高血压患者豆纹动脉数量减少与局部脑代谢物变化的相关性

目的:探讨高血压患者脑微小血管数量减少与局部脑代谢改变的关系。方法:将50例高血压患者和50例健康志愿者纳入本研究。所有研究对象均行三维时间飞跃法磁共振血管成像和磁共振波谱成像扫描,对所有图像进行后处理后计算豆纹动脉数量和基底节区脑代谢物NAA/Cr、Cho/Cr、MI/Cr比值。结果:高血压组和健康志愿者组双侧豆纹动脉数量分别为5.12±0.98、6.10±0.95,差异有统计学意义(P0.000 1)。高血压组患者NAA/Cr比值的降低与豆纹动脉数量减少具有一定相关性,单侧豆纹动脉数量≤3时,NAA/Cr比值下降得更显著。结论:高血压患者豆纹动脉数量减少至一定范围可引起基底节区脑代谢物NAA/Cr比值的降低。     

Carbohydrate metabolism enzymes in children with extrahepatic portal hypertension]

Glycogen and protein concentrations and the activities of liver glycogen metabolic enzymes were measured in 22 children aged 4 to 15, suffering from extrahepatic portal hypertension. Glucose-6-phosphatase, amylo-1,6-glucosidase, fructose-1,6-diphosphatase, phosphorylases alpha and beta, phosphoglucomutase, and phosphohexose isomerase levels were analyzed. Liver biopsy specimens obtained by surgical marginal biopsy were used in the study. No or drastic reduction of phosphorylase alpha activity and reduction of glycogen concentration and glucose-phosphatase activity were found characteristic of extrahepatic hypertension. Analysis of correlations of the findings has demonstrated a medium correlation in 4 cases and a strong correlation between the findings in 1 case, the possibility being estimated as 0.95-0.99. The highest number of correlations was observed with phosphorylase alpha and glucose-6-phosphatase (3 correlations). Liver blood stream impairments result in injury to one of its main biochemical functions, i.e., the maintenance of blood glucose homeostasis, this leading to reduction of the adaptation potential of the body; this should be borne in mind when planning therapeutic measures for patients with extrahepatic hypertension.     

Tolamolol in the treatment of hypertension: an open evaluation study

The effect of tolamolol 50-300 mg three times daily in the treatment of 30 patients with mild-severe hypertension was studied. The duration of therapy in the majority of cases was 3-6 months. There was a highly significant reduction of mean blood pressure (p less than 0.001) for the group as a whole. Overall, 61% of patients became normotensive or showed a reduction in severity of hypertension, In the majority of cases, this improvement occurred within the first four weeks of therapy. There was not postural hypertension. Apart from one patient with Prurigo Besnier who developed asthma, another patient who developed severe headache and a third patient who stopped treatment without giving a reason, treatment was well tolerated and there were no other serious side or toxic effects.     

Hypertension, coronary artery disease and insulin resistance--linked disorders with an impact on treatment.

Coronary artery disease is a very common disorder for which hypertension is a well-recognized risk factor. However many trials of antihypertensive therapy have failed to demonstrate a reduction in the incidence of coronary events. One explanation is that hypertension is a disorder associated with hyperinsulinaemia, obesity and non-insulin dependent diabetes. Furthermore certain antihypertensive drugs, notably thiazide diuretics, increase the hyperinsulinaemia and thereby increase one of the other coronary risk factors. In this review the links between hypertension and hyperinsulinaemia are explored and the mechanisms whereby an increased plasma insulin can lead to the more rapid development of coronary artery disease are explained. These observations may influence the choice of drugs used to treat hypertension.     

The impact of ACE inhibition on all-cause and cardiovascular mortality in contemporary hypertension trials: a review

The renin–angiotensin–aldosterone system is a key therapeutic target in hypertension. The latest meta-analysis of mortality reduction with angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) in hypertension features 158,998 patients from 20 contemporary hypertension trials. ACE inhibitors and ARBs significantly reduced relative risk for all-cause mortality by 5% (p = 0.032) and cardiovascular mortality by 7% (p = 0.018) in populations with a high prevalence of hypertension (≥66%). ACE inhibitors produced a 10% reduction in relative risk for all-cause mortality (p = 0.004) and a trend toward a 12% reduction in cardiovascular mortality (p = 0.051), whereas ARBs had no effect. On balance, mortality evidence suggests that in hypertension, ACE inhibitors should be considered ahead of ARBs, and ARBs restricted to patients intolerant of ACE inhibitors.     

