| Congestive heart failure (CHF) refers to a variety of causes impaired heart function, particularly ventricular systolic and diastolic function damaged, heart can not maintain an adequate cardiac output to meet the needs of the body metabolism and venous blood flow obstruction state, CHF is a group of clinical syndrome of the end stage of heart disease, and the main complaints are dyspnea and fatigue, and CHF is high morbidity and mortality. The main pathophysiology of CHF is the ventricular remodeling and nerve-endocrine-cytokine activation system. Activation of these neurons - endocrine - cytokines system include: adrenergic system, renin-angiotensin-aldosterone system(RASS), cytokines and signal peptide systems which include endothelin system and natriuretic peptide system, endothelin is a shrinking role of the vascular system and natriuretic peptide is expansion of the vascular function, neurons - endocrine - cytokines system are a series of compensatory activities of circulatory function after CHF, but these also led to the left ventricular remodeling and CHF symptoms increase, and the condition worsened. Brain natriuretic peptide (BNP) and atrial natriuretic peptide (ANP) are the principal members of natriuretic peptide system. BNP is secreted by ventricular, half-life is 18 min, with the CHF increased secretion increased, and it compensatory antagonism the activity of adrenergic antagonist, renin - angiotensin - aldosterone and endothelin system, and it relaxates the vascular smooth muscle cells and expansese the peripheral arteriovenous, and increasese sodium excretion and natriuretic, these reduce the preload and afterload of heart, so BNP can release CHF conditions.RhBNP that using recombinant DNA technologies to produce is high-purity freeze-dried powder, and it with the same 32 amino acid sequence and three-dimensional structure of the endogenous BNP ,and therefore they have the same biological activity and mechanisms. BNP binding natriuretic peptide receptor to activate the combination guanylate cyclase, and increasing guanosine monophosphate (cGMP) concentration inner the cell,it is a class new drug of blood vessel dilation , it does not have strong hearts, not inhibit phosphodiesterase, do not rely onβ-adrenergic receptors, BNP increasing cGMP plays roles of natriuretic and reducing pulmonary capillary pressure and systemic vascular resistance and pulmonary artery pressure,increasing cardiac index and ejection fraction, but also does not affect synthesis of renin-- angiotensin-aldosterone system of reducing plasma aldosterone levels. RhBNP first produced in the United States and has developed a new generation of intravenous treatment of decompensated CHF drugs. In more severe stages of heart failure, there may be a relative shortage of endogenous BNP or BNP resistance. Therefore, the exogenous BNP may be the treatment of decompensated heart failure (DHF).Objective To compare the clinical efficacy of recombinant human brain natriuretic peptide (rhBNP) and nitroglycerin on acute decompensated heart failure (ADHF). Methods 50 cases of ADHF patients were randomly divided into rhBNP group and the nitroglycerin groups. In all patients, dyspnea and global clinical status were assessed at 30 minutes, 6 hours and 24 hours after the use of study drug, and the input liquid and urine and hemodynamic parameters were recorded after administration 24 hours. First the nitroglycerin group used the dose of nitroglycerin 5μg / min, and then every three to five minutes increased 5μg / min, according to the hemodynamic parameters of the individual to adjust the dosage; and the rhBNP group use rhBNP (first 1.5μg per kilogram of body weight bolus intravenous followed by a infusion of 0.0075μg per kilogram of body weight per minute for 72 hours). Application SPSS15.0 software for statistical analysis, as a significant level of 0.05 (bilateral). Comparison of measurement data using independent samples t-test, compared with the count data using Pearson Chi-square test, grading information using Wilcoxon W test or Kruskal Wallis test . Results The improved level of dyspnea and global clinical status of the rhBNP group were significantly better than those of the nitroglycerin group at 30 minutes and 6 hours after the start of study drug (the P value is 0.042 and 0.019 for dyspnea ,and it is 0.018 and 0.044 for global clinical status, respectively); after 24 hours those were no significant difference in the two groups (P values were 0.192 and 0.179); After 24 hours ,the urine of rhBNP group (1513.8±242.9) ml were significantly more than that of the nitroglycerin group (1341.2±239.7) ml (the P value is 0.015) , and the increase in ejection fraction and the decrease in pulmonary arterial pressure and systolic blood pressure of the rhBNP group were significantly more than those of the nitroglycerin group (P values were 0.001,0.000 and 0.002, respectively); After 72 hours the number of premature ventricular contraction and couplets premature beats and paroxysmal ventricular tachycardia of the rhBNP group were significantly lower than those of the nitroglycerin group (P values were 0, 0.001 and 0.002). Conclusion RhBNP promote the excretion of urine, decrease pulmonary artery pressure and increase left ventricular ejection fraction, so rhBNP can significantly improved dyspnea and global clinical status for the patients of decompensated heart failure, and significantly reduce the onset of ventricular arrhythmias.
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