Treatment Of Elevated Blood Pressure Research Articles

Primary Prevention of Cardiovascular Disease and Type 2 Diabetes in Patients at Metabolic Risk: An Endocrine Society Clinical Practice Guideline

The objective was to develop clinical practice guidelines for the primary prevention of cardiovascular disease (CVD) and type 2 diabetes mellitus (T2DM) in patients at metabolic risk. Healthcare providers should incorporate into their practice concrete measures to reduce the risk of developing CVD and T2DM. These include the regular screening and identification of patients at metabolic risk (at higher risk for both CVD and T2DM) with measurement of blood pressure, waist circumference, fasting lipid profile, and fasting glucose. All patients identified as having metabolic risk should undergo 10-yr global risk assessment for either CVD or coronary heart disease. This scoring will determine the targets of therapy for reduction of apolipoprotein B-containing lipoproteins. Careful attention should be given to the treatment of elevated blood pressure to the targets outlined in this guideline. The prothrombotic state associated with metabolic risk should be treated with lifestyle modification measures and in appropriate individuals with low-dose aspirin prophylaxis. Patients with prediabetes (impaired glucose tolerance or impaired fasting glucose) should be screened at 1- to 2-yr intervals for the development of diabetes with either measurement of fasting plasma glucose or a 2-h oral glucose tolerance test. For the prevention of CVD and T2DM, we recommend that priority be given to lifestyle management. This includes antiatherogenic dietary modification, a program of increased physical activity, and weight reduction. Efforts to promote lifestyle modification should be considered an important component of the medical management of patients to reduce the risk of both CVD and T2DM.

Beyond Established and Novel Risk Factors

Dyslipidemia, hypertension, and diabetes mellitus have been appropriately highlighted as established predictors of cardiovascular disease. These risk factors have become preeminent targets for influencing cardiovascular risk; their assessment, treatment, and monitoring are major emphases of clinical care, research investigation, treatment guidelines, organization position papers, and measures of physician and hospital performance. Notably, lifestyle risk factors, including dietary habits, physical inactivity, smoking, and adiposity, strongly influence the established cardiovascular risk factors and also affect novel pathways of risk such as inflammation/oxidative stress, endothelial function, thrombosis/coagulation, and arrhythmia. Furthermore, modest alterations of these lifestyle risk factors are achievable and have substantial effects on cardiovascular risk. Thus, basic lifestyle habits should be considered fundamental risk factors for cardiovascular disease. Although efforts to combat established and novel risk factors with pharmacological treatments are important and should continue, we call for a systematic rebalancing of current research, clinical care, and policy efforts to focus more on lifestyle. The rising costs of healthcare and the epidemics of overweight and obesity highlight the inadequacies of our current strategy. Substantially more resources should be directed toward research on lifestyle risk factors, their determinants, and effective interventions to change them. The clinical evaluation and treatment of dietary, physical activity, and smoking habits must become as routine and familiar as assessment of blood pressure, cholesterol, and glucose levels. Major policy initiatives and reimbursement guidelines must also be rebalanced to emphasize lifestyle risk factors. Cardiovascular diseases are leading causes of death and disability among men and women in nearly all nations.1 Identification of persons at higher or lower risk for cardiovascular events is important to facilitate effective use of resources and interventions to reduce disease burden among individuals and in society. Each of the established risk factors for cardiovascular disease—age, gender, dyslipidemia, hypertension, diabetes mellitus, and smoking—have been appropriately highlighted …

Sex differences in risk factor control of treated hypertensives: a national primary healthcare-based study in Sweden

