title: Amiodarone decreases plasma brain natriuretic peptide level in patients with heart failure and ventricular tachyarrhythmia.
abstract: Brain natriuretic peptide (BNP) is a powerful neurohormonal marker of left ventricular function and prognosis. Amiodarone either has no effect or improves the haemodynamics in patients with left ventricular dysfunction, but its effect on BNP is unknown. This study evaluated the effect of amiodarone on plasma BNP level in patients with heart failure and ventricular tachyarrhythmia. Plasma BNP level was studied in 46 patients with heart failure ventricular tachyarrhythmia, before (baseline) and at week 2 and months 1, 3 and 6 of amiodarone treatment. In addition, 21 patients with heart failure and ventricular tachyarrhythmia, who received an implantable cardioverter defibrillator, but not amiodarone, were studied on the same schedule. All patients had previously received potent vasodilator and beta-blocker therapy. Echocardiography and Holter monitoring were also performed. Amiodarone significantly decreased plasma BNP levels at week 2 to month 6 during therapy. Heart rates and frequencies of premature ventricular complexes were markedly reduced by amiodarone. Echocardiographic findings did not show a change in left ventricular end-diastolic dimensions, despite a slight increase in fraction shortening at month 6 during amiodarone therapy. The above parameters showed no change in patients without amiodarone. The effect of heart rate, premature ventricular complexes, fraction shortening, serum creatinine or thyroid stimulating hormone level was not significantly associated with decrease in BNP level during amiodarone therapy by a multivariate analysis. Among amiodarone-treated patients, mortality was higher in 24 with BNP levels >/=100 pg/ml at month 6 than in 22 with BNP levels <100 pg/ml during a mean follow-up period of 31 months. Amiodarone appears to have a decreasing effect on plasma BNP level, as well as an antiarrhythmic effect, in patients with heart failure and ventricular tachyarrhythmia.
authors: Department of Cardiology, The Heart Institute of Japan, Tokyo Women's Medical University, Tokyo, Japan. mshiga@hij.twmu.ac.jp
authors: Tsuyoshi
authors: T
authors: Shiga
authors: Fumitaka
authors: F
authors: Hosaka
authors: Michi
authors: M
authors: Wakaumi
authors: Naoki
authors: N
authors: Matsuda
authors: Kohei
authors: K
authors: Tanizaki
authors: Katsuya
authors: K
authors: Kajimoto
authors: Morio
authors: M
authors: Shoda
authors: Nobuhisa
authors: N
authors: Hagiwara
authors: Hiroshi
authors: H
authors: Kasanuki
mesh_terms: D000638:Amiodarone / Q000627:therapeutic use*; D000889:Anti-Arrhythmia Agents / Q000627:therapeutic use*; D015415:Biomarkers / Q000097:blood; D004562:Electrocardiography; D005260:Female; D006333:Heart Failure / Q000000981:diagnostic imaging / Q000188:drug therapy* / Q000503:physiopathology; D006801:Humans; D008297:Male; D008875:Middle Aged; D020097:Natriuretic Peptide, Brain / Q000097:blood*; D017180:Tachycardia, Ventricular / Q000000981:diagnostic imaging / Q000188:drug therapy* / Q000503:physiopathology; D014463:Ultrasonography; D018487:Ventricular Dysfunction, Left / Q000000981:diagnostic imaging / Q000503:physiopathology
chemical_list: D000889:Anti-Arrhythmia Agents; D015415:Biomarkers; D020097:Natriuretic Peptide, Brain; D000638:Amiodarone