Evidence map›Paper›PMID 30155803›Full record

ArticleJournal of medical ultrasonics (2001)2019

Association of left ventricular myocardial dysfunction with diabetic polyneuropathy.

Satoshi Tabako, Masahiko Harada, Kunio Sugiyama, Hiroshi Ohara, Takanori Ikeda

Abstract read
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In one paragraph

Article in Journal of medical ultrasonics (2001), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.7field-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

2 citing papers in PubMed, 5 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

5 authors at 1 institution in 1 country.

Satoshi TabakoDepartment of Clinical Functional Physiology, Toho University Medical Center Omori Hospital, 6-11-1 Omorinishi, Ota-ku, Tokyo, 143-8541, Japan. satochin@med.toho-u.ac.jp.ORCID http://orcid.org/0000-0001-5935-0951
Masahiko HaradaDepartment of Clinical Functional Physiology, Toho University Medical Center Omori Hospital, 6-11-1 Omorinishi, Ota-ku, Tokyo, 143-8541, Japan.
Kunio SugiyamaDepartment of Clinical Functional Physiology, Toho University Medical Center Omori Hospital, 6-11-1 Omorinishi, Ota-ku, Tokyo, 143-8541, Japan.
Hiroshi OharaDivision of Cardiovascular Medicine, Department of Internal Medicine, Toho University Medical Center Omori Hospital, 6-11-1 Omorinishi, Ota-ku, Tokyo, 143-8541, Japan.
Takanori IkedaDivision of Cardiovascular Medicine, Department of Internal Medicine, Toho University Medical Center Omori Hospital, 6-11-1 Omorinishi, Ota-ku, Tokyo, 143-8541, Japan.
Toho University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe pathogenesis of left ventricular (LV) dysfunction in diabetes has been attracting attention. It has been reported that LV longitudinal systolic myocardial function determined by speckle tracking echocardiography (STE) is associated with diabetic polyneuropathy (DPN). However, the relationship between the severity of peripheral neuropathy and LV myocardial dysfunction is unknown. This study examined the relationship between the severity of DPN and echocardiographic parameters as well as clinical features.

methodsThe subjects were 166 patients (57 ± 14 years old) with diabetes who had a normal LV ejection fraction (≥ 55%). To assess LV longitudinal systolic function, global longitudinal strain (GLS) was calculated by two-dimensional STE as the average peak strain of 18 LV segments in three standard apical views. A nerve conduction study (NCS) was performed in each subject to assess the severity of neuropathy based on the NCS Baba Classification (Grade 0: no apparent abnormalities-Grade IV: abolition). Three nerves in the lower extremity were examined: tibial nerve (F-wave latency, motor nerve conduction velocity, and amplitude), sural nerve (sensory conduction velocity and amplitude), and peroneal nerve (motor nerve conduction velocity and amplitude).

resultsOf the 166 subjects, 112 subjects (67.5%) were confirmed to have DPN, and all the subjects were divided into two groups according to the presence/absence of DPN. When multivariate analysis was performed using significant factors from univariate logistic regression analysis as explanatory variables, GLS was found to be an independent determinant of DPN (odds ratio: 0.55, p < 0.001). In multivariate analysis of NCS data, F-wave latency was the most important determinant of DPN (odds ratio: 1.43, p < 0.001). There was a significant negative correlation between F-wave latency and GLS (r = - 0.43, p < 0.001). Regarding the relation between GLS and the severity of DPN, GLS was significantly lower in patients with Grade I or higher DPN than in patients without DPN, but showed no significant difference between the grades of neuropathy. In addition, GLS was significantly lower when 2-3 lower extremity nerves were affected by DPN than in patients without DPN.

conclusionPatients with diabetes may already have subclinical LV myocardial dysfunction when DPN is Grade I. Assessment of LV longitudinal systolic function by GLS may be important in diabetic patients with DPN.

Indexed as

AdultAgedDiabetic NeuropathiesEchocardiographyFemaleHeart VentriclesHumansMaleMiddle AgedMultivariate AnalysisNeural ConductionObserver VariationOdds RatioReproducibility of ResultsRetrospective StudiesSeverity of Illness IndexDiabetic cardiomyopathyDiabetic polyneuropathyEchocardiographyGlobal longitudinal strainNerve conduction study

Identifiers

PMID30155803
OpenAlexW2889513342

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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.