CLINICAL RESEARCH: BNP AND HEART FAILURE
Obesity and suppressed B-type natriuretic peptide levels in heart failure
Mandeep R. Mehra, MD, FACC*,*,
Patricia A. Uber, PharmD*,
Myung H. Park, MD*,
Robert L. Scott, MD*,
Hector O. Ventura, MD, FACC*,
Bobbett C. Harris, RN* and
Edward D. Frohlich, MD, FACC*
* Department of Cardiovascular Medicine, Ochsner Clinic Foundation, New Orleans, Louisiana, USA
Manuscript received July 24, 2003;
revised manuscript received October 6, 2003,
accepted October 7, 2003.
* Reprint requests and correspondence: Dr. Mandeep R. Mehra, 1514 Jefferson Highway, New Orleans, Louisiana 70121, USA.
mmehra{at}ochsner.org
 |
Abstract
|
|---|
OBJECTIVES: This investigation evaluated the relationship between obesity and B-type natriuretic peptide (BNP) in heart failure.
BACKGROUND: Obesity is a major risk factor for the development of heart failure, but the precise mechanisms remain uncertain. Physiologically, natriuretic peptides and lipolysis are closely linked.
METHODS: A total of 318 patients with heart failure were evaluated between June 2001 and June 2002. Levels of BNP were compared in obese (body mass index [BMI]  30 kg/m2) and nonobese (BMI <30 kg/m2) patients with respect to New York Heart Association functional class and lean body weight–adjusted peak aerobic oxygen consumption. In a subset of 36 patients, plasma levels of tumor necrosis factor-alpha, interleukin-6, and soluble intercellular adhesion molecule-1 were measured.
RESULTS: The population's BMI was 29.4 ± 6.6 kg/m2; 24% were lean (BMI <25 kg/m2), 31% overweight (BMI 25 to 29.9 kg/m2), and 45% obese (BMI 30 kg/m2). Obese patients were younger, more often African American, and more likely to have a history of antecedent hypertension, but less likely to have coronary artery disease and with only a trend toward diabetes mellitus. Levels of BNP were significantly lower in obese than in nonobese subjects (205 ± 22 and 335 ± 39 pg/ml, respectively; p = 0.0007), despite a similar severity of heart failure and cytokine levels. Multivariate regression analysis identified BMI as an independent negative correlate of BNP level. There were no differences in emergency department visits, heart failure hospitalization, or death between the obese and nonobese patients at 12-month follow-up.
CONCLUSIONS: Our investigation indicates that a state of reduced natriuretic peptide level exists in the obese individual with heart failure.
|
Abbreviations and Acronyms
| | BMI | = body mass index | | BNP | = B-type natriuretic peptide | | CHF | = chronic heart failure | | CI | = confidence interval | | CPX | = cardiopulmonary stress testing | | LV | = left ventricular | | LVEF | = left ventricular ejection fraction | | NYHA | = New York Heart Association | | VO2 | = oxygen consumption |
|
The role of natriuretic peptides in the clinical expression of chronic heart failure (CHF) has been established (1). Contemporary investigations have correlated the levels of circulating B-type natriuretic peptide (BNP) with the severity of heart failure, and it can provide incremental refinement for improving the diagnosis of heart failure (1,2). Other studies have alluded to variations in the expression of this hormone as a function of age, gender, and renal dysfunction (3,4).
The influence of obesity on the development of cardiovascular disease has also been well established (5). In particular, obesity is a known factor that has an impact on systolic and diastolic ventricular function and has also been identified as a major risk factor for the development of coronary artery disease and heart failure (6–8). Physiologically, natriuretic peptides and lipolysis have been closely linked, and adipose tissues are intimately related to the natriuretic clearance receptor (9,10). Hence, this raises the possibility that the pathophysiologic mechanisms underlying the relationship between obesity and cardiovascular disease outcomes could at least partially be related to the impact of natriuretic peptides (9,10).
Therefore, we hypothesized that the state of obesity and heart failure could be associated with alterations in the peripheral expression of natriuretic peptides. Thus, this investigation was designed to evaluate the relationship between obesity and circulating levels of BNP.
|
Methods
|
|---|
Study design.
