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

Inflammation occurs in the vasculature as a response to injury, lipid peroxidation, and perhaps infection. Various risk factors, including hypertension, diabetes, and smoking, are amplified by the harmful effects of oxidized low-density-lipoprotein cholesterol, initiating a chronic inflammatory reaction, the result of which is a vulnerable plaque, prone to rupture and thrombosis. Epidemiological and clinical studies have shown strong and consistent relationships between markers of inflammation and risk of future cardiovascular events. Inflammation can potentially be detected locally by imaging techniques as well as emerging techniques, such as identification of temperature or pH heterogeneity. It can be detected systemically by measurement of inflammatory markers. Of these, the most reliable and accessible for clinical use is currently high-sensitivity C-reactive protein. A combination of methods may provide the best identification of persons at risk for cardiovascular events who would benefit from treatment. In randomized, controlled trials, 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, in the form of statins, have been shown to provide effective therapy for lowering CRP, in conjunction with their lipid-lowering effects. Although the magnitude of risk reduction associated with statin use appears to be largest for those with the highest serum levels of CRP, whether CRP reduction per se lowers cardiovascular risk is unknown.
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PMID:Inflammation as a cardiovascular risk factor. 1517 56

Common conditions predisposing to atherosclerosis, such as hypercholesterolemia, hypertension, diabetes, and smoking, are associated with endothelial dysfunction. Endothelial function has largely been assessed as endothelium-dependent vasomotion, at least in part based on the assumption that impaired endothelium-dependent vasodilation also reflects the alteration of other important functions of the endothelium. An important rationale for this approach has been the observation that endothelium-derived nitric oxide (NO), a major mediator of endothelium-dependent vasodilation, has important anti-inflammatory and antithrombotic properties, ie, inhibiting leukocyte adhesion, limiting platelet adhesion and aggregation, and the expression of plasminogen activator inhibitor-1 (PAI-1), a prothrombotic protein. Accumulating data suggest that the degree of impairment of endothelium-dependent vasomotion has profound and independent prognostic implications. A common mechanism underlying endothelial dysfunction relates to increased vascular production of reactive oxygen species. Recent studies also suggest that inflammation per se and C-reactive protein in particular may directly contribute to endothelial dysfunction. These findings raise the question of whether assessment of endothelial function can be used in the clinical setting to identify patients at high risk. New insights into mechanisms of endothelial dysfunction, such as a better understanding of the regulation of important vascular sources of oxygen radicals, may lead to novel therapeutic strategies with the potential to improve prognosis.
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PMID:Endothelial function: a critical determinant in atherosclerosis? 1517 60

Mechanisms underlying biological effects of statin and angiotensin-converting enzyme inhibitor therapies differ. Thus, we studied vascular responses to combination therapy in hypercholesterolemic patients. A randomized, double-blind, placebo-controlled, crossover trial was conducted with 50 hypercholesterolemic patients with simvastatin and either placebo or ramipril (study I) and in 45 hypercholesterolemic diabetic patients with simvastatin or ramipril with placebo or simvastatin combined with ramipril (study II) for 2 months with 2 months washout. In study I simvastatin combined with ramipril significantly reduced blood pressure after 2 months. Simvastatin alone or combined with ramipril significantly changed lipoproteins, improved percent flow-mediated dilator response to hyperemia by 30+/-5% and 53+/-6%, respectively (P<0.001), and reduced plasma levels of malondialdehyde by 4+/-7% (P=0.026) and 25+/-4% (P<0.001), respectively. Monocyte chemoattractant protein-1 levels decreased by 3+/-3% and 12+/-2%, respectively (P=0.049 and P=0.001, respectively), C-reactive protein levels changed by 0% and 18%, respectively (P=0.036 and P<0.001, respectively), and plasminogen activator inhibitor-1 antigen levels changed by -7+/-7% and 17+/-5%, respectively (P=0.828 and P<0.001, respectively). In study II ramipril alone did not significantly change lipoproteins and C-reactive protein levels, however, simvastatin combined with ramipril significantly changed lipoproteins and C-reactive protein levels more than ramipril alone (P<0.001 and P=0.048 by ANOVA, respectively). Ramipril alone or simvastatin combined with ramipril significantly improved the percent flow-mediated dilator response to hyperemia (both P<0.001), however, simvastatin combined with ramipril showed significantly more improvement than ramipril alone (P<0.001 by ANOVA). Simvastatin combined with ramipril significantly improved endothelium-dependent vasodilation and fibrinolysis potential and reduced plasma levels of oxidant stress and inflammation markers in hypercholesterolemic patients.
Hypertension 2004 Aug
PMID:Simvastatin combined with ramipril treatment in hypercholesterolemic patients. 1518 51

