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

Heart failure is a major and still growing medical and epidemiological problem, but in the last 10-20 years great progress has been made in its treatment. Alleviating symptoms is not (any longer) the only aim of the treatment; improving the life expectation or reducing the mortality has become a different, at least as important aim. Left ventricular dysfunction, even if asymptomatic, should be regarded, just as hypertension and hypercholesterolaemia, as a risk factor for which efficacious treatment is available and which consequently should be treated. A problem in this respect is that the effect of treatment of asymptomatic left ventricular dysfunction and of mild forms of heart failure is difficult to measure. Beta-blocking agents have proved to be the greatest gain in the treatment of heart failure in recent years, in addition to ACE inhibitors, diuretics and digoxin. These preparations should be prescribed with caution and due consideration. However, their favourable influence is such that use on a much larger scale than currently appears to be justified.
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PMID:[Revised insights and therapeutic goals in the treatment of chronic heart failure]. 1044 72

Arterial distensibility reflects mechanical properties of the arterial wall and have, thus a clearcut clinical relevance. This because an arterial distensibility reduction is associated with an increased pulse pressure, an increased cardiac work and a reduced diastolic vital organ perfusion. In recent years it has been demonstrated that arterial distensibility is reduced in marked and mild hypercholesterolemia, in a manner independent from arterial blood pressure values. Arterial mechanical properties are also impaired in heart failure, this leading to a further cardiac damage. This important vascular properties however, can be improved by appropriate treatment, while the time needed for that can be extremely long.
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PMID:Pharmacological improvement of large arteries properties. 1052 65

Heart failure (HF) is a common and expensive cardiovascular disease, in economic terms as well as in lives lost. Angiotensin converting enzyme (ACE) inhibitors have been shown to significantly reduce mortality and hospitalisation in HF. However, recent surveys show that the prescription rate of ACE inhibitors for HF is far below what is considered to be optimal. Furthermore, prescribed dosages are usually lower than those recommended based on evidence from clinical trials. This article estimates the consequences, both economic and human, of underprescribing ACE inhibitors in patients with HF. The indication for prescribing an ACE inhibitor varies, and clinical trials have included different categories of patients; it is inappropriate to assess costs in all eligible patients without taking these factors into account. Therefore, we analysed the data with respect to 4 different groups: (i) asymptomatic left ventricular systolic dysfunction (LVSD)--an early stage leading to chronic HF; (ii) chronic HF; and post-myocardial infarction (MI) LVSD differentiated into (iii) post-MI asymptomatic LVSD and (iv) post-MI chronic HF. We also estimated the cost effectiveness of adding an ACE inhibitor to the treatment of patients with HF for whom an ACE inhibitor is not currently prescribed. If only patient populations in which large trials have shown a significant effect of ACE inhibition on mortality are included in the analysis (i.e. excluding asymptomatic patients with LVSD), increasing the number of Swedish patients receiving an ACE inhibitor could save in excess of 3700 lives each year, in addition to reducing the annual number of hospitalisations by 8400. The additional cost would be 101.5 million Swedish kronor (SEK), a cost per life saved of SEK27 200. Chronic HF is the most cost-effective patient population to treat, generating cost savings under certain assumptions. A further 6700 hospitalisations can be avoided should the use of ACE inhibitors be extended to asymptomatic patients with LVSD. Increasing dosages to those used in the large clinical trials may generate additional savings in lives and hospitalisations. In conclusion, the use of ACE inhibitors in HF and LVSD has clearly been proven to be cost effective, and compares favourably with the cost effectiveness of treating hypertension or hypercholesterolaemia. At present, however, ACE inhibitors are not optimally utilised. Given the increasingly constrained resources for healthcare, every effort should be made to increase the use of cost-effective treatments, such as ACE inhibitors in chronic HF and post-MI LVSD.
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PMID:Angiotensin converting enzyme (ACE) inhibitors and heart failure. The consequences of underprescribing. 1053 27

