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

EPIDEMIOLOGY OF DIABETES: Diabetes mellitus and arterial hypertension are closely related diseases that strongly predispose an individual to atherosclerotic cardiovascular disease and to renal failure. High blood pressure is twice as frequent in diabetics compared with the general population, and often precedes and contributes to the development of diabetic nephropathy. The prevalence of coexisting arterial hypertension and non-insulin-dependent diabetes mellitus (NIDDM) is increasing as populations age, giving an increased prevalence of both diseases. TREATMENT OF HYPERTENSIVE DIABETIC PATIENTS: The goal of treating arterial hypertension in diabetic patients is to prevent death and disability associated with high blood pressure. In addition, other reversible risk factors for cardiovascular disease, seen so frequently in hypertensive diabetics, also need to be addressed. The optimal goal of blood pressure control in diabetics has not been established, but there are indications that it should be lower than the 130/85 mmHg systolic/diastolic pressure recommended by current guidelines. In the presence of multiple associated risk factors, most guidelines suggest a threshold for intervention of > or = 140/90 mmHg. In particular, in hypertensive diabetic patients intervention must be early and aggressive.
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PMID:How far should blood pressure be reduced in diabetic hypertensive patients? 921 1

Monumental advances in the field of lipid metabolism and its relationship to atherosclerotic cardiovascular disease have been achieved during the last half century. Epidemiologic studies have defined lipid disorders as highly significant independent risk factors for coronary heart disease, along with diabetes mellitus, hypertension and smoking. Primary and secondary prevention studies including the Coronary Primary Prevention Trial, Helsinki Heart Study, and the Coronary Drug Project have shown that lowering the atherogenic low density lipoproteins (LDL) and very low density lipoproteins (VLDL) whilst raising the high density lipoproteins (HDL) significantly decreases the risk for coronary disease. Striking evidence that aggressive therapy (to sharply lower LDL and raise HDL with newer drugs) prevents progression and induces regression of coronary narrowing has been obtained in numerous recent studies using quantitative coronary arteriography. An interesting and unexpected lesson learned from these arteriographic studies was that a highly significant reduction within months in several studies in coronary events was out of proportion to improvements in luminal narrowing. Recently, three major clinical trials to assess the effects of cholesterol reduction by the newly discovered HMG CoA reductase inhibitors (statins) have been published. Pravastatin significantly reduced coronary events in hypercholesterolemic patients [mean LDL-Chol. = 5.0 mM/L (192 mg/dl)] without a history of myocardial infarction. In a secondary prevention study, simvastatin also reduced coronary complications in hypercholesterolemic patients [mean LDL-Chol. = 4.9 mM/L (190 mg/dl)] with pre-existing coronary disease. Very recently, pravastatin treatment significantly reduced coronary events and stroke in patients with a history of myocardial infarction and average cholesterol levels [mean LDL-Chol. = 3.6 mM/L (139 mg/dl)], representing the majority of patients with coronary disease. In all these studies, reduction in cardiovascular events was approximately one-third. In subgroup analyses, men, women, elderly, smokers and hypertensives benefited from cholesterol lowering. There was no significant increase in non-cardiovascular causes of death. In the United States of America, the National Cholesterol Education Program (NCEP) Adult Treatment Panel, representing major health organizations, developed national guidelines on the detection, evaluation and treatment of high blood cholesterol in adults. In a given patient, the Panel recognizes the importance of weighing all cardiovascular disease risk factors including age (men > 45 years, postmenopausal women), family history of premature coronary disease, smoking, hypertension, diabetes and HDL-Cholesterol (< 35 mg/dl) in determining how aggressive therapy should be. The patient with manifest coronary heart disease (CHD) is given a special position as such patients are at highest risk for recurrent events. Major goals of therapy are to lower the LDL-Cholesterol to 2.6 mM/L (< 100 mg/dl) in the CHD patient. In non-CHD patients with two or more risk factors, the LDL-Cholesterol goal is 3.4 mM/L (130 mg/dl). In those with fewer risk factors, the goal is 4.2 mM/L (160 mg/dl). These guidelines should be modified as appropriate for Singapore. Patients with elevated triglycerides usually have low HDL-Cholesterol levels and often represent a heterogeneous group who may have other concurrent abnormalities including the presence of small dense LDL, insulin resistance, hypertension, obesity, overt diabetes and combined hyperlipidemia. Such patients merit individualized treatment. The prevalence of this syndrome may be more common in Singapore and requires further investigation. Current therapeutic guidelines emphasize the need for weight loss and dietary restriction of total and especially saturated fat (< 7% to 10% total calories), cholesterol (< 200 to 300 mg/day), and exercise. (ABSTRACT TRUNCATED)
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PMID:Cholesterol and atherosclerosis: a contemporary perspective. 939 24