A total of 318 patients with CHF were evaluated in our heart failure center between June 2001 and June 2002. All patients received a careful history and physical examination by a heart failure specialist physician who was blinded to BNP data. To be included in this analysis, patients had to have CHF (with or without obesity) for at least six months and receive stable doses of their medications with no recent increases in symptoms or the need for intravenous medication support for at least six weeks before evaluation. Thus, this cohort did not selectively comprise those with obesity-induced heart failure. Those patients with an acute coronary syndrome, new-onset atrial arrhythmia, percutaneous or surgical coronary revascularization or other cardiac surgery, or severe renal dysfunction (serum creatinine >3.0 mg/dl or current dialysis) within the previous three months were likewise excluded. The severity of CHF was categorized by New York Heart Association (NYHA) functional class criteria, as well as by performance of cardiopulmonary stress testing (CPX) in order to establish peak aerobic capacity in all patients. Detailed demographic variables and clinical data were collected at the time of study performance. Additionally, a subgroup of patients underwent evaluation of pro-inflammatory cytokines in order to assess the status of CHF with BNP levels and obesity. Our Institutional Review Board approved the study.
Measurement of BNP.
The bioactive BNP level was analyzed at the time of clinical assessment. For each BNP measurement, 5 ml of whole blood was collected into tubes containing potassium EDTA (1 mg/ml blood) and measured using the Triage BNP test (Biosite Diagnostics Inc., San Diego, California). This test is a fluorescence immunoassay for the quantitative determination of BNP in whole blood and plasma specimens. The turnaround time for the assay is 15 to 20 min.
Assessment of obesity parameters, CPX, and echocardiography.
Obesity was defined on the basis of a body mass index (BMI) of 30 kg/m2. Levels of BNP were compared in the obese and nonobese (BMI <30 kg/m2) patients with respect to NYHA functional class and lean body weight–adjusted peak aerobic oxygen consumption (VO2). Cardiopulmonary stress testing was accomplished using a ramping treadmill protocol, and breath-to-breath on-line gas analysis was performed using a MedGraphics CPXID metabolic cart (St. Paul, Minnesota). Incremental data, including minute ventilation, VO2, and carbon dioxide production, were collected, and maximal VO2, anaerobic threshold, and respiratory exchange ratio were calculated. Oxygen consumption was corrected for body fat and was reported as lean body mass–adjusted VO2, as we reported previously (11). Echocardiography was performed in all patients and interpreted by investigators blinded to the clinical data and BNP data. Renal function was evaluated by using serum creatinine measurements (mg/dl) and by the calculated glomerular filtration rate.
Cytokine substudy.
In a subset of 36 patients with NYHA class III heart failure, we measured plasma levels of tumor necrosis factor-alpha, interleukin-6, and soluble intercellular adhesion molecule-1 by means of enzyme-linked immunoassay. These cytokines were determined in obese and nonobese patients who were matched with respect to the clinical severity of heart failure, left ventricular ejection fraction (LVEF), peak exercise VO2, and medications used.
Outcomes analysis.
We also evaluated the combined end points of emergency department visits or hospitalizations for CHF or death in obese heart failure patients compared with nonobese subjects at 12 months after study entry.
Statistical analysis.
Normally distributed data are reported as the mean value ± SD. Categorical variables were compared using the likelihood ratio chi-square test. With continuous variables, group mean values were compared using the unpaired Student t test, as long as the variables were normally distributed within each group and the variation of scores in the two groups were not reliably different. The normality assumption was evaluated by examining the distribution of data (via histograms). If the data distribution did not follow the normality assumption, the Wilcoxon rank-sum test was utilized. Further multivariate analyses were performed to evaluate the independent relationship of BMI and BNP levels in concert with demographic variables (age, race, and gender), structural cardiac functional indexes (LVEF and LV end-diastolic diameter), severity of heart failure (NYHA class, lean peak VO2), and renal function. Cox proportional hazard regression analysis was used to determine the independent predictors of event-free survival and included BMI, age, gender, ischemic versus nonischemic cardiomyopathy, functional classification, LVEF, renal function, BNP levels, and peak VO2. All analyses were performed using StatView version 4.5 (Abacus Concepts Inc., Berkeley, California), and statistical significance was set at p < 0.05.
|
Results
|
|---|
Patients.
