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

The ability of insulin to stimulate glucose disposal varies more than six-fold in apparently healthy individuals. The one third of the population that is most insulin resistant is at greatly increased risk to develop cardiovascular disease (CVD), type 2 diabetes, hypertension, stroke, nonalcoholic fatty liver disease, polycystic ovary disease, and certain forms of cancer. Between 25-35% of the variability in insulin action is related to being overweight. The importance of the adverse effects of excess adiposity is apparent in light of the evidence that more than half of the adult population in the United States is classified as being overweight/obese, as defined by a body mass index greater than 25.0 kg/m(2). The current epidemic of overweight/obesity is most-likely related to a combination of increased caloric intake and decreased energy expenditure. In either instance, the fact that CVD risk is increased as individuals gain weight emphasizes the gravity of the health care dilemma posed by the explosive increase in the prevalence of overweight/obesity in the population at large. Given the enormity of the problem, it is necessary to differentiate between the CVD risk related to obesity per se, as distinct from the fact that the prevalence of insulin resistance and compensatory hyperinsulinemia are increased in overweight/obese individuals. Although the majority of individuals in the general population that can be considered insulin resistant are also overweight/obese, not all overweight/obese persons are insulin resistant. Furthermore, the cluster of abnormalities associated with insulin resistance - namely, glucose intolerance, hyperinsulinemia, dyslipidemia, and elevated plasma C-reactive protein concentrations -- is limited to the subset of overweight/obese individuals that are also insulin resistant. Of greater clinical relevance is the fact that significant improvement in these metabolic abnormalities following weight loss is seen only in the subset of overweight/obese individuals that are also insulin resistant. In view of the large number of overweight/obese subjects at potential risk to be insulin resistant/hyperinsulinemic (and at increased CVD risk), and the difficulty in achieving weight loss, it seems essential to identify those overweight/obese individuals who are also insulin resistant and will benefit the most from weight loss, then target this population for the most-intensive efforts to bring about weight loss.
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PMID:Obesity, insulin resistance, and cardiovascular disease. 1474 3

Elevated levels of C-reactive protein (CRP) led to a 52% increase in the risk of developing hypertension. Results were significant even in women with low blood pressure. The study raises the possibility that lowering blood pressure might lower CRP levels.
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PMID:Women's high CRP levels can predict hypertension. 1487 May 24

Cardiovascular disease (CVD) is the leading cause of mortality in women and a major cause of morbidity. Coronary heart disease (CHD) accounts for nearly half of all CVD deaths. Gender differences in CHD include a later age of onset for women, a greater prevalence of comorbid diseases, and differences in the initial manifestations of the disease. Traditional risk factors for CHD include tobacco use, hypertension, diabetes mellitus, dyslipidemia, obesity, sedentary lifestyle, and atherogenic diet. More recently identified risk factors in women include high sensitivity C-reactive protein (hsCRP), homocysteine, and lipoprotein (a). Appropriate management of risk factors is associated with a reduced incidence of CHD, yet poor implementation in women is widely documented. Barriers to optimal risk factor management in women should be identified and overcome in an effort to maximize the cardiovascular health of women.
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PMID:Epidemiology of coronary heart disease in women. 1496 52

