Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Carvedilol is a dual-acting drug designed to produce two complementary effects: beta-blockade and vasodilation. These effects are induced in the same dose range, a prerequisite for utilizing both properties in an appropriate manner. The vasodilation is mediated predominantly by specific alpha 1-adrenoceptor blockade. At markedly higher concentrations, additional vasodilating actions besides alpha 1-blockade can be observed. These effects resemble those of Ca(2+)-antagonistic properties. However, they do not contribute to the acute blood pressure-lowering activity of carvedilol but may be responsible for the increased blood flow to specific organs. At beta-blocking doses, carvedilol reduces the regional and systemic vascular resistance in various experimental models, healthy volunteers, and in patients with cardiovascular diseases such as hypertension, coronary artery disease, and heart failure. The profile of carvedilol thus insures beneficial treatment of hemodynamic disorders characterized by increased sympathetic tone and increased vascular resistance.
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PMID:Vasodilatory action of carvedilol. 137 50

Factors that can influence cardiovascular growth are becoming increasingly important for our understanding of such complex diseases as cardiac hypertrophy, coronary artery disease, atherosclerosis, and hypertension. Several proto-oncogenes were found to be involved in the regulation of abnormal cell growth in cardiovascular disease. It is also evident that some peptide hormones, which are well known to be involved in blood pressure control, may play a role as growth modulators. Angiotensin II is one such peptide. It elevates blood pressure through its direct vasoconstrictor, sympathomimetic, and (through release of aldosterone) sodium-retaining activity but also appears to have mitogenic actions. Interestingly, all components of the renin-angiotensin system were found locally in cardiovascular tissues. The question remains whether angiotensin can act directly as a growth factor or whether it does so indirectly by influencing or modulating cell growth factors. A better understanding of the renin-angiotensin system as a direct or indirect mediator for cardiovascular hypertrophy would offer new and interesting insights into the pathophysiology of hypertension and possibly novel options for the treatment of cardiovascular disease.
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PMID:The molecular basis of cardiovascular hypertrophy: the role of the renin-angiotensin system. 138 95

Coronary reserve has been defined as the ratio of coronary resistance under control (rest) conditions and of coronary resistance after maximal coronary vasodilation. The latter can be achieved by various interventions, the most important and clinically relevant example being intravenous administration of dipyridamole at 0.5 mg/kg of body weight. For patients without coronary artery disease, the coronary reserve is about 400 to 500%, i.e., the normal heart is capable of reducing its coronary resistance to minimal values of 0.18 to 0.2 mm Hg/ml/min/100 g or to increase coronary flow by approximately four- to fivefold. The determination of coronary reserve in humans implies the availability of adequate methods. Systematic analyses of different coronary blood flow measurements have proved the gas chromatographic argon method to be the most appropriate and accurate method for clinical conditions, as previously described in detail. In this report, our findings on the coronary reserve analysis in various clinical conditions are described as follows: (a) coronary artery disease, (b) inflammatory disturbances of the microcirculation, (c) hypertensive microangiopathy, (d) rheologic abnormalities of the heart, and (e) pressure and volume overload due to hypertension and heart valve lesions (metabolic overload).
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PMID:The concept of coronary flow reserve. 138 97

Atrial fibrillation is a common disorder and the incidence increases with each decade of life. Previously, rheumatic mitral valve disease has been the condition most highly associated with atrial fibrillation. However, with the decreasing incidence of rheumatic heart disease, other conditions have assumed greater importance and now congestive cardiac failure, coronary artery disease, and hypertension are the most commonly associated conditions. Nonrheumatic atrial fibrillation is associated with an approximately five-fold increase in the risk of ischemic stroke and a 5% to 7% yearly risk that increases with age. In addition, atrial fibrillation is associated with an increased incidence of silent cerebral infarction and increased mortality. However, whether atrial fibrillation is independently associated with the risk of stroke or is a marker of underlying cardiac disease is contentious. Until recently, the use of preventive therapy has been controversial. However, data from four recently published, prospective randomized studies clearly support the use of warfarin prophylaxis in nonrheumatic atrial fibrillation. Within the diverse group of patients with nonrheumatic atrial fibrillation there are high and low risk subgroups and identification of these may influence decisions regarding antithrombotic prophylaxis. With a few exceptions, however, this remains an area in which there are contradictory findings in the literature. The role of aspirin for prophylaxis in nonrheumatic atrial fibrillation remains unclear and further evaluation awaits the publication of ongoing studies.
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PMID:Atrial fibrillation: epidemiology and the risk and prevention of stroke. 138 92

