Plasma Brain Natriuretic Peptide Levels In Patients Research Articles

Effects of high-absorption curcumin for the prevention of hypertensive heart disease: a double-blind, placebo-controlled, randomized clinical study.

AimsHypertension is a strong risk factor for heart failure with preserved ejection fraction. Curcumin has p300-specific histone acetyltransferase inhibitory activity, suppresses cardiomyocyte hypertrophy and fibrosis, and significantly reduces myocardial brain natriuretic peptide (BNP) expression without altering blood pressure in a rat model of hypertensive heart disease. This double-blind, placebo-controlled, randomized study, for the first time, aimed to examine the efficacy of a high-absorption curcumin for the prevention of hypertensive heart disease in humans.Methods and resultsPatients exhibiting initial signs of hypertensive heart disease with left ventricular ejection fraction ≥60% and stable blood pressure <140/90 mmHg orally took a double-blinded capsule (either a 90 mg curcumin capsule or placebo) twice daily for 24 weeks. The primary endpoint was per cent changes in left ventricular diastolic function (E/E′) from baseline to 6 months after administration. The secondary endpoint was the per cent change in plasma BNP levels. The E/E′ ratio per cent change from baseline to 6 months after administration was similar between the placebo (n = 69) and the curcumin (n = 73) groups. The per cent change in plasma BNP levels was significantly lower in the curcumin group than in the placebo group. In patients <65 years, BNP per cent changes were significantly lower in the curcumin group than in the placebo group, but similar between groups in ≥65 years (<65 vs. ≥65 years: P for interaction = 0.011).ConclusionsA high-absorption curcumin agent did not affect the E/E′ ratio, rather it significantly inhibited the increase in plasma BNP levels in patients with initial signs of hypertensive heart disease.

Influences of Donepezil on Cardiovascular System—Possible Therapeutic Benefits for Heart Failure—DOnepezil Cardiac TEst Registry (DOCTER) Study

To study prospectively influences of donepezil, an acetylcholinesterase inhibitor against Alzheimer disease, on cardiovascular system, we evaluated cardiovascular changes occurring during new initialized treatment with donepezil in 49 dementia patients over 6 months. No patient suffered from cardiovascular events. In clinical changes between baseline and the first evaluation after donepezil treatment, heart rate and plasma brain natriuretic peptide (BNP) levels as a marker for heart failure did not change (BNP: 59.62 ± 62.71 pg/mL at baseline to 53.18 ± 42.34 pg/mL at first evaluation; P = 0.262). We further examined plasma BNP levels in 2 groups into which the patients were divided at baseline according to the cut-off plasma BNP level of 60 pg/mL. In patients with high level of BNP, the BNP levels decreased after administration of donepezil (116.39 ± 76.58 pg/mL at baseline to 82.24 ± 46.64 pg/mL at first evaluation; P = 0.011) with the tendency to be reduced in the follow-up period. BNP did not change in patients with low level of BNP. Donepezil seemed to be safe in patients with dementia without symptomatic heart disease and significantly decreased plasma BNP levels in patients with subclinical chronic heart failure.

Relationship between CT Findings and the Plasma Levels of Brain Natriuretic Peptide in 29 Patients with Acute Cardiogenic Pulmonary Edema

Brain natriuretic peptide (BNP) is a useful biomarker for the assessment of cardiogenic pulmonary edema. This study evaluated the relationship between computed tomography (CT) findings and plasma BNP levels in patients with cardiogenic pulmonary edema. Twenty-nine consecutive outpatients with severe respiratory failure from cardiogenic edema presenting to emergency departments were enrolled. They underwent chest CT and plasma BNP levels were measured in the emergency room. CT findings were independently evaluated by two radiologists who were unaware of the patients' clinical information. The plasma BNP levels only correlated with the volume of pleural effusion in each side (right: r(s) = 0.519, P = .004; left: r(s) = 0.460, P = .012). No significant correlation was observed between the BNP levels and the findings of lung parenchyma or cardiovascular enlargement. Estimating the pleural effusion volume with CT may be a feasible method as well as measuring the plasma BNP level in the assessment of acute cardiogenic pulmonary edema.