To evaluate potential sex differences, this study aimed to investigate blood pressure and lipid control and other risk factors for cardiovascular disease in treated hypertensive (tHT) patients from primary healthcare. This cross-sectional survey of tHT patients was carried out between 2002 and 2005 by 264 primary care physicians from Sweden who consecutively recruited 6537 tHT patients (48% men and 52% women) from medical records. tHT men more often reached the treatment goal for systolic/diastolic blood pressure, less than 140/90 mmHg, than tHT women (30 vs. 26%, P<0.01). Men had lower systolic blood pressure than women, however, women had lower diastolic blood pressure and higher pulse pressure. More tHT women had total cholesterol>or=5.0 mmol/l than corresponding men (75 vs. 64% P<0.001). Men more often had diabetes (25 vs. 20% P<0.001), left ventricular hypertrophy (20 vs. 16% P<0.001), and microalbuminuria (24 vs. 16% P<0.001). Women were more often treated with diuretics (64 vs. 48%) and beta-receptor blockers (54 vs. 51%), and men more often treated with angiotensin-converting enzyme inhibitors (27 vs. 18%), calcium channel blockers (34 vs. 26%), and lipid-lowering drugs (34 vs. 29%). A need still exists for more intensified treatment of elevated blood pressure and hypercholesterolemia, especially in women. In hypertensives of both sexes, smoking and other risk factors also need to be addressed to reduce the risk of cardiovascular disease.

Effect of Treatment of Elevated Blood Pressure on Neurological Deterioration in Patients with Acute Intracerebral Hemorrhage

Treatment of elevated blood pressure after acute intracerebral hemorrhage (ICH) is controversial. There is a risk of hematoma expansion with elevated blood pressure, and risk of ischemia with blood pressure control. This study was done to determine the effect of blood pressure control on outcome. We retrospectively studied 122 patients with ICH. We collected 24-h blood pressure readings on all patients. The Glasgow Coma Score (GCS) at baseline and at 24 h was used to determine neurological deterioration (GCS decline > or = 2). Baseline computerized tomography (CT) scans were reviewed for hematoma volume, intraventricular hemorrhage, and location of hemorrhage. Drops in systolic blood pressure and mean arterial pressures over 24 h were divided in quartiles to determine the risk of neurological deterioration among quartiles. A logistic regression model was used to determine the association between variables of interest and neurological deterioration. Neurological deterioration was observed in 12 patients (10%). Baseline blood pressure and GCS were only two variables significantly different among quartiles of blood pressure drop. Multivariable adjusted analysis for these variables demonstrated significant trend toward reduced neurological deterioration with maximum blood pressure drop (systolic or mean). The risk of neurological deterioration was significantly lower in the quartile of maximum drop of systolic (odds ratio [OR] 0.02, 95% confidence interval [CI] 0.0-0.68) or mean (OR 0.03, 95% CI 0.0-0.98) blood pressure when compared to the quartile with least drop. This study supports that reduction of blood pressure in patients with acute ICH is safe and suggests that aggressive reduction might reduce the risk of neurological deterioration in first 24 h of admission.

So, What’s New?

See related article, pages 1557-1564. Does reduced medication access after a stroke increase the risk of recurrent stroke and subsequent disability? How many recurrent strokes in the population are attributable to poor control of risk factors, such as lack of treatment of elevated blood pressure (BP), high cholesterol, diabetes or the use of antiplatelet agents, etc? The article by Levine et al1 notes that ≈9% or an estimated 76 000 stroke survivors in the US were unable to afford their necessary medications. The characteristics of such individuals are, as would be expected from previous studies, lower income, lack of insurance, multiple diseases requiring high cost of treatments, lack of usual source of care and lack of disposable income to pay for the drugs. The critical question is if we could enhance adherence, would it have any effect on outcomes? The current report by Levine et al did not measure whether the lack of funds to pay for the drug therapy had any impact on the control of risk factors or whether it had any effect on the clinical outcomes of poststroke patients. However, other studies have clearly documented that adherence to drug therapies is an important component of reducing risk of disease. Most likely, levels of risk factors and adherence to therapies are the 2 critical variables that determine risk of both incident stroke and recurrent stroke.2–7 In 2001, Qureshi reported in 1252 survivors of myocardial infarction and stroke from the National Health And Nutrition Examination Survey (NHANES) III that only 53% of hypertensives were controlled. Blood glucose in diabetics was controlled in only about 50% and cholesterol was poorly controlled in 46%. About 18% of individuals were also still smoking cigarettes.8 In January 2002, Dr Claude Lenfant, then Director of the National Heart, Lung, …

Long-Term and Short-Term Changes in Antihypertensive Prescribing by Office-Based Physicians in the United States

