Observational Study Open Access
Copyright ©The Author(s) 2024. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Diabetes. Jun 15, 2024; 15(6): 1280-1290
Published online Jun 15, 2024. doi: 10.4239/wjd.v15.i6.1280
Evaluation of left ventricular systolic function in type 2 diabetes mellitus patients with and without peripheral vascular disease
Guang-An Li, Jun Huang, Li Fan, Department of Echocardiography, The Affiliated Changzhou Second People’s Hospital with Nanjing Medical University, Changzhou 213000, Jiangsu Province, China
ORCID number: Jun Huang (0000-0002-4680-5344).
Author contributions: Li GA and Huang J designed the study and carried out the study, data collection and analysis; Li GA wrote the manuscript; Huang J revised the manuscript; Huang J and Fan L collected the type 2 diabetes mellitus patients and normal controls; and Fan L performed the statistical analysis.
Supported by The Science and Technology Project of Changzhou Health Commission, No. ZD202342.
Institutional review board statement: This research was approved by the Human Research and Ethics Committee of the Affiliated Changzhou Second People’s Hospital of Nanjing Medical University, No. 2016-YLJSE009.
Informed consent statement: All the normal controls and type 2 diabetes mellitus patients underwent echocardiography. When they underwent this examination, we told them that we would like to do research on their cardiac function, and if they provided consent, we analysed their data; if they did not consent, we did not analyse their data.
Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article.
Data sharing statement: All data collected during the study are available from the corresponding author by request: Huang J, E-mail: 305669112@qq.com.
STROBE statement: The authors have read the STROBE Statement-checklist of items, and the manuscript was prepared and revised according to the STROBE Statement-checklist of items.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Jun Huang, MD, PhD, Chief Doctor, Doctor, Postdoc, Teacher, Department of Echocardiography, The Affiliated Changzhou Second People’s Hospital with Nanjing Medical University, No. 68 Gehu Road, Changzhou 213000, Jiangsu Province, China. 305669112@qq.com
Received: January 20, 2024
Revised: February 29, 2024
Accepted: April 26, 2024
Published online: June 15, 2024
Processing time: 143 Days and 8.5 Hours

Abstract
BACKGROUND

Peripheral vascular disease (PVD) is a common complication of type 2 diabetes mellitus (T2DM). Patients with T2DM have twice the risk of PVD as nondiabetic patients.

AIM

To evaluate left ventricular (LV) systolic function by layer-specific global longitudinal strain (GLS) and peak strain dispersion (PSD) in T2DM patients with and without PVD.

METHODS

Sixty-five T2DM patients without PVD, 57 T2DM patients with PVD and 63 normal controls were enrolled in the study. Layer-specific GLS [GLS of the epimyocardium (GLSepi), GLS of the middle myocardium (GLSmid) and GLS of the endocardium (GLSendo)] and PSD were calculated. Receiver operating characteristic (ROC) analysis was performed to calculate the sensitivity and specificity of LV systolic dysfunction in T2DM patients with PVD. We calculated Pearson’s correlation coefficients between biochemical data, echocardiographic characteristics, and layer-specific GLS and PSD.

RESULTS

There were significant differences in GLSepi, GLSmid and GLSendo between normal controls, T2DM patients without PVD and T2DM patients with PVD (P < 0.001). Trend tests revealed a ranking of normal controls > T2DM patients without PVD > T2DM patients with PVD in the absolute value of GLS (P < 0.001). PSD differed significantly between the three groups, and the trend ranking was as follows: normal controls < T2DM patients without PVD < T2DM patients with PVD (P < 0.001). ROC analysis revealed that the combination of layer-specific GLS and PSD had high diagnostic efficiency for detecting LV systolic dysfunction in T2DM patients with PVD. Low-density lipoprotein cholesterol was positively correlated with GLSepi, GLSmid and PSD (P < 0.05), while LV ejection fraction was negatively correlated with GLSepi, GLSmid and GLSendo in T2DM patients with PVD (P < 0.01).

