The goal of this clinical trial is to evaluate the effect of spironolactone in the primary prevention of cardiotoxicity in cancer patients who are undergoing chemotherapy with anthracycline within 12 months. The main question it aims to answer is: • Does spironolactone reduce the incidence of cardiotoxicity in patients undergoing anthracycline chemotherapy? Participants will: * Be cancer patients over 18 years starting treatment with anthracycline; * Be randomized to receive either spironolactone or a placebo for 1 year; * Undergo assessments of their left ventricular ejection fraction (LVEF), global longitudinal strain, and cardiac biomarkers over the 12-month period. Researchers will compare the spironolactone group to the placebo group to see if cardiotoxicity incidence differs between the two.
Objective: To assess the potential of spironolactone in preventing anthracycline-induced cardiotoxicity among cancer patients. Background: There's ongoing debate and a dearth of evidence regarding the role of mineralocorticoid receptor antagonists, such as spironolactone, in averting anthracycline-induced cardiotoxicity. Study Design: A randomized, double-blind, placebo-controlled trial conducted at a single center. Sample Size: 264 patients. Intervention: Eligible participants will be randomized on a 1:1 basis to either receive spironolactone or a placebo over a 12-month period. Primary Outcome: Incidence of cardiotoxicity at the 12-month mark.
Study Type
INTERVENTIONAL
Allocation
RANDOMIZED
Purpose
PREVENTION
Masking
TRIPLE
Enrollment
264
Spironolactone 25 mg capsule
Placebo capsule
Instituto do Coração
São Paulo, Brazil
Cardiotoxicity
Incidence of cardiotoxicity, defined as: * A decrease in ejection fraction (LVEF) by 10% or more to LVEF \< 50%, as seen on transthoracic echocardiogram; OR * Relative drop in global longitudinal strain greater than 15% compared to baseline, observed on transthoracic echocardiogram; OR * New increase in cardiac biomarkers (troponin T \> 99th percentile and/or NT-proBNP \> 125 pg/mL).
Time frame: 12 months
Left ventricular dysfunction
Decrease in ejection fraction (LVEF) ≥ 10% to LVEF \< 50% seen on transthoracic echocardiogram and cardiac magnetic resonance imaging
Time frame: 3, 6 and 12 months
Ventricular function
Relative reduction in global longitudinal strain ≥ 15%, observed on transthoracic echocardiogram and cardiac magnetic resonance imaging
Time frame: 3, 6 and 12 months
Incidence of myocardial injury
Elevation of biomarkers (troponin T \> 99th percentile and/or NT-proBNP \> 125 pg/mL).
Time frame: 6 and 12 months
Oxygen consumption
Measurement of oxygen consumption (VO2), ventilatory equivalents for oxygen (VE/VO2) and for carbon dioxide (VE/VCO2) by cardiopulmonary exercise test
Time frame: 6 and 12 months
Ventricular diameters
Ventricular diameters measured by transthoracic echocardiogram
Time frame: 3, 6 and 12 months
Myocardial work
Global work index (GWI) and global constructive work (GCW) measured by transthoracic echocardiogram
Time frame: 3, 6 and 12 months
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: 3, 6 and 12 months
Composite endpoint of mortality or major cardiovascular outcomes
Composite endpoint of mortality or major cardiovascular outcomes (defined as acute myocardial infarction, symptomatic heart failure or complex arrhythmia).
Time frame: 3, 6 and 12 months
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