Determinants of plasma brain natriuretic peptide levels in untreated hypertensive patients

Plasma brain natriuretic peptide (BNP) level is elevated in patients with left ventricular (LV) hypertrophy reflecting not only altered LV geometry but LV systolic and/or diastolic dysfunction. However, the values and limitations of BNP measurements are unclear in patients with untreated hypertension. In this study, plasma BNP level was compared with LV geometric and functional characteristics in patients with untreated hypertension. Plasma BNP level was measured in 115 patients with untreated hypertension (72 males, 43 females, aged 60±12years). Routine echo parameters of LV geometry and LV systolic and diastolic performance were also determined. LV ejection fraction was 67±6% and plasma BNP level was 32±30pg/ml. Plasma BNP levels correlated with age, LV mass index (LVMI), and mitral E velocity, respectively (r=0.46, p<0.05; r=0.21, p<0.05; r=0.29, p<0.05, respectively), but not with systolic blood pressure or relative wall thickness (r=0.01; r=-0.02). Plasma BNP level correlated with E/E' ratio (r=0.27, p<0.05, n=77). When a stepwise multivariate analysis was performed, E velocity was selected in addition to age and LVMI as significant correlates of plasma BNP level. LVMI and E velocity were independent determinants of plasma BNP level in patients with untreated hypertension. Plasma BNP level is substantially useful for the screening of abnormalities of LV geometry and/or function in patients with untreated hypertension. Additional echocardiography is useful to assess the mechanism of the elevation of plasma BNP level in untreated hypertensive patients.

MRI of Cardiac Sarcoidosis: Basal and Subepicardial Localization of Myocardial Lesions and Their Effect on Left Ventricular Function

The objective of our study was to use MRI to analyze the topographic localization of myocardial lesions and their relationship to plasma brain natriuretic peptide (BNP) levels and several cardiac function parameters in patients with cardiac sarcoidosis. Delayed contrast-enhanced MRI was performed in 40 patients with sarcoidosis (11 cardiac, 29 extracardiac cases). Using a 29-segment model of the left ventricle (LV), the extent of myocardial hyperenhancement was visually scored (0 = no hyperenhancement, 1 = 1-25%, 2 = 26-50%, 3 = 51-75%, 4 = 76-100% hyperenhancement) and was compared with plasma BNP level and several parameters of cardiac function. Ten of the 11 patients with cardiac sarcoidosis showed myocardial hyperenhancement, whereas none of the 29 patients without cardiac sarcoidosis did. In patients with cardiac sarcoidosis, hyperenhancement was significantly more extensive in basal short axis slices than in apical short axis slices (p < 0.0005). Myocardial hyperenhancement was significantly more frequent in subepicardial layers than in subendocardial layers. The global extent of myocardial hyperenhancement was significantly correlated with plasma BNP levels and the LV end-diastolic volume index and was negatively correlated with the LV ejection fraction. In patients with cardiac sarcoidosis, myocardial lesions detected on delayed contrast-enhanced MRI were predominantly localized in the basal and subepicardial myocardium. The extent of myocardial lesions may be related to LV dysfunction and plasma BNP level in patients with cardiac sarcoidosis.

Assessment of factors affecting plasma BNP levels in patients with chronic atrial fibrillation and preserved left ventricular systolic function