Advances in our understanding of the ways in which the traditional cardiovascular risk factors, including standard lipid (eg, total cholesterol, low-density lipoprotein cholesterol, and high-density lipoprotein cholesterol) and nonlipid (eg, hypertension) risk factors, interact to initiate atherosclerosis and promote the development of cardiovascular disease have enhanced our ability to assess risk in the individual patient. In addition, the ongoing identification and understanding of so-called novel risk factors may further improve our ability to predict future risk when these are included along with the classic risk factors in assessing the global risk profile. This review briefly summarizes the evidence that some newer risk factors, including impaired fasting glucose, triglycerides and triglyceride-rich lipoprotein remnants, lipoprotein(a), homocysteine, and high-sensitivity C-reactive protein, contribute to an increased risk of coronary and cardiovascular diseases.
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PMID:New risk factors for atherosclerosis and patient risk assessment. 1519 61

Neutrophil functions are impaired in patients with diabetes mellitus. Bacterial phagocytosis and oxidative burst activity are reduced at high glucose concentrations in diabetic patients. Defects in neutrophil oxidative burst capacity are of multifactorial origin in diabetes mellitus and correlate with glucose levels. It has been reported that neutrophil NADPH oxidase activity is impaired and superoxide production is reduced in diabetic patients with or without any infections. Nicotinamide is a vitamin B3 derivative and a NAD precursor with immunomodulatory effects. In vitro studies demonstrated that nicotinamide increases NAD and NADH content of beta cells. The authors hypothesized that nicotinamide may restore the impaired oxidative burst capacity of neutrophils in diabetic patients by increasing the NADH content as an electron donor and possibly through NADPH oxidase activity of the cell. In order to test the hypothesis, this placebo-controlled and open study was designed to evaluate neutrophil functions in infection-free poorly controlled type 2 diabetic patients as compared to healthy subjects and assess the effects of nicotinamide on neutrophil phagocytosis as well as oxidative burst activity. Thirty patients with type 2 diabetes mellitus were enrolled in the study. Sixteen were females and 14 were males, with a mean age 58 +/- 10. All patients were on sulphonylurea treatment and their hemoglobin A(1c) (HbA(1c)) levels were above 7.5%. The control group consisted of 10 voluntary healthy subjects. Diabetic and control subjects were not significantly different in terms of age, body mass index (BMI), leucocyte and neutrophil counts, C-reactive protein (CRP) level, and erythrocyte sedimentation rate (ESR), but HbA(1c) and fasting glucose levels were significantly higher in patients with diabetes mellitus. Phagocytic activity and respiratory burst indexes were measured by flow cytometric analyses as previously described by Rothe and Valet (Methods Enzyml., 233, 539-548, 1994) and compared in diabetic subjects and healthy controls. Diabetic patients were grouped to receive either 50 mg/kg oral nicotinamide (n = 15) or placebo (n = 15) for a period of 1 month. The 2 groups did not differ in terms of treatment, frequency of hypertension, BMI, diabetes duration, age, fasting plasma glucose (FPG), HbA(1c), CRP, ESR, polymorphonuclear leukocyte (PNL) and neutrophil counts. Neutrophil functions were reassessed after the treatment period. Phagocytic activity represented as indexes were lower in diabetic patients when compared to healthy subjects, but the differences were not statistically significant (P >.05). Patients with diabetes mellitus had significantly lower oxidative burst indexes when compared to healthy controls (P values <.05). In diabetic patients, a negative correlation between neutrophil functions and HbA(1c) was found which was not statistically significant (P values >.05). Phagocytic indexes were similar in nicotinamide and placebo groups after treatment period (P >.05). But oxidative burst activity in patients receiving nicotinamide was greater when compared with placebo and the difference was statistically significant at 30 and 45 minutes (P values.04 and.03). This effect of nicotinamide may be due to increased NADH content and NADPH oxidase activity of the cell, which needs to be further studied. Impaired neutrophil functions may aggravate various infections in patients with diabetes mellitus and blood glucose regulation is an important target of treatment to improve neutrophil functions. But nicotinamide treatment may help to improve prognosis in diabetic patients with severe infections.
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PMID:Nicotinamide effects oxidative burst activity of neutrophils in patients with poorly controlled type 2 diabetes mellitus. 1520 86

Carotid stenosis is frequent in patients with coronary artery disease (CAD). In the literature, 9-28% of patients with CAD have additional carotid artery stenosis, predictors of which are advanced age, smoking, diabetes mellitus, arterial hypertension, coronary multivessel disease, and peripheral arterial disease. Moreover, patients with unstable coronary syndromes and those with elevated inflammatory markers such as C-reactive protein or fibrinogen more often have concomitant CAD and carotid artery stenosis. The long-term prognosis of these patients is worse than with CAD only. Therefore, patients with CAD should be screened for additional carotid artery stenosis, especially if coronary artery bypass grafting is planned. Continuous wave Doppler sonography and color-coded duplex sonography are suitable methods to screen for carotid artery stenosis.
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PMID:[Carotid stenosis concomitant to coronary artery disease]. 1522 Oct 90