The study included 318 consecutive patients (age 57 ± 14 years; 57% men; 53% white) with CHF (LVEF 31 ± 17%). All patients received maximal treatment using conventional therapy. Thus, 89% received angiotensin-converting enzyme inhibitors or angiotensin receptor blockers and 71% received beta-blockers. All received diuretics to "dry" weight. The total population's BMI was 29.4 ± 6.6 kg/m2; 24% were lean (BMI <25 kg/m2), 31% overweight (BMI 25–29.9 kg/m2), and 45% obese (BMI 30 kg/m2). Obese patients with CHF were younger, more often African American, and more likely to have a history of antecedent hypertension, but less likely to have coronary artery disease and with only a trend toward diabetes mellitus (Table 1).
Comparison of BNP levels in obese and nonobese patients.
Levels of BNP were significantly lower in obese than in nonobese subjects (205 ± 22 and 335 ± 39 pg/ml, respectively; p = 0.0007). These differences persisted even when the patients were regrouped into lean (BNP 366 ± 47 pg/ml), overweight (BNP 309 ± 34 pg/ml), or obese (BNP 205 ± 22 pg/ml, p < 0.01 for trend). However, there was no significance between the lean and overweight groups (p = 0.3), although the BNP level in overweight versus obese subjects was significantly less (p = 0.009). Thus, the group of overweight subjects was similar to the lean group with regard to BNP levels (Figs. 1A and B), but the differences in BNP levels between the obese and nonobese groups persisted even though they had a similar functional class. Thus, the LVEF, VO2 corrected for lean body mass, serum creatinine, and glomerular filtration rate were similar between the two groups. To further evaluate the influence of age and its possible interaction with BNP levels in the context of obesity, we divided the cohort into the elderly (65 years old) and nonelderly (<65 years old) and found that the relationship of obesity and decreased BNP levels persisted. Thus, the elderly obese patients had 28% lower BNP levels compared with elderly nonobese patients (BNP 290 ± 50 vs. 405 ± 48 pg/ml, p = 0.03). Similarly, the younger (<65 years old) obese patients demonstrated 40% lower BNP levels compared with younger nonobese patients (175 ± 24 vs. 294 ± 35 pg/ml, p = 0.006). No significant interaction of diabetes mellitus as a determinant of BNP levels in the obese and nonobese subjects was noted. Regression analysis of BNP levels and BMI as a continuous variable revealed a weak but significantly inverse relationship between the two variables (r = –0.36, p = 0.002) (Fig. 2).
View larger version (14K):
[in this window]
[in a new window]
|
Figure 1 (A) Obese patients have lower circulating levels of B-type natriuretic peptide (BNP) compared with both lean and overweight patients with heart failure. (B) Difference in circulating levels of BNP in obese and nonobese patients (lean and overweight).
|
|
View larger version (26K):
[in this window]
[in a new window]
|
Figure 2 This figure depicts the raw data demonstrating a significant inverse correlation between circulating B-type natriuretic peptide (BNP) levels and body mass index (BMI).
|
|
Multivariable predictors of BNP levels.
Multivariate regression analysis identified BMI as an independent negative correlate of BNP levels (t = –3.428, p = 0.0007). Other independent correlates included age (t = 3.001, p = 0.0003), female gender (t = 2.584, p = 0.01), serum creatinine concentration (t = 3.677, p = 0.0003), NYHA class (t = 4.731, p = 0.0001), and LVEF (t = –3.430, p = 0.0007). In particular, we did not find any significant independent influence of diabetes mellitus on BNP levels.
Cytokine substudy findings.
Although BNP levels were significantly lower in the obese (n = 16, 305 ± 124 pg/ml) versus nonobese (n = 20, 510 ± 141 pg/ml, p = 0.01 by Wilcoxon rank-sum test) comparison, there were no differences (p = NS by Wilcoxon rank-sum test) in the three cytokines between these subgroups (Table 2). These findings suggest that the differences in BNP levels in obese patients were not related to differences in circulating levels of pro-inflammatory cytokines.
Outcomes.
