Evidence mapPaperPMID 19815124Full record

ArticleJournal of the American College of Cardiology2009

Altered myocardial substrate metabolism and decreased diastolic function in nonischemic human diabetic cardiomyopathy: studies with cardiac positron emission tomography and magnetic resonance imaging.

Luuk J Rijzewijk, Rutger W van der Meer, Hildo J Lamb, Hugo W A M de Jong, Mark Lubberink, Johannes A Romijn, Jeroen J Bax, Albert de Roos, Jos W Twisk, Robert J Heine and 3 more

Registry-linked trialOpen access · greenAbstract readComparative Study
PubMed Publisher
In one paragraph

Article in Journal of the American College of Cardiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT01761318 (Magnetic Resonance Assessment of Victoza Efficacy in the Regression of Cardiovascular Dysfunction In Type 2 Diabetes Mellitus), which is not on this map. Cited by 149 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
149citing papers in PubMed, 1 pooled it
10.0field-weighted citation impact, top 1% 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.

NCT01761318 phase4completedstarted 2013, after this paper: background citation

Magnetic Resonance Assessment of Victoza Efficacy in the Regression of Cardiovascular Dysfunction In Type 2 Diabetes Mellitus

Ran2013Enrolled50Registered outcomes48Posted comparisons0ConditionsCardiovascular Disease, Diabetes Mellitus Type 2, Diastolic Dysfunction, Fatty LiverArmsliraglutide, Liraglutide - Placebo
Open the trial in the graph
3 · Its place in the literature

Who cites it

149 citing papers in PubMed, 1 synthesis or guideline pooled it, 304 citations in OpenAlex.

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  16. The heart of diabetes: unraveling metabolic drivers of cardiomyopathy.Cardiovascular diabetology. Endocrinology reports · 2025
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89 more citing papers are in PubMed but not listed here.

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

13 authors at 2 institutions in 1 country.

Luuk J RijzewijkDiabetes Center, VU University Medical Center, Amsterdam, the Netherlands.
Rutger W van der Meer
Hildo J Lamb
Hugo W A M de Jong
Mark Lubberink
Johannes A Romijn
Jeroen J Bax
Albert de Roos
Jos W Twisk
Robert J Heine
Adriaan A Lammertsma
Johannes W A Smit
Michaela Diamant
Amsterdam UMC Location Vrije Universiteit Amsterdam · NLLeiden University Medical Center · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesThis study was designed to evaluate myocardial substrate and high-energy phosphate (HEP) metabolism in asymptomatic men with well-controlled, uncomplicated type 2 diabetes with verified absence of cardiac ischemia, and age-matched control subjects, and to assess the association with myocardial function.

backgroundMetabolic abnormalities, particularly an excessive exposure of the heart to circulating nonesterified fatty acids and myocardial insulin resistance are considered important contributors to diabetic cardiomyopathy in animal models of diabetes. The existence of myocardial metabolic derangements in uncomplicated human type 2 diabetes and their possible contribution to myocardial dysfunction still remain undetermined.

methodsIn 78 insulin-naive type 2 diabetes men (age 56.5 +/- 5.6 years, body mass index 28.7 +/- 3.5 kg/m(2), glycosylated hemoglobin A(1c) 7.1 +/- 1.0%; expressed as mean +/- SD) without cardiac ischemia and 24 normoglycemic control subjects (age 54.5 +/- 7.1 years, body mass index 27.0 +/- 2.5 kg/m(2), glycosylated hemoglobin A(1c) 5.3 +/- 0.2%), we assessed myocardial left ventricular (LV) function by magnetic resonance imaging, and myocardial perfusion and substrate metabolism by positron emission tomography using H(2)(15)O, carbon (11)C-palmitate, and 18-fluorodeoxyglucose 2-fluoro-2-deoxy-D-glucose. Cardiac HEP metabolism was assessed by phosphorous P 31 magnetic resonance spectroscopy.

resultsIn patients, compared with control subjects, LV diastolic function (E/A ratio: 1.04 +/- 0.25 vs. 1.26 +/- 0.36, p = 0.003) and myocardial glucose uptake (260 +/- 128 nmol/ml/min vs. 348 +/- 154 nmol/ml/min, p = 0.015) were decreased, whereas myocardial nonesterified fatty acid uptake (88 +/- 31 nmol/ml/min vs. 68 +/- 18 nmol/ml/min, p = 0.021) and oxidation (85 +/- 30 nmol/ml/min vs. 63 +/- 19 nmol/ml/min, p = 0.007) were increased. There were no differences in myocardial HEP metabolism or perfusion. No association was found between LV diastolic function and cardiac substrate or HEP metabolism.

conclusionsPatients versus control subjects showed impaired LV diastolic function and altered myocardial substrate metabolism, but unchanged HEP metabolism. We found no direct relation between cardiac diastolic function and parameters of myocardial metabolism.

Indexed as

AgedCardiomyopathiesChromatography, High Pressure LiquidDiabetes Mellitus, Type 2DiastoleGlucoseGlycated HemoglobinHumansMagnetic Resonance ImagingMaleMiddle AgedMyocardiumPositron-Emission TomographyReproducibility of ResultsVentricular Function, LeftGlucoseGlycated Hemoglobin

Identifiers

PMID19815124
OpenAlexW1519485868

What Socratic holds

Textmetadata
Read underepoch 390

Registered trials

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 Socratic graph.