The effect of a four weeks oral treatment with 100 mg isosorbide dinitrate (ISDN) daily on platelet function was evaluated in 40 patients (aged 40-65 years) with proven coronary artery disease. Isosorbide dinitrate decreased platelet reactivity to ADP (p less than 0.001), increased platelet sensitivity to PGI2 (p less than 0.01) while the production of TXB2 from exogenous arachidonic acid substrate and from endogenous substrate were both significantly reduced. Circulating platelet aggregates as measured by the Wu-test were markedly reduced (p less than 0.001) but there was little change in the plasma concentration of the platelet proteins beta-thromboglobulin and platelet factor 4. Overall, platelet activation correlated with smoking, hypertension and a family history of coronary artery disease. The reduced platelet activation seen during treatment with isosorbide dinitrate may contribute to the therapeutic benefit seen with this drug in patients with coronary artery disease.
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PMID:Modification of platelet function by isosorbide dinitrate in patients with coronary artery disease. 138 8

This study was undertaken to study the effects of hyperlipidemia and hypertension on the coronary circulation and on the myocardium of Watanabe heritable hyperlipidemic (WHHL) rabbits. Surgery to induce hypertension by the one-kidney, one-clip technique was performed on the WHHL rabbits at 3 months of age. At 3 and 6 months after surgery, the right and left coronary arteries and the left ventricle and posterior papillary muscle from normotensive and hypertensive animals were assessed. Atherosclerotic involvement was found at the coronary origin in 94% of the arteries evaluated. Lesions were usually confined to the proximal 1-2 mm of the coronary artery. The prevalence of coronary atherosclerosis in the WHHL rabbit was found to be higher than previously reported in rabbits of the same age. Hypertension-induced muscular and vascular changes such as left ventricular hypertrophy, medial thickening of the arteries, and hyaline arteriolosclerosis were found in most of the hypertensive animals. These changes were rarely seen in the normotensive rabbits. Characteristics of ischemia and cell injury such as eosinophilic fibers, fiber vacuolization, and contraction band necrosis were found more often in hypertensive than in normotensive WHHL rabbits. Confluent areas of severe necrosis indicative of myocardial infarction were not found; myocardial damage was diffuse and involved individual cells and small microscopic areas. This model may be valuable in further studies of coronary artery disease and myocardial injury that result from the combination of hypercholesterolemia and hypertension.
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PMID:Effects of hypertension and hyperlipidemia on the myocardium and coronary vasculature of the WHHL rabbit. 138 26

The correlations of the coronary artery disease (CAD) and hypertension, smoking and/or the levels of lipoproteins and apolipoproteins, were studied in 100 patients with CAD diagnosed by coronary arteriography and 141 non-CAD controls. The findings are: 1. There are: significant positive dose-response relationships between the degrees of CAD and the levels of diastolic pressure, cumulative smoking consumptions, the levels of high-density lipoprotein subclasses and apolipoproteins A1 and/or B. 2. The degrees of CAD in patients with the hypertension and smoking at same time were more serious than those with only a single risk factor. It's suggested that there are some synergy between hypertension and smoking in the occurrence of CAD. The synergic mechanism may be related to lipids metabolism.
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PMID:[Study on the interaction between hypertension, smoking and the disorder of lipids metabolism in the coronary artery disease]. 139 81