There were no significant differences in the time to first event (emergency department visit or hospitalization for CHF or death) between the obese and nonobese patients (Fig. 3). Moreover, the event rate for the entire cohort at one year was 27%, and this was not different between the obese (25%) and nonobese (29%) patients. In a Cox proportional hazards model stratified by obese and nonobese patients and including age (95% confidence interval [CI] 0.97 to 1.02), female gender (95% CI 0.68 to 2.8), LVEF (95% CI 0.97 to 1.01), serum creatinine (95% CI 0.73 to 1.7), and BNP level (95% CI 0.99 to 1.01) as covariates, there were no significant interactions noted. Only a higher NYHA class predicted a worse survival (CI 1.17 to 2.9, p = 0.02).
View larger version (16K):
[in this window]
[in a new window]
|
Figure 3 No difference in emergency department visits, heart failure hospitalization, or death between obese (triangles) and nonobese (circles) patients at 12-month follow-up was noted in the obese and nonobese patients with heart failure.
|
|
|
Discussion
|
|---|
This study demonstrates that obesity is an important and independent determinant of peripheral BNP expression in patients with CHF. The implications of these findings not only extend to the usefulness of BNP as a diagnostic test in obese patients with heart failure, but also provide important insight into certain potential underlying pathophysiologic mechanisms that relate to the development of heart failure in obese patients. Thus, patients with obesity, even before development of heart failure, have an expanded intravascular (plasma) volume associated with an increased cardiopulmonary volume (6). Several recent studies have shown that natriuretic peptide levels are reduced in the obese state, partly related to altered clearance receptors and peptide degradation (9,10). These lines of evidence, coupled with our findings, provide endorsement for the presence of a reduced natriuretic response in the state of obesity. The suggestion that there may be increased clearance of BNP by adipose tissue raises the interesting possibility that there may be early loss of natriuretic-mediated vasodilation, lesser antagonism of the rennin-angiotensin system, or loss of natriuretic ability in obese patients.
Several investigations have alluded to obesity as a major risk factor for the development of heart failure (5–8),regardless of gender (8). Why the heart fails as a result of obesity continues to be a matter of intense investigative scrutiny. Several lines of evidence have pointed to hemodynamic overload, lipoapoptosis, impaired fatty acid oxidation, or the concerted effects of diffuse vascular damage, which are present early in childhood (12–15). Obesity is associated with an increased prevalence of most cardiovascular risk factors, including systemic hypertension, diabetes mellitus, hyperlipidemia, and LV hypertrophy (16). Moreover, because of coexistent volume overload with obesity and pressure overload with frequent hypertension, eccentric and concentric LV hypertrophy is expected (6). Our study supports this notion, as obese heart failure patients were younger and had a more prevalent history of hypertension and perhaps diabetes mellitus. Nevertheless, the precise mechanisms linking obesity to heart failure remain unresolved.
As already suggested, the natriuretic peptide system and adiposity are closely linked. Lipolysis is mediated by catecholamines (stimulation of lipolysis) and insulin (inhibition of lipolysis) (17). More recently, natriuretic peptides have been shown to be important stimuli for lipolysis in humans and similar in potency to catecholamines (18). Furthermore, since adipose cells express the natriuretic clearance receptor (19), in obese patients, a state of reduced natriuretic peptide concentration could occur, explaining the increased sodium retention and volume expansion characteristic of obesity-related hypertension (6). Fasting and weight loss are known to decrease expression of adipose cellular natriuretic peptide clearance receptors (20). Conversely, obesity is common after menopause, and it has been suggested that the decreased availability of circulating natriuretic peptides due to increased expression of the natriuretic clearance receptor could explain, at least in part, the increase in cardiovascular disease after menopause (21). Our study lends credence to these potential mechanisms and suggests that one possible explanation for the earlier expression of heart failure in the presence of obesity could be related to reduced circulating natriuretic peptides.
Thus, a paradox has emerged in the obese patient. On one hand, heart failure is increased in obese patients, but alternatively, a survival advantage in heart failure has been reported (22–24). Several lines of evidence have been suggested for diminished activation of natriuretic peptides, enhanced protection against endotoxin/inflammatory cytokines, and increased nutritional and metabolic reserve. All of these possibilities may explain the observation of better survival in obese patients with heart failure (25–28). As noted in our study, event-free survival was not different in obese and nonobese heart failure patients. Other studies have demonstrated this apparent obesity paradox by including patients with severe heart failure and cardiac cachexia. In the current study, no differences in the circulating pro-inflammatory cytokines were found, and the severity of heart failure (as evaluated by lean body weight–adjusted VO2) was similar in obese and nonobese patients. These observations suggest that the lower levels of natriuretic peptides in obesity did not confer a more favorable prognosis. This finding lends further credence to the concept that a state of reduced BNP level exists in obese patients with heart failure.
