Brain natriuretic peptide response is heterogeneous during β-blocker therapy for congestive heart failure

Yoshizawa, Akihiro; Yoshikawa, Tsutomu; Nakamura, Iwao; Satoh, Tsuyoshi; Moritani, Kazunori; Suzuki, Masahiro; Baba, Akira; Iwanaga, Shiro; Mitamura, Hideo; Ogawa, Satoshi

doi:10.1016/j.cardfail.2003.10.011

Cited by 24 publications

(29 citation statements)

References 22 publications

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“…This might be due to small sample sizes, different kits with variable analytic specificity [29], variable follow-up time and differences between study populations [13,26,[30][31][32][33].…”

Section: Discussionmentioning

confidence: 90%

Effect of Beta-blockade and ACE Inhibition on B-type Natriuretic Peptides in Stable Patients with Systolic Heart Failure

Rosenberg

Gustafsson

Remme³

et al. 2008

Cardiovasc Drugs Ther

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Treatment of HF patients with carvedilol alone does not reduce levels of natriuretic peptides, but treatment with enalapril does. Both BNP and NT-proBNP predict death and hospitalisation in HF patients treated with carvedilol for six months. The clinical implication of our results is that NT-proBNP and BNP can be used as risk markers of death and cardiovascular hospitalisations in systolic HF patients receiving carvedilol without ACE inhibition.

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“…This might be due to small sample sizes, different kits with variable analytic specificity [29], variable follow-up time and differences between study populations [13,26,[30][31][32][33].…”

Section: Discussionmentioning

confidence: 90%

Effect of Beta-blockade and ACE Inhibition on B-type Natriuretic Peptides in Stable Patients with Systolic Heart Failure

Rosenberg

Gustafsson

Remme³

et al. 2008

Cardiovasc Drugs Ther

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“…Many studies are available which demonstrate possible benefits of repeated determinations of BNP levels to guide further heart failure therapy [1,18]. Only few studies report no changes in BNP levels despite marked clinical improvement [21,25].…”

Section: Discussionmentioning

confidence: 99%

Clinical Status and B-Type Natriuretic Peptide Levels in Patients with Heart Failure at Hospital Discharge

Oral

Mistrík²,

Náplava³

2007

Herz

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“…However, this is a well-known phenomenon when initiating β-blocker treatment in patients with a normal or near-normal NT-proBNP. 39,40 Finally, an extensive reduction in HR (eg, >−20 minute −1 ) appeared to inhibit the compensatory increase in SV and to reduce cardiac index ( Figure 3A and 3B). This may diminish any favorable effect achieved by metoprolol and increase the risk of adverse effects.…”

Section: Safety Of Metoprolol In Patients With Asymptomatic Asmentioning

confidence: 96%

Metoprolol Reduces Hemodynamic and Metabolic Overload in Asymptomatic Aortic Valve Stenosis Patients

Hansson

Sørensen

Harms

et al. 2017

Circ: Cardiovascular Imaging

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Background— Currently, no pharmacological treatment can modify the natural history of aortic valve stenosis (AS). This underlines the critical need to explore novel treatment strategies, which could postpone or prevent the need for aortic valve replacement in patients with asymptomatic AS. The objectives of this study were to investigate whether metoprolol reduce the hemodynamic and metabolic burden imposed by AS. Methods and Results— In a double-blinded design, 40 patients with moderate-severe asymptomatic AS (aortic valve area, 0.5±0.1 cm 2 /m 2 ; peak gradient, 53±19 mm Hg) were randomized to placebo or metoprolol treatment for 22 weeks. Patients were evaluated by echocardiography, cardiovascular magnetic resonance, and 11 C-acetate positron emission tomography. Compared with placebo, metoprolol (100±53 mg/d) decreased heart rate; mean difference (95% confidence interval) −8 minute − 1 (−13, −3; P =0.003) and increased ejection time 26 ms (2, 50; P =0.03). Furthermore, metoprolol reduced aortic valve peak −7 mm Hg (−13, 0; P =0.05) and mean −4 mm Hg (−7, −1; P =0.03) gradients, without affecting stroke volume 3 mL/m 2 (−2, 8; P =0.16). Valvuloarterial impedance (ie, global afterload) and myocardial oxygen consumption were reduced by −11% and −12% ( P =0.03 and 0.01), respectively; and decreased heart rate correlated with lower valvuloarterial impedance, myocardial oxygen consumption, and improved myocardial efficiency defined as stroke work/myocardial oxygen consumption ( r =0.63–0.65; all P <0.01). There were 2 adverse cardiovascular events in the metoprolol group and none in the placebo group. Conclusions— In patients with asymptomatic AS, metoprolol increases systolic ejection time and reduces aortic valve gradients, global afterload, and myocardial oxygen requirements. Thus, metoprolol displays favorable hemodynamic and metabolic effects and could improve outcome in patients with asymptomatic AS. Clinical Trial Registration— URL: http://www.clinicaltrials.gov . Unique identifier: NCT02076711.

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Brain natriuretic peptide response is heterogeneous during β-blocker therapy for congestive heart failure

Cited by 24 publications

References 22 publications

Effect of Beta-blockade and ACE Inhibition on B-type Natriuretic Peptides in Stable Patients with Systolic Heart Failure

Effect of Beta-blockade and ACE Inhibition on B-type Natriuretic Peptides in Stable Patients with Systolic Heart Failure

Clinical Status and B-Type Natriuretic Peptide Levels in Patients with Heart Failure at Hospital Discharge

Metoprolol Reduces Hemodynamic and Metabolic Overload in Asymptomatic Aortic Valve Stenosis Patients

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