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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Uterine fibroids are the most common benign tumour of the female genital tract. However, their true prevalence is probably under-estimated, as the incidence at histology is more than double the clinical incidence. Recent longitudinal studies have estimated that the lifetime risk of fibroids in a woman over the age of 45 years is more than 60%, with incidence higher in blacks than in whites. The cause of fibroids remains unclear and their biology poorly understood. No single candidate gene has been detected for commonly occurring uterine fibroids. However, the occurrence of rare uterine fibroid syndromes, such as multiple cutaneous and uterine leiomyomatosis, has been traced to the gene that codes for the mitochondrial enzyme, fumarate hydratase. Cytogenetic abnormalities, particularly deletions of chromosome 7, which are found in up to 50% of fibroid specimens, seem to be secondary rather than primary events, and investigations into the role of tumour suppressor genes have yielded conflicting results. The key regulators of fibroid growth are ovarian steroids, both oestrogen and progestogen, growth factors and angiogenesis, and the process of apoptosis. Black race, heredity, nulliparity, obesity, polycystic ovary syndrome, diabetes and hypertension are associated with increased risk of fibroids, and there is emerging evidence that familial predisposition to fibroids is associated with a distinct pattern of clinical and molecular features compared with fibroids in families without this prevalence.
Best Pract Res Clin Obstet Gynaecol 2008 Aug
PMID:Incidence, aetiology and epidemiology of uterine fibroids. 1853 13

Over the last 15 years, a number of long-term health risks associated with reduced fetal growth have been identified, including cardiovascular diseases, hypertension, dyslipidaemia and type 2 diabetes. A common feature of these conditions is insulin resistance, which is thought to play a pathogenic role. However, despite abundant data in the literature, it is still difficult to trace the pathway by which fetal events, environmental or not, may lead to increased morbidity later in life. To explain this association, several hypotheses have been proposed pointing to the role of a detrimental fetal environment, a genetic susceptibility or an interaction between the two, and of the particular dynamic changes in adiposity that occur during catch-up growth. The relative impact of early postnatal events in relation to fetal growth has to be considered for designing health policy strategies for early interventions aimed at decreasing disease risk throughout life.
Best Pract Res Clin Endocrinol Metab 2008 Jun
PMID:Pathophysiology of insulin resistance in subjects born small for gestational age. 1853 89

The aims of critical care management are broad. Critical illness in pregnancy is especially pertinent as the patient is usually young and previously fit, and management decisions must also consider the fetus. Assessment must consider the normal physiological changes of pregnancy, which may complicate diagnosis of disease and scoring levels of severity. Pregnant women may present with any medical or surgical problem, as well as specific pathologies unique to pregnancy that may be life threatening, including pre-eclampsia and hypertension, thromboembolic disease and massive obstetric haemorrhage. There are also increasing numbers of pregnancies in those with high-risk medical conditions such as cardiac disease. As numbers are small and clinical trials in pregnancy are not practical, management in most cases relies on general intensive care principles extrapolated from the non-pregnant population. This chapter will outline the aims of management in an organ-system-based approach, focusing on important general principles of critical care management with considerations for the pregnant and puerperal patient.
Best Pract Res Clin Obstet Gynaecol 2008 Oct
PMID:Aims of obstetric critical care management. 1869 71

VENTRICULAR ARRHYTHMIAS: Different factors--like hypertrophy, fibrosis, ischemia and apoptosis increase the risk of ventricular arrhythmias and sudden arrhythmic death. ACE inhibitors and Angiotensin receptor antagonists offer a curative therapeutic approach. Beta-blocker are strongly recommended. Amiodarone may be used for symptomatic arrhythmia suppression--but with no proven favourable prognostic effect. The use of class-1 antiarrhythmic drugs is obsolete in the presence of left ventricular hypertrophy and heart failure. Implantable cardioverter/defibrillators (ICD) have been proven to have a positive effect on survival in secondary and primary prevention of sudden cardiac death, and so has cardiac synchronization in severe cardiac dysfunction and widened QRS complex. Atrial fibrillation (AF): Arterial hypertension represents the main risk factor for AF. Patients' age, left ventricular hypertrophy, left atrial dilatation and angiotensin-II activation play an important role in the induction and maintenance of AF. Angiotensin-receptor and beta-blockers seem to be efficacious in AF suppression and also on the regression of hypertrophy. The use of antiarrhythmic agents (AA) is limited because of their relatively low long-term efficacy and pro-arrhythmia properties. Best results may be achieved with class 1C AA drugs in patients with no or minimal structural heart disease. In all other cases amiodarone is suitable but is limited by its side effects. In patients with no or only a few symptoms rate control may be sufficient, but if there are symptoms interventional left atrial ablation of pulmonary veins should be attempted as a real curative strategy.
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PMID:[Arterial hypertension and cardiac arrhythmias]. 1908 3