Conclusions.
Obesity is associated with significantly lower peripheral expression of natriuretic peptides in heart failure. Our investigation indicates that a state of reduced natriuretic peptide level exists in the obese individual with heart failure.
|
Acknowledgments
|
|---|
We are indebted to Barbara Siede for graphic assistance.
|
Footnotes
|
|---|
Dr. Mehra has served as a consultant to Biosite Diagnostics, Inc., the makers of the BNP assay used in this study. However, this potential conflict has in no way biased the author's viewpoint. Dr. Mitchell Finkel acted as Guest Editor of this paper.
|
References
|
|---|
- Adams KF Jr., Mathur VS, Gheorghiade M. B-type natriuretic peptide: from bench to bedside. Am Heart J. 2003;145(Suppl):34–46
- Maisel AS, Krishnaswamy P, Nowak RM, et al. Rapid measurement of B-type natriuretic peptide in the emergency diagnosis of heart failure. N Engl J Med. 2002;347:161–167[Abstract/Free Full Text]
- Redfield MM, Rodeheffer RJ, Jacobsen SJ, Mahoney DW, Bailey KR, Burnett JC Jr. Plasma brain natriuretic peptide concentration: impact of age and gender. J Am Coll Cardiol. 2002;40:976–982[Abstract/Free Full Text]
- Breathing Not Properly Multinational Study InvestigatorsMcCullough PA, Duc P, Omland T, et al. B-type natriuretic peptide and renal function in the diagnosis of heart failure: an analysis from the Breathing Not Properly Multinational Study. Am J Kidney Dis. 2003;41:571–579[CrossRef][Medline]
- Hubert HB, Feinleib M, McNamara PM, Castelli WP. Obesity as an independent risk factor for cardiovascular disease: a 26-year follow-up of participants in the Framingham Heart Study. Circulation. 1983;67:968–977[Abstract/Free Full Text]
- Frohlich ED, Messerli FH, Reisin E, Dunn FG. The problem of obesity and hypertension. Hypertension. 1983;5 Suppl:III71–78
- Alpert MA, Lambert CR, Panayiotou H, et al. Relation of duration of morbid obesity to left ventricular mass, systolic function, and diastolic filling, and effect of weight loss. Am J Cardiol. 1995;76:1194–1197[CrossRef][Medline]
- Kenchaiah S, Evans JC, Levy D, et al. Obesity and the risk of heart failure. N Engl J Med. 2002;347:358–359[Free Full Text]
- Sarzani R, Dessi-Fulgheri P, Paci VM, Espinosa E, Rappelli AJ. Expression of natriuretic peptide receptors in human adipose and other tissues. J Endocrinol Invest. 1996;19:581–585[Medline]
- Sengenes C, Berlan M, De Glisezinski I, Lafontan M, Galitzky J. Natriuretic peptides: a new lipolytic pathway in human adipocytes. FASEB J. 2000;14:1345–1351[Abstract/Free Full Text]
- Osman AF, Mehra MR, Lavie CJ, Nunez E, Milani RV. Incremental prognostic importance of body fat adjusted peak oxygen consumption in chronic heart failure. J Am Coll Cardiol. 2000;36:2126–2131[Abstract/Free Full Text]
- Messerli FH, Sundgaard-Riise K, Reisin ED, et al. Dimorphic cardiac adaptation to obesity and arterial hypertension. Ann Intern Med. 1983;99:757–761[Medline]
- Zhou YT, Grayburn P, Karim A, et al. Lipotoxic heart disease in obese rats: implications for human obesity. Proc Natl Acad Sci USA. 2000;97:1784–1789[Abstract/Free Full Text]
- Young ME, Guthrie PH, Razeghi P, et al. Impaired long-chain fatty acid oxidation and contractile dysfunction in the obese Zucker rat heart. Diabetes. 2002;51:2587–2595[Abstract/Free Full Text]
