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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

After the discovery by Furchgott and colleagues in 1980 that the endothelium plays an obligatory role in acetylcholine-induced vasodilation many investigators have elucidated the role of the endothelium in the regulation of vascular tone. While the sympathetic nervous system serves the organism as a whole, the endothelium appears to act as a local regulator adapting blood flow to local metabolic needs. A variety of endothelium-derived relaxing and contracting factors such as nitric oxide, prostacyclin, endothelium-derived hyperpolarizing factor, endothelin and thromboxane A2 play a role in the endothelium-dependent control of vascular tone. Furthermore, nitric oxide inhibits thrombocyte aggregation and adhesion. Many diseases have been reported to be associated with an impaired endothelium-dependent vasodilation which may contribute to an increased susceptibility to vasospasm, decreased inhibition of thrombus formation and an impaired ability to reduce vascular resistance in ischaemic conditions. In hypertension, hypercholesterolaemia and diabetes mellitus this impairment may be interpreted as an early marker of a process that ultimately will lead to atherosclerosis. The impaired endothelium-dependent vasodilation probably contributes to the increased peripheral vascular resistance in hypertension and heart failure. The role of the endothelium does not seem to be restricted to cardiovascular diseases. Several mediators of inflammation stimulate the endothelium to release nitric oxide, suggesting an important role of the endothelium in the haemodynamic sequelae of sepsis.
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PMID:Endothelium and the regulation of vascular tone with emphasis on the role of nitric oxide. Physiology, pathophysiology and clinical implications. 820 3

Major advances in the management of acute myocardial infarction have been achieved by a combination of careful experimental work and development of effective pharmacologic and interventional strategies in conjunction with the conduct of large, reliable randomized trials. Current trials indicate that a combination of thrombolytic therapy, aspirin, and intravenous followed by oral beta blockers reduces mortality. There are a number of additional promising interventions, such as intravenous magnesium, nitrates, and the newer antithrombin agents. However, before these agents are used widely in clinical practice, clear proof of benefit and adequate safety should be available from the ongoing randomized trials. Following discharge from the hospital, long-term therapy with aspirin and beta blockers should be considered in all patients. In patients with heart failure and low ejection fraction, angiotensin-converting enzyme (ACE) inhibitors have been shown to reduce mortality, reinfarction, and the need for further hospitalizations for heart failure. Therefore, these therapies, in conjunction with risk factor modification (cessation of cigarette smoking, treatment of hypercholesterolemia, treatment of hypertension), should be considered in all appropriate patients. A number of new strategies for the prevention of atherosclerosis and its complications are currently being evaluated in prospective randomized trials. These include the natural antioxidant vitamins, estrogen replacement therapy, tamoxifen therapy, and ACE inhibitors in patients without evidence of heart failure or left ventricular dysfunction.
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PMID:Maximizing benefits of therapies in acute myocardial infarction. 827 52

We investigated a change in vascular reactivity as a potential adaptive mechanism to chronic exercise. The study consisted of 2 separate protocols with 10 male athletes and 10 age-matched sedentary male control subjects participating in each. Protocol 1 investigated forearm blood flow responses to intra-arterial infusions of acetylcholine and sodium nitroprusside by use of venous occlusion plethysmography. Protocol 2 used identical techniques to study responses to norepinephrine, angiotensin II (ANG II), and NG-monomethyl-L-arginine (L-NMMA). The percent reduction in forearm vascular resistance to acetylcholine was significantly greater in the athletic compared with the sedentary group (multivariate analysis of variance for repeated measures, P = 0.03). Covariance analysis suggested that the lower total cholesterol level of the athletic group (P = 0.03) may contribute to their enhanced responsiveness to acetylcholine. There were no differences between athletic and sedentary groups in the forearm vascular resistance responses to norepinephrine, ANG II, sodium nitroprusside, or L-NMMA. These data support the hypothesis that long-term endurance training is associated with enhanced endothelium-dependent dilator reserve due to altered lipoprotein levels in athletes. This finding may have therapeutic application in conditions of elevated cholesterol and impaired vasodilator capacity including hypertension, hypercholesterolemia, atherosclerosis, and cardiac failure.
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PMID:Enhanced vasodilation to acetylcholine in athletes is associated with lower plasma cholesterol. 876 51

In this review, a rationale is presented for how hypercholesterolemia, hypertension, diabetes mellitus, end-stage renal disease, renal dialysis, and prolonged stress can all lead to atherosclerosis, ischemic heart disease, and stroke. The data indicate that Mg deficiency caused either by poor diet and/or errors in Mg metabolism may be a missing link between diverse cardiovascular risk factors and atherosclerosis. Data from our laboratories and others indicate that reduction in extracellular and intracellular free Mg ions (Mg2+) can induce an entire array of pathophysiological phenomena known to be important in atherogenesis, that is, vasospasm, increased vascular reactivity, elevation in [Ca2+]i, formation of proinflammatory agents, oxygen radicals, platelet aggegation, reduction in cardiac bioenergetics, cardiac failure, oxidation of lipoproteins, gender-related modulation of endothelial-derived relaxing factor/NO, changes in membrane fatty acid saturation, changes in membrane plasmalogens and N-phospholipids (suggesting changes in intracellular phospholipid signals), and probably transcription factors.
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PMID:Magnesium and cardiovascular biology: an important link between cardiovascular risk factors and atherogenesis. 886 81

