共同作用的结果,纠正代谢异常是高粘血症的防治关键.     

高血压前期动脉弹性与胰岛素抵抗的相关性研究

目的探讨高血压前期大动脉、小动脉弹性与胰岛素抵抗的相关关系。方法选择高血压前期36人、1-2级高血压患者46例、理想血压健康者30人,使用CVProfilorDO-2020动脉弹性功能测定仪检测桡动脉脉搏波形和动脉弹性指数C1和C2,采用HOMA-IR公式计算胰岛素抵抗指数（IR）;比较各组间大动脉、小动脉弹性情况,对高血压前期者动脉弹性与IR进行相关分析。结果校正了年龄和病程后,高血压组与理想血压组、高血压前期组比较,C1和C2均降低（P〈0.05）;高血压前期组与理想血压组比较,C2降低（P〈0.05）,高血压前期组和高血压组与理想血压组比较,HOMA-IR升高（P〈0.05）。C2与HOMA-IR负相关（r=-0.687,P〈0.05）。结论高血压前期者已经存在小动脉弹性的减退及胰岛素抵抗,且两者之间呈负相关。     

慢性肺原性心脏病患者肺动脉压力及血浆B型尿钠肽变化分析

目的探讨慢性肺原性心脏病（PHD）患者肺动脉高压及血浆B型尿钠肽（BNP）的水平及临床意义。方法80例PHD患者同时行心脏超声测定肺动脉压以及采用免疫荧光法测定BNP,根据肺动脉压力水平分为正常、轻度、中度、重度肺动脉高压组,比较各组BNP水平。结果重度肺动脉高压组BNP水平显著高于以及正常轻中度肺动脉高压组（P〈0．01）。肺动脉压力与BNP水平有较强的正相关性（r=0．79,P〈0．001）。结论慢性肺原性心脏病患者肺动脉高压增高血浆BNP水平也增高,BNP增高的程度与肺动脉压有较强的正相关。     

先天性心脏病合并肺动脉高压患者血清B型尿钠肽、血管内皮生长因子及高敏C反应蛋白水平变化的研究

目的 探讨血清B型尿钠肽(BNP)、血管内皮生长因子(VEGF)、高敏C反应蛋白(hs-CRP)水平与先天性心脏病(简称先心病)合并肺动脉高压患者肺动脉压的关系.方法 体肺分流性先心病41例.正常对照组20例.先心病患者分为无肺动脉高压组16例.轻中度肺动脉高压组13例和重度肺动脉高压组12例.应用酶联免疫吸附法(ELISA)测定患者血清标本BNP、VEGF及hs-CRP水平,并探讨其与肺动脉压相关性.结果 先心病患者血清BNP、VEGF及hs-CRP水平较对照组明显升高(P均<0.05),并且BNP、VEGF水平与肺动脉压力呈正相关(r=0.754,P<0.001;r=0.641,P<0.001).结论 先心病早期虽未发生肺动脉高压,但已有炎症的激活,肺血管的重构.血清BNP、VEGF水平对于先心病合并肺动脉高压患者肺动脉压的评估有一定意义及临床价值.     

Pulmonary veno-occlusive disease.

Pulmonary veno-occlusive disease has recently been recognized as a distinct pathological entity and a cause of pulmonary arterial hypertension. Twenty previously reported cases and a new patient are here reviewed. The majority presented with breathlessness and in the early stages of the disease, when the abnormal signs were not striking, some patients were wrongly diagnosed as suffering from an anxiety state. The condition usually has an insidious onset but is remorselessly progressive and since no effective treatment is available at present, invariably fatal and the majority of patients have died within two years. The fully developed clinical picture is dominated by symptoms and signs of pulmonary arterial hypertension, similar to those found with other diseases causing a raised pulmonary arterial blood pressure. However, some patients with pulmonary veno-occlusive disease show, in addition, signs of pulmonary venous and capillary hypertension, which can lead to its clinical recognition when associated with a normal left atrial blood pressure. In this condition the pulmonary wedge pressure would appear to be unreliable as a record of the left atrial blood pressure. Pulmonary angiography and lung scanning will differentiate pulmonary veno-occlusive disease from massive thromboembolic pulmonary arterial hypertension but not from primary pulmonary arterial hypertension or micro thromboembolism. Although in some patients it should now be possible to recognise pulmonary veno-occlusive disease in life, there will be others where, even after full investigation, it will still be impossible to differentiate the condition from primary pulmonary arterial hypertension or micro thromboembolism and in these the diagnosis will only be made when the distinctive histological pattern of the disease is demonstrated. In pulmonary veno-occlusive disease there is a widespread occlusion of the pulmonary veins and venules by a loose intimal fibrosis which is often basophilic. Recanalization of the occluded veins is common and in some cases may be very striking. These occlusive lesions in the pulmonary veins lead to an elevation of pulmonary arterial pressure with associated disease of these vessels, and are also responsible for chronic oedema of the elveolar walls with subsequent development of interstitial pulmonary fibrosis. In the present case organised thrombi were present in the pulmonary arteries in addition to the pulmonary venous lesions.     