Controlling hypertension in patients with diabetes

Hypertension and diabetes mellitus are common diseases in the United States. Patients with diabetes have a much higher rate of hypertension than would be expected in the general population. Regardless of the antihypertensive agent used, a reduction in blood pressure helps to prevent diabetic complications. Barring contraindications, angiotensin-converting enzyme inhibitors are considered first-line therapy in patients with diabetes and hypertension because of their well-established renal protective effects. Calcium channel blockers, low-dose diuretics, beta blockers, and alpha blockers have also been studied in this group. Most diabetic patients with hypertension require combination therapy to achieve optimal blood pressure goals.     

Hypertension in children and adolescents

Normal blood pressure and hypertension were defined according to age and sex based on the data on Japanese children. When high blood pressure is found, both white-coat and secondary hypertension should be excluded. Subsequently lifestyle modifications should be initiated in children and adolescents with essential hypertension. These modifications include: weight reduction, reduction of dietary salt intake, high dietary potassium intake and increased physical activity. When nonpharmacologic treatment is not effective after 3 to 6 months, or when there is an evidence of target organ injury, antihypertensive drugs such as ACE inhibitors and Ca antagonists will be started to control blood pressure. Lifestyle modifications are also important for primary prevention of hypertension in normotensive children.     

Cerebral complications in the treatment of accelerated hypertension.

The malignant phase of hypertension is invariably fatal unless treated, and rapid reduction of arterial pressure is thought to be the treatment of choice. Ten patients with accelerated hypertension are described in whom abnormal neurological signs developed following the rapid reduction of arterial pressure. Three patients died without recovering from the neurological damage. A fourth died of an unrelated cause a month later. Areas of ischaemic damage were found in the brains of three of these cases. Of the six survivors, four were left with some permanent neurological disability. It is likely that these changes resulted from the inability of the cerebral circulation in patients with severe hypertension to autoregulate blood flow to the brain, so that a rapid reduction in arterial pressure led to ischaemia, especially of the watershed areas of the brain. Cerebrovascular autoregulation is likely to be compromized in patients with cerebral oedema, stenosis of major cranial vessels or in those patients with long-standing severe hypertension. It is suggested that the blood pressure in patients with accelerated hypertension should be lowered gently over a period of several hours or even days in order to allow time for the cerebrovascular autoregulatory mechanisms to recover.     

Can prevention of hypertension work?

In this article, the clinical trials that have most effectively demonstrated the effectiveness of hypertension nonpharmacologic prevention interventions are presented and discussed. Thus, data from weight reduction, dietary interventions, and lifestyle modifications are shown and discussed. It is concluded that these interventions lead to control of hypertension either by themselves or in association with pharmacologic interventions. Over the years, many controlled clinical trials have demonstrated the efficacy of pharmacologic treatment of hypertension. However, such treatment has its shortcomings. First, it usually requires a lifelong commitment to therapy because, although this approach can control hypertension and reduce its consequences, it does not cure the condition. Next, the cost of pharmacologic interventions can be very high and, thus, prohibitive for poorer individuals and nations. In addition, many patients experience problems with compliance and adherence, which almost certainly contribute to the low level of hypertension control that is so widely observed. Finally, the pharmacologic approach requires a strong commitment by public health officials for detection and treatment of hypertension if there is to be any hope of limiting this condition's impact. All of these negative considerations are compounded by the fact that the prevalence of hypertension is increasing worldwide. For all these reasons, nonpharmacologic interventions should be implemented to prevent or delay the occurrence of hypertension.     

Volume is not the only key to hypertension control in dialysis patients

There is a widely held belief that hypervolaemia due to excess intake or inadequate removal of salt and water is the principal cause of hypertension in dialysis patients. The risk of failing to consider additional pathophysiological elements is that inadequate or inappropriate therapeutic strategies may be adopted. This review aims to highlight multiple alternative mechanisms for hypertension in this setting along with the risks of probing for normotension by empirical dry weight reduction if dry weight is imprecisely defined.     