Congestive heart failure (CHF) is a common manifestation of hypertension, coronary artery disease, and dilated cardiomyopathy. The Framingham study showed that the incidence of CHF increases twofold with each decade of age. The presence of CHF increases the age-adjusted death rate 5.5-fold for women and 8-fold for men, and it increases the sudden death rate 5.5-fold in both men and women. Ventricular arrhythmias are a common accompaniment of CHF. Ambient ventricular premature complexes occur in most of these patients, and nearly one half of all CHF patients will have nonsustained ventricular tachycardia on a 24-h ambulatory electrocardiographic (Holter) recording. In addition, low left ventricular ejection fraction (LVEF) predicts inducible sustained ventricular tachycardia on electrophysiologic study. One-year mortality increases with worsening New York Heart Association (NYHA) Functional Class and decreasing LVEF. As the overall yearly mortality increases, the proportion of patients who die of arrhythmias decreases. The precise mechanism of death is frequently difficult to assess. Nonarrhythmic causes of death include CHF, shock, electromechanical dissociation, and myocardial rupture. Arrhythmic causes are most commonly due to ventricular tachycardia/ventricular fibrillation. Bradycardic events (asystole or heart block) are usually associated with progressively worsening CHF. Noncardiac causes that may confuse classification include pulmonary embolus and cerebrovascular accident. Because many patients have ischemic heart disease as the etiology of the CHF, a recurrent ischemic event can likewise make classification difficult. Overall, approximately one half of all deaths in CHF are arrhythmic and one half are nonarrhythmic.
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PMID:Clinical significance and management of arrhythmias in the heart failure patient. 139 10

Cardiac constituents affected in arterial hypertension comprise the myocardium, interstitium and coronary circulation. With regard to coronary circulation, arterial hypertension is an important risk factor in coronary artery disease, but even in the absence of coronary artery disease, hypertensive patients frequently have angina pectoris or reveal electrocardiographic abnormalities suggestive of myocardial ischaemia due to coronary insufficiency. Under clinical conditions, determination of coronary flow reserve (dipyridamole; Argon-method) allows for the evaluation of impairment of coronary regulatory reserve. In comparison to healthy normotensives, coronary haemodynamics in hypertensive patients with microvascular angina are characterized by a severely increased minimal coronary resistance and reduced maximal coronary blood flow to dipyridamole. Accordingly, coronary reserve is markedly reduced by about 40%, and metabolic, myocardial and vascular factors may be involved in this reduction. In the compensated stage of arterial hypertension, with concentric left ventricular hypertrophy, myocardial factors, such as myocyte hypertrophy, extravascular compressing forces and functional implications of impaired relaxation, as well as metabolic factors, contribute to impairment in coronary reserve to a minor extent. The reduction in coronary flow reserve is not proportional to the elevation in left ventricular muscle mass and thus the degree of left ventricular hypertrophy does not seem to determine the reduction in vasodilator reserve directly. Thus the reduction in coronary reserve seems to be primarily the consequence of an impaired vasodilating capacity of the coronary resistance vessels, as indicated by a severely increased minimum coronary resistance to dipyridamole, i.e. a severely reduced overall coronary conductance capacity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Coronary haemodynamics in hypertensive heart disease. 139 59

Diabetes mellitus leads to acute and chronic complications. Acute complications include hypoglycaemia, diabetic keto-acidosis, hyperglycaemic hyperosmolar non-ketotic syndrome and lactic acidosis. Chronic complications are neuropathies, nephropathy, retinopathy, peripheral arterial disease, cerebrovascular disease, coronary artery disease, cardiomyopathy, hypertension, infection, delayed wound healing and stiff joint disease. End-organ pathology is in part responsible for the increased morbidity and mortality seen in diabetic patients in the peri-operative period. A thorough pre-operative search for end-organ pathology is essential to optimise patient management. Relevant diabetic complications and their anaesthetic risk are discussed.
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PMID:Diabetic complications with special anaesthetic risk. 141 8


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