In the current economic climate it is important to demonstrate that healthcare resources are being used efficiently. As a consequence, pharmacoeconomic analyses are invaluable for assessing the cost-effectiveness of new therapeutic strategies. A condition with recurrent morbid events that are costly to treat provides the greatest potential for cost savings. In contrast, there is less opportunity to redeem original treatment costs when a condition is associated with infrequent and inexpensive morbidity. Consequently, treatment strategies that have a rapid onset and substantial impact on disease progression are likely to be the most highly cost-effective forms of therapy. Elevated blood pressure in the elderly and established coronary heart disease (CHD) are both associated with high rates of costly cardiovascular events (eg, stroke, myocardial infarction, and heart failure). Clinical trials have shown that administration of blood-pressure-lowering agents to elderly hypertensives and the treatment of hypercholesterolemia with statins in the secondary prevention of CHD are highly effective strategies for reducing this morbidity. Pharmacoeconomic analyses of the data from these clinical trials now provide an additional assessment of their cost-effectiveness. The results of these analyses suggest that blood-pressure-lowering therapy for the elderly and the use of statins to control hypercholesterolemia in patients at high risk of CHD are extremely cost-effective, compared with many other routine medical interventions.
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PMID:The health economics of the treatment of hyperlipidemia and hypertension. 1055 9

BACKGROUND: We investigated the association of cigarette smoking with high-grade carotid artery stenosis in patients with ischemic stroke and transient ischemic attacks. METHODS: Prospectively collected data from 404 patients with focal brain ischemia were used for a cross-sectional study estimating the association between cigarette smoking and high-grade carotid artery stenosis (diagnosed by Doppler-ultrasound and defined as a luminal narrowing of > or = 70%). Cerebral ischemia patients with normal sonographic findings served as a comparison group. Multivariate logistic regression models were used for statistical tests to determine the association between smoking and high-grade carotid stenosis. Age, gender, hypertension, diabetes mellitus, hypercholesterolemia and co-existing heart disease (myocardial infarction, angina, heart failure) were considered potential confounders. RESULTS: High-grade carotid stenoses were found in 25% (n = 101) of the patients; 39% (n = 156) were classified as smokers. Smoking (odds ratio 3.6, 95% confidence interval [CI] 2.2 to 5.8), hypercholesterolemia (odds ratio 1.8; CI 1.1 to 2.8) and preexisting heart disease (odds ratio 1.7; CI 1.1 to 2.7) were significantly associated with carotid stenosis > or = 70%. The impact of smoking augmented with increasing degree of stenosis (odds ratio for stenoses > or = 80%: 4.3, CI 2.3 to 7.7), whereas the association with hypercholesterolemia, and co-existing heart disease decreased in strength for stenoses greater than 80%. Hypertension and diabetes mellitus were not found to be significantly with high-grade carotid artery stenoses. CONCLUSION: Smoking is an independent determinant of severe carotid artery stenosis in patients with focal cerebral ischemia.
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PMID:[In Process Citation] 1059 30

Terminalia arjuna is a deciduous tree found throughout India growing to a height of 60-90 feet. The thick, white-to-pinkish-gray bark has been used in India's native Ayurvedic medicine for over three centuries, primarily as a cardiac tonic. Clinical evaluation of this botanical medicine indicates it can be of benefit in the treatment of coronary artery disease, heart failure, and possibly hypercholesterolemia. It has also been found to be antibacterial and antimutagenic. Terminalia's active constituents include tannins, triterpenoid saponins (arjunic acid, arjunolic acid, arjungenin, arjunglycosides), flavonoids (arjunone, arjunolone, luteolin), gallic acid, ellagic acid, oligomeric proanthocyanidins (OPCs), phytosterols, calcium, magnesium, zinc, and copper.
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PMID:Terminalia arjuna. 1060 17