原发性高血压社区护理干预效果评价

目的了解社区原发性高血压患者的知、形、态,探讨社区护理对控制原发性高血压的效果。方法自行设计问卷,对475例原发性高血压患者进行问卷调查,并实施针对性的护理干预。结果干预后原发性高血压患者对原发性高血压相关知识的了解、行为方式、态度、血压控制率明显优于干预前。结论对社区原发性高血压患者实施护理干预,可提高患者对原发性高血压的认识和遵医行为,建立健康的生活方式,密切护患关系,提高治疗率和控制率,减少并发症。     

原发性高血压社区护理干预效果评价

目的　了解社区原发性高血压患者的知、形、态，探讨社区护理对控制原发性高血压的效果。方法　自行设计问卷，对475例原发性高血压患者进行问卷调查，并实施针对性的护理干预。结果　干预后原发性高血压患者对原发性高血压相关知识的了解、行为方式、态度、血压控制率明显优于干预前。结论　对社区原发性高血压患者实施护理干预，可提高患者对原发性高血压的认识和遵医行为，建立健康的生活方式，密切护患关系，提高治疗率和控制率，减少并发症。     

Prevention of migraine with olmesartan in patients with hypertension/prehypertension

OBJECTIVE: To explore the effects of olmesartan on frequency and severity of migraine attacks in patients with comorbid hypertension and prehypertension. BACKGROUND: A randomized, double-blind, placebo-controlled, crossover study with a total of 60 patients has demonstrated the efficacy and safety of the angiotensin II receptor blocker candesartan in migraine prophylaxis. We study the potential efficacy and tolerability of olmesartan in preventing migraine in patients with hypertension and prehypertension. DESIGN/METHODS: Twenty-four adults, aged 27 through 76, with either hypertension or prehypertension, were included in this open-label study. Participants suffered from migraines (diagnosed according to International Headache Society classifications) for at least 3 months. Patients were treated with 10 to 40 mg of olmesartan per various observational periods of at least 3 months. Frequency and severity were recorded by office visits or by telephonic interview. RESULTS: Patients reported an 82.5% average reduction in the frequency of migraine attacks. Patients also experienced a 45% average reduction in the severity of migraine attacks measured on a numeric pain scale of 1 to 10. The only undesired effect was dizziness or presyncope. No serious adverse events occurred and no adverse event caused a premature termination. Two patients had no reduction in headache frequency, intensity, and blood pressure. CONCLUSIONS: The favorable results and low rate of adverse effects, in this open migraine prevention study in patients with hypertension or prehypertension, are similar to results of the randomized, double-blind, placebo-controlled, crossover study in patients taking candesartan. Olmesartan shows a potential as an effective and well-tolerated migraine prophylactic agent for patients with comorbid hypertension and prehypertension.     

Hypertension in obstructive sleep apnea: risk and therapy

Obstructive sleep apnea (OSA) is a common form of sleep-disordered breathing that occurs due to recurrent collapse of the upper airway with inspiration. Large epidemiologic studies have established that OSA is a risk factor for developing hypertension. The pathophysiologic mechanism of this relationship is due to the distinctive pattern of intermittent hypoxia seen in OSA. This pattern increases sympathetic tone, oxidative stress, inflammation and endothelial dysfunction. These processes can all lead to persistent elevation of blood pressure beyond the obstructive events. OSA should be considered as part of the workup of patients with hypertension. Treatment of OSA with continuous positive airway pressure has an effect on hypertension control and risk reduction of cardiovascular diseases. This review discusses the pathophysiology and causal relationship between OSA and hypertension, along with the cardiovascular effects of treatment of OSA.     

Modulation of the molecular composition of large conductance,Ca(2+) activated K(+) channels in vascular smooth muscle during hypertension

Hypertension is a clinical syndrome characterized by increased vascular tone. However, the molecular mechanisms underlying vascular dysfunction during acquired hypertension remain unresolved. Localized intracellular Ca2+ release events through ryanodine receptors (Ca2+ sparks) in the sarcoplasmic reticulum are tightly coupled to the activation of large-conductance, Ca2+-activated K+ (BK) channels to provide a hyperpolarizing influence that opposes vasoconstriction. In this study we tested the hypothesis that a reduction in Ca2+ spark-BK channel coupling underlies vascular smooth muscle dysfunction during acquired hypertension. We found that in hypertension, expression of the beta1 subunit was decreased relative to the pore-forming alpha subunit of the BK channel. Consequently, the BK channels were functionally uncoupled from Ca2+ sparks. Consistent with this, the contribution of BK channels to vascular tone was reduced during hypertension. We conclude that downregulation of the beta1 subunit of the BK channel contributes to vascular dysfunction in hypertension. These results support the novel concept that changes in BK channel subunit composition regulate arterial smooth muscle function.     