Background Several studies have reported that plasma brain natriuretic peptide (BNP) levels are increased in patients with chronic atrial fibrillation (AF). The objective of this study was to assess the factors influencing plasma BNP levels in patients with chronic AF and preserved left ventricular (LV) systolic function. Methods Transthoracic echocardiography was performed in 104 patients (48 men, 56 women; mean age, 63.9 ± 10.7 years) with chronic AF. At the same time, plasma BNP levels were measured with a Triage R kit (Biosite, San Diego, CA). Results Women, long duration of AF, and hypertension were more prevalent in the highest quartile group of BNP levels than in the lowest quartile of BNP. Significant correlations were observed between plasma BNP levels and the following: mitral E velocity ( r = 0.343), mitral annular E′ velocity ( r = − 0.402), ratio of mitral E velocity and mitral annular E′ velocity ( r = 0.487), left atrial(LA) size ( r = 0.653), LA volume index ( r = 0.775), right atrial (RA) volume index ( r = 0.563), maximal velocity ( V max) of mitral regurgitation (MR) ( r = 0.448), tricuspid regurgitation (TR) V max ( r = 0.532) and LV mass index ( r = 0.581). In stepwise multiple linear regression analysis, LA volume index ( β = 0.326, p < 0.001), LV mass index ( β = 0.395, p < 0.001) and duration of AF ( β = 0.492, p < 0.001) independently predicted plasma BNP levels in the study subjects. The patients with increased LA volume index exhibited a longer duration of AF, larger RA volume index and LV mass index, higher MR V max, TR V max and plasma BNP level. Conclusions LA volume index, LV mass index and duration of AF are independent predictors of plasma BNP levels in patients with chronic AF and preserved LV systolic function.

Elevated Plasma BNP Level in Patients with Diabetes Mellitus Correlates with Prevalence of Heart Failure After Acute Myocardial Infarction

Patients with Diabetes Mellitus (DM) are more likely to develop heart failure than non-DM patients after acute myocardial infarction (MI), though there is no significant difference in LV ejection fraction or infarct size. We test the hypothesis that diabetes is associated with the increased level of Brain natriuretic peptide (BNP) in patients with first anterior MI.

Assessment of Factors Influencing Plasma BNP Level in Patients with Chronic Atrial Fibrillation and Preserved Left Ventricular Systolic Function

Background and Objectives:Several studies have reported that Brain Natriuretic Peptide (BNP) were increased in patients with chronic atrial fibrillation (AF). The objective of this study was to assess the factors influencing plasma BNP levels in patients with chronic AF and preserved left ventricular (LV) systolic function. Subjects and Methods:Transthoracic echocardiography was performed in 55 patients (25 men, 30 women; mean age 66.6± 11.5 years) with chronic AF. At the same time, plasma BNP was measured with a Triage kit (Biosite, San Diego, California). Results:Women, long duration of AF and hypertension were more prevalent in the highest quartile group of BNP levels than in the lowest quartile group of BNP levels. Significant correlations were observed between plasma BNP levels and the following: mitral E velocity (r=0.339), mitral annular E’-velocity (r=-0.396), ratio of mitral E-velocity and mitral annular E’ velocity (r=0.473), left atrium (LA) size (r=0.648), LA volume index (r=0.744), right atrium (RA) volume index (r=0.554), maximal velocity (Vmax) of mitral regurgitation (MR) (r=0.444), tricuspid regurgitation (TR) Vmax (r=0.544), MR grade (r=0.431), TR grade (r=0.427) and LV mass index (r=0.570). In stepwise multiple linear regression analysis, LA volume index (β=0.299, p=0.014), LV mass index (β=0.404, p<0.001) and duration of AF (β=0.488, p<0.001) independently predicted plasma BNP levels in this study subjects. The patients with increased LA volume index exhibited longer duration of AF, larger RA volume index and LV mass index, higher MR Vmax, TR Vmax, MR and TR grade and plasma BNP level. Conclusion:LA volume index, LV mass index and duration of AF were independent predictors of plama BNP level in patients with chronic AF and preserved LV systolic function. (Korean Circulation J 2005;35:605-612)

