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)

Beta blockers are known to suppress renin release in hypertension and in patients taking angiotensin-converting enzyme (ACE) inhibitors. This study sought to explore the effect of additional beta blockade on neurohumoral modulation in patients with severe heart failure (HF) who received ACE inhibitors. Forty-nine patients with chronic HF who received ACE inhibitors were given metoprolol 50 mg or carvedilol 25 mg twice daily after a 4-week dose titration period in addition to standard therapy in a prospective trial. Samples of plasma renin activity (PRA), aldosterone, aminoterminal B-type natriuretic peptide (N-BNP), and atrial natriuretic peptide (ANP) were taken at baseline and at 4, 12, and 52 weeks after starting therapy. Treatment with either beta blocker significantly lowered PRA at 4 weeks compared with baseline (-2.0 +/- 0.6 nmol/L/hour, p = 0.006), but at 12 weeks, PRA had reduced to -1.1 +/- 0.6 nmol/L/hour (p = 0.08), but at 52 weeks, it was not significantly different from baseline (+1.05 +/- 0.6 nmol/L/hour, p = 0.13). Aldosterone levels did not change significantly from baseline at 4 or 12 weeks, although there was a nonsignificant trend for lower levels at 52 weeks (baseline 232 +/- 154 pmol/L, 52 weeks 192 +/- 100 pmol/L, p = 0.09). There was significant reduction in N-BNP and ANP together with an improvement in symptom and left ventricular systolic function at 1-year follow-up. These results indicate that the suppressive effect of beta blockers on PRA in patients with HF taking ACE inhibitors is temporary, and that there is no significant effect on serum aldosterone levels.
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PMID:Effect of beta blockade (carvedilol or metoprolol) on activation of the renin-angiotensin-aldosterone system and natriuretic peptides in chronic heart failure. 1291 70

We monitored the change in plasma ANP and BNP levels (as markers for left ventricular dysfunction (LVD)) in DM2 patients treated with pioglitazone (Pio) for 4 weeks. Thirty DM2 patients with no sign of heart failure were treated with Pio (15 mg/day), and their plasma ANP (normal levels <or=43 pg/ml) and BNP levels (normal levels <or=18.4 pg/ml) were examined. We also examined those levels in no drug-treatment group (n = 10) as well as buformine treatment group (n = 10). Among these groups, there were no significant differences in clinical profiles related to DM control. Pio treatment was terminated when BNP (above 100 pg/ml) and ANP levels (above 50 pg/ml) suggested the left ventricular dysfunction (LVD). The patients (n = 12) whose BNP levels reached to the LVD-positive levels showed the basal BNP levels above the normal upper limit (18 pg/ml), while the rest of subjects (n = 18) whose basal BNP levels within normal limits did not showed the LVD-positive levels in the Pio-treatment. On the other hand basal ANP levels did not predict the development to LVD. In conclusion, BNP levels are suggested to be a good marker of Pio-induced LVD, and the Pio treatment of DM2 patients with BNP levels above the normal limit should be carefully carried out by monitoring BNP levels.
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PMID:Plasma BNP levels in the treatment of type 2 diabetes with pioglitazone. 1291 98

In the present study, we assessed the use of urinary natriuretic peptides [N-terminal proatrial natriuretic peptide (N-ANP) and N-terminal pro-brain natriuretic peptide (N-BNP) and C-type natriuretic peptide (CNP)] in the diagnosis of heart failure. Thirty-four consecutive hospitalized heart failure patients (median age, 75.5 years; 14 female) were compared with 82 age- and gender-matched echocardiographically normal controls. All subjects provided plasma and urine specimens. Plasma was assayed for N-BNP, and urine was assayed for N-ANP, N-BNP and CNP. The diagnostic efficiency of peptides was assessed using receiver operating characteristic (ROC) curve analysis. All three urinary natriuretic peptides were significantly elevated in heart failure patients ( P <0.001). Urine N-BNP was correlated with plasma N-BNP ( r (s)=0.53, P <0.0005). Areas under the ROC curves for urinary N-ANP, N-BNP and CNP were 0.86, 0.93 and 0.70 and for plasma N-BNP was 0.96. Correcting urinary peptide levels using urine creatinine produced ROC areas of 0.89, 0.93 and 0.76 respectively. A urine N-BNP level cut-off point of 11.6 fmol/ml had a sensitivity and specificity for heart failure detection of 97% and 78% respectively, with positive and negative predictive values of 64.7 and 98%. In conclusion, although all three natriuretic peptides were elevated in urine in heart failure, urinary N-BNP had diagnostic accuracy comparable with plasma N-BNP. Use of urinary N-BNP for heart failure diagnosis may be suitable for high-throughput screening, especially in subjects reluctant to provide blood samples.
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PMID:Diagnosis of heart failure using urinary natriuretic peptides. 1453 78

