Evidence map›Paper›PMID 32372287›Full record

ArticleClinical research in cardiology : official journal of the German Cardiac Society2021

Diagnostic value of the novel CMR parameter "myocardial transit-time" (MyoTT) for the assessment of microvascular changes in cardiac amyloidosis and hypertrophic cardiomyopathy.

Grigorios Chatzantonis, Michael Bietenbeck, Anca Florian, Claudia Meier, Philipp Stalling, Dennis Korthals, Holger Reinecke, Ali Yilmaz

Open access · hybridAbstract read
In one paragraph

Article in Clinical research in cardiology : official journal of the German Cardiac Society, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

13 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. [Diagnostics of cardiac amyloidosis].Innere Medizin (Heidelberg, Germany) · 2023
    Review
  8. Coronary microvascular disease in hypertrophic and infiltrative cardiomyopathies.Journal of nuclear cardiology : official publication of the American Society of Nuclear Cardiology · 2023
    Article
  9. Article
  10. Article
  11. Cardiac amyloidosis CT sign.Clinical research in cardiology : official journal of the German Cardiac Society · 2021
    Article
  12. Prognostic implications of pericardial and pleural effusion in patients with cardiac amyloidosis.Clinical research in cardiology : official journal of the German Cardiac Society · 2021
    Article
  13. Review
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

8 authors at 1 institution in 1 country.

Grigorios ChatzantonisDepartment of Cardiology I, University Hospital Münster, Albert-Schweitzer-Campus 1, Building A1, 48149, Münster, Germany.
Michael BietenbeckDepartment of Cardiology I, University Hospital Münster, Albert-Schweitzer-Campus 1, Building A1, 48149, Münster, Germany.
Anca FlorianDepartment of Cardiology I, University Hospital Münster, Albert-Schweitzer-Campus 1, Building A1, 48149, Münster, Germany.
Claudia MeierDepartment of Cardiology I, University Hospital Münster, Albert-Schweitzer-Campus 1, Building A1, 48149, Münster, Germany.
Philipp StallingDepartment of Cardiology I, University Hospital Münster, Albert-Schweitzer-Campus 1, Building A1, 48149, Münster, Germany.
Dennis KorthalsDepartment of Cardiology I, University Hospital Münster, Albert-Schweitzer-Campus 1, Building A1, 48149, Münster, Germany.
Holger ReineckeDepartment of Cardiology I, University Hospital Münster, Albert-Schweitzer-Campus 1, Building A1, 48149, Münster, Germany.
Ali YilmazDepartment of Cardiology I, University Hospital Münster, Albert-Schweitzer-Campus 1, Building A1, 48149, Münster, Germany. ali.yilmaz@ukmuenster.de.ORCID http://orcid.org/0000-0003-4526-8679
University Hospital Münster · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCoronary microvascular dysfunction (CMD) is present in various non-ischemic cardiomyopathies and in particular in those with left-ventricular hypertrophy. This study evaluated the diagnostic value of the novel cardiovascular magnetic resonance (CMR) parameter "myocardial transit-time" (MyoTT) in distinguishing cardiac amyloidosis from other hypertrophic cardiomyopathies.

methodsN = 20 patients with biopsy-proven cardiac amyloidosis (CA), N = 20 patients with known hypertrophic cardiomyopathy (HCM), and N = 20 control patients without relevant cardiac disease underwent dedicated CMR studies on a 1.5-T MR scanner. The CMR protocol comprised cine and late-gadolinium-enhancement (LGE) imaging as well as first-pass perfusion acquisitions at rest for MyoTT measurement. MyoTT was defined as the blood circulation time from the orifice of the coronary arteries to the pooling in the coronary sinus (CS) reflecting the transit-time of gadolinium in the myocardial microvasculature.

resultsMyoTT was significantly prolonged in patients with CA compared to both groups: 14.8 ± 4.1 s in CA vs. 12.2 ± 2.5 s in HCM (p = 0.043) vs. 7.2 ± 2.6 s in controls (p < 0.001). Native T1 and extracellular volume (ECV) were significantly higher in CA compared to HCM and controls (p < 0.001). Both parameters were associated with a higher diagnostic accuracy in predicting the presence of CA compared to MyoTT: area under the curve (AUC) for native T1 = 0.93 (95% confidence interval (CI) = 0.83-1.00; p < 0.001) and AUC for ECV = 0.95 (95% CI = 0.88-1.00; p < 0.001)-compared to the AUC for MyoTT = 0.76 (95% CI = 0.60-0.92; p = 0.008). In contrast, MyoTT performed better than all other CMR parameters in differentiating HCM from controls (AUC for MyoTT = 0.93; 95% CI = 0.81-1.00; p = 0.003 vs. AUC for native T1 = 0.69; 95% CI = 0.44-0.93; p = 0.20 vs. AUC for ECV = 0.85; 95% CI = 0.66-1.00; p = 0.017).

conclusionThe relative severity of CMD (measured by MyoTT) in relationship to extracellular changes (measured by native T1 and/or ECV) is more pronounced in HCM compared to CA-in spite of a higher absolute MyoTT value in CA patients. Hence, MyoTT may improve our understanding of the interplay between extracellular/intracellular and intravasal changes that occur in the myocardium during the disease course of different cardiomyopathies.

Indexed as

AmyloidosisBiopsyCardiomyopathiesCardiomyopathy, HypertrophicCoronary CirculationCoronary VesselsFollow-Up StudiesMagnetic Resonance Imaging, CineMicrovesselsMyocardiumPredictive Value of TestsProspective StudiesTime FactorsVentricular Function, LeftCMDCMRECVHCMMVDMyoTT

Identifiers

PMID32372287
PMCPMC7806531
OpenAlexW3021890945

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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.