This study examined possible selective impairment of endothelial dysfunction in the peripheral vascular bed in patients with chronic heart failure in the absence of confounding factors influencing endothelial function (i.e. hypertension, hypercholesterolaemia and diabetes mellitus). Several recent studies have suggested that endothelium-dependent peripheral vasodilation is impaired but endothelium-independent vasodilation is preserved in patients with chronic heart failure. However, a classical paper has demonstrated that sodium nitrite-mediated calf blood flow is clearly depressed in patients with valvular heart disease and cardiomyopathy. We examined forearm blood flow changes mediated by acetylcholine and nitroprusside in patients with valvular heart disease (n = 55) or congenital heart disease (n = 13), and a comparison was made with healthy volunteers (n = 21). The blood flow changes mediated by acetylcholine and nitroprusside were significantly impaired in both patient groups (P < 0.01). When blood flow responses were collected from all patients, two types of vasodilatory capacity were found to have decreased significantly with increasing clinical severity of heart failure (New York Heart Association functional class; P < 0.01). This suggests that the peripheral vasodilatory responses mediated by endothelium-dependent and endothelium-independent vasodilators are significantly impaired in patients with symptomatic chronic heart failure due to non-ischaemic heart disease.
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PMID:Endothelium-dependent vasodilatation is not selectively impaired in patients with chronic heart failure secondary to valvular heart disease and congenital heart disease. 896 Apr 11

In the Netherlands the general practitioner (GP) plays an important role in prevention. Every Dutch citizen has to be registered with one GP and GPs know their patients well. Face-to-face contact is a relatively effective means of influencing behavior; if preventive advice is related to a patient's state of health, compliance may be stimulated. However, Dutch GPs have shown reluctance toward preventive work. Curing rather than preventing disease is emphasized in medical school. Many GPs doubt that they are entitled to interfere with a patients' lifestyle unless asked. Some GPs are aware of their limited knowledge of nutrition. Preventive work requires some reorganization of medical practice and can lead to an increased workload, without financial compensation. Then there is the "prevention paradox": preventive actions that have a demonstrable effect on the whole population bring only small benefits for individuals. Since 1989 the Dutch College of General Practitioners has published 60 standards for general practice. Several of these include advice on lifestyle and diet, eg, for non-insulin-dependent diabetes mellitus, hypertension, hypercholesterolemia, peptic ulcer, and heart failure. Prevention work in general practice must use only interventions proved to be effective and they must be feasible in the context of general practice. A trial collaboration of 118 GPs and 5 public health authorities between 1988 and 1990 for screening and lifestyle management of hypertension was a limited success. It brought to light the practical problems of this type of work in general practice. Present government priorities for GP-public health collaboration are influenza vaccination and cervical screening.
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PMID:Challenges to prevention in Dutch general practice. 917 99

Atherosclerosis and its consequences account for most of the morbidity and mortality in Western countries. It is a disease of the intima and primarily involves four cell types, i.e., endothelial and vascular smooth muscle cells, monocytes and platelets. In recent years, knowledge on the cellular and molecular mechanisms of these cells and their alterations by cardiovascular risk factors and in atherosclerosis has greatly expanded. In particular, it has become clear that endothelial cells play a crucial role in the regulation of platelet function, coagulation, and vascular tone and structure. Interestingly, endothelial dysfunction occurs early, particularly if cardiovascular risk factors such as hyperlipidemia, hypertension and diabetes are present. This could lead to adhesion of circulating platelets and monocytes and increased accumulation of lipids in the intima, as well as increased contraction, migration and proliferation of vascular smooth muscle cells. One of the enzymes with a key role in vascular homeostasis is angiotensin I converting enzyme (ACE). ACE is located on the endothelial cell membrane and is responsible for the conversion of angiotensin I into angiotensin II, as well as for the breakdown of bradykinin. While the antihypertensive effect of ACE inhibitors probably contributes to their antiatherogenic effects, other mechanisms are likely to be of greater importance. These direct antiatherogenic effects attributable to ACE inhibition are related to their vasculoprotective properties, including antiproliferative and antimitogenic activity, effects on endothelial function, protection against plaque rupture, antithrombotic effects, and possible antioxidant properties. There is overwhelming evidence to demonstrate the beneficial effects of long-term ACE inhibitor treatment in heart failure, acutely for suspected myocardial infarction (MI), and following MI in patients with left ventricular dysfunction. Hypercholesterolemia is a health risk, and epidemiological studies have shown a line between total cholesterol levels and the risk of cardiac events. Studies have shown that lowering the levels of total and low-density lipoprotein cholesterol using HMG-CoA reductase inhibitors can result in a decrease in cardiac morbidity and mortality. Angiographic studies of coronary arteries have demonstrated a disparity between the decrease in cardiac events and the extent of regression of coronary artery lesions. Mechanisms other than the regression of coronary stenosis may therefore be important in the beneficial effect of cholesterol lowering. It may be of major importance that lipid-lowering therapy is associated with improved endothelial function and decreased platelet activity. Thus, both ACE inhibitors and HMG-CoA reductase inhibitors have vasculoprotective properties which may explain their beneficial effects on cardiovascular morbidity and mortality.
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PMID:[Pharmacotherapy of arteriosclerosis and its complications. Effect of ACE inhibitors and HMG-CoA-reductase inhibitors]. 919 90