Medication choices for the treatment of elevated blood pressure have a large potential impact on both patient outcomes and health care costs. Historic trends of prescribing for hypertension will advance the understanding of physician practice of evidence-based medicine. This study describes both long- and short-term trends in US antihypertensive prescribing from 1990 through 2004. Data were extracted from the National Disease and Therapeutic Index, a continuing survey of a national sample of US office-based physicians. Cox and Stuart and z tests were performed. Diuretics ranked among the top 3 antihypertensive drug classes throughout the entire study time span. Angiotensin-converting enzyme (ACE) inhibitors and calcium channel blockers (CCBs) were preferred over diuretics beginning in 1993, with diuretics surpassing CCBs in 2000. Beta-blockers were consistently the fourth most common class until 2002, when exceeded by angiotensin II receptor antagonists (ARBs). Most recent trends indicated an immediate but short-lived increase in the prescription of thiazide diuretics after the new clinical evidence released in December 2002 demonstrating clinical equivalence of thiazides to ACE inhibitors and CCBs. In contrast, prescription of ACE inhibitors declined, accompanied by continuation of a pre-existing increase in the prescription of ARBs, whereas prescription of CCBs remained essentially stable after the new evidence was released. The recorded long- and short-term trends indicate that evidence-based clinical recommendations had an impact on antihypertensive prescribing practices, but the magnitude of impact may be smaller and of more limited duration than desired.

The value of lowering blood pressure

According to the Canadian Heart Health Survey, only 14% of Canadian hypertensive patients are aware of their disease and are treated appropriately. One of the reasons for this could be that physicians are confused by an excess of confusing and contradictory information regarding the choice of drugs. Two recent publications may contribute to a much-needed simplification of the problem. The Blood Pressure Lowering Treatment Trialists' Collaboration published a meta-analysis based on 29 randomized trials that comprised a total of more that 162,000 participants. The treatment regimens were based on angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, diuretics, beta-blockers and calcium channel blockers. The main finding of the meta-analysis was that treatment with any of the blood pressure-lowering regimens reduced the risk of major cardiovascular events, and the extent of these risk reductions was directly related to the degree of blood pressure lowering. The Valsartan Antihypertensive Long-term Use Evaluation (VALUE) compared valsartan with amlodipine. At the end of the study, the reductions in blood pressure from baseline were 17.3/9.9 mmHg in the amlodipine group and 15.2/8.2 mmHg in the valsartan group (P<0.0001). There was a significantly lower incidence of myocardial infarction in the amlodipine group (4.1%) than in the valsartan group (4.8%). From these two studies, it would be reasonable to conclude that the treatment of elevated blood pressure has two main goals: to achieve a normal blood pressure and to produce a happy patient. The agent or agents used to obtain these goals are relatively unimportant.

Why and how to implement sodium, potassium, calcium, and magnesium changes in food items and diets?

The present average sodium intakes, approximately 3000-4500 mg/day in various industrialised populations, are very high, that is, 2-3-fold in comparison with the current Dietary Reference Intake (DRI) of 1500 mg. The sodium intakes markedly exceed even the level of 2500 mg, which has been recently given as the maximum level of daily intake that is likely to pose no risk of adverse effects on blood pressure or otherwise. By contrast, the present average potassium, calcium, and magnesium intakes are remarkably lower than the recommended intake levels (DRI). In USA, for example, the average intake of these mineral nutrients is only 35-50% of the recommended intakes. There is convincing evidence, which indicates that this imbalance, that is, the high intake of sodium on one hand and the low intakes of potassium, calcium, and magnesium on the other hand, produce and maintain elevated blood pressure in a big proportion of the population. Decreased intakes of sodium alone, and increased intakes of potassium, calcium, and magnesium each alone decrease elevated blood pressure. A combination of all these factors, that is, decrease of sodium, and increase of potassium, calcium, and magnesium intakes, which are characteristic of the so-called Dietary Approaches to Stop Hypertension diets, has an excellent blood pressure lowering effect. For the prevention and basic treatment of elevated blood pressure, various methods to decrease the intake of sodium and to increase the intakes of potassium, calcium, and magnesium should be comprehensively applied in the communities. The so-called 'functional food/nutraceutical/food-ceutical' approach, which corrects the mineral nutrient composition of extensively used processed foods, is likely to be particularly effective in producing immediate beneficial effects. The European Union and various governments should promote the availability and use of such healthier food compositions by tax reductions and other policies, which make the healthier choices cheaper than the conventional ones. They should also introduce and promote the use of tempting nutrition and health claims on the packages of healthier food choices, which have an increased content of potassium, calcium, and/or magnesium and a lowered content of sodium. Such pricing and claim methods would help the consumers to choose healthier food alternatives, and make composition improvements tempting also for the food industry.