Cardiovascular disease is the leading cause of death in the industrialized world, and a number of well-characterized factors, including advanced age, hypertension, dyslipidemia, diabetes, and smoking, contribute to cardiovascular risk. Integration of these factors using the Framingham calculation estimates the absolute 10-year risk for coronary heart disease (CHD), which can be used to guide therapy. Recent studies have demonstrated that additional markers, including elevated lipoprotein(a), homocysteine, sitosterol, and particularly C-reactive protein (CRP), are also associated with increased risk for CHD. In particular, high-sensitivity CRP has been shown to identify patients with high CHD risk who may not have elevated low-density lipoprotein cholesterol (LDL-C) and may add to the predictive value of the Framingham functions for CHD risk assessment. Assessment of global risk is particularly important in lipid management, as the LDL-C target goals are determined by risk category.
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PMID:Assessing coronary heart disease risk with traditional and novel risk factors. 1523 85

The cardiovascular risk in patients with hypothyroidism is related to an increased risk of functional cardiovascular abnormalities and to an increased risk of atherosclerosis. The pattern of cardiovascular abnormalities is similar in subclinical and overt hypothyroidism, suggesting that a lesser degree of thyroid hormone deficiency may also affect the cardiovascular system. Hypothyroid patients, even those with subclinical hypothyroidism, have impaired endothelial function, normal/depressed systolic function, left ventricular diastolic dysfunction at rest, and systolic and diastolic dysfunction on effort, which may result in poor physical exercise capacity. There is also a tendency to increase diastolic blood pressure as a result of increased systemic vascular resistance. All these abnormalities regress with L-T4 replacement therapy. An increased risk for atherosclerosis is supported by autopsy and epidemiological studies in patients with thyroid hormone deficiency. The "traditional" risk factors are hypertension in conjunction with an atherogenic lipid profile; the latter is more often observed in patients with TSH >10 mU/L. More recently, C-reactive protein, homocysteine, increased arterial stiffness, endothelial dysfunction, and altered coagulation parameters have been recognized as risk factors for atherosclerosis in patients with thyroid hormone deficiency. This constellation of reversible cardiovascular abnormalities in patient with TSH levels <10 mU/L indicate that the benefits of treatment of mild thyroid failure with appropriate doses of L-thyroxine outweigh the risk.
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PMID:Hypothyroidism as a risk factor for cardiovascular disease. 1524 98

The majority of end-stage renal disease (ESRD) patients are hypertensive. Drug therapy for hypertension in hemodialysis (HD) patients includes all classes of antihypertensive drugs, with the sole exception of diuretics. Angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor blockers may decrease morbidity and mortality by reducing the mean arterial pressure (MAP), aortic pulse wave velocity, and aortic systolic pressure augmentation, as well as left ventricular hypertrophy (LVH) and probably reduction of C-reactive protein (CRP) and oxidant stress. Potential risk factors include hyperkalemia, anaphylactoid reaction with AN69 membranes (particularly ACE inhibitors), and aggravation of renal anemia. beta-blockers decrease not only mortality, blood pressure (BP), and ventricular arrhythmias, but also improve left ventricular function in ESRD patients. Nonselective beta-blockers can cause an increase in serum potassium (particularly during fasting or exercise). Lisinopril and atenolol have a predominant renal excretion and therefore a prolonged half life in ESRD patients. Thus thrice-weekly supervised administration of these drugs after HD can enhance BP control. The use of calcium channel blockers is also associated with lower total and cardiovascular-specific mortality in HD patients. Minoxidil is a very potent vasodilator that is generally reserved for dialysis patients with severe hypertension. Hypertensive dialysis patients who are noncompliant with their medications may benefit from transdermal clonidine therapy once a week. The majority of dialysis patients need a combination of several antihypertensive drugs for adequate BP control.
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PMID:Drug therapy for hypertension in hemodialysis patients. 1525 Sep 20

THREE DEFINITIONS: The metabolic or X syndrome is defined by an association of metabolic anomalies leading to an increased risk of cardiovascular complications. Today, there are at least 3 definitions of X syndrome: those of WHO, EGIR and NCEP. To varying degrees they associate increased abdominal fat, hypertension, glucose tolerance abnormality (ranging from hyperinsulinism to diabetes), and hypertriglyceridemia with low HDL cholesterol. FROM AN EPIDEMIOLOGICAL POINT OF VIEW: The prevalence of metabolic syndrome depends on the definition used and varies with the country or ethnic group considered. About 25% of the US and 10% of the French adult populations are concerned. THE RISK OF COMPLICATIONS: According to clinical trials, people with metabolic syndrome have a 2 to 4-fold increase in risk for coronary heart disease. Some of them have a particularly high risk (association of most features of the syndrome, association of an increased waist circumference and hypertriglyceridemia, presence of biological markers such as elevated C-reactive protein or microalbuminuria). Metabolic syndrome is also associated with a 4-fold increase in risk for developing diabetes.
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PMID:[Epidemiological data and screening criteria of the metabolic syndrome]. 1525 40


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