CONCLUSION

PVD may aggravate the deterioration of LV systolic dysfunction in T2DM patients. Layer-specific GLS and PSD can be used to detect LV systolic dysfunction accurately and conveniently in T2DM patients with or without PVD.

Key Words: Type 2 diabetes mellitus; Peripheral vascular disease; Speckle tracking echocardiography; Global longitudinal strain; Peak strain dispersion

Core Tip: Left ventricular (LV) systolic function is impaired in type 2 diabetes mellitus (T2DM) patients, especially those with peripheral vascular disease (PVD). Layer-specific global longitudinal strain (GLS) and PSD can be used to detect LV systolic dysfunction flexibly, accurately and conveniently. The level of low-density lipoprotein cholesterol was positively correlated with global longitudinal strain of the epimyocardium, global longitudinal strain of the middle myocardium and PSD. PVD may aggravate the LV systolic dysfunction in T2DM patients. Layer-specific GLS and PSD can be used to detect LV systolic dysfunction flexibly, accurately and conveniently in T2DM patients with or without PVD.
INTRODUCTION

Peripheral vascular disease (PVD) of the lower extremities affects more than 200 million people worldwide, and its prevalence is expected to increase in the coming years[1,2]. Compared with coronary heart disease (CHD) and/or carotid artery disease, PVD has not been well studied[3]. PVD is a common complication of type 2 diabetes mellitus (T2DM), as are cardiovascular events, neural degeneration, kidney failure, blindness, and dementia. Patients with T2DM have twice the risk of PVD in as nondiabetic patients[4]. Both the microvasculature and large vessels are affected by classical cross-talk[5].

T2DM may progress to heart failure even in the absence of myocardial ischaemia and hypertension[6,7]. Cardiac magnetic resonance imaging and echocardiography are the most commonly used methods for detecting subclinical left ventricle (LV) systolic and diastolic dysfunction in T2DM patients[8-10]. Layer-specific global longitudinal strain (GLS) and peak strain dispersion (PSD), derived from two-dimensional speckle tracking echocardiography (STE), accurately detect LV systolic dysfunction in patients with most cardiovascular diseases, such as cardiomyopathy[11,12], coronary artery disease (CAD)[13], and hypertension[14].

Even in the subclinical stage of LV ejection fraction (LVEF) preservation, the LV systolic function of T2DM patients may be impaired, and subclinical dysfunction can be evaluated by STE[15-17]. Whether PVD aggravates the impairment of LV systolic function in T2DM patients has not been further investigated. We propose that the LV systolic function of T2DM patients is further impaired by PVD. We added STE to the diagnostic repertoire of this patient population to evaluate LV systolic function impairment early in T2DM patients with PVD and provide a further reference for reducing the incidence of adverse cardiovascular events. The purpose of this study was to evaluate LV systolic function in T2DM patients with PVD by layer-specific GLS and PSD, observe whether LV systolic function in T2DM patients with PVD is further impaired, and calculate the sensitivity and specificity of the two techniques in evaluating LV systolic function in T2DM patients with PVD.

MATERIALS AND METHODS
Study population

We enrolled 65 T2DM patients without PVD and 57 T2DM patients with PVD. T2DM was diagnosed according to the American Diabetes Association criteria[18]. T2DM patients with PVD were defined by an ankle-brachial index < 0.9. Patients with a history of arrhythmia, CAD, myocardial infarction, cardiomyopathy, valvular disease, thyroid disease, neoplastic disease, or kidney failure were excluded from the study. Sixty-three normal subjects of similar age and sex were enrolled as controls.

Biochemistry

The levels of fasting plasma glucose (FPG), glycated haemoglobin (HbA1c), total cholesterol, triglyceride (TG), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), lipoprotein a (LPA), blood urea nitrogen (BUN), and serum creatinine (SCr) were measured in hospital.

