Q2. What have the authors stated for future works in "University of groningen spironolactone in patients with heart failure, preserved ejection fraction, and worsening renal function beldhuis," ?
Future studies investigating epidemiology, pathophysiology, and treatment strategies related to renal dysfunction in HFpEF are warranted.
Q3. What are the contributions mentioned in the paper "University of groningen spironolactone in patients with heart failure, preserved ejection fraction, and worsening renal function beldhuis," ?
The purpose of this study was to investigate the association between WRF, spironolactone treatment, and clinical outcomes in patients with HFpEF. In 1,767 patients randomized to spironolactone or placebo in the TOPCAT ( Treatment of Preserved Cardiac Function Heart Failure With an Aldosterone Antagonist Trial ) -Americas study, the authors examined the incidence of WRF ( doubling of serum creatinine ) by treatment assignment. Associations between incident WRF and subsequent risk for the primary study endpoint of cardiovascular ( CV ) death, HFH, or aborted cardiac arrest and key secondary outcomes, including CV death, HFH, and all-cause mortality according to treatment assignment, were examined in time-updated Cox proportional hazards models with an interaction term. 12. 057 m the Cardiovascular Division, Brigham and Women ’ s Hospital, Boston, Massachusetts, USA ; University of Groningen, iversity Medical Center Groningen, Department of Cardiology, Groningen, the Netherlands ; Division of Medicine, Akershus iversity Hospital, Lorenskog, Norway ; Division of Cardiology, University of Colorado Anschutz Medical Campus, Aurora, lorado, USA ; University of Utah School of Medicine, Salt Lake City, Utah, USA ; National Heart, Lung, and Blood Institute, tional Institutes of Health, Bethesda, Maryland, USA ; New England Research Institutes, Watertown, Massachusetts, USA ; ontreal Heart Institute, Montreal, Quebec, Canada ; University of Michigan School of Medicine, Ann Arbor, Michigan, USA ; vision of Cardiology, Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, Illinois, USA ; d the Minneapolis VA Center for Care Delivery and Outcomes Research, University of Minnesota, Minneapolis, Minnesota, A. e authors attest they are in compliance with human studies committees and animal welfare regulations of the authors ’ titutions and Food and Drug Administration guidelines, including patient consent where appropriate. For more information, it the Author Center.
Q4. What future works have the authors mentioned in the paper "University of groningen spironolactone in patients with heart failure, preserved ejection fraction, and worsening renal function beldhuis," ?
Future studies investigating epidemiology, pathophysiology, and treatment strategies related to renal dysfunction in HFpEF are warranted.
Q5. What is the effect of RAAS in HFpEF?
RAAS activation in HF leads to glomerular efferent arteriolar vasoconstriction that increases glomerular filtration, and RAAS inhibitors counteract this effect (6).
Q6. What is the role of spironolactone in the HFpEF?
Careful monitoring of renal function during treatment with spironolactone and interpretation of these measurements in context of the disease progression are of utmost importance for optimal patient care.
Q7. Why did the authors restrict their analyses to the subset of TOPCAT subjects in Russia and the Republic?
Due to previously reported differences in patient demographics, event rates, adherence to study medication, responses to treatment, and outcomes among TOPCAT subjects enrolled in Russia and the Republic of Georgia, the authors restricted their analyses to the subset of TOPCAT subjects enrolled in the Americas (United States, Canada, Argentina, Brazil; N ¼ 1,767) (9,10,14).
Q8. What is the way to treat HFpEF?
Future studies investigating epidemiology, pathophysiology, and treatment strategies related to renal dysfunction in HFpEF are warranted.
Q9. What is the effect of spironolactone on cardiovascular mortality?
Despite increased incidence of WRF associated with spironolactone use in patients with HFpEF, the beneficial effects of spironolactone compared with placebo on cardiovascular mortality were more pronounced in those who developed WRF versus those that did not develop WRF.
Q10. How many patients had a HF hospitalization after a WRF?
During a mean follow-up of 3.3 years, the primary outcome of CV death, aborted cardiac arrest, or HF hospitalization occurred in 522 (29.5%) patients.
Q11. What was the recommendation for down-titration for patients with serum potassium measurements?
Study drug instructions included a recommendation for down-titration for patients with serum potassium measurements $5.5 mmol/l and discontinuation for serum potassium $6.0 mmol/l or serum creatinine $3.0 mg/dl.
Q12. What is the effect of ACEi/ARB on WRF?
In addition, ACEi/ARB treatment and lower baseline creatinine were associated with WRF in patients allocated to spironolactone, and higher NYHA functional class in patients allocated to placebo (Table 2).
Q13. What was the effect of WRF on the outcomes of the primary endpoint?
After adjustment for age, sex, race, BMI, NYHA functional class, systolic blood pressure, baseline potassium, diabetes, ACEi/ARB treatment, and diuretic requirement, the strength of the interaction between treatment and WRF with regard to cardiovascular outcomes was attenuated (interaction p ¼ 0.113),but remained statistically significant for CV death (interaction p ¼ 0.003) and all-cause mortality (interaction p ¼ 0.001) (Table 4).
Q14. What is the hazard ratio of spironolactone and WRF?
In a recent meta-analysis, patients with HFpEF and RAAS inhibitor–induced WRF experienced increased mortality risk and no benefit from RAAS inhibition when compared with placebo (5).