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

The majority of persons sustaining acute myocardial infarction are older, and in these older persons morbidity and mortality are high. Clinical presentations and characteristics are significantly different between older and younger infarction patients. Older infarction patients are more likely to be female and to have a history of heart failure, but they are less likely to have a family history of myocardial infarction, elevated cholesterol, or to smoke. Older patients will frequently have unrecognized or silent myocardial infarctions or, when present, symptoms will be atypical. Instead of chest pain, older patients may have shortness of breath or neurological symptoms, such as confusion. Also, older infarction patients will delay longer in seeking medical assistance after onset of symptoms, and often will not demonstrate ST elevation or Q waves on their electrocardiograms. Not infrequently, older infarction patients will demonstrate major complications such as heart failure or right ventricular infarction on hospital admission, and their presenting complaints will reflect these complications. Because of these atypical presentations and the wide variability of symptoms, physicians must be highly suspicious of the presence of an acute myocardial infarction in older patients who have an unexplained acute change in their physical condition.
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PMID:Management of the older patient with acute myocardial infarction: difference in clinical presentations between older and younger patients. 973 13

ALTERATIONS OF THE ENDOTHELIUM: Because of its anatomic position between circulating blood and smooth muscle cells, the vascular endothelium is a prime target for cardiovascular diseases such as hypertension, hypercholesterolemia, diabetes or ischemia. The morphological changes occurring in the endothelium have been known for many years, but it was only recently that the functional alterations have been described. IMPACT OF NO: Under physiological conditions, the vascular endothelium plays a protective role by secreting relaxation factors. In the disease state, the synthesis and release of NO may be reduced or even abolished. The exact significance of endothelium-dependent vasodilatation disorders remains a topic of research, but the properties of NO strongly suggest it is involved in several diseases. For some diseases it is still a question as to whether the observed anomalies are the cause or the consequence of the underlying disease. DISEASE-SPECIFIC CHANGES: NO is known to be reduced in atherosclerosis, either because of less synthesis or accelerated degradation. In different experimental modules of hypertension, the baseline level of NO release appears to be decreased. Conversely, NO release can be normal, reduced or increased in diabetes. In heart failure, there appears to be not only a permanent alteration in NO secretion, but also an increase in factors stimulating vascular contraction, contributing to an altered capacity for vascular adaptation in these patients.
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PMID:[Nitric oxide (NO), vascular protection factor. NO related cardiovascular diseases]. 976 31

Several botanicals, including Crataegus oxycantha, Terminalia arjuna, Inula racemosa, and Astragalus membranaceus, have been found to have therapeutic benefit for the treatment of cardiovascular disease. Crataegus oxycantha has been used traditionally as a cardiac tonic and current uses include treatment for angina, hypertension, arrhythmias, and congestive heart failure. Animal studies have also indicated that Crataegus extracts may also have potential use as anti-ischemic and lipid-lowering agents. The bark of the Terminalia arjuna tree has a long history of use as a cardiac tonic as well, and has been indicated in the treatment of coronary artery disease, heart failure, hypercholesterolemia and for relief of anginal pain. Additionally, it has been found to have antibacterial and antimutagenic properties. Inula racemosa, also known as Pushkarmoola, is another traditional Ayurvedic botanical that has potential cardioprotective benefit. In human trials, a combination of Inula racemosa and Commiphora mukul was shown to be superior to nitroglycerin in reducing the chest pain and dyspnea associated with angina. Astragalus membranaceus, a Chinese herb, is often used as a "Qi tonifier" and has been studied for its therapeutic benefit in treatment of ischemic heart disease, myocardial infarction, heart failure, and relief of anginal pain. Clinical studies have indicated that its in vitro antioxidant activity is the mechanism by which it affords its cardioprotective benefit.
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PMID:Botanical influences on cardiovascular disease. 985 67

Health economics is about spending limited resources wisely and, as with so many fields in medicine, combines science with art and ingenuity. In order to know whether money is well spent it is necessary to have some reference points to make comparisons. Many accepted cardiovascular interventions, such as revascularization for multivessel disease (US$50000 per life year gained) or the use of a statin for hypercholesterolaemia in middle-aged men at high risk of cardiovascular events (US$30000 per life year gained) are associated with moderate expense. By contrast heart failure is one of the few conditions in which, under some circumstances, lives may be saved while significantly reducing costs. This article seeks to review currently available reports on the health economic consequences of interventions for heart failure and describes the development of a new health economic model. Digoxin, ACE inhibitors and beta-blockers all appear to be cost-effective under widely differing sets of assumptions. Estimates range from a substantial cost-saving to a few thousand dollars per life year gained. The major factor limiting the reduction in costs associated with effective treatment for heart failure (with the exception of digoxin) is the costs incurred as a consequence of improved longevity. Money spent on treating heart failure well is money wisely spent.
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PMID:Health economic consequences of the pharmacological treatment of heart failure. 988 10

