EXPRESS: Routine use of natriuretic peptides: lessons from a Big Data analysis

2021 ◽  
pp. 000456322110207
Author(s):  
Francois-Xavier Goudot ◽  
Sonia Msadek ◽  
Tanissia Boukertouta ◽  
Pierre-Olivier Schischmanoff ◽  
Christophe Meune
Keyword(s):  
Heart Failure ◽  
Big Data ◽  
Natriuretic Peptides ◽  
Ventricular Dysfunction ◽  
Big Data Analysis ◽  
Left Ventricular ◽  
Routine Practice ◽  
Cardiac Diseases ◽  
Biological Tests ◽  
Risk Patients

Background: Natriuretic peptides (NPs) have broad indications during heart failure (HF) and the detection of left ventricular dysfunction in high-risk patients. They can also be used for the diagnosis/management of other cardiac diseases. However, very little is known regarding their use in routine practice. Methods: We examined all biological tests performed from February 2010 to August 2015 in two districts from the French Brittany, covering 13,653 km2 and including 22,265 physicians. We report the settings and conditions of N-terminal pro-B-type Natriuretic Peptide (NT-proBNP) measurements (the only locally NP available). Results: From a total of 3,606,432 tests requested in 557,650 adult (older than 20 years) patients, only 56,653 (1.6%) included at least one NT-proBNP measurement. NT-proBNP measurements gradually increased, from 9,188 in 2011 to 12,938 in 2014 (p<0.001). Most NT-proBNP tests were measured in urban laboratories (72.7%) and in private (62.9%) non-hospital/clinics laboratories, they were mostly ordered by general practitioners (66% compared with 11% by cardiologists). The number of NT-proBNP measurements increased with age up to 80-90 years, and 70.3% of tests were measured in ≥75y patients. Creatinine and electrolytes were not associated with NT-proBNP in 15.8% and 19.7% of tests, respectively. Conclusion: Among a very large cohort, we observed that NPs remain largely undermeasured. NT-proBNP is mostly measured in elderly patients, and its interpretation may be hazardous in up to 16% of all individuals because no measurement of creatinine was associated to NT-proBNP.

Anthracycline cardiotoxicity: an update on mechanisms, monitoring and prevention

Heart ◽  
2017 ◽  
Vol 104 (12) ◽  
pp. 971-977 ◽  
Author(s):  
Peter A Henriksen
Keyword(s):  
Heart Failure ◽  
High Risk ◽  
Left Ventricular Dysfunction ◽  
Ventricular Dysfunction ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Anthracycline Cardiotoxicity ◽  
High Risk Patients ◽  
Risk Patients ◽  
Clinical Heart Failure

Anthracycline chemotherapy causes dose-related cardiomyocyte injury and death leading to left ventricular dysfunction. Clinical heart failure may ensue in up to 5% of high-risk patients. Improved cancer survival together with better awareness of the late effects of cardiotoxicity has led to growing recognition of the need for surveillance of anthracycline-treated cancer survivors with early intervention to treat or prevent heart failure. The main mechanism of anthracycline cardiotoxicity is now thought to be through inhibition of topoisomerase 2β resulting in activation of cell death pathways and inhibition of mitochondrial biogenesis. In addition to cumulative anthracycline dose, age and pre-existing cardiac disease are risk markers for cardiotoxicity. Genetic susceptibility factors will help identify susceptible patients in the future. Cardiac imaging with echocardiographic measurement of global longitudinal strain and cardiac troponin detect early myocardial injury prior to the development of left ventricular dysfunction. There is no consensus on how best to monitor anthracycline cardiotoxicity although guidelines advocate quantification of left ventricular ejection fraction before and after chemotherapy with additional scanning being justified in high-risk patients. Patients developing significant left ventricular dysfunction with or without clinical heart failure should be treated according to established guidelines. Liposomal encapsulation reduces anthracycline cardiotoxicity. Dexrazoxane administration with anthracycline interferes with binding to topoisomerase 2β and reduces both cardiotoxicity and subsequent heart failure in high-risk patients. Angiotensin inhibition and β-blockade are also protective and appear to prevent the development of left ventricular dysfunction when given prior or during chemotherapy in patients exhibiting early signs of cardiotoxicity.

scholarly journals Natriuretic peptides in cardiovascular diseases

2008 ◽  
Vol 13 (2) ◽  
Author(s):  
Mariusz Piechota ◽  
Maciej Banach ◽  
Anna Jacoń ◽  
Jacek Rysz
Keyword(s):  
Heart Failure ◽  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Cardiovascular Diseases ◽  
Natriuretic Peptide ◽  
Natriuretic Peptides ◽  
Ventricular Dysfunction ◽  
Left Ventricular ◽  
Peptide Family ◽  
Artery Disease

AbstractThe natriuretic peptide family comprises atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), C-type natriuretic peptide (CNP), dendroaspis natriuretic peptide (DNP), and urodilatin. The activities of natriuretic peptides and endothelins are strictly associated with each other. ANP and BNP inhibit endothelin-1 (ET-1) production. ET-1 stimulates natriuretic peptide synthesis. All natriuretic peptides are synthesized from polypeptide precursors. Changes in natriuretic peptides and endothelin release were observed in many cardiovascular diseases: e.g. chronic heart failure, left ventricular dysfunction and coronary artery disease.

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