The improving survival rate of patients with childhood cancer has led to a growing awareness of the long-term effects of malignant disease and its treatment. Various endocrine abnormalities have been reported as frequent long-term adverse effects of cancer treatment in childhood, and among these growth hormone (GH) deficiency is the most common one, especially after cranial irradiation. Besides promoting growth, GH has well-established metabolic effects. Patients with GH deficiency tend to be obese, and obesity per se is also associated with insulin resistance which plays a key role in a cluster of metabolic derangements including glucose intolerance, hypertension, lipid abnormalities and atherosclerotic cardiovascular disease. This condition is known as the metabolic syndrome. Our recent observations indicate that a combination of obesity, glucose intolerance, hyperinsulinaemia and an abnormal lipid profile can be observed in long-term survivors of childhood cancer. Every sixth patient had the triad of obesity, hyperinsulinaemia and low HDL cholesterol, whereas this combination was not seen in any of the controls. The survivors with such a high-risk profile for cardiovascular disease had markedly reduced spontaneous GH secretion, and also additional features of the metabolic syndrome, such as higher systolic blood pressure and higher plasma glucose and serum triglyceride levels. Accordingly, decreased GH secretion, or alternatively some other disturbance in the hypothalamic-pituitary axis, emerging as a consequence of cranial radiation, may expose long-term survivors of childhood cancer to premature evolution of the metabolic syndrome. This can have an important impact on the long-term prognosis in these patients, because the syndrome as such results in an increased risk of cardiovascular morbidity and mortality.
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PMID:Childhood cancer and later development of the metabolic syndrome. 945 78

Mild-to-moderate hypertension is common, and its natural history is reasonably well defined. The association of elevated blood pressure with left ventricular hypertrophy, insulin resistance, renal dysfunction, and increased propensity toward atherosclerotic cardiovascular disease and ventricular arrhythmias has been characterized. These associations, however, are not well predicted by the level of blood pressure elevation, suggesting some independence between blood pressure levels and cardiovascular complications. Although the reduction in pressure-related outcomes caused by therapeutic interventions (e.g., stroke) has been demonstrated, a similar reduction in many atherosclerotic outcomes has not been definitively demonstrated. The latter observation may be related to a number of factors but may be partly explained by the lack of direct correlation between blood pressure and cardiovascular outcome. This review attempts to update available information on the intermediating factors mitigating the relation among blood pressure, adverse cardiovascular outcome, and the treatment of hypertension.
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PMID:Hypertension, hypertrophy, hormones, and the heart. 948 8

A variety of medical, surgical, social, and psychiatric problems affect the renal allograft rejection, thromboembolic disease, infectious events and gastrointestinal disorders. Hypertension and hyperlipidemia appear around 3 months and may remain throughout the posttransplant period. The late complication are atherosclerotic cardiovascular disease, malignancy hepatic failure, chronic rejection, denovo and recurrent renal disease, posttransplant diabetes, musculoskeletal problems, cataracts and skin lesions. Routine follow up of all transplanted patients at specialized centers is critical for early detection and management of these complications. Such practice would reduce the patient morbidity and mortality and lead to an improved long-term outcome.
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PMID:Posttransplant medical complications. 953 39

Angiotensin-converting enzyme (ACE) inhibitors are now established drugs in the treatment of hypertension and heart failure. The renin-angiotensin-aldosterone system is complex and acts as a circulating hormonal system, a local endogenous tissue system and neuromodular. Current experimental evidence suggests that ACE inhibitors reduce the risk associated with atherosclerotic cardiovascular disease. The antiatherogenic action of ACE inhibitors is related to complex effects mediated by these agent, including an antiproliferative and antimitotic action, beneficial effects on endothelial function, plaque-stabilizing effects and the action of these agents on the sympathetic nervous system. The role of ACE inhibitors in preventing the clinical sequale of atherosclerotic cardiac disease has been evaluated in various patient populations. Several small trial assess the effects of ACE inhibitors in severity of angina pectoris have reported conflicting results, with benefit is some patients and no benefit or even exacerbation of angina in others, indicating that ACE inhibitors do not have consistent antianginal effects in short-term study. ACE inhibitors have the theoretical potential to prevent restenosis after PTCA but they do not prevent restenosis and has no effect on overall clinical outcome. New data suggest that ACE inhibitors may be effective therapy fir patients following acute myocardial infarction. The renin-angiotensin system, is activated during new myocardial infarction and has an impact on the process of remodeling of the left ventricle which causes ist dysfunction and heart failure. In most of the large mortality trials the rationale for early treatment with ACE inhibitors after myocardial infarction was stated. ACE inhibitors have a positive effect in preventing the ventricular dilatation and they reduce the rate of reinfarctions and the mortality rate.
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PMID:[The significance of converting enzyme inhibitor angiotensin I to angiotensin II in treatment of patients with coronary disease]. 955 7