- Haszon I, Papp F, Kovacs J, et al. Platelet aggregation, blood viscosity and serum lipids in hypertensive and obese children. Eur J Pediatr. 2003;162:385–390[Medline]
- The National Task Force on the Prevention and Treatment of Obesity. Overweight, obesity, and health risk. Arch Intern Med. 2000;160:898–904[Abstract/Free Full Text]
- Kalra PR, Tigas S. Regulation of lipolysis: natriuretic peptides and the development of cachexia. Int J Cardiol. 2002;85:125–132[CrossRef][Medline]
- Lafontan M, Berlan M, Stich V, et al. Recent data on the regulation of lipolysis by catecholamines and natriuretic peptides. Ann Endocrinol. 2002;63:86–90[Medline]
- Dessi-Fulgheri P, Sarzani R, Rappelli A. The natriuretic peptide system in obesity-related hypertension: new pathophysiological aspects. J Nephrol. 1998;11:296–299[Medline]
- Sarzani R, Paci VM, Zingaretti CM, et al. Fasting inhibits natriuretic peptides clearance receptor expression in rat adipose tissue. J Hypertens. 1995;13:1241–1246[CrossRef][Medline]
- Rappelli A. Hypertension and obesity after the menopause. J Hypertens. 2002;20(Suppl 2):26–28
- Horwich TB, Fonarow GC, Hamilton MA, MacLellan WR, Woo MA, Tillisch JH. The relationship between obesity and mortality in patients with heart failure. J Am Coll Cardiol. 2001;38:789–795[Abstract/Free Full Text]
- Lavie CJ, Osman AF, Milani RV, Mehra MR. Body composition and prognosis in chronic systolic heart failure: the obesity paradox. Am J Cardiol. 2003;91:891–894[CrossRef][Medline]
- Mosterd A, Cost B, Hoes AW, et al. The prognosis of heart failure in the general population: the Rotterdam Study. Eur Heart J. 2001;22:1318–1327[Abstract/Free Full Text]
- Ross C, Langer RD, Barrett-Connor E. Given diabetes, is fat better than thin? Diabetes Care. 1997;20:650–652[Abstract]
- Mohamed-Ali V, Goodrick S, Bulmer K, et al. Production of soluble tumor necrosis factor receptors by human subcutaneous adipose tissue in vivo. Am J Physiol. 1999;277:E971–975[Medline]
- Weber MA, Neutel JM, Smith DHG. Contrasting clinical properties and exercise responses in obese and lean hypertensive patients. J Am Coll Cardiol. 2001;37:169–174[Abstract/Free Full Text]
- Anker SD, Ponikowski P, Varney S, et al. Wasting as independent risk factor for mortality in chronic heart failure. Lancet. 1997;349:1050–1053[CrossRef][Medline]
This article has been cited by other articles:
|
|
|
|
 
L. Frankenstein, A. Remppis, M. Nelles, B. Schaelling, D. Schellberg, H. Katus, and C. Zugck
Relation of N-terminal pro-brain natriuretic peptide levels and their prognostic power in chronic stable heart failure to obesity status
Eur. Heart J.,
November 1, 2008;
29(21):
2634 - 2640.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
L Ingle, J G F Cleland, and A L Clark
Perception of symptoms is out of proportion to cardiac pathology in patients with "diastolic heart failure"
Heart,
June 1, 2008;
94(6):
748 - 753.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
E. D. Abel, S. E. Litwin, and G. Sweeney
Cardiac Remodeling in Obesity
Physiol Rev,
April 1, 2008;
88(2):
389 - 419.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
L. B. Daniels and A. S. Maisel
Natriuretic Peptides
J. Am. Coll. Cardiol.,
December 18, 2007;
50(25):
2357 - 2368.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
S. Kenchaiah, S. J. Pocock, D. Wang, P. V. Finn, L. A.M. Zornoff, H. Skali, M. A. Pfeffer, S. Yusuf, K. Swedberg, E. L. Michelson, et al.
