Cardiovascular effects of BNP

BNP and ANP are both natural antagonists of renin angiotensin aldosterone system (RAAS). They also resist the sodium and water retention and hypertension raising effects of vasopressin and sympathetic nerve. BNP, together with ANP, participates in the regulation of blood pressure, blood volume and water salt balance, improves glomerular filtration rate, natriuretic diuresis, dilates blood vessels, reduces systemic vascular resistance and plasma volume, which all play a role in maintaining cardiac function. BNP is different from ANP. ANP is mainly synthesized in the atrium. When the atrium is overloaded or dilated, the secretion increases, and the plasma concentration increases, which mainly reflects the changes of pulmonary vascular pressure. Some other hormones such as antidiuretic hormone and catecholamines can directly stimulate the secretion of ANP. Because ANP precursors are stored in secretory granules, they are decomposed into ANP during secretion, Its rapid regulation is mainly carried out in the amount of hormone secretion; BNP is mainly synthesized in the ventricle and increases when the ventricle is overloaded or dilated; Therefore, it is more sensitive and specific to reflect the changes of ventricular function. Because BNP precursors are not stored in secretory granules, the rapid regulation of BNP synthesis and secretion is carried out at the level of gene expression.

Diagnostic value of BNP in cardiac function

Heart failure is the final stage of many diseases. Heart failure can be divided into acute heart failure (AHF) and chronic heart failure (CHF). CHF is divided into grades I, II, III and IV according to the cardiac function classification of New York Heart Association (NYHA). Grade I cardiac function has no clinical symptoms of heart failure, which can be called left ventricular dysfunction (LVD). The symptoms of acute decompensation of chronic heart failure are similar to those of acute heart failure. The reliability of clinical diagnosis of heart failure is very poor, especially in primary health care institutions. Echocardiography is the most useful and reliable non-invasive method for the diagnosis of cardiac insufficiency. There are 120000 suspected new cases of heart failure in the UK each year. It is difficult to diagnose such a large number of patients by echocardiography. Based on the close relationship between BNP and cardiac function, many researchers have done a lot of work to explore its clinical application. The importance of BNP has been affirmed in the pathophysiological changes and diagnosis of CHF. Mukoyama et al reported that the plasma BNP concentration in patients with CHF was higher than normal and was directly proportional to the severity of heart failure. Comparing the heart and plasma BNP levels between normal group and CHF group, it was found that the ventricular BNP content in normal people was 7.2% of that in atrium and 30% of that in the whole heart, while that in patients with CHF increased to 22% and 52% respectively. The plasma BNP concentration in normal people was about 0.9 ± 0.07fmol/ml, and the BNP / ANP value was about 0.16 ± 0.02, BNP concentration in patients with different degrees of CHF (NYHA grade Ⅰ ~ Ⅳ): grade Ⅰ is about 14.3 ± 1.8fmol/ml; Grade II: About 68.9 ± 37.9 fmol / ml; Grade III: about 155.4 ± 39.1fmol/ml; Grade IV is about 267.3 ± 79.9fmol/ml. In grade III and IV patients, the plasma BNP / ANP values were 1.44 and 1.72 respectively. BNP increased 200 ~ 300 times compared with normal, while ANP was only 20 ~ 30 times. Therefore, it is considered that the increase of ventricular synthesis and secretion of BNP in CHF patients is part of the reason for the increase of plasma BNP, and the severity of heart failure increases. Selvais and others believed that BNP was superior to ANP in the diagnosis of CHF and its severity. They compared the concentrations of ANP and BNP in normal people, patients with coronary heart disease with normal left ventricular ejection fraction (LVEF) and patients with different degrees of CHF. They found that the concentration of BNP (205 ± 143pg / ml) in severe heart failure (NYHA grade III ~ IV) was significantly higher than that in mild heart failure (NYHA ~ II) (51 ± 28pg / ml) (P < 0.001), The ability of BNP to distinguish CHF from normal people and patients with normal LVEF is better than ANP (P < 0.01), the correlation between BNP concentration and LVEF is better than ANP (rbnp = -0.59, ranp = -0.30, P < 0.05), and it is stronger than LVEF (P < 0.05). It is considered that BNP can be used to diagnose outpatients with cardiovascular disease.

At present, the clinical research on BNP mainly focuses on left ventricular dysfunction (LVD), where left ventricular function refers to systolic function. BNP is mainly synthesized and secreted by left ventricular cardiomyocytes in both normal people and patients with LVD. It enters the small vein and flows back to the ventricular septal vein and enters the circulation through the coronary sinus. Its secretion is mainly regulated by the tension of the left ventricular wall. The severity of LVD is positively correlated with its secretion. The level of BNP in peripheral blood can reflect the ventricular secretion rate and the degree of LVD.

At present, moderate and severe LVD can be easily diagnosed according to clinical examination, while mild LVD (NYHA grade I) is difficult to do, but it is very important for the diagnosis of LVD, especially for those patients who return to normal after myocardial infarction. The concentrations of plasma BNP, ANP and other peptide hormones and cGMP measured at rest or 3 minutes after exercise are higher than those in the normal control group, but only BNP has significant statistical significance, Through ROC curve analysis, it was found that the areas under the curve of BNP at rest and after exercise were 0.70 and 0.75 respectively, which was significantly better than ANP and cGMP in distinguishing normal from LVD. BNP was the best marker of natriuretic peptide system for LVD. Huang Yansheng and others reported that the combined detection of BNP and n-anp was more suitable for the diagnosis of LVD. They screened patients with LVD and CHF through radionuclide gated heart blood pool imaging, and selected healthy people with normal cardiac function as control, Results the levels of plasma BNP (98.72 ± 48.96 ng / L) and n-anp (1382.25 ± 549.51 ng / L) in LVD group were significantly higher than those in control group (39.06 ± 18.20 ng / L and 422.06 ± 255.38 ng / L, respectively, P < 0.05 and P > 0.001), but significantly lower than those in CHF group (150.90 ± 83.66 ng / L and 4020.43 ± 2090.95 ng / L, respectively, P < 0.05 and P > 0.001); When plasma BNP > 75.00ng/l, the sensitivity and specificity for the diagnosis of LVD were 91% and 94%; When plasma n-anp > 923.00ng/l, the sensitivity and specificity of diagnosing LVD were 75% and 94%. It was considered that BNP and n-anp could be used to diagnose LVD. BNP > 75.00ng/l and n-anp > 923.00ng/l were suitable as diagnostic indexes.

More and more literatures support the determination of BNP after myocardial infarction (MI). This can not only identify the presence or absence of left ventricular systolic dysfunction, but also may be superior to echocardiography in judging left ventricular remodeling and risk of death. In clinical practice, BNP also helps to distinguish asthma caused by heart failure from asthma caused by other causes. Normal BNP can almost exclude asthma caused by left ventricular dysfunction.