Evidence map›Paper›PMID 33754487›Full record

ArticleESC heart failure2021

Myocardial work index: a marker of left ventricular contractility in pressure- or volume overload-induced heart failure.

Bálint Károly Lakatos, Mihály Ruppert, Márton Tokodi, Attila Oláh, Szilveszter Braun, Christian Karime, Zsuzsanna Ladányi, Alex Ali Sayour, Bálint András Barta, Béla Merkely and 2 more

Open access · goldAbstract read
In one paragraph

Article in ESC heart failure, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
4.9field-weighted citation impact, top 4% 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

21 citing papers in PubMed, 34 citations in OpenAlex.

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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

12 authors at 2 institutions in 2 countries.

Bálint Károly LakatosHeart and Vascular Center, Semmelweis University, Városmajor St. 68, Budapest, H-1122, Hungary.
Mihály RuppertHeart and Vascular Center, Semmelweis University, Városmajor St. 68, Budapest, H-1122, Hungary.
Márton TokodiHeart and Vascular Center, Semmelweis University, Városmajor St. 68, Budapest, H-1122, Hungary.
Attila OláhHeart and Vascular Center, Semmelweis University, Városmajor St. 68, Budapest, H-1122, Hungary.
Szilveszter BraunHeart and Vascular Center, Semmelweis University, Városmajor St. 68, Budapest, H-1122, Hungary.
Christian KarimeHeart and Vascular Center, Semmelweis University, Városmajor St. 68, Budapest, H-1122, Hungary.
Zsuzsanna LadányiHeart and Vascular Center, Semmelweis University, Városmajor St. 68, Budapest, H-1122, Hungary.
Alex Ali SayourHeart and Vascular Center, Semmelweis University, Városmajor St. 68, Budapest, H-1122, Hungary.
Bálint András BartaHeart and Vascular Center, Semmelweis University, Városmajor St. 68, Budapest, H-1122, Hungary.
Béla MerkelyHeart and Vascular Center, Semmelweis University, Városmajor St. 68, Budapest, H-1122, Hungary.
Tamás RadovitsHeart and Vascular Center, Semmelweis University, Városmajor St. 68, Budapest, H-1122, Hungary.
Attila KovácsHeart and Vascular Center, Semmelweis University, Városmajor St. 68, Budapest, H-1122, Hungary.
Semmelweis University · HUZero to Three · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsWhile global longitudinal strain (GLS) is considered to be a sensitive marker of left ventricular (LV) function, it is significantly influenced by loading conditions. We hypothesized that global myocardial work index (GMWI), a novel marker of LV function, may show better correlation with load-independent markers of LV contractility in rat models of pressure-induced or volume overload-induced heart failure. METHODS AND

resultsMale Wistar rats underwent either transverse aortic constriction (TAC; n = 12) or aortocaval fistula creation (ACF; n = 12), inducing LV pressure or volume overload, respectively. Sham procedures were performed to establish control groups (n = 12/12). Echocardiographic loops were obtained to determine GLS and GMWI. Pressure-volume analysis with transient occlusion of the inferior caval vein was carried out to calculate preload recruitable stroke work (PRSW), a load-independent 'gold-standard' parameter of LV contractility. Myocardial samples were collected to assess interstitial and perivascular fibrosis area and also myocardial atrial-type natriuretic peptide (ANP) and brain-type natriuretic peptide (BNP) relative mRNA expression. Compared with controls, GLS was substantially lower in the TAC group (-7.0 ± 2.8 vs. -14.5 ± 2.5%; P < 0.001) and was only mildly reduced in the ACF group (-13.2 ± 2.4 vs. -15.4 ± 2.0%, P < 0.05). In contrast with these findings, PRSW and GMWI were comparable with sham in TAC (110 ± 26 vs. 116 ± 68 mmHg; 1687 ± 275 mmHg% vs. 1537 ± 662 mmHg%; both P = NS), while it was found to be significantly reduced in ACF (58 ± 14 vs. 111 ± 40 mmHg; 1328 ± 411 vs. 1934 ± 308 mmHg%, both P < 0.01). In the pooled population, GMWI (r = 0.70; P < 0.001) but not GLS (r = -0.23; P = 0.12) showed a strong correlation with PRSW. GLS correlated with interstitial (r = 0.61; P < 0.001) and perivascular fibrosis area (r = 0.54; P < 0.001), and also with myocardial ANP (r = 0.85; P < 0.001) and BNP relative mRNA expression (r = 0.75; P < 0.001), while GMWI demonstrated no or only marginal correlation with these parameters.

conclusionsBeing significantly influenced by loading conditions, GLS may not be a reliable marker of LV contractility in heart failure induced by pressure or volume overload. GMWI better reflects contractility in haemodynamic overload states, making it a more robust marker of systolic function, while GLS should be considered as an integrative marker, incorporating systolic function, haemodynamic loading state, and adverse tissue remodelling of the LV.

Indexed as

Heart FailureHeart VentriclesAnimalsMaleMyocardiumRatsRats, WistarVentricular Function, LeftEchocardiographyHeart failureMyocardial workPressure overloadVolume overload

Identifiers

PMID33754487
PMCPMC8120402
OpenAlexW3137038939

What OpenQuestion holds

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LicenceCC BY-NC
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Registered trials

None linked

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.