Although the role of nitric oxide (NO) in the modulation of vascular tone has been studied and well understood, its potential role in the control of myocardial metabolism is only recently evident. Several lines of evidence indicate that NO regulates myocardial glucose metabolism; however, the details and mechanisms responsible are still unknown. The aim of this study was to further define the role of NO in the control of myocardial glucose metabolism and the nitric oxide synthase (NOS) isoform responsible using transgenic animals lacking endothelial NOS (ecNOS). In the present study, we examined the regulation of myocardial glucose uptake using isometrically contracting Langendorff-perfused hearts from normal mice (C57BL/6J), mice with defects in the expression of ecNOS [ecNOS (-/-)], and its heterozygote [ecNOS (+/-)], and wild-type mice [ecNOS (+/+)] (n=6, respectively). In hearts from normal mice, little myocardial glucose uptake was observed. This myocardial glucose uptake increased significantly in the presence of N(omega)-nitro-L-arginine methyl ester (L-NAME). Similarly, in the hearts from ecNOS (-/-), glucose uptake was much greater than in normal mice, whereas myocardial glucose uptake of ecNOS (+/-) and ecNOS (+/+) mice was not different from normal mice. In addition, myocardial glucose uptake of ecNOS (+/-) and ecNOS (+/+) mice increased significantly in the presence of L-NAME. At a workload of 800 g. beats/min, L-NAME increased glucose uptake from 0.1+/-0.1 to 3+/-0.4 microg/min x mg in ecNOS (+/-) mice and from 0.2+/-0.1 to 2.7+/-0.7 microg/min x mg in ecNOS (+/+) mice. Furthermore, in the hearts from ecNOS (-/-) mice, 8-bromoguanosine 3':5'-cyclic monophosphate (8-Br-cGMP), a cGMP analog or S-nitroso-N-acetylpenicillamine (SNAP), a NO donor essentially shut off glucose uptake, and in hearts from ecNOS (+/-) mice, 1H-[1,2,4]oxadiazolo[4,3,-a]quinoxalin-1-one (ODQ), an inhibitor of cGMP, increased the glucose uptake significantly. These results indicate clearly that cardiac NO production regulates myocardial glucose uptake via a cGMP-dependent mechanism and strongly suggest that ecNOS plays a pivotal role in this regulation. These findings may be important in the understanding of the pathogenesis of the diseases such as ischemic heart disease, heart failure, diabetes mellitus, hypertension, and hypercholesterolemia, in which NO synthesis is altered and substrate utilization by the heart changes.
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PMID:Myocardial glucose uptake is regulated by nitric oxide via endothelial nitric oxide synthase in Langendorff mouse heart. 1067 77

Enhanced oxidant stress involved in the pathogenesis of cardiovascular (heart failure, atherosclerosis, ischemia-reperfusion injury), neurodegenerative (M. Alzheimer), metabolic (hypercholesterolemia, diabetes) and inflammatory disorders is mimicked by non-intermittent therapy with nitrovasodilators. We used this latter therapy model to study urinary 3-nitrotyrosine (n-tyr) excretion as a potential biomarker that may reflect the enhanced generation of reactive oxygen species. Namely, free or protein-bound n-tyr is formed in the organism by nitration of tyrosine (residues) via peroxynitrite (reaction product of NO&z.ccirf; and O(2)(-)&z. ccirf;). Free n-tyr content was analyzed by gas chromatography in urine obtained from healthy human subjects under a nitrite-limited diet during a two-day non-intermittent transdermal administration of glyceroltrinitrate (GTN; 0.4 mg/h) with or without vitamin C (Vit-C; 55 microg/kg/min) as antioxidant. Concomitant with the development of complete vascular tolerance (loss of dilator action), a progressive increase in urinary n-tyr excretion (up to 186+/-9 microg/day) was demonstrated in volunteers given GTN only. In contrast, when Vit-C was added, the GTN-induced increases in urinary n-tyr content were significantly suppressed (up to 130.20+/-6.91 microg/day), whereas Vit-C alone even decreased urinary n-tyr content (down to 34.00+/-5.66 microg/day), which was below control values (56.0+/-3.4 microg/day). Thus, urinary n-tyr may serve as a biomarker to detect changes in oxidant stress and thereby to evaluate the efficacy of therapeutic interventions aimed at reducing oxidant stress under various pathophysiological conditions.
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PMID:How urine analysis reflects oxidative stress--nitrotyrosine as a potential marker. 1084 22

