BACKGROUND: The aim of this study was to determine whether spironolactone therapy has an effect on serum apelin-12 levels in heart failure with reduced ejection fraction (HFrEF) patients. METHODS: Eighty outpatients previously diagnosed with HFrEF were enrolled in the current study. Included patients were taking only standard heart failure therapy (ST) (angiotensin converting enzyme or angiotensin receptor blocker, beta-blockers, loop diuretics and anticoagulant or antiagregan agents) without a mineralocorticoid receptor antagonists (MRA) because of its side effects, and were designated the non-MRA group; those patients taking 25 mg/daily spironolactone in addition to the ST were deemed the MRA group. Patient blood samples were collected to measure serum apelin-12 levels. RESULTS: After adjustment for all clinical and demographic factors, plasma apelin-12 levels were significantly higher and NT pro-BNP levels were significantly lower in the MRA group compared to the non-MRA group (p < 0.001, p < 0.001; respectively). In multiple linear regression analyses, there was no association between baseline apelin-12 level and clinical parameters. MRA using initial apelin-12 levels were lower and NT pro-BNP levels were higher in patients with stricken event than in event-free patients (p = 0.042, p < 0.001, and p < 0.001; respectively). CONCLUSIONS: Blocking the aldosterone receptors by spironolactone, in addition to maximal standard therapy, may increase serum apelin-12 levels among patients with HFrEF.
BACKGROUND: The aim of this study was to determine whether spironolactone therapy has an effect on serum apelin-12 levels in heart failure with reduced ejection fraction (HFrEF) patients. METHODS: Eighty outpatients previously diagnosed with HFrEF were enrolled in the current study. Included patients were taking only standard heart failure therapy (ST) (angiotensin converting enzyme or angiotensin receptor blocker, beta-blockers, loop diuretics and anticoagulant or antiagregan agents) without a mineralocorticoid receptor antagonists (MRA) because of its side effects, and were designated the non-MRA group; those patients taking 25 mg/daily spironolactone in addition to the ST were deemed the MRA group. Patient blood samples were collected to measure serum apelin-12 levels. RESULTS: After adjustment for all clinical and demographic factors, plasma apelin-12 levels were significantly higher and NT pro-BNP levels were significantly lower in the MRA group compared to the non-MRA group (p < 0.001, p < 0.001; respectively). In multiple linear regression analyses, there was no association between baseline apelin-12 level and clinical parameters. MRA using initial apelin-12 levels were lower and NT pro-BNP levels were higher in patients with stricken event than in event-free patients (p = 0.042, p < 0.001, and p < 0.001; respectively). CONCLUSIONS: Blocking the aldosterone receptors by spironolactone, in addition to maximal standard therapy, may increase serum apelin-12 levels among patients with HFrEF.
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