Body Mass Index and Prognosis in Patients With Chronic Heart Failure: Insights From the Candesartan in Heart failure: Assessment of Reduction in Mortality and morbidity (CHARM) Program
Circulation,
August 7, 2007;
116(6):
627 - 636.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
T. Tsutamoto, T. Tanaka, H. Sakai, C. Ishikawa, M. Fujii, T. Yamamoto, and M. Horie
Total and high molecular weight adiponectin, haemodynamics, and mortality in patients with chronic heart failure
Eur. Heart J.,
July 2, 2007;
28(14):
1723 - 1730.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
A. Meirhaeghe, M. S. Sandhu, M. I. McCarthy, P. de Groote, D. Cottel, D. Arveiler, J. Ferrieres, C. J. Groves, A. T. Hattersley, G. A. Hitman, et al.
Association between the T-381C polymorphism of the brain natriuretic peptide gene and risk of type 2 diabetes in human populations
Hum. Mol. Genet.,
June 1, 2007;
16(11):
1343 - 1350.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
G. Kwan, S. R. Isakson, J. Beede, P. Clopton, A. S. Maisel, and R. L. Fitzgerald
Short-Term Serial Sampling of Natriuretic Peptides in Patients Presenting With Chest Pain
J. Am. Coll. Cardiol.,
March 20, 2007;
49(11):
1186 - 1192.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
T. J. Wang, M. G. Larson, M. J. Keyes, D. Levy, E. J. Benjamin, and R. S. Vasan
Association of Plasma Natriuretic Peptide Levels With Metabolic Risk Factors in Ambulatory Individuals
Circulation,
March 20, 2007;
115(11):
1345 - 1353.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
A. Bayes-Genis, D. M. Lloyd-Jones, R. R. J. van Kimmenade, J. G. Lainchbury, A. M. Richards, J. Ordonez-Llanos, M. Santalo, Y. M. Pinto, and J. L. Januzzi Jr
Effect of Body Mass Index on Diagnostic and Prognostic Usefulness of Amino-Terminal Pro-Brain Natriuretic Peptide in Patients With Acute Dyspnea
Arch Intern Med,
February 26, 2007;
167(4):
400 - 407.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
A. Y. Chang, S. M. Abdullah, T. Jain, H. G. Stanek, S. R. Das, D. K. McGuire, R. J. Auchus, and J. A. de Lemos
Associations Among Androgens, Estrogens, and Natriuretic Peptides in Young Women: Observations From the Dallas Heart Study
J. Am. Coll. Cardiol.,
January 2, 2007;
49(1):
109 - 116.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
I J Bujalska, M Quinkler, J W Tomlinson, C T Montague, D M Smith, and P M Stewart
Expression profiling of 11{beta}-hydroxysteroid dehydrogenase type-1 and glucocorticoid-target genes in subcutaneous and omental human preadipocytes.
J. Mol. Endocrinol.,
October 1, 2006;
37(2):
327 - 340.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
S. Jelic and T. H. Le Jemtel
Diagnostic Usefulness of B-Type Natriuretic Peptide and Functional Consequences of Muscle Alterations in COPD and Chronic Heart Failure.
Chest,
October 1, 2006;
130(4):
1220 - 1230.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
G. M. Felker, J. W. Petersen, and D. B. Mark
Natriuretic peptides in the diagnosis and management of heart failure.
Can. Med. Assoc. J.,
September 12, 2006;
175(6):
611 - 617.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
J. V. St. Peter, G. G. Hartley, M. M. Murakami, and F. S. Apple
B-Type Natriuretic Peptide (BNP) and N-Terminal Pro-BNP in Obese Patients without Heart Failure: Relationship to Body Mass Index and Gastric Bypass Surgery
Clin. Chem.,
April 1, 2006;
52(4):
680 - 685.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
R. van Kimmenade, F. van Dielen, J. Bakker, J. Nijhuis, H. Crijns, W. Buurman, M. van Dieijen-Visser, J.-W. Greve, and Y. Pinto
Is Brain Natriuretic Peptide Production Decreased in Obese Subjects?
J. Am. Coll. Cardiol.,
February 21, 2006;
47(4):
886 - 887.
[Full Text]
[PDF]
|
|
|
|
|
|
|
A. Nohria and M. M. Givertz
B-Type Natriuretic Peptide and the Stressed Heart
J. Am. Coll. Cardiol.,
February 21, 2006;
47(4):
749 - 751.
[Full Text]
[PDF]
|
|
|
|
|
|
|
S. E. Litwin
The Growing Problem of Obesity and the Heart: The Plot "Thickens"
J. Am. Coll. Cardiol.,
February 7, 2006;
47(3):
617 - 619.
