Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We investigated the effects of the aldosterone blocker eplerenone alone and in combination with angiotensin II type 1 receptor antagonist on ventricular remodeling in rats with left ventricular (LV) dysfunction after extensive myocardial infarction (MI). Adding an aldosterone antagonist to an ACE inhibitor reduces mortality and morbidity in heart failure. Starting 1 day after MI, rats were treated with placebo, eplerenone (100 mg/kg/day), the angiotensin type 1 receptor antagonist candesartan (1 mg/kg/day), or a combination of both for nine weeks. Both monotherapies attenuated the rise in LV end-diastolic dimension (LVDd) and LV end-diastolic volume (LVEDV) compared with placebo, whereas combined treatment further attenuated LVDd and LVEDV and significantly improved LV function. Increased collagen type I and III gene expressions in the noninfarcted LV myocardium from MI placebo rats was attenuated by candesartan, but almost completely prevented by eplerenone and eplerenone/candesartan. The addition of eplerenone to candesartan prevented the increases in LV gene expression of ANP and BNP more effectively than either monotherapy. The aldosterone blocker eplerenone improved LV remodeling in rats with LV dysfunction after extensive MI. Combination therapy with an candesartan substantially potentiates this effect by a complementary prevention of LV fibrosis, cardiac hypertrophy, and molecular alterations.
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PMID:Additive improvement of left ventricular remodeling by aldosterone receptor blockade with eplerenone and angiotensin II type 1 receptor antagonist in rats with myocardial infarction. 1527 26

Elevated plasma brain natriuretic (BNP) concentrations correlate with increased cardiac filling pressures. Therefore, increased BNP has been proposed as a marker for asymptomatic ventricular dysfunction, as an aid in the diagnosis of cardiac dyspnea, as an end point to assess the efficacy of heart failure therapy, and as a prognostic marker in heart failure. An understanding of the utility of BNP requires an appreciation of the sensitivity, specificity, and diagnostic accuracy of BNP in each of these clinical situations. At this time, there is strong evidence for the value of BNP in the evaluation of dyspnea of uncertain cause. Further population studies will need to be performed to refine the application of BNP to community cohorts and to determine its clinical value and cost-effectiveness as a screening tool in the early diagnosis of ventricular dysfunction. To make optimal use of BNP for the assessment of heart failure therapy and prognosis in individual patients, physicians will require additional information on the biological variability of BNP. Studies comparing the sensitivity, specificity, and predictive value of the available BNP and N-terminal pro-BNP assays need to be conducted in each of these clinical settings.
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PMID:Measuring plasma B-type natriuretic peptide in heart failure: good to go in 2004? 1531 52

Angiogenic gene therapy in angina pectoris has been disappointing so far. Reasons might be that the administered genes already are overexpressed in ischemic myocardium, or that atrial and brain natriuretic peptides (ANP and BNP) are overexpressed, as they have anti-angiogenic effects. Five stable angina pectoris patients without heart failure were studied. Left ventricular biopsies were taken during coronary by-pass surgery from a region with stress-inducible ischemia and from a normal region. Both ANP and BNP but not vascular endothelial growth factor (VEGF) and VEGF-receptor 1 and 2 were overexpressed in ischemic regions compared to non-ischemic regions as measured by real-time PCR. The expression of 15 other angiogenic genes measured by oligonucleotide arrays was not consistently increased in ischemic regions. The overexpression of ANP and BNP suggests an anti-angiogenic effect in ischemic heart disease. The lack of overexpression of angiogenic genes supports the concept of therapeutic overexpression of these genes.
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PMID:ANP and BNP but not VEGF are regionally overexpressed in ischemic human myocardium. 1531 4

Current evidence favors the view that regardless of etiology, there is a predictable sequence of neuroendocrine activation that operates in most dogs and cats with progressive heart disease and that it is largely, but not entirely, independent of etiology. The natriuretic peptides and sympathetic nervous system seem to be early responders to developing cardiac and hemodynamic perturbations in both species. BNP plays a particularly prominent role in cats, possibly as a reflection of disease etiology. Shortly thereafter, plasma endothelin concentrations rise, reflecting the impact of the hemodynamic alterations on the vasculature. Endothelin and the natriuretic peptides directly suppress plasma renin release but have divergent effects on aldosterone. Activation of the tissue RAAS may operate early on to further the progression of heart failure, but evidence of plasma RAAS activation occurs comparatively late and near the time of development of overt CHF. Finally, in animals with severe CHF that are prone to hypotension,vasopressin levels may also rise, contributing to the retention of free water and congestion that is refractory to diuretics. Although oversimplified, this scenario seems to be consistent with data obtained in human, canine, and feline patients. These observations provide some impetus for evaluating ACE inhibitors in cats and beta-receptor-blocking drugs in dogs and cats. Perhaps we are also a little closer to identifying useful biochemical markers that can aid in the diagnosis of heart disease, guide therapy, and improve our understanding of the biologic processes occurring in our patients.
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PMID:Neuroendocrine evaluation of cardiac disease. 1532 72