Measurement and treatment of elevated blood pressure in the pediatric patient with chronic kidney disease

Hypertension, as in adults, is a frequent complication found in children with chronic kidney disease (CKD). Indeed, hypertension has now become one of the most prevalent chronic diseases of childhood. The most recent data available (2003) indicate that at least 38% of children with CKD in the United States are receiving antihypertensive therapy. Only recently has it been shown in children that hypertension, traditionally considered a marker for disease severity in children, is additionally a significant and independent risk factor for accelerated deterioration of kidney function and progression of CKD and a significant risk factor for cardiovascular disease. The following review outlines the differences and similarities of childhood versus adult hypertension with respect to measurement, diagnosis, treatment, and consequence in CKD. The definition of hypertension changes continually as a child grows with or without CKD. Despite numerous guidelines, the diagnosis of childhood hypertension continues to be based on epidemiologic data rather than evidence. For children, the current definition includes 2 categories: high normal, which is blood pressure (BP) between the 90th and 95th percentile, and hypertensive, which is BP above the 95th percentile. The evaluation of all hypertensive children should include a complete assessment of end-organ damage, including eyes, cardiovascular system (including blood vessels), kidneys, and nervous system. For children with CKD and end-stage renal disease (ESRD), a high percentage have left ventricular hypertrophy (LVH). The finding of end-organ damage or comorbidity (CKD, diabetes) in any child is an absolute indication for immediate pharmacologic therapy, whereas the presence of hypertension above the 95th percentile in children without CKD warrants initial intervention such as life style modification. The guidelines for measurement of BP in children with CKD are similar to those in children without CKD and include casual BP measurement, self-measured BP, and ambulatory BP monitoring. The recommendation for BP measurement in children is, when permitted, by auscultative method with a well-calibrated mercury manometer. Most casual BP measurements are performed with an automated oscillometric device whose validation has not been confirmed in children with CKD. The ambulatory BP monitor (ABPM) has 2 advantages: it significantly correlates with the presence of end-organ damage, and it identifies abnormal BP patterns that are frequently present in CKD patients, such as hypertension during the sleep period. An abnormal ABPM pattern can also be predictive of the development of end-organ damage. Treatment of hypertension in children, with and without CKD, is based on 3 factors: degree of BP elevation, the presence of cardiovascular risk factors, and the presence of end-organ damage. Additionally, the initial antihypertensive agent may be selected on available and age-appropriate formulations (eg, suspension and dosage selection). A physician treating a hypertensive child with CKD faces multiple challenges. They include selecting the convenience of available automated devices and the ABPM versus traditional auscultatory techniques upon which all normative standards have been based. Current research initiatives propose to develop pharmacokinetic and pharmacodynamics properties of antihypertensive medications and to study the effect of early intervention on end-organ damage.

Undiagnosed Hypertension in the ED Setting—An Unrecognized Opportunity by Emergency Nurses

Introduction Hypertension is often undiagnosed, untreated, undertreated, and poorly controlled. Many patients use the emergency department as their primary source of health care, and the emergency department represents an opportunity to identify undiagnosed hypertension. We sought to (1) identify the prevalence of elevated blood pressures in low-acuity patients and (2) describe the existing practice of reassessment, treatment, and referral of abnormal vital signs in these patients. Methods We conducted a retrospective study of 88 ED patients at an academic medical center. All patients meeting Emergency Severity Index level 4 or 5 criteria (low acuity) were eligible. The following variables were recorded: triage level, medical history and medications, disposition, and all blood pressures. The investigators independently reviewed and reached consensus regarding the following outcome variables: the need for and actual treatment of elevated blood pressure, and the need for and referral for blood pressure recheck after discharge. Results Thirty-seven patients (45%) had hypertension by definition on arrival. Systolic hypertension was more common. Ten of the patients (27%) with elevated blood pressures had documented rechecks prior to discharge in the emergency department, and only one patient was referred for follow-up. Twenty-seven out of 37 low-acuity patients (73%) who presented with elevated blood pressures had no documentation of the blood pressure being rechecked and no documentation of the patient being referred. Conclusion Our data suggest that important opportunities for education and follow-up of hypertension are being missed.