Conventional 2D Doppler echocardiography

Conventional echocardiography was performed with a GE Vivid E9 ultrasound diagnostic system equipped with an M5s 3.5-5 MHz transducer (GE Vingmed Ultrasound, Horten, Norway). M-mode in the parasternal long-axis view of the LV was used to measure the left atrial diameter (LAd), interventricular septum thickness (IVSd), LV posterior wall thickness (LVPWd), and LV diameter (LVDd) in the end-diastole period, and the mitral annular plane systolic excursion (MAPSE) was measured in the apical four-chamber view. Simpson′s biplane method was used to measure LV end-diastolic (LVEDV) and end-systolic volume (LVESV) and to calculate LVEF. Pulsed wave Doppler imaging of the mitral valve was used to measure the peak early and late diastolic mitral annular velocities (E and A, respectively), and the ratio of E/A was then calculated. The peak early (e′) diastolic annular velocities were obtained by averaging the values at the septum and lateral positions using tissue Doppler imaging, and E/e′ was calculated.

Two-dimensional speckle tracking echocardiography

Three consecutive cardiac cycles of apical three-, four- and two-chamber views were recorded for off-line analyses. Layer-specific GLS and PSD were measured by EchoPAC software (EchoPAC Version: 203, GE Vingmed Ultrasound, Norway).

Statistical analysis

All the data analyses were performed with SPSS 26.0 software (SPSS, Chicago, IL, United States). The normality of all variables was assessed by the Shapiro-Wilk test. Variables were compared between the T2DM patients, T2DM patients with PVD and normal controls by one-way analysis of variance or the Kruskal-Wallis rank sum test, as appropriate. We defined layer-specific GLS and PSD values in the normal controls as the normal state and considered the values of T2DM patients with PVD to be abnormal. These values in T2DM patients with PVD were determined through receiver operating characteristic (ROC) curve analysis by MedCalc software. Correlations between biochemical, echocardiographic, and layer-specific GLS and PSD values were tested using Pearson or Spearman correlation tests, as appropriate. The categorical variables are presented as frequencies and percentages. Normally distributed data are presented as mean ± SD, non-normally distributed data as median (interquartile range). A P value < 0.05 was considered significant for all tests.

Reproducibility and repeatability

Twenty random patients among all enrolled subjects were selected for interobserver and interobserver variability analysis of the GLS of the epimyocardial region (GLSepi), GLS of the middle myocardial region (GLSmid), GLS of the endomyocardial region (GLSendo) and PSD.

RESULTS
Clinicodemographic characteristics and laboratory results

Significant differences were detected in weight, body mass index, SBP, DBP, HR, HbA1c, HDL-C, FPG and BUN between normal controls, T2DM patients without PVD and T2DM patients with PVD (P < 0.05). No significant differences were found in age, sex, height, BSA, TG, TC, LDL-C, LPA or SCr between the normal controls, T2DM patients without PVD and T2DM patients with PVD (P > 0.05; Table 1).