Treatment of isolated systolic hypertension in the elderly

Systolic hypertension is a major health economy problem within our aging society. Increased arterial stiffness is the vascular phenotype of systolic hypertension, especially of the large arteries. Elevated systolic blood pressure is even more associated with cardiovascular morbidity and mortality than diastolic blood pressure. Treatment of systolic hypertension in the elderly should be based on nonpharmacological measures and medical therapy if the systolic hypertension cannot be controlled by conservative therapy alone. The HYVET study provided evidence-based medicine data showing that, in the very elderly, lowering blood pressure to a level of 150/80 mmHg is still very beneficial. Antihypertensive therapy needs to be tailored in the elderly because of comorbid conditions, such as ischemic heart disease, heart failure, atrial fibrillation, renal insufficiency and diabetes. Angiotensin-converting enzyme inhibitors or angiotensin II-receptor blockers should be considered in combination with diuretics or with a dihydropyridine calcium antagonist. β-blockers seem to be less effective for cardiovascular disease protection in comparison with other antihypertensive drug classes, such as diuretics, dihydropyridines, angiotensin-converting enzyme inhibitors or angiotensin II-receptor blockers. Major effort is required to reduce the therapeutic inertia and increase therapeutic adherence for better blood pressure control in the elderly with systolic hypertension.     

高血压合并冠心病患者血压变异性及动态血压的变化

[目的]分析高血压合并冠心痛患者的血压变异性与动态血压变化特点.[方法]选取2014年6月至2015年6月本院收治的160例高血压患者的临床资料.根据冠脉造影(CGA)结果或冠脉CT成像(CTA)诊断结果将其分为冠心病合并高血压组(n=80,观察组),单纯性高血压组(n=80,对照组),对两组患者动态血压和血压变异性指标进行分析比较.[结果]观察组患者日间平均收缩压、夜间平均收缩压、24h平均收缩压、日间平均脉压、夜间平均脉压、24h平均脉压、日间平均收缩压标准差、夜间平均收缩压标准差、24h平均收缩压标准差均显著高于对照组,差异有统计学意义(均P＜0.05);观察组与对照组患者在日间平均舒张压、夜间平均舒张压、24h平均舒张压、日间平均舒张压标准差、夜间平均舒张压标准差、24h平均舒张压标准差方面比较,差异均无统计学意义(均P＞0.05).[结论]高血压合并冠心病患者其动态血压波动比较大,且血压变异性相对增大,加强其血压动态血压与血压变异性监测对冠心病合并高血压的临床诊治有着一定的作用.     

Heart disease in the hypertensive patient.

Uncontrolled hypertension increases the workload of the left ventricle causing the development of hypertrophy and an increase in myocardial oxygen consumption that may precipitate ischemia because of inadequate oxygen delivery related to accelerated coronary atherosclerosis. Control of the hypertension should prevent the further development of hypertrophy, delay the development of fibrosis and possibly also slow the rate of development of atherosclerosis. Furthermore, when myocardial function is impaired because of hypertrophy or other myocardial diseases, the level of blood pressure becomes an important determinant of left ventricular performance. Regardless of the level of arterial pressure, vasodilator drugs that lower arterial pressure may result in marked improvement in left ventricular performance and relief of symptoms of left ventricular failure. Therefore, control of blood pressure in the presence of heart disease may involve treatment of normotensive patients to bring them into a lower normotensive range as well as the more traditional treatment of hypertensives to bring them into the normotensive range. Although this scenario is consistent with conventional wisdom and clinical experience, intricacies of the relationship between hypertension, hypertrophy, myocardial oxygen delivery, atherosclerosis and intramyocardial blood flow distribution remain poorly understood. Until these aspects of the natural history of heart disease are better worked out therapy will remain largely empirical.     