C-reactive protein (CRP) and microalbuminuria reflect intimately related components of the atherosclerotic disease process. Epidemiological studies found only modest associations between CRP and microalbuminuria. Blood pressure, one of the components of the metabolic syndrome in the general population, is the main determinant of microalbuminuria in diabetes and hypertension. We questioned whether CRP modifies the relationship of blood pressure and other cardiovascular risk factors with microalbuminuria in a cross-sectional study in 8592 inhabitants from Groningen, The Netherlands. The crude data showed an increase in the prevalence of microalbuminuria with increasing CRP quartiles (4.8, 9.6, 14.5, and 18.6%, P<0.0001). On stratification for cardiovascular risk factors, the data revealed a significant and positive interaction between mean arterial pressure (MAP) and quartiles of CRP with respect to the risk of microalbuminuria (Wald statistic 9.2, P=0.03). In subjects with a MAP <90 mm Hg, a nonsignificant trend in the association between CRP quartiles and microalbuminuria was found (prevalence: 3.9%, 5.8%, 6.6%, 8.7%; P=0.11). This trend was much steeper and significant in subjects with an MAP >90 mm Hg (prevalence: 6.7%, 13.6%, 20.4%, 25.1%; P<0.0001). Controlling for other risk factors in multivariate analyses, the positive interaction persisted (P=0.0004). No significant interactions between other risk factors and CRP with respect to the risk of microalbuminuria were encountered. Thus, CRP modifies the relation between blood pressure and microalbuminuria.
Hypertension 2004 Apr
PMID:C-reactive protein modifies the relationship between blood pressure and microalbuminuria. 1496 37

We sought to assess the relation between circulating levels of inflammation markers, such as neopterin and C-reactive protein, and the development of adverse cardiovascular events in patients with hypertension but without obstructive coronary artery disease. We observed that patients who developed adverse events during follow-up had significantly higher neopterin levels compared with patients without events.
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PMID:Prognostic value of neopterin levels in treated patients with hypertension and chest pain but without obstructive coronary artery disease. 1499 95

As a population-based, longitudinal study of nearly 6000 older American adults, the Cardiovascular Health Study provides an excellent opportunity to assess the roles of traditional and novel cardiovascular risk factors in the development of coronary heart disease. Cardiovascular Health Study investigators have analyzed both traditional risk factors, such as diabetes, hypertension, and smoking, and new risk factors, such as hemostatic factors, inflammatory markers, exposure to infectious agents, and genetic determinants. These analyses have led to several important conclusions. First, older adults without previous cardiovascular events have a tremendous burden of subclinical vascular disease, which may change how physicians view risk factor modification in this age group. Second, some traditional cardiovascular risk factors lose importance as predictors of cardiovascular disease among older adults. Third, even modest elevations in fasting blood glucose or systolic blood pressure-below the levels used to define diabetes or hypertension-may have prognostic implications. Fourth, novel cardiovascular risk factors may add further information about cardiovascular disease risk in older adults. Promising potential candidates identified in the Cardiovascular Health Study include markers of hemostatic activation, fibrinogen, factor VIII coagulant activity, C-reactive protein, and exposure to herpes simplex virus-1 and possibly chlamydia. Future Cardiovascular Health Study investigations will help to clarify which combination of traditional and newer risk factors provides the best estimate of cardiovascular risk for older adults.
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PMID:Traditional and novel risk factors in older adults: cardiovascular risk assessment late in life. 1501 Jun 53

A rapidly growing body of evidence demonstrates important associations between the metabolic syndrome, characterized by a cluster of risk factors or phenotypes that include dyslipidemia, central obesity, hypertension, and hyperinsulinemia, and both cardiovascular disease and type 2 diabetes. The purpose of the present study was to characterize the metabolic syndrome in a sample of 432 individuals from 68 Japanese-American families, using factor analysis of quantitative phenotypes, and to estimate the heritability of these independent factors. Using nine characteristic phenotypes that included LDL particle size and C-reactive protein (CRP), factor analysis identified three multivariate factors interpreted as lipids, body fat/insulin/glucose/CRP, and blood pressure, explaining 65% of the variance. Heritability analysis revealed significant genetic effects on all of the factors: lipids (h(2) = 0.52, P < 0.001), body fat/insulin/glucose/CRP (h(2) = 0.27, P = 0.016), and blood pressure (h(2) = 0.25, P = 0.026). This analysis shows that independent, multivariate factors of the metabolic syndrome are heritable, demonstrating genetic influences on the underlying pathophysiological mechanisms of the syndrome.
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PMID:Heritability of multivariate factors of the metabolic syndrome in nondiabetic Japanese americans. 1504 37

