Preface
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Main Text
BNP is synthesized and secreted by ventricular myocardial cells. Changes in ventricular load and wall tension stimulate BNP secretion. In simple terms, when myocardial cells deform or are stretched (even before actual deformation), BNP levels in the blood increase.
Note that unlike TnI and TnT, which are specific to myocardial cells, BNP and NT-proBNP are mainly expressed in ventricular myocardial cells, but also in atrial myocardial cells and brain tissue, thus they are not specific to myocardial cells. Besides heart failure, other factors can also cause changes in natriuretic peptide levels.
Natriuretic Peptide Cutoff Points
BNP cutoff:
(1) Chronic heart failure: <35 ng/L generally excludes diagnosis, >150 ng/L indicates diagnosis;
(2) Acute heart failure: <100 ng/L generally excludes diagnosis, >400 ng/L indicates diagnosis.
NT-proBNP cutoff: Unlike BNP, NT-proBNP is significantly affected by aging and renal function, requiring stratification
- Chronic heart failure: <125 ng/L generally excludes diagnosis, >600 ng/L indicates diagnosis;
- Acute heart failure: <300 ng/L generally excludes diagnosis; >450 ng/L for under 50 years old, >900 ng/L for 50–75 years old, and >1800 ng/L for over 75 years old indicate diagnosis;
- In renal insufficiency (glomerular filtration rate <60 ml·min^-1·1.73 m^-2), cutoff should be >1200 ng/L;
- In patients with atrial fibrillation, the NT-proBNP cutoff should be increased by 20%–30%.
Factors Leading to Elevated Natriuretic Peptides
- Cardiovascular factors: acute coronary syndrome, myocardial diseases (such as left ventricular hypertrophy), myocarditis, pulmonary embolism, valvular heart disease, hypertrophic cardiomyopathy, congenital heart disease, and atrial and ventricular arrhythmias;
- Cardiac contusion, infiltration or malignancy: electrical cardioversion, pericardial diseases, invasive cardiac procedures or surgeries, pulmonary hypertension (right ventricular failure), infiltrative cardiomyopathy, and use of cardiotoxic drugs;
- Non-cardiovascular factors: advanced age, renal insufficiency, critical illness (sepsis syndrome and cytokine syndrome), stroke, lung diseases (severe pneumonia, sleep apnea, chronic obstructive pulmonary disease), liver diseases, severe anemia, severe metabolic and endocrine diseases (hyperthyroidism and diabetic ketoacidosis), and severe burns;
- Neprilysin is a BNP degradation enzyme; neprilysin inhibitor sacubitril can temporarily increase BNP levels but does not affect NT-proBNP. Patients treated with sacubitril/valsartan should be tested for NT-proBNP.
Factors Leading to Decreased Natriuretic Peptides
Obesity or increased body mass index, acute pulmonary edema, constrictive pericarditis, and cardiac tamponade.
Efficacy Evaluation
A decrease of ≥30% in BNP/NT-proBNP levels can be used as a criterion for effective treatment.