With the increasing prevalence of heart failure, the greater spectrum of proven therapies, the broader spectrum of cardiac dysfunction qualifying for treatment and the recognition that heart failure is difficult to diagnose, the need for an indicator of both the diagnosis and the efficacy of treatment in this condition is clear. Plasma concentrations of the B-type natriuretic peptides are related to cardiac function and cardiovascular prognosis. They parallel hemodynamic indicators of cardiac dysfunction and may therefore act as indicators of the adequacy of therapy. In the one published trial of outpatient treatment of heart failure guided by plasma BNP, 69 patients (LVEF < 40%, NYHA II-IV) were randomised to treatment according to plasma peptide levels or a clinical score. The primary end point of total cardiovascular events was reduced in BNP-guided patients (19 versus 54 events) with p < 0.001 in a multivariate analysis. The natriuretic peptides and particularly plasma BNP and aminoterminal proBNP promised to provide an objective guide for optimising treatment in heart failure.
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PMID:Outpatient management of heart failure. 1457 55

While measurement of plasma BNP concentration has been shown to be useful in the diagnosis of heart failure, its role as a screening test for detection of pre-clinical ventricular remodeling or dysfunction in the general population has not been established. Here we review available population-based studies assessing the predictive characteristics of BNP for the detection of pre-clinical structural heart disease (Stage B Heart Failure).
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PMID:The role of brain natriuretic peptide in population screening. 1457 56

The evolving paradigm of heart failure has now been expanded to include the favorable neurohormonal, structural and hemodynamic profile of B-type natriuretic peptide [BNP]. As a marker of left ventricular dysfunction, BNP is a practical tool that facilitates diagnosis, contributes to prognostic evaluations and tracks disease severity. BNP elevations vary according to gender, disease states and perhaps obesity but in general elevated levels are consistent not only with left ventricular stress but likely represent the best surrogate for ongoing left ventricular remodeling. The full utility of BNP surveys has not yet been realized but emerging areas of use include clinical assessment by physician extenders, post-MI assessment, and a target of tailored therapy for heart failure. New biomarkers for heart failure similar to BNP are on the horizon but their clinical niche has yet to be determined.
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PMID:Practical considerations for BNP use. 1457 60

Heart failure is the leading cause for hospitalization in the United States, resulting in over $8 billion in costs annually. Over 4.8 million Americans are afflicted with the disease and the number is increasing as the baby boomer generation continues to age. It is imperative that new and innovative modalities of therapy and diagnosis evolve as we continue to redefine the nature of heart failure and discover more about this debilitating disease. This article addresses the implications for endogenous brain (B-type) natriuretic peptide (BNP) testing in patients diagnosed with heart failure as well as the implications for the first available form of exogenous BNP, nesiritide. In addition, the pathophysiology of heart failure and traditional treatment modalities are discussed.
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PMID:Brain (B-type) natriuretic peptide: implications for heart failure management. 1459 12