Using a model of chronic ischemic heart disease (recurring coronary insufficiency against the background of chronic hypercholesterolemia), regularities were studied of the microcirculation rearrangements in the myocardium. Employed in the studies were methods of light optics, electron microscopy, injection, as was morphometry. All structural and functional links of the myocardial microcirculation system were put to study, such as resistive, metabolic and blood-drawing segments of the microhemocirculatory channel, intramyocardial tracts of lymph outflow, and interstitium as a direct carrier of the intratissue milieu, as well as subepicardial portion of the lymphatic network of the heart. There have been determined the morphofunctional equivalents and morphogenesis of those changes disorganizing the transport processes in the myocardium under the above type disorder, such as changes in microhaemodynamics, permeability of the histohematic barrier, lymph outflow, and intermediary exchange; there have also been analysed the pathogenetic interrelations thereof. The results obtained suggest that dysfunction of the myocardial system of microcirculation should have a part as a local tissue factor of pathogenesis of cardiac insufficiency in ischemic heart disease.
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PMID:[The transport-trophic support of myocardial function in the modelling of chronic ischemic heart disease]. 947 76

To measure myocardial blood flow, Nitrogen-13 ammonia. Oxygen-15 water, Rubidium-82 and et al. are used. Each has merit and demerit. By measuring myocardial coronary flow reserve, the decrease of flow reserve during dipyridamole in patients with hypercholesterolemia or diabetes mellitus without significant coronary stenosis was observed. The possibility of early detection of atherosclerosis was showed. As to myocardial metabolism, glucose metabolism is measured by Fluorine-18 fluorodexyglucose (FDG), and it is considered as useful for the evaluation of myocardial viability. We are using FDG to evaluate insulin resistance during insulin clamp in patients with diabetes mellitus by measuring glucose utilization rate of myocardium and skeletal muscle. FFA metabolism has been measured by 11C-palmitate, but absolute quantification has not been performed. Recently the method for absolute quantification was reported, and new radiopharmaceutical 18F-FTHA was reported. Oxygen metabolism has been estimated by 11C-acetate. Myocardial viability, cardiac efficiency was evaluated by oxygen metabolism. As to receptor or sympathetic nerve end, cardiac insufficiency or cardiac transplantation was evaluated. Imaging of positron emitting radiopharmaceutical by gamma camera has been performed. Collimator method is clinically useful for cardiac imaging of viability study.
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PMID:[The review of myocardial positron emission computed tomography and positron imaging by gamma camera]. 964 28

We prospectively studied the gender differences of baseline variables, therapies, and outcomes among a cohort of 369 Chinese patients with acute myocardial infarction from 1990 to 1995. There were 277 male and 92 female patients. The male gender had a younger mean (+/-SD) age (61.5+/-10.7 vs. 67.1+/-11.7 years, P<0.0001). Hypercholesterolemia (201.2+/-44.2 vs. 187.5+/-43.7 mg/dl, P=0.0111) and obesity (25.0 vs. 15.9%, P=0.0494) were more prominent in the female. Smoking was more prevalent in the male (78.3 vs. 18.5%, P<0.0001). The male group also had more frequent use of thrombolytic agents (19.1 vs. 9.8%, P=0.0377), beta-blockers (61.7 vs. 47.8%, P=0.0191) and heparin (25.3 vs. 12.0%, P=0.0075); but less use of angiotensin-converting enzyme inhibitors (6.9 vs. 15.2%, P=0.0149). The condition on admission was worse in the female group (Killip classification (1.5+/-0.9 vs. 1.9+/-1.0, P=0.0022), myocardial failure (8.7 vs. 2.9%, P=0.0178) and cardiomegaly (65.2 vs. 53.1%, P=0.0419). During a follow-up duration of 26.4+/-24.1 and 22.9+/-23.9 months respectively, the mortality rate was lower in the male (19.5 vs. 30.4%, P=0.0288). However after adjustment for the effect of age, the differences in Killip classification, myocardial failure, cardiomegaly and mortality became insignificant.
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PMID:Gender differences in baseline variables, therapies and outcomes in Chinese patients with acute myocardial infarction. 969 35


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