Plasma Brain Natriuretic Peptide
Plasma Brain Natriuretic Peptide
Background: Plasma brain natriuretic peptide (BNP) is a sensitive and specific marker of left ventricular (LV) function. In the treatment of heart failure, especially in idiopathic dilated cardiomyopathy (IDC),
-blocker (BB) therapy has been established as a powerful strategy. The purpose of this study was to analyze relationships between changes in BNP level and LV function during BB therapy in patients with IDC.
Methods: In 30 patients with IDC who had already received conventional therapy, measurement for plasma BNP and norepinephrine levels and echocardiographic indices were evaluated before and 2 and 6 months after carvedilol in 21 patients and at baseline and after 6 months in 9 patients who did not receive carvedilol.
Results: After 6 months carvedilol treatment significantly improved LV end-diastolic dimension (LVEDD) (65 ± 8 to 61 ± 8 mm) and LV ejection fraction (LVEF) (34% ± 13% to 43% ± 12%) with intergroup differences; it significantly decreased BNP (127 ± 113 to 69 ± 92 pg/mL) with no intergroup difference; however, it did not decrease norepinephrine. BNP correlated strongly with LVEDD, LVEF, and LV mass index in carvedilol-treated patients. The degree of change in BNP correlated with that in LVEDD or LVEF 6 months after carvedilol. All 14 patients with decreased or unchanged BNP levels showed an increase in LVEF, and 4 of 7 with a rise in BNP had decreased or unchanged LVEF. According to receiver operating characteristic analysis, the optimal BNP levels for detecting LVEF <35% before and after carvedilol were 75.5 and 69 pg/mL, respectively.
Conclusion: Plasma BNP levels may accurately reflect alteration in LV function and structure and can be used as a therapeutic indicator for risk stratification in patients with IDC during BB therapy.
Because the number of patients with heart failure is increasing, new and more efficient diagnostic modalities (other than echocardiography and radionuclide ventriculography) have been expected to be developed to identify and treat patients at risk for the development of congestive heart failure. The plasma brain natriuretic peptide (BNP) level is known to be increased in established chronic heart failure and appears to be the most powerful neurohormonal predictor of left ventricular (LV) function and prognosis. According to recent large-scale trials,
-blocker (BB) treatment for chronic heart failure significantly reduced all-cause mortality and hospital admissions compared with placebo. Moreover, recent studies, including ours, disclosed that reverse ventricular remodeling with neurohormonal antagonism in heart failure was associated with a better outcome. More recently, BNP-guided heart failure treatment including angiotensin-converting enzyme (ACE) inhibitors, diuretics, and digitalis has been shown to reduce total cardiovascular events compared with intensive clinically guided treatment. However, there is no consensus on the changes in plasma BNP during BB therapy, and the usefulness of BNP as a guide to BB administration, especially in patients with idiopathic dilated cardiomyopathy (IDC). The aims of the current study were (1) to investigate the changes in plasma BNP during BB therapy in patients with IDC over 6 months of follow-up, (2) to determine whether BNP concentrations correlate with cardiac function and structure assessed with echocardiography during therapy, (3) to determine whether there is a correlation between changes in BNP and echocardiographic findings during BB, and (4) to ascertain that measurement of BNP may distinguish patients with relatively preserved or improved LV function from those with persistently depressed LV function.
Background: Plasma brain natriuretic peptide (BNP) is a sensitive and specific marker of left ventricular (LV) function. In the treatment of heart failure, especially in idiopathic dilated cardiomyopathy (IDC),
-blocker (BB) therapy has been established as a powerful strategy. The purpose of this study was to analyze relationships between changes in BNP level and LV function during BB therapy in patients with IDC.
Methods: In 30 patients with IDC who had already received conventional therapy, measurement for plasma BNP and norepinephrine levels and echocardiographic indices were evaluated before and 2 and 6 months after carvedilol in 21 patients and at baseline and after 6 months in 9 patients who did not receive carvedilol.
Results: After 6 months carvedilol treatment significantly improved LV end-diastolic dimension (LVEDD) (65 ± 8 to 61 ± 8 mm) and LV ejection fraction (LVEF) (34% ± 13% to 43% ± 12%) with intergroup differences; it significantly decreased BNP (127 ± 113 to 69 ± 92 pg/mL) with no intergroup difference; however, it did not decrease norepinephrine. BNP correlated strongly with LVEDD, LVEF, and LV mass index in carvedilol-treated patients. The degree of change in BNP correlated with that in LVEDD or LVEF 6 months after carvedilol. All 14 patients with decreased or unchanged BNP levels showed an increase in LVEF, and 4 of 7 with a rise in BNP had decreased or unchanged LVEF. According to receiver operating characteristic analysis, the optimal BNP levels for detecting LVEF <35% before and after carvedilol were 75.5 and 69 pg/mL, respectively.
Conclusion: Plasma BNP levels may accurately reflect alteration in LV function and structure and can be used as a therapeutic indicator for risk stratification in patients with IDC during BB therapy.
Because the number of patients with heart failure is increasing, new and more efficient diagnostic modalities (other than echocardiography and radionuclide ventriculography) have been expected to be developed to identify and treat patients at risk for the development of congestive heart failure. The plasma brain natriuretic peptide (BNP) level is known to be increased in established chronic heart failure and appears to be the most powerful neurohormonal predictor of left ventricular (LV) function and prognosis. According to recent large-scale trials,
-blocker (BB) treatment for chronic heart failure significantly reduced all-cause mortality and hospital admissions compared with placebo. Moreover, recent studies, including ours, disclosed that reverse ventricular remodeling with neurohormonal antagonism in heart failure was associated with a better outcome. More recently, BNP-guided heart failure treatment including angiotensin-converting enzyme (ACE) inhibitors, diuretics, and digitalis has been shown to reduce total cardiovascular events compared with intensive clinically guided treatment. However, there is no consensus on the changes in plasma BNP during BB therapy, and the usefulness of BNP as a guide to BB administration, especially in patients with idiopathic dilated cardiomyopathy (IDC). The aims of the current study were (1) to investigate the changes in plasma BNP during BB therapy in patients with IDC over 6 months of follow-up, (2) to determine whether BNP concentrations correlate with cardiac function and structure assessed with echocardiography during therapy, (3) to determine whether there is a correlation between changes in BNP and echocardiographic findings during BB, and (4) to ascertain that measurement of BNP may distinguish patients with relatively preserved or improved LV function from those with persistently depressed LV function.