[Full Text]
[PDF]
|
|
|
|
|
|
|
L. C. Costello-Boerrigter, G. Boerrigter, M. M. Redfield, R. J. Rodeheffer, L. H. Urban, D. W. Mahoney, S. J. Jacobsen, D. M. Heublein, and J. C. Burnett Jr
Amino-Terminal Pro-B-Type Natriuretic Peptide and B-Type Natriuretic Peptide in the General Community: Determinants and Detection of Left Ventricular Dysfunction
J. Am. Coll. Cardiol.,
January 17, 2006;
47(2):
345 - 353.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
T. B. Horwich, M. A. Hamilton, and G. C. Fonarow
B-Type Natriuretic Peptide Levels in Obese Patients With Advanced Heart Failure
J. Am. Coll. Cardiol.,
January 3, 2006;
47(1):
85 - 90.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
C. Bionda, C. Bergerot, D. Ardail, C. Rodriguez-Lafrasse, and R. Rousson
Plasma BNP and NT-proBNP Assays by Automated Immunoanalyzers: Analytical and Clinical Study
Ann. Clin. Lab. Sci.,
January 1, 2006;
36(3):
299 - 306.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
R. Talens-Visconti, M. Rivera Otero, M. J. Sancho-Tello, F. G. de Burgos, L. Martinez-Dolz, B. Sevilla, V. Climent, R. Cortes, A. Salvador, F. Sogorb, et al.
Left ventricular cavity area reflects N-terminal pro-brain natriuretic peptide plasma levels in heart failure
Eur J Echocardiogr,
January 1, 2006;
7(1):
45 - 52.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
A. Clerico, F. A. Recchia, C. Passino, and M. Emdin
Cardiac endocrine function is an essential component of the homeostatic regulation network: physiological and clinical implications
Am J Physiol Heart Circ Physiol,
January 1, 2006;
290(1):
H17 - H29.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
S. R. Das, M. H. Drazner, D. L. Dries, G. L. Vega, H. G. Stanek, S. M. Abdullah, R. M. Canham, A. K. Chung, D. Leonard, F. H. Wians Jr, et al.
Impact of Body Mass and Body Composition on Circulating Levels of Natriuretic Peptides: Results From the Dallas Heart Study
Circulation,
October 4, 2005;
112(14):
2163 - 2168.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
M. Lafontan, C. Moro, C. Sengenes, J. Galitzky, F. Crampes, and M. Berlan
An Unsuspected Metabolic Role for Atrial Natriuretic Peptides: The Control of Lipolysis, Lipid Mobilization, and Systemic Nonesterified Fatty Acids Levels in Humans
Arterioscler. Thromb. Vasc. Biol.,
October 1, 2005;
25(10):
2032 - 2042.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
M. H. Olsen, T. W. Hansen, M. K. Christensen, F. Gustafsson, S. Rasmussen, K. Wachtell, K. Borch-Johnsen, H. Ibsen, T. Jorgensen, and P. Hildebrandt
N-Terminal Pro Brain Natriuretic Peptide Is Inversely Related to Metabolic Cardiovascular Risk Factors and the Metabolic Syndrome
Hypertension,
October 1, 2005;
46(4):
660 - 666.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
Developed in Collaboration With the American Colle, Endorsed by the Heart Rhythm Society, S. A. Hunt, W. T. Abraham, M. H. Chin, A. M. Feldman, G. S. Francis, T. G. Ganiats, M. Jessup, M. A. Konstam, et al.
ACC/AHA 2005 Guideline Update for the Diagnosis and Management of Chronic Heart Failure in the Adult--Summary Article: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Update the 2001 Guidelines for the Evaluation and Management of Heart Failure)
J. Am. Coll. Cardiol.,
September 20, 2005;
46(6):
1116 - 1143.
[Full Text]
[PDF]
|
|
|
|
|
|
|
C. Kistorp, J. Faber, S. Galatius, F. Gustafsson, J. Frystyk, A. Flyvbjerg, and P. Hildebrandt
Plasma Adiponectin, Body Mass Index, and Mortality in Patients With Chronic Heart Failure
Circulation,
September 20, 2005;
112(12):
1756 - 1762.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
Top
Abstract
Methods