Exercise release of cardiac natriuretic peptides is markedly enhanced when patients with coronary artery disease are treated medically by beta-blockers

Marie, Pierre-Yves; Mertès, Paul-Michel; Hassan-Sebbag, Nathalie; Talence, Nicole de; Djaballah, Karim; Djaballah, W.; Friberg, Johan; Olivier, Pierre; Karcher, Gilles; Zannad, F.; Bertrand, Alain

doi:10.1016/j.jacc.2003.07.047

Cited by 42 publications

(32 citation statements)

References 33 publications

(38 reference statements)

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“…The effect of BB on plasma NP has been reported in population-based studies, 15 in healthy control subjects, 16 during exercise, in hypertension, 17,18 in coronary disease, 19 and in HF. 20 -30 The reported responses are widely divergent, presumably reflecting differences between specific ␤-blockers and the effects of dose and duration of treatment and clinical state.…”

Section: Clinical Perspective P 985mentioning

confidence: 97%

Introduction of Metoprolol Increases Plasma B-Type Cardiac Natriuretic Peptides in Mild, Stable Heart Failure

et al. 2006

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Background-The effect of ␤-blockade on the cardiac natriuretic peptides is poorly understood but could contribute to their beneficial treatment effect and may be relevant to clinical use of plasma brain natriuretic peptide (BNP)/N-terminal pro brain natriuretic peptide (NTproBNP) measurements in risk stratification and in titration of anti-heart failure therapy. Methods and Results-Sixteen men with mild, stable heart failure (NYHA class II to III; left ventricular ejection fraction Ͻ40%) underwent serial blood sampling for plasma natriuretic peptide levels and received infusions of atrial natriuretic peptide (ANP) and BNP before and 6 weeks after the introduction and uptitration of metoprolol or 6 weeks unchanged therapy in a randomized, parallel-group design. Plasma natriuretic peptides (BNP, NTproBNP, ANP, and NTproANP) were increased by metoprolol (PϽ0.01 for all). The natriuretic responses to ANP and BNP infusions were sustained with the introduction of metoprolol despite reduced renal perfusion pressure. The levels of the noninfused natriuretic peptide were increased by both ANP and BNP infusions, and this effect was enhanced by metoprolol. The early plasma half-life (t 1 ⁄2␣) of BNP was prolonged by metoprolol (5.6Ϯ0.45 to 11Ϯ1.3 versus 5.7Ϯ0.8 to 6.6Ϯ1.3 minutes in control subjects; Pϭ0.019). Conclusions-Plasma cardiac natriuretic peptide levels increase significantly with the introduction of metoprolol in heart failure as a result of effects on secretion and clearance. Natriuretic responses to NP infusions are sustained with ␤-blockade despite reduced renal perfusion pressure. Clinicians should be aware that the introduction of metoprolol causes a rise in plasma BNP/NTproBNP that is unrelated to deterioration in clinical status and must be considered when measurements are undertaken for risk stratification or titration of treatment.

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Section: Clinical Perspective P 985mentioning

confidence: 97%

Introduction of Metoprolol Increases Plasma B-Type Cardiac Natriuretic Peptides in Mild, Stable Heart Failure

et al. 2006

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“…On the other hand, some older in vivo studies indicate the opposite, that b-adrenergic stimulation ''alone'' is not an important stimulus for release of ANP in vivo (Lachance and Garcia, 1991;Rankin et al, 1987;Ruskoaho et al, 1989). Regarding the plasma levels of ANP, a recent study has shown that patients with chronic coronary artery disease exhibit higher plasma levels of ANP when exercising and when their treatment includes bblockers compared to exercising patients with no bblocking treatments (Marie et al, 2004). Hence, it seems unclear whether adrenergic nerves have stimulatory or inhibitory effects on the ANP expression and/ or release in the heart.…”

Section: Importance Of the Natriuretic Peptide Receptorsmentioning

confidence: 99%

Receptor binding occurrence and plasma levels of natriuretic peptides in response to sympathectomy

Hansson

2005

Microsc. Res. Tech.

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In the present investigation the relationship between the sympathetic nervous system and the endocardial levels of receptor binding sites for natriuretic peptides and the plasma content of atrial natriuretic peptide were analyzed in rats. In order to destruct the cardiac sympathetic nerve terminals, chemical sympathectomy with 6-hydroxydopamine was made in parallel with intravenous measurements of blood pressure and heart frequency. By use of immunohistochemical and enzyme-linked-immunosorbent techniques the expression of tyrosine hydroxylasepositive sympathetic nerve terminals and plasma levels of pro-atrial natriuretic peptide were determined, respectively. The occurrence of receptor binding sites for natriuretic peptides was examined by in vitro receptor autoradiography. In contrast to the marked occurrence of natriuretic peptide receptor binding sites seen in the ventricular endocardium of control rats, the sympathectomized rats exhibited a decreased number of binding sites for natriuretic peptides in the endocardium of both the right and left chambers. Interestingly, this was found in parallel with a significant decrease of systolic and diastolic blood pressure and increased plasma levels of pro-atrial natriuretic peptide in the treated group of rats. These findings, together with those in previous studies, give support to an idea that one part of the blood pressure-decreasing effects, seen in patients treated with b-adrenergic blockade, might be through a reduction of the natriuretic clearance receptor C, then giving rise to increased levels of atrial natriuretic peptide. Microsc. Res. Tech. 67:90-99, 2005. V