The Therapeutic Implications of Left Ventricular Hypertrophy in the Hypertensive Patient

Hypertension can be considered a syndrome broader than the condition of an increased blood pressure per se. Epidemiologic studies have established that high blood pressure is associated with an increased risk of cardiovascular events. Clinical trials of antihypertensive therapy have failed to show a consistent reduction in cardiovascular endpoints. The incidence of coronary disease has been reduced minimally, suggesting that factors beyond just measuring mm Hg in the hypertensive may be important in the genesis of atherosclerotic disease in hypertensive patients. Patients with hypertension appear to have an exaggerated vulnerability to the consequences of lipid abnormalities. In addition, hypertension is associated with insulin resistance and altered glucose tolerance. The increased plasma concentrations of insulin may produce proliferative effects on vascular smooth muscle and connective tissue, and these changes may adversely affect vascular integrity, leading to hypertrophy and facilitation of the arthersclerosis process. The left ventricle also appears to be involved in hypertension and this involvement may be independent of blood pressure. An increase in the muscle mass of the left ventricle as well as changes in its diastolic-filling characteristics occur early on with hypertension and may contribute to an adverse cardiovascular outcome. The arterial circulation is also involved. Alterations in structure or function of the vascular tree are reflected in diminished arterial compliance. These changes can be demonstrated prior to the appearance of clinical manifest hypertension. Based on these observations, treatment designed to reduce cardiovascular risk in hypertensive patients from cardiovascular events must not be based on blood pressure reduction alone but must take into account all the components of the hypertension syndrome.     

Pulmonary hypertension in congenital heart disease

Over the past 40 years, significant advances have been made in the diagnosis and management of congenital heart defects. Improvements in diagnostic and interventional cardiology, surgical technique, cardiopulmonary bypass and post-operative intensive care have all contributed to a reduction in mortality and morbidity. Despite these advances, pulmonary hypertension caused by congenital heart defects remains a significant problem in the immediate post-operative period, as well as long-term. This article reviews the pathophysiology of pulmonary hypertension due to congenital heart disease and discusses the options available for the management of this condition.     

The Mayo Three-Community Hypertension Control Program. II. Outcome of intervention in entire communities.

A pronounced decline in blood pressure levels of hypertensive patients occurred in each of three rural Minnesota communities 1 to 2 years after the inception of community programs to control high blood pressure in these populations. An experimental hypertension clinic was established in one community to integrate a nurse practitioner into a physician-supervised program of long-term patient management. In the community with this innovative, partially subsidized practice arrangement, we observed declines in diastolic pressures of hypertensives. However, comparable degrees of blood pressure reduction occurred in the two other communities, with traditional solo or small group practice arrangements, where intervention was limited to detection and referral alone or was supplemented with continuing education of physicians in the management of hypertension. The evaluation of these three community programs suggests, among other conclusions, that this innovative community model for hypertension control, based on the recommendations of the Inter-Society Commission for Heart Disease Resources, contributed to favorable short-term blood pressure outcomes for the community. The observation of similar overall outcomes as measured by blood pressure reduction in all three communities was unexpected; the clinic's impact appears to have been matched by the effectiveness of screening and referral, alone or with continuing education, in the two other communities.     

Frataxin and endothelial cell senescence in pulmonary hypertension

Pulmonary hypertension (PH), increased blood pressure within the lungs, is classified into five diagnostic groups based on etiology, with treatment assigned on this basis. Currently, only Group 1 pulmonary arterial hypertension (PAH) and Group 4 chronic thromboembolic PH (CTEPH) have pharmacological treatments available. The role of the endothelial cell in pulmonary hypertension has long been debated, and in this issue of the JCI, Culley et al. present evidence for the reduction in frataxin expression across multiple groups of PH. Reduced frataxin expression led to endothelial cell senescence and associated with the development of PH. Removal of the senescent cells using the senolytic drug Navitoclax in multiple models of PH effectively treated PH, suggesting a new class of treatments that may work beyond Group 1 and Group 4 PH in patients with evidence of pulmonary vascular endothelial senescence.     

Combination therapy with beta-adrenergic blockade and amlodipine as second line treatment in essential hypertension

In hypertension both beta-blockers and calcium antagonists are drugs with proved efficacy. Because only half the patients respond to a single drug, even at full dosage, a second hypotensive agent is frequently required to obtain adequate blood pressure control. The combination of a dihydropyridine calcium antagonist and a beta-blocker can be justified by their different mechanisms of action. A randomised double blind parallel group study versus placebo was performed, in order to assess the efficacy of atenolol combined with amlodipine in the treatment of stage I-II essential hypertension not controlled by atenolol alone. Twenty-four-hour arterial blood pressure monitoring showed that amlodipine added to atenolol produced a statistically significant reduction of blood pressure values compared with placebo in patients whose blood pressure was not controlled by atenolol alone. Blood pressure circadian rhythm was unchanged. The reduction of side-effects, obtained by adding a dihydropyridine derivate to a beta-blocker, confirms the effectiveness of this combination.