Table 1 Clinical parameters of patients among normal controls, type 2 diabetes mellitus patients without peripheral vascular disease and type 2 diabetes mellitus patients with peripheral vascular disease.
Clinical parameters
Normal controls (n = 63)
T2DM without PVD (n = 65)
T2DM with PVD (n = 57)
P value
Age, yr53.29 ± 7.5554.75 ± 7.7256.73 ± 7.760.053
Male, n (%)31 (49)38 (58)38 (67)0.103
Height, cm164.84 ± 7.07165.83 ± 8.61164.20 ± 6.980.492
Weight, kg63.56 ± 10.0968.95 ± 11.76a67.32 ± 11.350.021
BMI, kg/m223.33 ± 2.9124.97 ± 3.1224.89 ± 3.40a0.005
BSA, m21.67 ± 0.161.74 ± 0.191.71 ± 0.170.054
SBP, mmHg77.90 ± 0.5782.17 ± 10.81a80.18 ± 10.580.001
DBP, mmHg123.38 ± 11.12132.77 ± 16.29a130.70 ± 17.30a0.049
HR, bpm66.95 ± 8.6175.58 ± 9.91a74.80 ± 8.20a< 0.001
HbA1c, %5.48 ± 0.359.47 ± 2.39a9.94 ± 2.39a< 0.001
TC, mmol/L4.53 ± 0.854.36 ± 1.064.55 ± 1.030.550
TG, mmol/L1.30 (0.89, 1.80)1.52 (0.93, 2.43)1.64 (1.01, 2.07)0.073
HDL-C, mmol/L1.25 ± 0.331.08 ± 0.291.08 ± 0.340.013
LDL-C, mmol/L2.65 ± 0.702.58 ± 0.842.70 ± 0.830.729
LPA, g/L0.17 (0.09, 0.29)0.12 (0.06, 0.32)0.16 (0.09, 0.25)0.772
FPG, mmol/L4.99 (4.57, 5.28)10.02 (7.44, 13.64)a10.25 (8.29, 14.07)a< 0.001
BUN, mmol/L4.90 (3.60, 6.40)5.65 (4.70, 6.58)6.00 (4.70, 7.40)a0.015
SCr, μmol/L65.00 (56.00, 76.00)61.00 (51.75, 81.95)61.70 (52.20, 73.00)0.772
Medication (%)
ACEI/ARB-13 (20)12 (21)
Calcium channel blocker-10 (15)20 (35)
β-blocker-1 (2)2 (4)
SGLT-2 inhibitor-14 (22)19 (33)
Metformin-36 (55)36 (63)
Insulin-41 (63)42 (74)
aP < 0.05, indicates significantly different when type 2 diabetes mellitus (T2DM) patients without peripheral vascular disease (PVD) or T2DM patients with PVD compared with the normal controls.
T2DM: Type 2 diabetes mellitus; BMI: Body mass index; BSA: Body surface area; SBP: Systolic blood pressure; DBP: Diastolic blood pressure. HR: Heart rate; FPG: Fasting plasma glucose; HbA1c: Glycated haemoglobin; TC: Total cholesterol; TG: Triglyceride; HDL-C: High density lipoprotein cholesterol; LDL-C: Low-density lipoprotein cholesterol; LPA: Lipoprotein a; BUN: Blood urea nitrogen; SCr: Serum creatinine.
Echocardiographic parameters

The LAd and E/e′ in the T2DM patients were significantly higher than those in the normal controls, while the E, A, E/A and e′ were significantly lower. No significant differences were found in IVSd, LVPWd, LVDd, LVEDV, LVESV or LVEF between normal controls, T2DM patients without PVD and T2DM patients with PVD (P > 0.05; Table 2).