A slightly elevated urinary albumin excretion rate (UAER) is a predictor of atherosclerotic cardiovascular disease. The mechanism is unknown, but moderate office blood pressure elevation has been demonstrated as part of a clustering of known atherosclerotic risk factors in subjects with elevated UAER. Because 24-hour ambulatory blood pressure is a superior predictor of hypertensive target organ involvement, we aimed to investigate blood pressure profile in clinically healthy subjects with elevated UAER. Ambulatory blood pressure monitoring was performed with a portable recorder in 27 subjects with an elevated UAER (>6.6 microg/min, overnight urine collection) and 46 normoalbuminuric control subjects. Mean+/-SD systolic and diastolic ambulatory blood pressures (24-hour) were significantly higher in subjects with elevated UAER than in normoalbuminuric controls (134+/-12 versus 128+/-11 mm Hg and 78+/-7 versus 75+/-6 mm Hg, P<0.05), as were systolic and diastolic blood pressure loads [median (range): 42% (6 to 94%) versus 23% (1 to 89%) and 20% (0 to 68%) versus 6% (0 to 62%), P<0.05]. The circadian variation of blood pressure was normal in subjects with elevated UAER. However, the increased urinary loss of albumin could not be solely related to the higher blood pressure. In conclusion, apparently healthy subjects with elevated UAER had slightly but significantly higher 24-hour systolic and diastolic blood pressure levels in addition to increased blood pressure loads but normal circadian variation. The demonstrated differences in blood pressure may offer a partial explanation for the association between elevated urinary albumin excretion and atherosclerotic cardiovascular risk.
Hypertension 1998 Jul
PMID:Ambulatory blood pressure and urinary albumin excretion in clinically healthy subjects. 967 40

Body iron status has been implicated in atherosclerotic cardiovascular disease. The main hypothesis was that high iron status was associated with increased oxidation of LDL. The associations of serum ferritin (a marker of iron status) and dietary iron intake with the susceptibility of LDL to in vitro oxidation (lag phase) and autoantibodies against MDA-modified LDL (two markers of oxidation stress) were examined among 281 men and 192 women with a mean age of 59 years (S.D. = 5) who participated in the Atherosclerosis Risk in Communities (ARIC) Study visit 2 in 1990 through 1992. Lag phase duration and the autoantibodies against MDA-modified LDL were weakly correlated with each other (r = 0.19, P = 0.001 in men; r = 0.15, P = 0.03 in women). In linear regression analysis adjusting for age, field center, blood storage time, and carotid atherosclerosis case-control status, there was no association between ferritin level and the lag-phase, or between ferritin level and autoantibodies against MDA-modified LDL in either sex. Further adjustment for traditional cardiovascular risk factors (smoking, vitamin supplement use, body mass index, LDL cholesterol, hypertension and diabetes) did not alter these null results. Ferritin was significantly and positively correlated with body mass index in both sexes (r = 0.21 among men and r = 0.22 among women) and with the waist-to-hip ratio among women (r = 0.26). In addition, among women, ferritin was positively correlated with orosomucoid (r = 0.24) and with sialic acid (r = 0.19). Dietary iron was not associated with the parameters of LDL oxidation or with ferritin level. These findings do not support a role of body iron stores in promoting oxidation of LDL.
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PMID:Lack of association between ferritin level and measures of LDL oxidation: the ARIC study. Atherosclerosis Risk in Communities. 969 7

Prior to 1972, the increased cardiovascular morbidity and mortality that diabetics endure had been attributed to vascular disease. In 1972, Rubler et al. proposed the existence of a diabetic cardiomyopathy based on their expereince with four adult diabetic patients who suffered from congestive heart failure (CHF) in the absence of discernable coronary artery disease, valvular or congenital heart disease, hypertension, or alcoholism. Alternative explanations for CHF, such as anemia and vascular and renal disease in these four patients, gave rise to criticisms, but a wave of subsequent studies in the 1970s and 1980s provided credence to this new disease entity. This review of the studies done since 1972 appears to support the concept of a diabetic cardiomyopathy independent of atherosclerotic cardiovascular disease. The exact mechanism is still questionable, and several mechanisms have been proposed including small and microvascular disease, autonomic dysfunction, metabolic derangements, and interstitial fibrosis. However, the weight of evidence leans toward the development of fibrosis, possibly caused by the accumulation of a peroxidase acid schiff (PAS)-positive glycoprotein, leading to myocardial hypertrophy and diastolic dysfunction.
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PMID:Diabetic cardiomyopathy. 985 79

Endothelial dysfunction is a feature of the early stages of atherosclerotic cardiovascular disease. It also is almost invariably associated with recognized cardiovascular risk factors, including those that are irreversible (such as age and family history) and those that are reversible (such as hypertension and hypercholesterolemia). It remains the subject of debate whether endothelial dysfunction can be considered an independent risk factor or, perhaps more plausibly, an intermediate or surrogate end point. However, although the relevance to research into cardiovascular pathophysiology is not in dispute, there remains uncertainty about its relevance as a therapeutic target. Overall, the available evidence suggests that targeting of the conventional major risk factors remains the primary strategy, but an ancillary effect on intermediate end points, such as an improvement or reversal of endothelial dysfunction, constitutes an additional potential benefit.
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PMID:Endothelial dysfunction in cardiovascular disease: risk factor, risk marker, or surrogate end point? 988 52


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