Since the recognition that L-arginine (LA) is the natural metabolic donor of nitric oxide, this amino acid has reached the medical spotlight. LA exerts favorable effects in the prevention and treatment of endothelial damage and the restoration of endothelial function in patients with cardiovascular risk factors (hypercholesterolemia, smoking, hypertension, diabetes and advanced age) or with several chronic cardiovascular disorders (coronary, peripheral and cerebral vascular disease, and mild-to-moderate heart failure). LA administration is likely to represent a potentially novel therapeutic strategy during angioplasty, coronary bypass grafting and cardiac transplantation. More conclusive research findings for the rediscovered role of this well-known substance merit close attention.
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PMID:L-Arginine: rediscovery in progress. 989 62

The vascular endothelium plays a key role in the local regulation of vascular tone by the release of vasodilator substances (i.e. endothelium-derived relaxing factor (EDRF = nitric oxide, NO) and prostacyclin) and vasoconstrictor substances (i.e. thromboxane A2, free radicals, or endothelin). Using either agents like acetylcholine or changes in flow to stimulate the release of EDRF (NO), clinical studies have revealed the importance of EDRF in both basal and stimulated control of vascular tone in large epicardial coronary arteries and in the coronary microcirculation. The regulatory function of the endothelium is altered by cardiovascular risk factors or disorders such as hypercholesterolemia, chronic smoking, hypertension or chronic heart failure. Endothelial dysfunction appears to have detrimental functional consequences as well as adverse longterm effects, including vascular remodelling. Endothelial dysfunction is associated with impaired tissue perfusion particularly during stress and paradoxical vasoconstriction of large conduit vessels including the coronary arteries. These effects may cause or contribute to myocardial ischemia. Several mechanisms may be involved in the development of endothelial dysfunction, such as reduced synthesis and release of EDRF or enhanced inactivation of EDRF after its release from endothelial cells by radicals or oxidized low-density lipoprotein (LDL). Increased plasma levels of oxidized LDL have been noted in chronic smokers and are related to the extent endothelial dysfunction, raising the possibility that chronic smoking potentiates endothelial dysfunction by increasing circulating and tissue levels of oxidized LDL. In heart failure, cytokines and/or reduced flow (reflecting reduced shear stress) may be involved in the development of endothelial dysfunction and can be reversed by physical training. Other mechanisms include an activated renin-angiotensin system (i.e. postmyocardial infarction) with increased breakdown of bradykinin by enhanced angiotensin converting enzyme (ACE) activity. There is evidence that endogenous bradykinin is involved in coronary vasomotor control both in coronary conduit and resistance vessels. ACE inhibitors enhance endothelial function by a bradykinin-dependent mechanism and probably also by blunting the generation of superoxide anion. Endothelial dysfunction appears to be reversible by administering L-arginine, the precursor of nitric oxide, lowering cholesterol levels, physical training, antioxidants such as vitamin C, or ACE inhibition.
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PMID:Endothelial dysfunction in human disease. 1007 15

The contention that female gender is an independent factor that affects survival after acute myocardial infarction (AMI) is still controversial. The aim of this retrospective study was to assess whether or not early and late mortality after AMI is greater in women than in men. Data of 464 consecutive patients (130 women and 334 men) who had a documented acute myocardial infarction in our Department of Cardiology between 1990 and 1993 were eligible for the study. We excluded 48 patients from the study for the following reasons: the location of infarct could not be determined in 18 patients: 16 patients refused to take part in the study and we were not able to contact 14 patients. The remaining 416 patients were analyzed in the study. The mean follow-up period was 36 months (from 1 to 72 months). Women were significantly older than men (62.1 +/- 11.2 vs 58.1 +/- 11.6; p < 0.001), especially those who died in hospital (70.7 +/- 9.3 vs 64.4 +/- 8.7; p < 0.01). In hospital died 26 women (20%) and 39 men (11.7%)--p < 0.05. However, age-adjusted in-hospital mortality did not differ between women and men (p = 0.256). We did not find any significant difference in 3-year survival after AMI between women and men (22% vs 20.7%; NS). Total mortality was also similar (38% vs 30.2%; NS). QMI was diagnosed in 85 women and 234 men (73% vs 78%; NS), NQMI in 31 women and 66 men (27% vs 22%; NS). The rate complications of acute phase of AMI (acute heart failure and/or rhythm disturbances) was similar in women and men. Fibrinolytic treatment was introduced in 27.2% of women and in 26.4% of men. Hypercholesterolemia and hypertension were more often associated with female gender. In multivariate analysis we found that age, acute heart failure, previous MI, hypercholesterolemia and diabetes mellitus were significant factors which affects survival after AMI. Of these only age and diabetes mellitus appeared to be significant in women.
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PMID:[Survival of women and men after myocardial infarction does not differ. Results of several years' observation]. 1008 14