Impaired stress-induced pressure natriuresis, ie, an inadequate compensatory increase in urinary sodium excretion (U(Na)V) in response to a stress-induced blood pressure increase, may lead to the premature development of essential hypertension. To assess the heritability of baseline U(Na)V, stress U(Na)V, and the U(Na)V response to stress (Delta U(Na)V=stress U(Na)V- baseline U(Na)V), we studied 396 black and 494 white twins, including monozygotic and dizygotic twins of the same as well as the opposite sex (mean age: 17.6+/-3.3 years; range: 11.9 to 30.0 years). Bivariate genetic model fitting was performed to examine the extent to which genetic and environmental factors are common or specific to baseline and stress U(Na)V. Heritability estimates for Delta U(Na)V can be derived from these bivariate models. All of the bivariate analyses were performed separately in whites and blacks, because univariate models for baseline U(Na)V showed significant ethnic differences in heritability estimates. Best-fitting models showed that the heritability of stress U(Na)V was 0.42 in whites and 0.58 in blacks. Only 15% and 11% of the total variance could be attributed to genetic factors common to baseline and stress U(Na)V in whites and blacks, respectively. After removal of all of the shared influences with baseline U(Na)V, heritabilities for stress U(Na)V were 0.32 in whites and 0.57 in blacks. Heritability estimates for Delta U(Na)V were 0.36 in whites and 0.39 in blacks. In summary, this study establishes Delta U(Na)V and stress U(Na)V as heritable phenotypes that may be used to study the genetic etiology of early hypertension development.
Hypertension 2009 Feb
PMID:Stress-induced sodium excretion: a new intermediate phenotype to study the early genetic etiology of hypertension? 1910 6

Epidemiological observations support a positive relationship between cardiovascular diseases (CVD) and osteoporosis, where cholesterol has been indicated to be a possible link. Only a few studies have investigated the relation between lipids and BMD, but the association remains unclear. We studied the relationship between serum lipids and BMD of the calcaneus. A cross-sectional population-based study was performed, based on data from the Longitudinal Aging Study Amsterdam, including 620 men and 635 women, 65-88 yr of age. BMD was measured by quantitative ultrasound (QUS), velocity of sound (VOS; m/s), and broadband ultrasound attenuation (BUA; dB/MHz). Models were adjusted for age, body mass index, physical activity, smoking, alcohol, diabetes mellitus, hypertension, testosterone, and 25-hydroxyvitamin D. No association was found between total cholesterol (TC) and QUS. Men and women in the highest quartile of high-density lipoprotein cholesterol (HDL-c) had a significantly lower QUS (men-VOS: beta = -20.8, p = 0.00; BUA: beta = -5.2, p = 0.02; women-VOS: beta = -18.6, p = 0.00) compared with men and women in the lowest quartile. An even stronger positive association was seen between TC/HDL-c ratio and QUS (men-VOS: beta = 21.8, p = 0.00; BUA: beta = 5.5, p = 0.01; women-VOS: beta = 19.2, p = 0.00; BUA: beta = 3.6, p = 0.05). Our analysis shows that the lipid profile that is favorable in the prevention of CVD (i.e., high levels of HDL-c and low TC/HDL-c ratio) is unfavorable for QUS. These results indicate that HDL-c levels do not explain the association between osteoporosis and CVD.
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PMID:Lipid levels: a link between cardiovascular disease and osteoporosis? 1911 6