Table 2 Echocardiographic parameters among normal controls, type 2 diabetes mellitus patients without peripheral vascular disease and type 2 diabetes mellitus patients with peripheral vascular disease.
Echocardiographic parameters
Normal controls (n = 63)
T2DM without PVD (n = 65)
T2DM with PVD (n = 57)
P value
LAd, mm34.42 ± 2.7635.47 ± 3.2536.17 ± 3.82a0.015
IVSd, mm9.39 ± 0.749.20 ± 0.979.27 ± 0.970.477
LVPWd, mm9.05 ± 0.778.98 ± 0.999.13 ± 1.060.685
LVDd, mm46.35 ± 2.9745.42 ± 3.6046.60 ± 3.240.110
LVEDV, mL76.76 ± 14.8974.02 ± 16.7478.04 ± 15.980.358
LVESV, mL26.75 ± 6.5326.12 ± 7.1326.63 ± 6.470.857
LVEF, %65.19 ± 3.9864.98 ± 3.3965.81 ± 4.160.478
MAPSE, mm14.44 ± 1.4914.16 ± 1.8513.23 ± 1.87a,b0.001
E, m/s0.84 ± 0.130.75 ± 0.15a0.79 ± 0.13a0.001
A, m/s0.70 ± 0.150.74 ± 0.180.81 ± 0.17a,b0.002
E/A1.24 ± 0.281.08 ± 0.34a1.01 ± 0.27a< 0.001
e′, m/s0.11 ± 0.020.09 ± 0.02a0.09 ± 0.02a< 0.001
E/e′8.09 ± 1.548.66 ± 1.539.45 ± 1.92a,b< 0.001
aP < 0.05, indicates significantly different when type 2 diabetes mellitus (T2DM) patients without peripheral vascular disease (PVD) or T2DM patients with PVD compared with the normal controls.
bP < 0.05, indicates significantly different when T2DM patients with PVD compared with T2DM patients without PVD.
LAd: Left atrial diameter; IVSd: Interventricular septal wall thickness in end-diastolic period; LVPWd: Left ventricular posterior wall thickness in end-diastolic period; LVDd: Left ventricular diameter in end-diastolic period; LVEDV: Left ventricular end-diastolic volume; LVESV: Left ventricular end-systolic volume; LVEF: Left ventricular ejection fraction; MAPSE: Mitral annular plane systolic excursion; E: Peak velocity during early diastole of anterior mitral leaflet; A: Peak velocity during late diastole of anterior mitral leaflet; e′: Peak early diastolic annular velocities using TDI by averaging the values at the septum and lateral positions; PVD: Peripheral vascular disease; T2DM: Type 2 diabetes mellitus.
Layer-specific GLS and PSD

GLSepi, GLSmid and GLSendo differed between normal controls, T2DM patients without PVD and T2DM patients with PVD (P < 0.001), the trend tests showing a ranking of normal controls > T2DM without PVD > T2DM with PVD for the absolute values of all three (P < 0.001). There was a significant difference in PSD between the three groups, and the trend test results were as follows: normal controls < T2DM without PVD < T2DM with PVD (P < 0.001; Figures 1 and 2, and Table 3).

Figure 1
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Figure 1 Line graph showing the differences in layer-specific global longitudinal strain and peak strain dispersion between normal controls, type 2 diabetes mellitus patients without peripheral vascular disease and type 2 diabetes mellitus patients with peripheral vascular disease. aP < 0.05; bP < 0.01. GLSEpi: Global longitudinal strain of the epimyocardium; GLSMid: Global longitudinal strain of the middle myocardium; GLSEndo: Global longitudinal strain of the endocardium; PSD: Peak strain dispersion; LDL-C: Low-density lipoprotein cholesterol; LVEF: Left ventricular ejection fraction; PVD: Peripheral vascular disease; T2DM: Type 2 diabetes mellitus.
Figure 2
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Figure 2 Trend analysis of layer-specific global longitudinal strain and peak strain dispersion between normal controls, type 2 diabetes mellitus patients without peripheral vascular disease and type 2 diabetes mellitus patients with peripheral vascular disease. bP < 0.01. GLSEpi: Global longitudinal strain of the epimyocardium; GLSMid: Global longitudinal strain of the middle myocardium; GLSEndo: Global longitudinal strain of the endocardium; PSD: Peak strain dispersion; LDL-C: Low-density lipoprotein cholesterol; LVEF: Left ventricular ejection fraction; PVD: Peripheral vascular disease; T2DM: Type 2 diabetes mellitus.
Table 3 Layer-specific global longitudinal strain and peak strain dispersion among normal controls, type 2 diabetes mellitus patients without peripheral vascular disease and type 2 diabetes mellitus patients with peripheral vascular disease.
Normal controls (n = 63)
T2DM without PVD (n = 65)
T2DM with PVD (n = 57)
P value
P trend
GLSepi, %-18.65 ± 1.55-17.37 ± 1.85a-16.92 ± 2.21a< 0.001< 0.001
GLSmid, %-21.57 ± 1.81-19.98 ± 2.08a-19.47 ± 2.50a< 0.001< 0.001
GLSendo, %-25.03 ± 2.21-23.12 ± 2.43a-22.72 ± 2.85a< 0.001< 0.001
PSD, msec30.63 ± 7.2935.03 ± 10.81a39.37 ± 12.42a,b< 0.001< 0.001
aP < 0.05, indicates significantly different when type 2 diabetes mellitus (T2DM) patients without peripheral vascular disease (PVD) or T2DM patients with PVD compared with the normal controls.
bP < 0.05, indicates significantly different when T2DM patients with PVD compared with T2DM patients without PVD.
GLS: Global longitudinal strain; GLSEpi: Global longitudinal strain of the epimyocardial; GLSMid: Global longitudinal strain of the middle myocardial; GLSEndo: Global longitudinal strain of the endomyocardial; PSD: Peak strain dispersion; T2DM: Type 2 diabetes mellitus; PVD: Peripheral vascular disease.

