Key result
Lisinopril treatment for 6 months in patients with mild to moderate heart failure did not significantly reduce plasma norepinephrine concentrations or alter heart rate variability indices of sympathetic tone, despite improving symptoms and left ventricular function.
Why the study?
Does lisinopril improve sympathetic tone and cardiac function in patients with mild to moderate heart failure?
Does lisinopril improve sympathetic tone and cardiac function in patients with mild to moderate heart failure?
Absolute Event Rate: 639.1% vs 701.6%
p-value: p=0.574
In patients with mild to moderate heart failure, lisinopril improves cardiac function and symptoms and reduces natriuretic peptides without significantly suppressing systemic sympathetic nervous activity.
Lisinopril improves symptoms and LV function without suppressing sympathetic markers in mild-moderate HF; leaves open whether sympathetic modulation is required for ACEI benefit.
Sixteen patients with mild to moderate heart failure were examined to investigate whether sympathetic deactivation plays a role in the improvement in the failing heart by chronic angiotensin converting enzyme (ACE) inhibition. Measurements, including echocardiography, blood examinations, neurohumoral samplings (atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), norepinephrine), and spectral heart rate variability analysis by Holter electrocardiography, were carried out before and 6 months after the administration of lisinopril (5-10 mg/day). Quality of life assessment was accomplished by the Specific Activity Scale (SAS) questionnaire. Treatment with lisinopril for 6 months resulted in a significant reduction in systolic blood pressure. The left ventricular diastolic dimension significantly decreased and fractional shortening significantly increased on echocardiography. Of the 16 patients, 8 had improvement in their symptoms as measured by the SAS. Lisinopril did not significantly reduce the plasma norepinephrine concentration, but there was a significant reduction in the plasma ANP and BNP concentrations. In the heart rate power spectral analysis, total spectral power, high-frequency components and low/high frequency ratios did not change significantly with lisinopril. The mechanism by which ACE inhibitors improve mild to moderate heart failure is not by suppressing sympathetic activity.
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Inoko et al. (2001) studied Mild to moderate heart failure (n=16). Lisinopril vs. Baseline (pre-treatment) was evaluated on Plasma norepinephrine concentration (pg/ml) (p=0.574). Lisinopril treatment for 6 months in patients with mild to moderate heart failure did not significantly reduce plasma norepinephrine concentrations or alter heart rate variability indices of sympathetic tone, despite improving symptoms and left ventricular function.
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