Correlation between brain natriuretic peptide and right ventricular systolic pressure

2016-06-08T08-54-21Z
Source: International Journal of Medical Science and Public Health
Khalid Al Sulaiman, Sarah Al Yousef, Abdulmalik Al Kathiri, Shmylan Al Harbi, Abdulkareem Al Bekairy, Hind Al Modaimegh, Saleh Al Dekhail, Thamer Al Sulaiman, Salahdein Aburuz.
Background: Brain natriuretic peptide (BNP) is a cardiac hormone with diuretic, natriuretic, and vasodilatory properties produced by the heart ventricles in response to volume expansion and pressure load. The concentration of BNP is highest in the artery of healthy individuals but in heart failure patients it is shifted to the ventricles. Plasma BNP levels are influenced by many factors including age, renal function, medications, and arrhythmias. BNP is released in response to improved myocardial relaxation and it also plays an important role in the regulatory response to acute elevation in ventricular volume by opposing the effects of the activated renin, angiotensin, and aldosterone system. Objective: To evaluate the correlation between BNP and right ventricular systolic pressure (RVSP) in patients with decompensated heart failure. Materials and Methods: In this retrospective-chart review study, electronic data and medical records between 1 January 2013 and 31 December 2013 were reviewed to screen patients for inclusion into the study. Inclusion criteria included patients admitted to King Abdulaziz Medical City - Cardiac Center (KAMC-CC) with diagnosis of decompensated heart failure and Right Ventricular Systolic Pressure (RVSP) more than 35 mmhg on admission, aged 50 years or older with ejection fraction ≤ 35%, Brain Natriuretic Peptide (BNP) value and Echocardiography (2D) were assessed at least once, the time difference between BNP measurement and Echocardiography less than 72 hours, and New York Hear Association (NYHA) Class III IV. On the other hand, patients with impaired renal function (serum creatinine > 133 μmol/l), atrial arrhythmia, congenital heart disease and cardiogenic shock were excluded. Demographic and clinical data including BNP and RVSP were recorded for eligible patients. Patients were divided into four groups according to their RVSP readings (30-40, 40-50, 50-60, and > 60 mmhg). ANOVA was utilized to assess for group differences. Result: 388 patients with decompensated heart failure were screened during the period from January to December 2013. Only 27 patients met inclusion criteria. The increase in RVSP was associated with an increase in BNP until RVSP reaches a value of > 60 mmhg where BNP starts to decline. The differences between the four groups were statistically significant (F = 5.3, p = 0.007). Post hoc analysis was performed to test the difference between the individual groups and indicated a significant difference between Group one vs. Group two (mean difference: 215.5 ± 71.7, CI: 17.1 to 413.8, p = 0.03) and Group one vs. Group three (mean difference: 234.3 ± 63.8, CI: 414.02 to 60.69, p = 0.006). Conclusion: The study results indicate an association between RVSP and BNP. The increase in RVSP was associated with an increase in BNP until RVSP reaches a value of > 60 mmhg where BNP starts to decline. This correlation can be clinically useful in assessing prognosis and in helping physicians to predict BNP values with known RVSP values and vice versa. Further studies with larger sample size are required to confirm these interesting results.


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