A 73-year-old woman with a history of hypertension and hyperlipidemia presented with a sharp pain ranging from the right shoulder to the upper limb. She had suffered a sharp pain at rest accompanied by general fatigue and nausea for about ten months prior to admission. Her white blood cell count was 12,800/microl, and her serum C-reactive protein was 17.5 mg/dl. A chest computed tomography scan revealed an aneurysmal change of the origin of the brachiocephalic artery. Pseudoaneurysm due to infection and aortic dissection was considered as a preoperative diagnosis. A total arch replacement was performed under cardiopulmonary bypass, deep hypothermia, and selective cerebral perfusion. Postoperatively, a bacteriologic culture of the contents of the aneurysm revealed Staphylococcus aureus. Perioperative administration of antibiotics was effective and the postoperative course was uneventful.
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PMID:Mycotic pseudoaneurysm of the brachiocephalic artery. 1507 52

Inflammation appears to be pivotal in all phases of atherosclerosis from the fatty streak lesion to acute coronary syndromes. An important downstream marker of inflammation is C-reactive protein (CRP). Numerous studies have shown that CRP levels predict cardiovascular disease in apparently healthy individuals. This has resulted in a position statement recommending cutoff levels of CRP <1.0, 1.0 to 3.0, and >3.0 mg/L equating to low, average, and high risk for subsequent cardiovascular disease. More interestingly, much in vitro data have now emerged in support of a role for CRP in atherogenesis. To date, studies largely in endothelial cells, but also in monocyte-macrophages and vascular smooth muscle cells, support a role for CRP in atherogenesis. The proinflammatory, proatherogenic effects of CRP that have been documented in endothelial cells include the following: decreased nitric oxide and prostacyclin and increased endothelin-1, cell adhesion molecules, monocyte chemoattractant protein-1 and interleukin-8, and increased plasminogen activator inhibitor-1. In monocyte-macrophages, CRP induces tissue factor secretion, increases reactive oxygen species and proinflammatory cytokine release, promotes monocyte chemotaxis and adhesion, and increases oxidized low-density lipoprotein uptake. Also, CRP has been shown in vascular smooth muscle cells to increase inducible nitric oxide production, increase NFkappa(b) and mitogen-activated protein kinase activities, and, most importantly, upregulate angiotensin type-1 receptor resulting in increased reactive oxygen species and vascular smooth muscle cell proliferation. Future studies should be directed at delineating the molecular mechanisms for these important in vitro observations. Also, studies should be directed at confirming these findings in animal models and other systems as proof of concept. In conclusion, CRP is a risk marker for cardiovascular disease and, based on future studies, could emerge as a mediator in atherogenesis.
Hypertension 2004 Jul
PMID:C-reactive protein: risk marker or mediator in atherothrombosis? 1514 94

Atherosclerosis is the major cause of cardiovascular disease. Hypercholesterolaemia, hypertension and cigarette smoking are the common risk factors for atherosclerosis. These risk factors unite behind a convergence of mechanism, involving oxidation and inflammation in the artery wall that, with time, gives rise to characteristic fatty-fibrous lesions. Physical trauma and inflammation produce lesion rupture, which can lead to clinical events such as heart attack and stroke, or resolve with plaque growth. Disease progression is marked by the inflammatory indicator CRP (C-reactive protein). Early indicators of heart attack are the inflammatory marker CD40, and the cardiac myofilament protein troponin. Coronary atherosclerosis is the common cause of heart failure (HF). Disordered calcium signalling to the myofilaments occurs in HF and in cardiomyopathy. Enhanced calcium signalling suppresses HF. Neuro-humoral and biomechanical processes, as seen in hypertension, produce cardiac hypertrophy, which predisposes to HF through apoptosis. Although in humans cardiac damage produces permanent loss of cells, because the heart cannot regenerate, developments in stem cell technology suggest that help is at hand.
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PMID:Pathophysiology and biochemistry of cardiovascular disease. 1517 70


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