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“…-Blocker scheinen dagegen einen komplexeren Effekt auf die Plasmaspiegel natriuretischer Peptide zu haben [10,13,24,35,38]; wäh-rend unmittelbar nach Therapiebeginn ein Anstieg der Plasmaspiegel zu beobachten ist, kommt es längerfris-tig korrespondierend zur Verbesserung der kardialen Funktion mit Abnahme der Füllungsdrücke und kardialen Volumina zu einer Verminderung unter das Ausgangsniveau [13]. Langfristig mit -Blockern therapierte Patienten mit koronarer Herzkrankheit weisen trotzdem unter Belastung signifikant größere Anstiege der Konzentrationen von ANP und BNP im Plasma auf als Patienten ohne diese Therapie [24]. Richards et al berichteten über eine signifikante Verringerung der Ereignisraten von Tod oder Herzinsuffizienz bei Patienten mit ischämisch bedingter Herzinsuffizienz unter Carvediloltherapie [35] und über im Rahmen der Studie gemessene BNP-Plasmaspiegel.…”

Section: Figureunclassified

Natriuretische Peptide?neue diagnostische Marker bei Herzerkrankungen

Angermann

Ertl²

2004

Herz

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In patients with heart failure, increased wall stretch due to volume and pressure overload leads to an increase in circulating natriuretic peptides (ANP and BNP and their N-terminal fragments NT-proANP and NT-proBNP). Plasma BNP levels commonly considered normal (< 20 pg/ml) are influenced by age, sex, and also by genetic factors. ANP and BNP are synthesized and released by atrial and ventricular myocytes (Figure 1). In subjects with acute dyspnea, a BNP plasma concentration of 100 pg/ml has been established as a cutoff value for the diagnosis of heart failure yielding a very high negative predictive value coupled with an acceptable positive predictive value (Figure 3). However, recent evidence suggests that much more subtle elevations of plasma BNP may also indicate an increased long-term risk of cardiovascular events and death (Figure 2). In acute heart failure, natriuretic peptides correlate with ventricular pressure and volume overload, as well as with NYHA functional class. They can, however, not reliably discriminate between heart failure due to reduced ejection fraction and heart failure with preserved systolic function (Figure 4). Thus, elevated BNP or NT-proBNP levels always demand further clarification of heart failure etiology using echocardiography as the method of choice. As indicated by the algorithm for a BNP-based differential diagnosis of acute heart failure symptoms (Figure 5), a variety of noncardiac causes may also lead to moderate elevations of the markers (BNP plasma concentrations of 100-400 pg/ml). In addition, normal marker levels may be observed in > 20% of patients with long-term stable heart failure. Thus, increased plasma concentrations of natriuretic peptides are not strictly specific for heart diseases and also lack sensitivity in the chronic compensated state. Diuretics, angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor antagonists, and spironolactone have been shown to decrease BNP and NT-proBNP in parallel with clinical and hemodynamic improvement. In patients hospitalized for decompensated heart failure, predischarge plasma BNP levels reflect the risk of future death and rehospitalization (Figure 6). Although adjusting heart failure treatment to reduce plasma NT-proBNP levels may improve outcome, a general recommendation for monitoring drug therapy using this marker should not be derived from this observation. General practitioners may, in the future, use BNP or NT-proBNP as a rule-out test for heart failure and preselect patients for further diagnostic work-up on the basis of an elevated plasma level. Within the framework of the German network for heart failure the multicentric "Handheld-BNP Study" will clarify, whether echocardiography using low-price simple handcarried devices could be used as an alternative or, more likely, as a complementary diagnostic tool to further improve heart failure diagnosis in primary care.

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Exercise release of cardiac natriuretic peptides is markedly enhanced when patients with coronary artery disease are treated medically by beta-blockers

Cited by 42 publications

References 33 publications

Introduction of Metoprolol Increases Plasma B-Type Cardiac Natriuretic Peptides in Mild, Stable Heart Failure

Introduction of Metoprolol Increases Plasma B-Type Cardiac Natriuretic Peptides in Mild, Stable Heart Failure

Receptor binding occurrence and plasma levels of natriuretic peptides in response to sympathectomy

Natriuretische Peptide?neue diagnostische Marker bei Herzerkrankungen

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