Urocortin (UCN), a member of the corticotrophin-releasing factor family, is expressed in heart, brain and gut. UCN has potent cardiostimulatory, cardioprotective, vasodilator and diuretic/natriuretic effects, and cardiac UCN expression is increased in heart failure (HF). In the present study, we investigated plasma levels of UCN in 119 patients with HF and 212 age- and gender-matched controls to clarify its relationship with gender and disease severity. UCN was elevated in HF [normal males, 19.5 (3.9-68.8) pmol/l and HF males, 50.2 (6.9-108.2) pmol/l, P < 0.0005; normal females, 14.2 (3.9-53.5) pmol/l and HF females, 21.8 (3.9-112.5) pmol/l, P < 0.001; values are medians (range)]. The relative increase was greater in males than females ( P < 0.03). UCN fell with increasing age, especially in HF patients ( r(s) = -0.56, P < 0.0005) and with increasing New York Heart Association (NYHA) class ( r(s) = -0.55, P < 0.0005). The fall in UCN levels with increasing NYHA class was reinforced by a significant correlation between UCN and ejection fraction ( r(s) = 0.45, P < 0.0005) in HF patients. Although receiver operating characteristic (ROC) curves for diagnosis of all HF cases yielded an area under the curve (AUC) of 0.76, ROC AUCs for patients with early HF (NYHA class I and II) were better (0.91). ROC AUCs for logistic models incorporating N-terminal probrain natriuretic peptide (N-BNP) and UCN were better than either peptide alone. In conclusion, plasma UCN is elevated in HF, especially in its early stages. Its decline with increasing HF severity may expedite disease progression due to diminished cardioprotective/anti-inflammatory effects. UCN measurement may also complement N-BNP in the diagnosis of early HF.
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PMID:Plasma urocortin in human systolic heart failure. 1465 73

The levels and pathophysiological role of amino terminal C-type natriuretic peptide in heart failure are unknown. The potential of plasma amino-terminal C-type natriuretic peptide (N-CNP) as a marker of cardiac function was investigated in symptomatic patients. In 305 patients with recent-onset dyspnea and/or peripheral edema, presenting to primary care, assay of plasma amino-terminal C-type natriuretic peptide and other plasma vasoactive hormones was conducted together with echocardiography. Heart failure was diagnosed in 77 (of the 305) patients by rigorous application of predefined criteria. Plasma amino-terminal C-type natriuretic peptide concentrations were elevated in patients with heart failure, and by univariate analysis were related to age, renal function, and other hormones. On multivariate analysis, tertile of plasma N-CNP interacted with tertile of plasma amino-terminal B-type natriuretic peptide to predict heart failure independent of age, gender, renal function, or echocardiographic left ventricular fractional shortening. N-CNP showed significant relations to concurrent plasma CNP, atrial natriuretic peptide (ANP), N-ANP, B-type (or brain) natriuretic peptide (BNP), N-BNP, endothelin-1, and adrenomedullin but not to echocardiographic indicators of left ventricular systolic function. Plasma amino-terminal C-type natriuretic peptide is elevated in heart failure and is related to other plasma hormones in heart failure. These findings suggest a possible compensatory response from the peripheral vasculature to heart failure by an endothelium-based vasodilator peptide and mandate further exploration of the role of C-type natriuretic peptide in this condition.
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PMID:Amino-terminal pro-C-type natriuretic peptide in heart failure. 1465 55

Congestive heart failure (CHF) is a major cardiovascular disorder that is increasing in incidence, prevalence, and lethality. The prognostic significance of cardiac troponin levels among symptomatic and asymptomatic CHF has attracted recent interest. We sought to assess the significance of cardiac troponins in heart failure. These cardiac markers are associated with decreased left ventricular ejection fraction and poor prognosis in patients with CHF and are related to the severity of heart failure. The mechanism for the release of these markers seems to be from ventricular remodeling, ongoing myocyte degeneration, the presence of coronary artery disease, and reduced coronary reserve. In addition to B-type (brain) natriuretic peptide (BNP), cardiac troponin levels measured in patients admitted to the hospital could help risk-stratify patients and manage them effectively. BNP and cardiac troponins are easy to measure and can be repeated many times to follow patients, without interobserver variability. Theoretically, BNP is a marker of heart failure status and cardiac troponin is a marker of myocyte injury. The first therapeutic goal could be relief of circulatory congestion and lowering of BNP. The second goal could be attenuation of myocyte injury and lowering of cardiac troponins. Measuring and monitoring the levels of both could be highly effective means to reliably stratify the patients into low-, intermediate-, and high-risk groups for cardiac events and progression of heart failure. Furthermore, large-scale trials are necessary to establish them as noninvasive monitoring markers of heart failure and effectiveness of treatment.
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PMID:Cardiac troponin levels in heart failure. 1466 59


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