Although the benefits of carvedilol in patients with heart failure and depressed ejection fraction (EF) have been elucidated, those in patients with preserved EF are not understood. We enrolled 40 patients with mild or moderate heart failure and EF >/=45%. They were randomly assigned to carvedilol (n = 19) or conventional therapy (n = 21). After 12 months of treatment, carvedilol significantly improved all end points (plasma concentration of B-type natriuretic peptide [BNP] from 175 (35 to 209) to 106 (52 to 160) pg/ml, mean (95% confidence interval) p <0.01; New York Heart Association functional class from 2.37 (2.13 to 2.61) to 1.56 (1.21 to 1.91), p <0.01; exercise capacity estimated with the Specific Activity Scale from 4.75 (4.50 to 5.00) to 5.68 (5.22 to 6.14) METs, p <0.02), whereas conventional therapy did not (plasma BNP concentration from 150 (114 to 186) to 174 (100 to 248) pg/ml; New York Heart Association functional class from 2.29 (2.08 to 2.50) to 2.11 (1.73 to 2.49); exercise capacity from 4.57 (4.34 to 4.80) to 4.72 (4.41 to 5.03) METs). Univariate regression analyses showed that only the use of carvedilol was correlated with the decrease in plasma BNP concentration (p <0.03). Multivariate analyses demonstrated that an ischemic cause of heart failure (p <0.02), high plasma concentration of BNP (p <0.02), left ventricular dilation (p <0.03), and use of carvedilol (p <0.04) at baseline were predictive of a decrease in plasma concentration of BNP. In conclusion, carvedilol potentially decreased neurohumoral activation, decreased symptoms, and increased exercise capacity in patients with heart failure and preserved EF.
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PMID:Effects of carvedilol on plasma B-type natriuretic peptide concentration and symptoms in patients with heart failure and preserved ejection fraction. 1532 27

Natriuretic peptides have proved useful in the diagnosis of heart failure in patients presenting to the emergency department with shortness of breath. Dyspnea and orthopnea in heart failure are clinical expressions of pulmonary capillary congestion and leakage, which may be assessed by the percentage of pulmonary hemosiderin-laden macrophages (HLM) in induced sputum. We found a significant difference in the percentage of HLM present in sputum among patients with acute heart failure, patients with noncardiac dyspnea with ventricular dysfunction, and patients without heart failure (p = 0.008). N-terminal pro-brain natriuretic peptide (N-BNP) concentrations were also different among these 3 patient groups (p = 0.006). N-BNP concentrations were positively associated with the percentage of HLM in patients with acute dyspnea (r = 0.6; p < 0.0001). N-BNP, in addition to being a ventricular dysfunction marker, may reflect the severity of pulmonary capillary congestion and leakage in patients with acute shortness of breath.
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PMID:N-terminal pro-brain natriuretic peptide reflects pulmonary capillary leakage in patients with acute dyspnea. 1534 7

Diagnosing or managing heart failure may still remain difficult. BNP and NT proBNP are neurohormones specifically secreted by myocytes. They have proved their effectiveness to improve clinician's diagnostic accuracy for diagnosing heart failure. BNP use is now recommended by European Society of Cardiology guidelines but multiplication of publications about BNP and NTProBNP show new possible applications for natriuretic peptides.
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PMID:[Brain natriuretic peptide and heart failure, from bench to bedside]. 1536 15

Medical treatment of acute decompensated heart failure has little changed in the last years, except with the advent of non-invasive ventilation. Doppler-echocardiography and BNP dosing have simplified the diagnostic approach and limited the need for invasion evaluation. Vasodilators remain probably underused whereas some doubts have emergency regarding the safety of positive inotropes. Analysis of the hemodynamic profile is mandatory for an optimal management of these patients. The next decade will be that of morbimortality trials in this common form of heart failure with severe prognosis.
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PMID:[Medical treatment of acute heart failure]. 1536 16

The cardiac natriuretic peptides, ANP (atrial natriuretic peptide) and BNP (brain natriuretic peptide), are secreted by the heart in proportion to cardiac transmural pressures. They possess a wide range of effects in multiple tissues facilitating overall pressure/volume homoeostasis. The close relationship between plasma concentrations of these peptides and 'cardiac load' has led to their use as biomarkers of cardiac health with diagnostic and prognostic applications in a variety of disorders affecting the cardiovascular system. BNP and its N-terminal fragment (NT-BNP) are especially sensitive indicators of cardiac dysfunction and remodelling, and correlate strongly with severity. Given that cardiac ischaemia is also an important trigger for the release of these ventricular peptides, they may likewise play a role in the detection of coronary artery disease. Measurement of BNP/NT-BNP shows particular promise as a 'rule out' test for suspected cases of HF (heart failure) in both emergency care and outpatient settings, and may assist in identifying individuals with asymptomatic ventricular impairment who will benefit from therapy preventing progression to overt HF. The BNP peptides also predict subsequent haemodynamic deterioration and adverse events in cardiovascular disease, and can therefore be used to monitor those at high risk and act as a guide to optimization of treatment. The favourable biological properties of the natriuretic peptides have also led to their use as therapeutic agents.
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PMID:Cardiac natriuretic peptides for cardiac health. 1547 36

Plasma levels of various neurohumoral factors are activated and have an important role of the pathophysiology of congestive heart failure (CHF). Atrial natriuretic peptide (ANP) and brain (or B-type) natriuretic peptide (BNP) are secreted from cardiomyocytes in response to atrial or ventricular wall stretch. The natriuretic peptides have a fundamental role in cardiovascular remodeling, volume homeostasis, and the response to myocardial injury. Clinical investigations of these peptides have focused on their diagnostic usefulness for heart failure and left ventricular dysfunction and their prognostic usefulness after acute coronary syndromes and heart failure. In patients with left ventricular systolic dysfunction, a high plasma BNP level is an independent prognostic predictor of CHF patients, suggesting that the compensatory activity of the cardiac natriuretic peptide system is attenuated as mortality increases in chronic CHF patients with high plasma levels of ANP and BNP. BNP is more useful than ANP for diagnosis and management of CHF. Recently, rapid BNP assay is available in our country, rapid measurement of BNP in the emergency department may improve the evaluation and treatment of patients with acute dyspnea and thereby reduced the time to discharge and the total cost of treatment. In addition, BNP-guided treatment of heart failure may reduce total cardiovascular events, and delayed time to first event combination with intensive clinically guided treatment.
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PMID:[Brain natriuretic peptide]. 1547 21


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