Plasma brain natriuretic peptide levels in patients with rheumatic heart disease

Brain natriuretic peptide (BNP) is a cardiac hormone secreted from the ventricular myocardium as a response to ventricular volume expansion and pressure overload. Rheumatic heart disease (RHD) is still an important cause of heart failure in developing countries. To measure BNP levels in patients with RHD and to determine whether BNP concentrations correlate with clinical and echocardiographic findings. Eighty-eight patients with rheumatic valve disease and 24 age- and sex-matched healthy subjects were entered in the study. BNP was measured using the Triage B-Type Natriuretic Peptide test (Biosite Diagnostics, San Diego, CA). Transthoracic echocardiography was performed in all patients to assess the severity of the valve disease and for the measurement of pulmonary artery pressure. The plasma concentrations of BNP were significantly higher in patients with rheumatic heart disease than in control subjects (232+/-294 vs. 14+/-12 pg/ml, p<0.0001). The plasma BNP level was significantly higher in NYHA class III+IV than in class II (463+/-399 vs. 192+/-243 pg/ml, p<0.0001) and in NYHA class II than in class I (192+/-243 vs. 112+/-135 pg/ml, p<0.001). The independent determinants of higher BNP levels were NYHA functional class and systolic pulmonary artery pressure in multivariate analysis. We found increased plasma BNP levels in patients with rheumatic heart disease compared with healthy subjects.

Diagnostic and prognostic value of plasma brain natriuretic peptide in non—dialysis-dependent CRF

Brain natriuretic peptide (BNP) is useful for the evaluation of ventricular dysfunction in patients with various cardiac diseases. However, its diagnostic value has been considered to be limited in patients with chronic renal failure (CRF) because renal dysfunction itself may affect BNP levels. This study is designed to clarify the diagnostic and prognostic value of plasma BNP level in patients with CRF. In 103 non-dialysis-dependent patients with CRF without heart failure and 60 hypertensive patients with normal renal function, echocardiographic examinations and BNP measurements were performed. Plasma BNP level was much greater in patients with CRF than in hypertensive controls; however, multiple regression analysis showed that left ventricular (LV) end-diastolic volume (EDV) index (LVEDVI) and the difference in mitral and pulmonary venous atrial wave duration (Ad-PVad), a marker of LV end-diastolic pressure, were independent determinants of plasma BNP levels in patients with CRF. The influence of LV overload (LVEDVI > or = 75 mL/m 2 and/or Ad-PVad < 0 milliseconds) on plasma BNP levels in subjects with CRF was independent of the severity of renal dysfunction. From Kaplan-Meier event-free curves (mean follow-up, 13 months), the incidence of heart failure was much greater in patients with a plasma BNP level of 150 pg/mL or greater ( P < 0.001). By means of multivariate Cox regression analysis, high plasma BNP level was the strongest predictor for heart failure events (hazard ratio, 6.31; P < 0.001). These findings support plasma BNP level as a reliable marker of LV overload, even in nondialysis patients with CRF. Also, a high BNP level (> or =150 pg/mL) may have powerful predictive potential for heart failure in these patients.

Increased Brain Natriuretic Peptide as a Marker for Right Ventricular Dysfunction in Acute Pulmonary Embolism

Right ventricular (RV) function is of major prognostic significance in patients with acute pulmonary embolism (PE). The aim of the present study was to evaluate the role of neurohormone plasma brain natriuretic peptide (BNP) in assessing RV function in patients with acute PE. BNP levels were measured in 16 consecutive patients with acute PE as diagnosed by high probability lung scintigraphy or pulmonary angiography. Twelve healthy age-matched volunteers served as controls. All 16 patients underwent standard echocardiography and blood tests during the first hour of presentation. In the patient group, survival was studied for a period of 30 days. Plasma BNP levels in patients with acute PE were higher than in controls (7.2 [95% CI 0.4 to 144.6] versus 1.4[95% CI 0.4 to 4.6] pmol/L, p = 0.0008). Plasma BNP was significantly higher in 5 patients with RV dysfunction compared to II patients with normal RV function (40.2 [95% CI 7.5 to 214.9] versus 3.3 [95% CI 0.4 to 24.9] pmol/L, p = 0.0003). RV systolic pressure was not significantly correlated with BNP (r = 0.42, p = ns). In conclusion, plasma BNP neurohormone levels might be of clinical importance as a supplementary tool for assessment of RV function in patients with acute PE.