Is blood pressure being measured?

The blood pressure measure is part of the physical exam and it should be accomplished in every medical consultation. To verify the blood pressure measured in the accomplished medical consultations record of first they were consulted it consults 500 patient's ambulatorial being 335 (67%) coming of medical and surgical clinics and 165 (33%) of the gynecological and obstetric clinics. The blood pressure was written down in 39% of the accomplished consultations (135 + 32 mm Hg 85 + 19 mm Hg), and 11% of this annotations the pressure diastólica was above 90 mm Hg. In relation to the previous diagnosis of hypertension it was verified that: a) in 62% of the records there was not this information; b) 20% referred to have hypertension, and in 79% of these the arterial pressure was scored; and c) 18% referred not to have hypertension and 46% of these had registration of the arterial pressure. Therefore, most of the patients didn't have its logged arterial pressure.     

Obesity hypertension

Obesity and hypertension are two major risk factors for the cardiovascular system. Whereas arterial hypertension increases afterload to the left ventricle, obesity produces an increase in stroke volume and increases preload. As a result of this double burden, the heart adapts with eccentric left ventricular hypertrophy. Contractility becomes impaired early in the course of obesity hypertension, and ventricular ectopy is observed. As a consequence, the obese hypertensive patient is at a high risk for congestive heart failure and sudden death. Despite the synergistic effects of obesity and hypertension on the heart, patients appear to be relatively protected from nephrosclerosis and coronary artery disease. These epidemiologic observations are supported by the pathophysiologic changes that take place in obesity hypertension. At any given level of arterial pressure, cardiac output and renal blood flow are elevated in obese hypertensive patients, whereas systemic and renal vascular resistance are decreased when compared to lean hypertensive patients. Because total peripheral resistance is considered the hemodynamic hallmark of arterial hypertension, systemic vascular complications may be less pronounced in obesity hypertension. Weight loss decreases preload, afterload to the left ventricle, and the sympathetic drive to the heart. Protecting the heart from these hypertrophic stimuli should be a major goal of preventive cardiology.     

5-HT in systemic hypertension: foe, friend or fantasy?

Since its discovery by Erspamer in the 1930s and identification by Page in the 1950s, 5-HT (5-hydroxytryptamine; serotonin) has been an elusive candidate as a substance that plays a role in the disease of high blood pressure, also known as hypertension. In both animal and human hypertension, arterial contraction to 5-HT is profoundly enhanced. Additionally, 5-HT is a vascular smooth muscle cell mitogen. Because both increased arterial contractility and smooth muscle growth contribute to the disease of hypertension, it is logical to believe that 5-HT is a potential cause of disease, and thus a foe. However, decades of research have produced conflicting results as to the potential role of 5-HT in hypertension. This review will discuss historical findings which both support and refute the involvement of 5-HT in hypertension, and pose some new questions that may reveal novel ways for 5-HT to modify vascular control of blood pressure.     

Activity of chymotrypsin-like proteinases in patients with ischemic heart disease, arterial hypertension and nonspecific aortic arteritis

AIM: To analyze activity of chymotrypsin-like plasma proteinases (CTP) in patients with various cardiovascular diseases. MATERIAL AND METHODS: CTP activity was studied in 82 patients with various cardiovascular diseases: 13 coronary heart disease patients with normal arterial pressure, 49 patients with essential hypertension (EH) and secondary arterial hypertension, 20 patients with nonspecific aortic arteritis. 28 donors served control. RESULTS: CTP activity in plasma of patients with EH rose 4 times compared to donors. If EH patients had concurrent diseases (CHD, chronic pyelonephritis, atherosclerosis of extracranial arteries), CTP activity may increase by 30-300%. In patients with nonspecific aortic arteritis CTP activity in blood plasma is 17.5 times higher than in donors. CONCLUSION: High CTP activity in cardiovascular patients may be explained by chymase and cathepsin G release into blood flow indicating activation of alternative to ACE pathway of angiotensin II production or the presence of the inflammatory process.