Increased intra-abdominal pressure (IAP) has received growing attention in critically ill patients. Pathophysiologically, it deranges cardiovascular haemodynamics, respiratory and renal functions and may eventually lead to multi-organ failure. It is primarily seen in surgical intensive care units and is frequently associated with abdominal trauma but also occurs after elective abdominal surgery. Non-surgical intensivists ought to be aware that the syndrome is also seen in a wide spectrum of medical conditions, e.g. acute pancreatitis. An expert panel has recently set up definitions of intra-abdominal hypertension (IAH, sustained or repeated pathological elevation in IAP > or = 12 mmHg) and abdominal compartment syndrome (ACS, sustained IAP > 20 mmHg associated with a new organ dysfunction or failure). As clinical signs of IAH are unreliable, IAP should be measured non-invasively by the 'bladder technique'. It is hoped that the consensus definitions will contribute to a broader recognition and effective treatment of this life-threatening syndrome.
Best Pract Res Clin Gastroenterol 2009
PMID:Abdominal compartment syndrome. 1925 84

Haematopoietic stem cell transplantation is currently the only curative option for many haematological malignancies, but is characterized by a wide spectrum of complications, including haemostatic changes. Bleeding and thrombotic events occur in the early and late phases after transplantation. In the early phase, thrombotic events have a variable clinical picture and present either as venous thrombosis, mainly at the site of central venous lines, veno-occlusive disease (also known as sinusoid occlusion syndrome) or transplant-associated microangiopathy. The latter two occur in the context of an acute graft-vs-host reaction, which involves various organs including the endothelium. In the late phase, years or decades after transplantation, thrombotic events present either as common venous thromboses or as arterial occlusions because of the development of premature atherosclerosis combined with diabetes, hypertension and dyslipidaemia, all of which are accelerated under the influence of the post-transplant treatment. This chapter will discuss the incidence, possible causative associations and treatment options of early and late thrombotic events after haematopoietic stem cell transplantation.
Best Pract Res Clin Haematol 2009 Mar
PMID:Thrombotic complications after haematopoietic stem cell transplantation: early and late effects. 1928 80

Better assessment of the association between cardiovascular disease and osteoporosis in older men may help identify shared etiologies for bone and heart health in this population. We assessed the association of BMD and bone turnover markers (BTMs) with risk of cardiovascular events (myocardial infarction or stroke) in 744 men >or=50 yr of age. During the 7.5-yr prospective follow-up, 43 strokes and 40 myocardial infarctions occurred in 79 men. After adjustment for confounders (age, weight, height, smoking, education, physical activity, self-reported history of diabetes, hypertension, and prevalent ischemic heart disease), men in the lowest quartile of BMD at the spine, whole body, and forearm had a 2-fold increased risk of cardiovascular events. Men in the highest quartile of bone resorption markers (deoxypyridinoline [DPD], C-telopeptide of type I collagen) had a 2-fold increased risk of cardiovascular events (e.g., multivariable-adjusted hazard ratio [including additional adjustment for BMD] was 2.11 [95% CI: 1.26-3.56], for the highest quartile of free DPD relative to the lowest three quartiles). The results were similar for men without prevalent ischemic heart disease and for myocardial infarction and stroke analyzed separately. Our data suggest that men with low BMD or high bone resorption may be at increased risk of myocardial infarction and stroke in addition to fracture. Thus, men with osteoporosis may benefit from screening for cardiovascular disease. Further study to elucidate the biological mechanism shared by bone and vascular disease may help efforts to identify men at risk or develop treatment.
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PMID:Increased bone resorption is associated with increased risk of cardiovascular events in men: the MINOS study. 1945 64

The primary systemic vasculitides are a group of autoimmune conditions characterised by occlusion, stenosis or aneurysmal dilatation of blood vessels secondary to intra-mural inflammation. Current therapy has converted the outlook of these diseases from death or severe morbidity to a remitting-relapsing condition in most instances. Longer survival, relapsing course of disease and chronic glucocorticoid therapy probably contribute to an increase in cardiovascular events and morbidity. This article reviews the available data for effect of primary systemic vasculitis on cardiovascular end points like coronary artery disease, congestive cardiac failure, hypertension and aortic aneurysm in all age groups. We examine the interplay between the activated endothelium, autoimmune mechanisms and treatment factors to produce a direct insult or increased atherogenic potential of primary systemic vasculitis. Recommendations to deal with cardiovascular end points are made.
Best Pract Res Clin Rheumatol 2009 Jun
PMID:Cardiovascular involvement in primary systemic vasculitis. 1950 48


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