Evidence map›Paper›PMID 39545930›Full record

ArticleEuropean heart journal. Cardiovascular Imaging2025

Prognostic implication of DPD quantification in transthyretin cardiac amyloidosis.

René Rettl, Franz Duca, Christina Kronberger, Christina Binder, Robin Willixhofer, Nikita Ermolaev, Michael Poledniczek, Felix Hofer, Christian Nitsche, Christian Hengstenberg and 6 more

Abstract read
In one paragraph

Article in European heart journal. Cardiovascular Imaging, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
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

5 citing papers in PubMed.

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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

16 authors.

René RettlDivision of Cardiology, Department of Internal Medicine II, Medical University of Vienna, Vienna, Austria.
Franz DucaDivision of Cardiology, Department of Internal Medicine II, Medical University of Vienna, Vienna, Austria.ORCID 0000-0002-7519-5274
Christina KronbergerDivision of Cardiology, Department of Internal Medicine II, Medical University of Vienna, Vienna, Austria.
Christina BinderDivision of Cardiology, Department of Internal Medicine II, Medical University of Vienna, Vienna, Austria.
Robin WillixhoferDivision of Cardiology, Department of Internal Medicine II, Medical University of Vienna, Vienna, Austria.
Nikita ErmolaevDivision of Cardiology, Department of Internal Medicine II, Medical University of Vienna, Vienna, Austria.
Michael PoledniczekDivision of Cardiology, Department of Internal Medicine II, Medical University of Vienna, Vienna, Austria.
Felix HoferDivision of Cardiology, Department of Internal Medicine II, Medical University of Vienna, Vienna, Austria.
Christian NitscheDivision of Cardiology, Department of Internal Medicine II, Medical University of Vienna, Vienna, Austria.
Christian HengstenbergDivision of Cardiology, Department of Internal Medicine II, Medical University of Vienna, Vienna, Austria.ORCID 0000-0002-8284-2994
Roza Badr EslamDivision of Cardiology, Department of Internal Medicine II, Medical University of Vienna, Vienna, Austria.
Johannes KastnerDivision of Cardiology, Department of Internal Medicine II, Medical University of Vienna, Vienna, Austria.
Jutta Bergler-KleinDivision of Cardiology, Department of Internal Medicine II, Medical University of Vienna, Vienna, Austria.ORCID 0000-0003-2591-1380
Marcus HackerDivision of Nuclear Medicine, Department of Biomedical Imaging and Image-guided Therapy, Medical University of Vienna, Waehringer Guertel 18-20, 1090 Vienna, Austria.
Raffaella CalabrettaDivision of Nuclear Medicine, Department of Biomedical Imaging and Image-guided Therapy, Medical University of Vienna, Waehringer Guertel 18-20, 1090 Vienna, Austria.ORCID 0000-0001-6409-5158
Andreas A KammerlanderDivision of Cardiology, Department of Internal Medicine II, Medical University of Vienna, Vienna, Austria.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsQuantification of cardiac [99mTc]-3,3-diphosphono-1,2-propanodicarboxylic acid (DPD) uptake enhances diagnostic capabilities and may facilitate prognostic stratification in patients with transthyretin cardiac amyloidosis (ATTR-CA). This study aimed to evaluate the association of quantitative left ventricular (LV) DPD uptake with myocardial structure and function, and their implications on outcome in ATTR-CA. METHODS AND

resultsConsecutive ATTR-CA patients (n = 100) undergoing planar DPD scintigraphy with Perugini grade 2 or 3, alongside quantitative DPD single-photon emission computed tomography/computed tomography imaging and speckle-tracking echocardiography between 2019 and 2023, were included and divided into two cohorts based on median DPD retention index (low DPD uptake: ≤5.4, n = 50; high DPD uptake: >5.4, n = 50). The DPD retention index showed significant, albeit weak to modest, correlations with LV global longitudinal strain (LV-GLS: r = 0.366, P < 0.001), right ventricular free wall longitudinal strain (RV-FW-LS: r = 0.316, P = 0.002), LV diastolic function (E/e' average: r = 0.304, P = 0.013), NT-proBNP (r = 0.332, P < 0.001), troponin T (r = 0.233, P = 0.022), 6 min walk distance (6MWD: r = -0.222, P = 0.033), and National Amyloidosis Centre (NAC) stage (r = 0.294, P = 0.003). ATTR-CA patients in the high DPD uptake cohort demonstrated more advanced disease severity regarding longitudinal cardiac function (LV-GLS: P = 0.012, RV-FW-LS: P = 0.036), LV diastolic function (E/e' average: P = 0.035), cardiac biomarkers (NT-proBNP: P = 0.012, troponin T: P = 0.044), exercise capacity (6MWD: P = 0.035), and disease stage (NAC stage I: P = 0.045, III: P = 0.006), and experienced adverse outcomes compared with the low DPD uptake cohort [composite endpoint: all-cause death or heart failure hospitalization, HR: 2.873 (95% CI: 1.439-5.737), P = 0.003; DPD retention index: adjusted HR 1.221 (95% CI: 1.078-1.383), P = 0.002].

conclusionIn ATTR-CA, enhanced quantitative LV DPD uptake indicates advanced disease severity and is associated with adverse outcome. DPD quantification may facilitate prognostic stratification when diagnosing patients with ATTR-CA.

Indexed as

Amyloid Neuropathies, FamilialCardiomyopathiesOrganotechnetium CompoundsAgedDiphosphonatesEchocardiographyFemaleHumansMaleMiddle AgedPrognosisRadiopharmaceuticalsRetrospective StudiesSingle Photon Emission Computed Tomography Computed TomographyDiphosphonatesOrganotechnetium CompoundsRadiopharmaceuticalstechnetium Tc 99m 1,1-diphosphonopropane-2,3-dicarboxylic acidATTR amyloidosisATTR-CADPD quantificationoutcomeprognosis

Identifiers

PMID39545930
PMCPMC11781830

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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.