Anthracyclines are associated with cardiotoxic effects. Previous studies suggest that enalapril, and or carvedilol, protect against cardiovascular effects of these drugs. Ivabradine selectively reduces heart rate through inhibition of the cardiac pace maker IF channel, thus prolonging the duration of spontaneous depolarization in the sinus node. Additionally, ivabradine might preserve myocardial perfusion without negative inotropic effect and probably maintain cardiac contractility despite the reduction of heart rate. Ivabradine has been shown to improve outcome in patients with heart failure and angina. The aim of this study is to evaluate whether ivabradine might prevent anthracycline-induced cardiotoxicity.
Study Type
INTERVENTIONAL
Allocation
RANDOMIZED
Purpose
PREVENTION
Masking
QUADRUPLE
Enrollment
160
Ivabradine capsule
Placebo oral capsule.
Instituto do Cancer do Estado de Sao Paulo
São Paulo, São Paulo, Brazil
RECRUITINGVentricular function
Reduction in global longitudinal strain of at least 10% (GLS)
Time frame: 365 days after randomization
Composite endpoint of mortality or major cardiovascular outcomes
Composite endpoint of mortality or major cardiovascular outcomes (defined as acute myocardial infarction, heart failure, inappropriate sinus tachycardia and arrhythmia)
Time frame: 365 days after randomization
Left ventricular dysfunction
Incidence of left ventricular (LV) dysfunction defined as reduction of LV ejection fraction by 10%.
Time frame: 365 days after randomization
Incidence of myocardial injury
Levels of NT-proBNP and high-sensitivity cardiac troponin T
Time frame: 90 days after randomization
Incidence of myocardial injury
Levels of NT-proBNP and high-sensitivity cardiac troponin T
Time frame: 180 days after randomization
Incidence of myocardial injury
Levels of NT-proBNP and high-sensitivity cardiac troponin T
Time frame: 365 days after randomization
Diastolic dysfunction
Assessment by echocardiography the incidence of diastolic dysfunction using the following parameters: peak E-wave velocity, peak A-wave velocity, mitral valve (MV) E/A ratio, MV deceleration time, pulsed-wave tissue doppler imaging e' velocity, Mitral E/e', left atrium maximum volume index, pulmonary vein(PV) systole(S) wave, PV diastole (D) wave, continuous wave (CW) doppler: tricuspid regurgitation, systolic jet velocity; Color M- mode.
Time frame: 365 days after randomization
Ventricular function
Reduction in global longitudinal strain of at least 10% (GLS)
Time frame: 180 days after randomization
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