The term oxidative stress refers to a situation in which cells are exposed to excessive levels of either molecular oxygen or chemical derivatives of oxygen (ie, reactive oxygen species). Three enzyme systems produce reactive oxygen species in the vascular wall: NADH/NADPH oxidase, xanthine oxidoreductase, and endothelial nitric oxide synthase. Among vascular reactive oxygen species superoxide anion plays a critical role in vascular biology because it is the source for many other reactive oxygen species and various vascular cell functions. It is currently thought that increases in oxidant stress, namely excessive production of superoxide anion, are involved in the pathophysiology of endothelial dysfunction that accompanies a number of cardiovascular risk factors including hypercholesterolemia, hypertension and cigarette smoking. On the other hand, vascular oxidant stress plays a pivotal role in the evolution of clinical conditions such as atherosclerosis, diabetes and heart failure.
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PMID:Vascular oxidant stress: molecular mechanisms and pathophysiological implications. 1087 82

The obese ZDFxSHHF-fa/fa(cp) model was developed by crossing lean female Zucker Diabetic Fatty (ZDF +/fa) and lean male Spontaneously Hypertensive Heart Failure (SHHF/Mcc-fa(cp), +/fa) rats. The purpose of the present study was to determine renal function and morphology, hemodynamics, and metabolic status in ZDFxSHHF rats. Two sets of experiments were conducted. First, we evaluated heart and kidney function and metabolic status in aged (46 weeks old) male obese ZDFxSHHF and age matched obese SHHF rats, lean Spontaneously Hypertensive (SHR) and lean normotensive Wistar Kyoto (WKY) rats. In the second set of experiments, renal function and structure as well as metabolic and lipid status were determined in lean (LN) and obese (OB) adult (29-weeks of age) ZDFxSHHF rats. At 46 weeks of age ZDFxSHHF rats are hypertensive expressing marked cardiac hypertrophy associated with diastolic dysfunction and preserved contractile function. Fasted hyperglycemia and hyperinsulinemia are accompanied by moderate hypercholesterolemia and hypertriglyceridemia. Obese aged ZDFxSHHF have marked renal hypertrophy, a 3-8 fold decrease in creatinine clearance (compared with SHHF, SHR and WKY), a high percent of segmental + global glomerulosclerosis (59.8%+/-10.8), and severe tubulointerstitial and vascular changes. Obese ZDFxSHHF rats die at an early age (approximately 12 months) from end-stage renal failure. Studies conducted in 29-week animals showed that, although both LN and OB 29-week old animals are hypertensive, OB animals have more severely compromised renal function and structure as compared with lean litter-mates (kidney weight: 2.56+/-0.16 vs. 1.61+/-0.12 g; creatinine clearance: 0.42+/-0.04 vs. 1.24+/-0.13 L/g kid/day; renal vascular resistance 12.39+/-1.4 vs. 6.14+/-0.42 mmHg/mL/min/g kid; protein excretion: 556+/-16 vs. 159+/-9mg/day/g kid, p < 0.05, OB vs. LN, respectively). Obesity is also associated with hyperglycemia (424+/-37 vs. 115+/-11 mg/dL), hyperinsulinemia (117.2+/-8.8 vs. 42.3+/-3.5 microU/mL), hypertriglyceridemia (5200+/-702 vs. 194+/-23 mg/dL), hypercholesterolemia (632+/-39 vs. 109+/-4mg/dL), and presence of segmental + global glomerulosclerosis (20.1+/-3.2% vs. 0.1+/-0.1%) with prominent tubular and interstitial changes (p < 0.05, OB vs. LN, respectively). In summary, the present study indicates that the crossing of rat strains of nephropathy produces hybrids that carry a high risk for severe renal dysfunction. The ZDFxSHHF rats express insulin resistance, hypertension, dislipidemia and obesity and develop severe renal dysfunction. In addition, the hybrids do not develop some of the complications (hydronephrosis or congestive heart failure) common for the parental strains that may compromise studies of renal function and structure. Therefore, the ZDFxSHHF rat may be a useful model fore valuating risk factors and pharmacological interventions in chronic renal failure.
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PMID:Renal function and structure in diabetic, hypertensive, obese ZDFxSHHF-hybrid rats. 1090 Nov 78


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