Elevated plasma brain natriuretic peptide levels in chronic respiratory failure with cor pulmonale

Elevated plasma brain natriuretic peptide (BNP) levels have been described in patients with congestive heart failure and acute myocardial infarction. We measured plasma BNP levels in patients with chronic respiratory failure to evaluate the correlation between plasma BNP levels and pulmonary haemodynamics. Plasma BNP levels were measured in 28 patients with chronic respiratory failure accompanied by three underlying diseases [14 with chronic obstructive pulmonary disease (COPD), seven with sequelae of pulmonary tuberculosis (sequelae Tbc) and seven with diffuse panbronchiolitis (DPB)] by immunoradiometric assay methods (IRMA). Twenty-one of 28 patients had already received oxygen supplementation and 16 of 21 patients were treated as outpatients with home oxygen therapy. Plasma BNP levels were significantly elevated in patients with chronic respiratory failure complicated by cor pulmonale (81·5 ± 13·1 pg ml −1) compared to patients without cor pulmonale (13·3 ± 2·7 pg ml −1, P<0·001). As controls, plasma BNP levels in 10 patients with primary lung cancer were studied, and the results (3·5 ± 1·0 pg ml −1) were not significantly different from those of patients with chronic respiratory failure without cor pulmonale. Plasma BNP levels in 12 healthy subjects were also studied, and the results (7·2 ± 1·0 pg ml −1) were not significantly different from those of the control subjects. Plasma BNP levels showed a weak linear correlation with systolic pulmonary arterial blood pressure, estimated by Doppler echocardiography ( r=0·43; P=0·068), but there was no significant correlation between BNP levels and the degree of hypoxaemia ( r=0·30; P=0·138). Plasma atrial natriuretic peptide (ANP) levels in patients with chronic respiratory failure were also measured using the same samples. Plasma ANP levels were also significantly elevated in patients with chronic respiratory failure complicated by cor pulmonale (80·8 ± 12·1 pg ml −1) compared to patients without cor pulmonale (26·1 ± 4·4 pg ml −1, P=0·003). A significant correlation was found between plasma BNP and ANP levels ( r=0·68; P<0·001). Our results suggest that the plasma BNP or ANP level may be a useful indicator for detecting the presence of cor pulmonale in patients with chronic respiratory failure.

Interactions of atrial and brain natriuretic peptides at pathophysiological levels in normal men

Atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) are both circulating plasma hormones that are secreted by the heart and have similar physiological effects. We have shown previously that abrupt increases in plasma BNP in normal humans impair the clearance of ANP from plasma and result in additive physiological effects. Because large increases in plasma ANP are reported to have no effect on plasma BNP levels in patients with heart failure, we have studied ANP-BNP interactions in eight normal male subjects receiving background infusions of BNP (2 pmol.kg-1.min-1 for 5 h). Each subject also received a coinfusion of ANP ("active" day, 2 pmol.kg-1.min-1 for 2 h) or vehicle ("placebo" day) using a balanced random order, single-blind design. Metabolic clearance rate of ANP (mean 4.1 +/- 0.6 l/min) and disappearance rate from the plasma (t1/2 3.4 +/- 0.3 min) were similar to values measured previously in the absence of exogenous BNP. In contrast, steady-state plasma BNP levels were reversibly increased (mean BNP increment 10 pmol/l) during the administration of ANP (P = 0.038). Associated with these changes were significant (additive) physiological effects. Thus the addition of ANP increased plasma and urine guanosine 3',5'-cyclic monophosphate (P < 0.001 for both) and lowered systolic blood pressure (P = 0.049). When ANP was coinfused, significant differences were also observed in urine volume (P = 0.001) and sodium excretion (P = 0.043) between the infusion period (when urine volume and sodium excretion were enhanced) and postinfusion period (when values decreased). Taken together, our findings of similar interactions between ANP-BNP and BNP-ANP infusions occurring at pathophysiological concentrations of these two peptides, suggest that the interactions result from dissociation of prebound hormone, presumably from biological or clearance receptors.