Pairwise comparisons of groups revealed a significant difference in PSD between T2DM patients without PVD and T2DM patients with PVD (P < 0.05). There was no significant difference in layer-specific GLS between these two groups (P > 0.05).

ROC analysis to measure the diagnostic value of layer-specific LV GLS and PSD for identifying LV systolic dysfunction in T2DM patients with PVD

The area under the ROC curve (AUC) of the combination of GLSepi, GLSmid, GLSendo and PSD was 0.801, and the best cut-off value was 0.44, which had a sensitivity of 75.44% and specificity of 77.78%. This AUC was greater than the AUCs of the individual indices alone.

There were no significant differences between the AUCs of layer-specific LV GLS and PSD (P > 0.05; Table 4 and Figure 3).

Figure 3
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Figure 3 Receiver operating characteristic analysis for detecting the accuracy of left ventricular systolic dysfunction in type 2 diabetes mellitus patients with peripheral vascular disease. GLSEpi: Global longitudinal strain of the epimyocardium; GLSMid: Global longitudinal strain of the middle myocardium; GLSEndo: Global longitudinal strain of the endocardium; PSD: Peak strain dispersion; LDL-C: Low-density lipoprotein cholesterol; LVEF: Left ventricular ejection fraction; PVD: Peripheral vascular disease; T2DM: Type 2 diabetes mellitus.
Table 4 Receiver operating characteristic curve analysis for the detection the left ventricular systolic function in type 2 diabetes mellitus patients with peripheral vascular disease.
ROC
GLSepi
GLSmid
GLSendo
PSD
Combined
Sensitivity, %50.8856.1466.1673.6875.44
Specificity, %85.7185.7177.7865.0877.78
Youden index0.36590.41850.40940.38760.5322
AUC (95%CI)0.735 (0.647-0.811)0.753 (0.666-0.827)0.750 (0.663-0.825)0.735 (0.646-0.811)0.801 (0.719-0.869)
Associated criterion-17.0-19.8-23.5320.44
P value0.0640.1270.1030.050
P values mean combined evaluation compare with global longitudinal strain and peak strain dispersion. GLSEpi: Global longitudinal strain of the epimyocardial; GLSMid: Global longitudinal strain of the middle myocardial; GLSEndo: Global longitudinal strain of the endomyocardial; PSD: Peak strain dispersion; ROC: Receiver operating characteristic; AUC: Area under the curve.
Correlations between layer-specific LV GLS and PSD and between clinical parameters, laboratory results, and echocardiographic parameters in T2DM patients with PVD

In T2DM patients with PVD, LDL-C was positively correlated with GLSepi, GLSmid and PSD (P < 0.05), while LVEF was negatively correlated with GLSepi, GLSmid and GLSendo (P < 0.01). BUN was positively correlated with GLSepi and PSD (P < 0.05). SCr was positively correlated with GLSepi (P < 0.05). MAPSE was negatively correlated with GLSmid (P < 0.05; Table 5 and Figure 4).