Hypertension and cerebrovascular disease

Stroke is a common problem in the United States and causes significant morbidity and mortality. In addition both the personal and economic costs of stroke are high. Chronic arterial hypertension is the most significant modifiable risk factor for stroke (ischemic and hemorrhagic), both because of it's high relative risk for stroke and also because of it's prevalence in the general population. In addition hypertension remains under-recognized and under-treated. Newer studies have demonstrated that more aggressive treatment of hypertension results in lower cardiovascular morbidity and mortality, including that due to stroke. Consequently, new definitions for hypertension and new recommendations for treatment have recently been published. Furthermore, certain conditions, such as stroke, have been determined to be a “compelling indication” for certain classes of antihypertension therapy. Chronic hypertension is an important cause of the vascular pathology which leads to stroke and intracerebral hemorrhage. Acute stroke and cerebral hemorrhage may also cause an acute rise in blood pressure. Treatment of elevated blood pressure during acute stroke must balance the theoretical risk of worsening the stroke due to reduced cerebral perfusion against the benefits of lowering blood pressure (reduced risk of hemorrhage, cerebral edema, and other end-organ damage). This has been made more challenging since the approval of thrombolytic therapy for acute ischemic stroke. Also, severely elevated blood pressure can also cause hypertensive encephalopathy which must be distinguished from stroke so that appropriate treatment can be instituted as quickly as possible.

Screening for high blood pressure: A review of the evidence for the U.S. Preventive Services Task Force

Context In 1996, the U.S. Preventive Services Task Force (USPSTF) recommended screening adults for hypertension. Since that time, the published literature on hypertension has expanded rapidly, necessitating a new examination of the evidence supporting screening. Objective Update the 1996 evidence review on screening for hypertension. Data sources The 1996 Guide to Clinical Preventive Services, recent systematic reviews, and focused searches of MEDLINE were used to identify new evidence relevant to detecting and treating hypertension. Study selection When a good quality, recent systematic review was available, it was used to summarize previous research; MEDLINE was searched only for more recent articles. Two authors reviewed abstracts (and full texts, if necessary) of potentially relevant articles to determine if they should be included. Data extraction One author extracted data from included studies into evidence tables. Data synthesis Hypertension can be effectively detected through office measurement of blood pressure. Treatment of elevated blood pressure in adults can reduce cardiovascular events. The magnitude of risk reduction depends on the degree of hypertension and the presence of other cardiovascular risk factors. Available studies have found no important adverse effects on psychological well-being and mixed effects on the absenteeism rates of adults who are screened and labeled as being hypertensive. Conclusions Substantial indirect evidence supports the effectiveness of screening adults to detect hypertension and treating them to reduce cardiovascular disease.

Sympathetic overactivity in hypertension: a risk factor for cardiovascular disease.

Numerous prospective studies have shown that high heart rate is related to the development of hypertension, atherosclerosis, and incidence of cardiovascular events. Experimental studies in monkeys have shown that high heart rate has direct atherogenic effects on the arteries as a result of increased wall stress. However, clustering of several risk factors for coronary artery disease in persons with high heart rate suggests that sympathetic overactivity also accounts for part of the increased cardiovascular morbidity that is observed in persons with tachycardia. Indeed, experimental studies have shown that heightened sympathetic tone can cause obesity, hyperinsulinemia, and insulin resistance, which in the long term can promote the development of atherosclerosis. Through its interaction with plasma insulin, sympathetic overactivity can promote the development of left ventricular hypertrophy. Sympathetic activation can also increase hematocrit and precipitate a procoagulant state. Angiotensin II has an effect both on the central nervous system, enhancing sympathetic outflow, and on the peripheral sympathetic nerves. Among the angiotensin II receptor antagonists, eprosartan showed a particular ability to block presynaptic angiotensin II receptor 1 (AT(1)) receptors at neuro-effector junctions in the sympathetic nervous system, as well as AT(1) receptors in blood vessels. This dual action may represent an important advance in treatment of elevated blood pressure.

