Abstract
Objective:To analyze the effects of glutamine and valsartan on the brain natriuretic peptide (BNP) and N-terminal pro-B-type natriuretic peptide (NT-proBNP) of patients with chronic heart failure (CHF).Methods:A total of 140 CHF patients were divided into a treatment group and a control group by random drawing, and were subjected to standard anti-heart failure treatment and administered with valsartan. Besides, the treatment group was also intravenously transfused glutamine. The treatment lasted eight weeks.Results: The overall efficacy of treatment group and control group were 98.6% and 90.0% respectively, with a statistically significant difference (P<0.05). The two groups had significantly increased left ventricular ejection fractions as well as significantly decreased left ventricular end-diastolic volumes and left ventricular end-diastolic dimensions after treatments (P<0.05) compared with those before. There were also inter-group differences between these values (P<0.05). After treatment, the levels of BNP, NT-proBNP and CD8+ in both groups significantly decreased (P<0.05), whereas those of CD4+ significantly increased (P<0.05). The two groups also had significantly different values (P<0.05).Conclusion: Glutamine in combination with valsartan enhanced the therapeutic effects by improving cardiac function, which may be associated with decreased expressions of BNP and NT-proBNP and beneficial effects of glutamine on immune function.
Highlights
Chronic heart failure (CHF), which is a clinically common and complex syndrome, has poor prognosis for being the ending of a variety of organicCorrespondence: August 19, 2014 September 18, 2014 October 3, 2014 heart diseases.[1,2] Currently, CHF has become one of the severe diseases endangering human health with population aging and has attracted global attention
brain natriuretic peptide (BNP) is active and decomposes rapidly, but the inactive NT-proBNP remains stable and allows easy detection.[7]. It is well-established that over-activations of the reninangiotensin-aldosterone system (RAAS) and the sympathetic nervous system dominantly control the vicious circle of cardiac remodeling and the deterioration of heart function.[8]
Inclusion criteria: The patients conforming to the diagnostic standards for CHF; the patients suffering from history or clinical manifestations of congestive heart failure for three months; the patients who had New York Heart Association (NYHA) Class III-IV; the patients with written consent
Summary
Chronic heart failure (CHF), which is a clinically common and complex syndrome, has poor prognosis for being the ending of a variety of organic. BNP is active and decomposes rapidly, but the inactive NT-proBNP remains stable and allows easy detection.[7] It is well-established that over-activations of the reninangiotensin-aldosterone system (RAAS) and the sympathetic nervous system dominantly control the vicious circle of cardiac remodeling and the deterioration of heart function.[8] it is of great significance to inhibit the over-activation and vicious circle of neurohumor, and to reverse ventricular remodeling.[9] Up to now, angiotensin II receptor blockers (ARBs) are drugs that block Ang II receptors, effectively inhibit Ang II or aldosterone escape, and provide clinical benefits for heart failure patients. Upon severe wasting diseases such as trauma, heart failure, major surgery and cancer, human body begins to require a large amount of glutamine that, if not supplemented in time, will give rise to various diseases when exhausted.[11,12] we analyzed the influences of glutamine and valsartan on the BNP and NT-proBNP of CHF patients
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