Figure 4
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Figure 4 The correlation test showed that low-density lipoprotein-cholesterol was positively correlated with global longitudinal strain of the epimyocardium, global longitudinal strain of the middle myocardium and peak strain dispersion, while left ventricular ejection fraction was negatively correlated with global longitudinal strain of the epimyocardium and global longitudinal strain of the middle myocardium and global longitudinal strain of the endocardium. GLSEpi: Global longitudinal strain of the epimyocardium; GLSMid: Global longitudinal strain of the middle myocardium; GLSEndo: Global longitudinal strain of the endocardium; PSD: Peak strain dispersion; LDL-C: Low-density lipoprotein cholesterol; LVEF: Left ventricular ejection fraction.
Table 5 Correlation test in type 2 diabetes mellitus patients with peripheral vascular disease.
Varibles
GLSepi
GLSmid
GLSendo
PSD
r value
P value
r value
P value
r value
P value
r value
P value
BMI0.0890.5100.0930.491-0.0090.945-0.0170.900
HbA1c-0.0110.9350.0280.839-0.0190.887-0.2250.095
TC0.1900.1580.1790.1820.0400.7670.2930.027
TG-0.1260.349-0.1530.257-0.1480.2710.0170.889
HDL-C-0.0330.812-0.0290.834-0.1650.2280.0930.499
LDL-C0.3400.0100.3270.0140.2040.1310.2900.030
LPA0.1590.2540.1340.3390.1840.187-0.1030.465
BUN0.2930.0330.2480.0740.1490.2870.2920.034
SCR0.3010.0270.2640.0530.1660.2310.2050.137
LVEF-0.4340.001-0.4390.001-0.447< 0.001-0.1090.420
MAPSE-0.2480.063-0.3130.018-0.2600.051-0.1110.411
BMI: Body mass index; HbA1c: Glycated haemoglobin; TC: Total cholesterol; TG: Triglyceride; HDL-C: High density lipoprotein cholesterol; LDL-C: Low-density lipoprotein cholesterol; LPA: Lipoprotein a; BUN: Blood urea nitrogen; SCR: Serum creatinine; GLS: Global longitudinal strain; GLSEpi: Global longitudinal strain of the epimyocardial; GLSMid: Global longitudinal strain of the middle myocardial; GLSEndo: Global longitudinal strain of the endomyocardial; PSD: Peak strain dispersion; LVEF: Left ventricular ejection fraction; MAPSE: Mitral annular plane systolic excursion.
Intraobserver and interobserver variability

The intraclass correlation coefficients of layer-specific GLS and PSD were both greater than 0.95 (Table 6).

Table 6 Intraclass correlation coefficients for intra- and inter-observer variability for layer specific global longitudinal strain and peak strain dispersion.
Variable
Inter-observer variability
Intra-observer variability
ICC
95%CI
ICC
95%CI
GLSendo0.9550.887-0.9820.9640.910-0.986
GLSmid0.9630.906-0.9850.9700.924-0.988
GLSepi0.9600.900-0.9840.9700.925-0.988
PSD0.9560.889-0.9830.9790.946-0.992
GLSEpi: Global longitudinal strain of the epimyocardial; GLSMid: Global longitudinal strain of the middle myocardial; GLSEndo: Global longitudinal strain of the endomyocardial; PSD: Peak strain dispersion; ICC: Intraclass correlation coefficient.
DISCUSSION

The findings of this study were as follows: (1) LV systolic function was impaired in both T2DM patients without PVD and T2DM patients with PVD, and LV systolic dysfunction was more serious in T2DM patients with PVD; (2) layer-specific GLS and PSD can be used to detect LV systolic dysfunction flexibly, accurately and conveniently; and (3) LDL-C was positively correlated with GLSepi, GLSmid and PSD.