Renin angiotensin system and ASCVD.

The renin angiotensin system was first described over 100 years ago and is still the focus of intense clinical and basic science investigation. The renin angiotensin system was demonstrated to play a major pathogenetic role in hypertension. The development of inhibitors of angiotensin-converting enzyme and specific receptor blockers for angiotensin-II represent a major advance in the treatment of elevated blood pressure. However, the renin angiotensin system is intimately involved in a number of conditions that increase the risk for atherosclerosis. Components of the renin angiotensin system have demonstrated to play a significant role in the initial phases of atherosclerosis. Additionally, plaque vulnerability and the potential for an acute atherosclerotic event are also modulated by the renin angiotensin system. Angiotensin-II plays a significant role in the balance between intravascular clot formation and fibrinolytic potential. Therefore, blocking the generation of angiotensin-II or inhibiting its binding to specific receptors may decrease the subsequent risk for unstable angina and acute myocardial infarction. Increased renin activity has been correlated as a statistical risk factor for coronary heart disease and converting enzyme inhibition has been demonstrated to decrease the incidence of acute ischemic events. This review will center on the role of modulation of the renin angiotensin system as a means to alter the clinical course of coronary atherosclerosis.

Cardiac hypertrophy depends upon sleep blood pressure: a study in rats.

The objective of this study was to determine whether cardiac hypertrophy in hypertensive rats could be reduced and normalized by intermittent reduction of blood pressure, and to determine whether left ventricular hypertrophy was related to 24 h workload or peak blood pressure responses. Hypertension was created by the application of a 0.20 mm clip to the left renal artery. Blood pressure response was monitored using a telemetry system (Data Science International). Blood pressure was reduced for varying periods of the day by giving different doses of captopril in the drinking water or by intra-peritoneal administration. Cardiac size was measured by weighing the ventricles and factoring by the body weight to obtain a cardiac index. Captopril 75 mg/kg per day and 25 mg/kg per day in the drinking water administered between 1800 and 2000 h lowered the 24 h blood pressure more than captopril 15 mg/kg per day or 5 mg/kg per day intra-peritoneally given at 0800 h. Captopril 75 mg/kg per day and captopril 15 mg/kg per day (intra-peritoneal) caused regression of cardiac hypertrophy whereas the other doses had no effect The best predictor of the cardiac hypertrophy response was the blood pressure between 0800 and 1200 h (i.e. the sleeping blood pressure). Twenty-four hour cardiac work did not correlate with the response. Cardiac hypertrophy can be reduced by intermittent treatment of elevated blood pressure. It is also caused by intermittent elevation of blood pressure. It appears that the crucial factor is when these alterations in blood pressure take place. An elevated blood pressure during the sleeping hours causes left ventricular hypertrophy, whereas a normal blood pressure during the sleeping hours allows reduction. It is suggested that acute wall stress is the signal to initiate the events that lead to cardiac hypertrophy but this only occurs if the hormonal milieu is appropriate.

Antihypertensive treatment: does the J-curve exist?

In the treatment of arterial hypertension, the optimal reduction in blood pressure is obviously the one that causes the maximum achievable prevention of hypertension-associated cardiovascular morbidity and mortality. This goal has clearly not been reached by today's approach to the treatment of elevated blood pressure. Treated hypertensive patients are still at increased risk of cardiovascular morbidity and mortality in spite of receiving antihypertensive treatment, as shown in many intervention studies. One possible explanation for this outcome could be that treated blood pressure is rarely brought down to strictly normotensive levels, again as shown in numerous studies. This finding would suggest that a more vigorous lowering of blood pressure would be advantageous when treating hypertensive patients. On the other hand, the fact that the relationship between the level of blood pressure and risk is J-shaped obviously means that vigorous lowering of blood pressure may increase cardiovascular risks, if blood pressure is brought down too far. Several open, retrospective, nonrandomized studies have been analyzed with this issue in mind, but so far only two prospective intervention trials have been specifically designed to address this problem: the BBB Study, published in 1994, and the much larger HOT Study, published in 1998. The rationale of these studies as well as some of their findings will be discussed briefly here, with emphasis on the HOT Study.

