Evidence map›Paper›PMID 37295665›Full record

Trial reportJournal of cardiac failure2023

The Cardiorenal Effects of Chronic Phosphodiesterase-V Inhibition in Preclinical Diastolic Dysfunction (Stage B Heart Failure).

Shravya Vinnakota, Fadi W Adel, Paul M McKie, Christopher G Scott, Horng H Chen

Open access · greenAbstract readRandomized Controlled Trial
In one paragraph

Trial report in Journal of cardiac failure, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact, top 84% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed, 0 citations in OpenAlex.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

Shravya VinnakotaDepartment of Cardiovascular Diseases, Mayo Clinic, Rochester, MN.
Fadi W AdelDepartment of Cardiovascular Diseases, Mayo Clinic, Rochester, MN.
Paul M McKieDepartment of Cardiovascular Diseases, Mayo Clinic, Rochester, MN.
Christopher G ScottDivision of Biomedical Statistics and Informatics, Mayo Clinic, Rochester, MN.
Horng H ChenDepartment of Cardiovascular Diseases, Mayo Clinic, Rochester, MN. Electronic address: Chen.horng@mayo.edu.
Mayo Clinic in Arizona · USMayo Clinic · US

Funding

MAYO CLINIC CENTER FOR TRANSLATIONAL SCIENCE ACTIVITIESUL1RR024150 · NCRR · MAYO CLINIC ROCHESTER · PI RIZZA, ROBERT A. · 2006 to 2011
$66.4M
Recruitment and Phenotyping CoreP01HL076611 · NHLBI · MAYO CLINIC ROCHESTER · PI BURNETT, JOHN C · 2005 to 2015
$19.6M
Human Cardiorenal SyndromeR01HL084155 · NHLBI · MAYO CLINIC ROCHESTER · PI HORNG H CHEN · 2009 to 2026
$5.5M
Preclinical Diastolic Dysfunction in Type 2 DiabetesR01HL136440 · NHLBI · MAYO CLINIC ROCHESTER · PI CHEN, HORNG H · 2018 to 2021
$2.8M
NCRR NIH HHS UL1 RR024150NHLBI NIH HHS P01 HL076611NHLBI NIH HHS R01 HL084155NHLBI NIH HHS R01 HL136440
6 · The paper itself

Abstract

objectiveTo determine whether chronic phosphodiesterase-V (PDEV) inhibition with tadalafil will improve urinary sodium excretion, glomerular filtration rate (GFR), plasma cyclic guanosine 3', 5'-monophosphate (cGMP), and urinary cGMP excretion in response to volume expansion (VE) in patients with preclinical diastolic dysfunction (PDD) or stage B heart failure.

backgroundPDD is defined as abnormal diastolic function with normal systolic function, without clinical heart failure. PDD is predictive of development of heart failure and all-cause mortality. Impaired renal function and attenuated cGMP response to VE are hallmarks of PDD.

methodsA double-blind, placebo-controlled, proof-of-concept study was conducted to compare 12 weeks of tadalafil 20 mg daily (n = 14) vs placebo (n = 7). Subjects underwent 2 study visits 12 weeks apart. Renal, neurohormonal and echocardiographic assessments were performed before and after intravascular VE (normal saline 0.25 mL/kg/min for 1 hour).

resultsBaseline characteristics were similar. There was no increase in GFR, plasma cGMP or urinary cGMP excretion in response to VE in either group at visit 1. At visit 2, tadalafil did not result in significant change in GFR but increased plasma cGMP and urinary cGMP excretion at baseline. In response to VE, tadalafil resulted in increased urine flow, urinary sodium excretion, GFR (7.00 [-1.0, 26.3] vs -9.00 [-24.5, 2.0] mL/min/1.73m2; P = 0.02) and plasma cGMP (0.50 [-0.1, 0.7] vs -0.25 [-0.6, -0.1] pmol/mL; P = 0.02). It did not improve urinary cGMP excretion after VE.

conclusionIn PDD, chronic PDEV inhibition with tadalafil improved renal response to VE through increased urine flow, urinary sodium excretion, GFR, and plasma cGMP. Further studies are required to determine whether this enhanced renal response can mitigate progression to clinical heart failure.

Indexed as

Phosphodiesterase 5 InhibitorsTadalafilAgedCyclic GMPDiastoleDouble-Blind MethodFemaleGlomerular Filtration RateHeart FailureHeart Failure, DiastolicHumansMaleMiddle AgedProof of Concept StudyTreatment OutcomeCyclic GMPPhosphodiesterase 5 InhibitorsTadalafilcGMPHeart failure with preserved ejection fractionPDE V inhibitiontadalafil

Identifiers

PMID37295665
PMCPMC10592474
OpenAlexW4379739692

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.