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The history of natriuretic peptides can be traced back to as early as 1956.1 However, the principal breakthrough came in 1981 when de Bold et al infused extracts of atrial tissue into rats and observed profuse natriuresis.1 The understanding of natriuretic peptides rapidly expanded thereafter as they were identified as neurohormones secreted form myocytes. From a clinical perspective, a major landmark was reached approximately 15 years later, the 1990s, when B-type natriuretic peptide (BNP) was shown to provide physicians with the ability to diagnose congestive heart failure in the urgent care setting.2 The prognostic properties of BNP and its inactive part, N-terminal pro BNP (NT-proBNP), were thereafter described and validated rapidly in patients with heart failure, stable and acute coronary artery disease, and even in asymptomatic community-dwelling cohorts during the initial years of 2000.3 These studies consistently found BNP or NT-proBNP to be independent and powerful risk markers for cardiovascular outcomes and mortality.3 The research of natriuretic peptides in patients with atrial fibrillation (AF) was more gradual. The initial studies during the first years of 2000 were predominantly of descriptive nature evaluating differences of natriuretic peptide levels, BNP and NT-proBNP, …
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Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
Competing interests ZH reports receiving lecture fees from Boehringer Ingelheim, Bristol-Myers Squibb, Pfizer, and Roche Diagnostics; consulting fees from Merck Sharp & Dohme, Bristol-Myers Squibb, Pfizer, and Roche Diagnostics. LW: institutional research grants, consultancy and lecture fees, and travel support from AstraZeneca, BMS and Pfizer, Boehringer Ingelheim, and GlaxoSmithKline; honoraria from GlaxoSmithKline; institutional research grant from Merck & Co. and Roche; consultancy fees from Abbot; holds two patents involving GDF-15.
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