Effect of medical therapy on progressive nephropathy: Influence of pregnancy, diabetes and hypertension

Nephropathy is a complication of diabetes mellitus that can affect women in their reproductive years. This article reviews the effects on treatment on the main factors associated with short- and long-term complications in pregnant women with diabetic nephropathy. Tight glycemic control, adequate treatment of elevated blood pressure, and renal function in early pregnancy are the most significant predictors of maternal and perinatal outcomes. Contemporary methods of perinatal care and adequate treatment of blood pressure allow fetal survival rates of 95%. Furthermore, pregnancy per se does not appear to worsen the natural progression to end-stage renal disease for most women with renal insufficiency. However, patients with moderate to severe renal impairment may experience acceleration of renal disease.

Determinants of elevated blood pressure in women around menopause: results from a cross-sectional study in Italy

Objective: To analyse the determinants of high blood pressure in women around menopause. Methods: Eligible women were consecutively identified among patients who asked for a visit of their general practitioner during the period March–November 1997. A total of 22 919 women aged 44–66 years (median age 55 years), were identified. Women whose mean of the second and third of the three measures of diastolic blood pressure values performed during interview was >90 mm of mercury and/or reporting any type of current pharmacological treatment for elevated blood pressure were considered hypertensive. Results: In comparison with women aged 40–50 years, the multivariate odds ratio (OR) of elevated blood pressure were 1.4 in women aged 51–55, 2.0 in those aged 56–60 and 2.7 in those aged ≥61. In comparison with women with a body mass index (kg m −2) <25, the OR of elevated blood pressure was 1.7 and 2.7, respectively, for women with a BMI of 25–28 and ≥29. In comparison with women reporting a low level of physical activity, the OR of elevated blood pressure were 0.9 (95%, confidence interval, CI 0.7–1.0) and 0.7 (95% CI 0.4–0.9), respectively, for those reporting an intermediate or high level of activity. In comparison with premenopausal women, the OR of elevated blood pressure was, after taking into account the confounding effect of age, 1.6 (95% CI 1.0–1.4) in post menopausal ones. The OR of elevated blood pressure was 0.8 (95% CI 0.7–0.9), for current users of hormone replacement therapy (HRT), but no clear association emerged with duration of HRT pressure. Conclusions: This study suggests that, after taking into account the effect of age, post-menopausal women are at higher risk of the condition, and current HRT use decreases the risk. Other main determinants of risk of elevated blood pressure were overweight and low physical activity.

Effect of medical therapy on progressive nephropathy: influence of pregnancy, diabetes and hypertension.

Nephropathy is a complication of diabetes mellitus that can affect women in their reproductive years. This article reviews the effects on treatment on the main factors associated with short- and long-term complications in pregnant women with diabetic nephropathy. Tight glycemic control, adequate treatment of elevated blood pressure, and renal function in early pregnancy are the most significant predictors of maternal and perinatal outcomes. Contemporary methods of perinatal care and adequate treatment of blood pressure allow fetal survival rates of 95%. Furthermore, pregnancy per se does not appear to worsen the natural progression to end-stage renal disease for most women with renal insufficiency. However, patients with moderate to severe renal impairment may experience acceleration of renal disease.

Diabetic nephropathy.

Renal involvement is one of the major microvascular complications of both type 1 and type 2 diabetes mellitus. Diabetic nephropathy is the major cause of end-stage renal failure in most Western nations and is associated with increased morbidity and mortality as compared to other causes of renal disease. The pathogenesis of renal involvement in diabetes is presumed to be the result of the interplay of metabolic and hemodynamic factors. Significant advances in the prevention and treatment of progression of diabetic nephropathy have been achieved with intensive glycemic control and the treatment of elevated blood pressure. Patients with diabetes should thus be screened regularly for the appearance of any of the risk factors for renal or other complications and treated intensively according to established guidelines for control of hyperglycemia and hypertension. Ancillary therapeutic measures include treatment of hyperlipidemia, low-protein diet, and the cessation of smoking.