Flow-dependent vasodilation has been recognized to play an important role in the perfusion of the myocardium and the occurrence of myocardial ischaemia. In the past few years, the role of the endothelium in the regulation of coronary artery dimensions has gained a lot of attraction. Changes in coronary artery size are caused through the contraction and relaxation of the smooth musculature within the vessel wall. Vasoactive substances released from the endothelium play a crucial role in the regulation of vessel size and coronary vasomotor tone. During physiologic exercise, normal coronary arteries dilate, whereas stenotic arteries constrict. This abnormal behaviour of the stenotic artery has been associated with the occurrence of myocardial ischaemia, and has been thought to be either due to: endothelial dysfunction with reduced release or production of the endothelial derived relaxant factor (EDRF); an increased sympathetic stimulation during exercise; enhanced platelet aggregation with release of thromboxane A2 and serotonin; and/or a passive collapse of the disease-free vessel segment within the stenosis when blood-flow velocity increases during exercise. Thus, a diseased coronary endothelium may have a dramatic effect on the function of the coronary arteries, and may cause or contribute to the occurrence of myocardial ischaemia under high-demand situations, e.g. physical exercise or mental stress. Changes in flow-dependent vasodilation have been described in various disease states, e.g. hypercholesterolaemia, hypertension, diabetes mellitus, but also in valvular heart disease, heart failure and transplantation. Most of these alterations are due to functional changes of the endothelium, but vascular remodelling of the coronary arteries with thickening of the intima and an enlargement of the artery may affect these functional changes importantly.
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PMID:Flow-dependent vasodilation in the coronary circulation: alterations in diseased states. 1009 79

Over the past 30 years the identification of high blood pressure and hypercholesterolaemia as major predictors of cardiovascular disease has led to an increasing expenditure on healthcare costs in pharmacological treatment of these risk factors. Most of the cost has been due to antihypertensive treatment, but evidence from randomised trials of the benefits of cholesterol-lowering drugs, along with the introduction of therapies with fewer side effects, suggests that expenditure on cholesterol treatment will rise dramatically. Cost-effectiveness analyses can aid decision making in the use of these treatments. For both hypertension and hypercholesterolaemia, the most favourable cost-effectiveness ratios were found in late middle age, in men compared to women, at the highest level of the risk factor, and in subjects with multiple risk factors. The most cost-effective treatments appear to be those which were the cheapest and which also produced the largest reductions in the risk factor. However, certain findings were based on assumptions which may be invalid. The most important of these in hypertension, and to a lesser extent in hypercholesterolaemia, is that different treatments have similar effects on morbidity and mortality for a given level of risk reduction. Experimental evidence that might confirm or refute this is not available for most treatments of hypertension. Moreover there are no trials in women or in the elderly of cholesterol-lowering treatments. The burden of disease due to these risk factors has been underestimated, and further research is required to establish the benefits of treatment on prevention of conditions such as heart failure, peripheral vascular disease, and vascular dementia.
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PMID:Pharmacoeconomic evaluation of risk factors for cardiovascular disease: an epidemiological perspective. 1014 38

Serum coenzyme Q10 (CoQ10: 2-(3,7,11,15,19,23,27,31,35,39-decamethyl-2,6,10,14,18,22,26,30,34 ,38 -tetracontadecaenyl)-5,6-dimethoxy-3-methyl-1,4-benzoquinone, CAS 303-98-0) and cholesterol levels were measured to assess the effect of cholesterol-lowering therapy in patients with non-insulin-dependent diabetes mellitus (NIDDM). Twenty healthy volunteers, 97 NIDDM patients and 2 patients with familial hypercholesterolemia were studied. None had overt heart failure or any other heart disease. Mean serum CoQ10 concentrations were significantly (p < 0.01) lower in diabetic patients with normal serum cholesterol concentrations, either with or without administration of 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (HMG-CoA RIs) including simvastatin (normal: 0.91 +/- 0.26 (mean +/- SD) mumol 1(-1); diabetic with HMG-CoA RI: 0.63 +/- 0.19; diabetic without HMG-CoA RI: 0.66 +/- 0.21). CoQ10 concentrations were higher (1.37 +/- 0.48, p < 0.001) in diabetic patients with hypercholesterolemia. Simvastatin or low density lipoprotein apheresis decreased serum CoQ10 concentrations along with decreasing serum cholesterol. Oral CoQ10 supplementation in diabetic patients receiving HMG-CoA RI significantly (p < 0.001) increased serum CoQ10 from 0.81 +/- 0.24 to 1.47 +/- 0.44 mumol 1(-1), without affecting cholesterol levels. It significantly (p < 0.03) decreased cardiothoracic ratios from 51.4 +/- 5.1 to 49.2 +/- 4.7%. In conclusion, serum CoQ10 levels in NIDDM patients are decreased and may be associated with subclinical diabetic cardiomyopathy reversible by CoQ10 supplementation.
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PMID:Effect of treatment with 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors on serum coenzyme Q10 in diabetic patients. 1033 51


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