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A. Basics
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01. History of Cardiology
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07. Syncope and Bradycardia
08. Ventricular Arrhythmias and Sudden Cardiac Death (SCD)
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20. Congenital Heart Disease and Pediatric Cardiology
21. Pulmonary Circulation, Pulmonary Embolism, Right Heart Failure
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28. Risk Factors and Prevention
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30. Cardiovascular Disease in Special Populations
31. Pharmacology and Pharmacotherapy
32. Cardiovascular Nursing
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CLEAR FILTERS
Sequential nephron blockade: a blocker in Heart Failure?
Session:
Posters - D. Heart Failure
Speaker:
Joana Brito
Congress:
CPC 2021
Topic:
D. Heart Failure
Theme:
10. Chronic Heart Failure
Subtheme:
10.4 Chronic Heart Failure – Treatment
Session Type:
Posters
FP Number:
---
Authors:
Joana Brito; João Agostinho; Pedro Alves da Silva; Beatriz Valente Silva; Beatriz Garcia; Ana Margarida Martins; Catarina Oliveira; Sara Couto Pereira; Joana Rigueira; Nuno Lousada; Fausto j. Pinto; Dulce Brito
Abstract
<p style="text-align:justify"><strong><span style="color:#000000"><span style="font-family:Calibri"><span style="font-size:medium">Introduction</span></span></span></strong></p> <p style="text-align:justify"><span style="color:#000000"><span style="font-family:Calibri"><span style="font-size:medium">In patients (pts) with Heart Failure with reduced ejection fraction (HFrEF), most decompensation episodes are characterized by volume overload requiring diuretic therapy, namely with loop diuretics and sometimes with sequential nephron blockade. Nevertheless, the impact of diuretic therapy on HFrEF prognostic is dubious. </span></span></span></p> <p style="text-align:justify"><span style="color:#000000"><span style="font-family:Calibri"><span style="font-size:medium"> </span></span></span></p> <p style="text-align:justify"><strong><span style="color:#000000; font-family:Calibri; font-size:medium">Aim</span></strong></p> <p style="text-align:justify"><span style="color:#000000"><span style="font-family:Calibri"><span style="font-size:medium">To evaluate the impact of thiazides and thiazide like diuretics (TZD) on pts with chronic HFrEF.</span></span></span></p> <p style="text-align:justify"><span style="color:#000000"><span style="font-family:Calibri"><span style="font-size:medium"> </span></span></span></p> <p style="text-align:justify"><strong><span style="color:#000000"><span style="font-family:Calibri"><span style="font-size:medium">Methods</span></span></span></strong></p> <p style="text-align:justify"><span style="color:#000000"><span style="font-family:Calibri"><span style="font-size:medium">Single-center retrospective study of patients with chronic HFrEF followed in a Heart Failure Ambulatory Unit. From a total population with 532 pts two groups were designed: study group - all pts medicated with TZD; control group - formed by a randomly selected quarter of the remaining population. Clinical and laboratory characteristics in three different time frames: baseline, time of maximal tolerated doses of HFrEF medication and last recorded follow-up visit were collected. The impact of TZD on prognosis was evaluated with Cox­ regression adjusted for age, left ventricular ejection fraction (LVEF), NT-proBNP, eTFG and NYHA functional class at the three different time frames.</span></span></span></p> <p style="margin-left:48px; text-align:justify"><strong><span style="color:#000000"><span style="font-family:Calibri"><span style="font-size:medium"> </span></span></span></strong></p> <p style="text-align:justify"><strong><span style="color:#000000"><span style="font-family:Calibri"><span style="font-size:medium">Results</span></span></span></strong></p> <p style="text-align:justify"><span style="font-size:medium"><span style="color:#000000"><span style="font-family:Calibri">A total of 212 pts (<span style="background-color:white">70±13 years,</span> 74.6% males) were included (73 pts in study group and 96 pts in control group).</span></span></span></p> <p style="text-align:justify"><span style="font-size:medium"><span style="color:#000000"><span style="font-family:Calibri">Baseline characteristics between the two groups were similar regarding NYHA functional class (NYHA II 57.5%; NYHA III 34.5%), HFrEF etiology, mean LVEF (28<span style="background-color:white">±9%)</span> and mean NT-proBNP (3674<span style="background-color:white">±5806pg/mL)</span>. eTGF was statistically lower in the study group (57<span style="background-color:white">±33 mL/min</span> versus 66<span style="background-color:white">±23mL/min</span>; p 0.07<span style="background-color:white">). </span></span></span></span></p> <p style="text-align:justify"><span style="font-size:medium"><span style="color:#000000"><span style="font-family:Calibri">Although at baseline the number of neurohumoral antagonist therapy classes<span style="background-color:white"> prescribed per pt was similar between groups (p<0.56), during follow-up a significant variation was observed and, at the last visit, the study group was under less optimized therapy (p<0.001). </span></span></span></span></p> <p style="text-align:justify"><span style="font-size:medium"><span style="color:#000000"><span style="font-family:Calibri"><span style="background-color:white">Likewise, during follow-up the study group presented worse NYHA functional class </span>(p 0.002) <span style="background-color:white">and higher NT-proBNP </span>(p 0.40) comparing with the control group.</span></span></span></p> <p style="text-align:justify"><span style="font-family:Calibri"><span style="font-size:medium"><span style="color:#000000">After a mean follow-up of 4.2±</span></span><span style="color:#000000"><span style="font-size:medium">3.9 years, mortality rate was 21.9% in study group and 5.2% in the control group, and heart failure hospitalization rate was 41.4% and 26.6%, respectively. Despite not being associated with heart failure or all-cause admissions (p=NS), TZD was an independent predictor of death on multivariate analysis (p 0.024, 95% IC 0.63-0.81 OR 0.27). On Kaplan-Meier survival analysis a negative impact on mortality becomes apparent as the follow-up time increases and becomes statistically significant after the 4</span><sup><span style="font-size:small">th</span></sup></span><span style="color:#000000"><span style="font-size:medium"> year of follow-up (p 0.047; Figure 1).</span></span></span></p> <p style="text-align:justify"><span style="color:#000000"><span style="font-family:Calibri"><span style="font-size:medium"> </span></span></span></p> <p style="text-align:justify"><strong><span style="color:#000000"><span style="font-family:Calibri"><span style="font-size:medium">Conclusion</span></span></span></strong></p> <p style="text-align:justify"><span style="color:#000000"><span style="font-family:Calibri"><span style="font-size:medium">Despite its role in HFrEF descompensation treatment and in keeping pts euvolemic, this study suggests that on the long term SNB using TZD may be deleterious and lead to higher mortality. These results also suggest that in HFrEF pts TZD may hinder therapy optimization and thus other drugs with diuretic properties, such as iSGLT2 or high dose sacubitril-valsartan may be more appropriate. </span></span></span></p>
Slides
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