The most important complications of T2DM are vascular complications, which are the primary cause of death in patients with T2DM. PVD is considered one of the macrovascular complications in T2DM patients, and the complications include CHD, heart failure, and cerebrovascular disease[19].

Layer-specific GLS and PSD can predict LV systolic function and synchronism. Huang et al[20] used layer-specific GLS to evaluate LV systolic function in primary hypertension patients and found that LV systolic function was impaired. Layer-specific GLS has also been used to detect LV systolic function in hypertrophic cardiomyopathy, acute coronary syndrome, Anderson-Fabry disease, and other conditions[12,21,22]. Ji and Zhang[23] used PSD to assess LV systolic synchrony in patients with systemic lupus erythematosus (SLE) and found that LV systolic synchrony was impaired. PSD can be used as a new, reliable index to evaluate LV systolic synchrony. PSD has also been used to evaluate LV systolic function and synchrony in hypertrophic cardiomyopathy, rheumatoid arthritis, and diabetes mellitus[24-26]. Therefore, using layer-specific GLS and PSD to evaluate LV systolic function is considered accurate and reliable.

Our research revealed that T2DM patients with and without PVD had decreased layer-specific GLS and increased PSD but similar LVEDV, LVESV, and LVEF to those of normal controls. Sustained hyperglycaemia can cause myocardial hypertrophy, fibrosis and decreased myocardial compliance, ultimately resulting in LV systolic dysfunction[27,28]. By comparing the three groups, we only found that the PSD in T2DM patients with PVD was greater than that in T2DM patients without a PVD and greater than that in normal controls. We concluded that T2DM patients with PVD are more likely to progress to more severe LV systolic dysfunction. PVD causes inflammatory damage to vessel walls due to endothelial cell dysfunction, resulting in stenosis and occlusion[29]. Hyperglycaemia blocks endothelial NO synthase and increases the amount of reactive oxygen species, causing vascular wall damage[30], and C-reactive protein, a risk factor for PVD, is elevated in patients with DM[3,31].

ROC analysis revealed that both layer-specific GLS and PSD had good predictive value for LV systolic dysfunction in T2DM patients with PVD. The combination of layer-specific GLS and PSD had a high AUC for evaluating LV systolic dysfunction, and the combined index also had the best predictive value for cardiac dysfunction in T2DM patients with PVD.

LDL-C was positively correlated with GLSepi, GLSmid and PSD in T2DM patients with PVD, which indicated that LDL-C should be controlled in T2DM patients when they have been diagnosed with PVD.

Limitations

First, the sample size of the study was relatively small. A larger sample size could improve the robustness and generalizability of the findings. Second, the study was conducted at a single centre, which may limit the generalizability of the findings to broader populations. Multicentre studies involving diverse demographic and geographic populations could enhance the external validity of the results.

CONCLUSION

PVD may aggravate the deterioration of LV systolic dysfunction in T2DM patients. Layer-specific GLS and PSD can be used to detect LV systolic dysfunction flexibly, accurately and conveniently in T2DM patients with or without PVD.

ACKNOWLEDGEMENTS

We would like to thank the Department of Echocardiography, Cardiology and Endocrinology, The Affiliated Changzhou Second People’s Hospital with Nanjing Medical University.

Footnotes

Provenance and peer review: Unsolicited article; Externally peer-reviewed.

Peer-review model: Single-blind

Specialty type: Endocrinology and metabolism

Country of origin: China

Peer-review report’s classification

Scientific Quality: Grade B, Grade B, Grade C, Grade C

Novelty: Grade B, Grade B

Creativity or Innovation: Grade B, Grade B

Scientific Significance: Grade B, Grade B

P-Reviewer: Horowitz M, Australia; Lee KS, South Korea; Roomi AB, Iraq; Wu QN, China S-Editor: Li L L-Editor: A P-Editor: Yuan YY

References
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