Left atrioventricular coupling and left atrial abnormality in patients with acute myocardial infarction with and without hyperglycemia assessed with 3.0T cardiac magnetic resonance imaging feature tracking

Introduction

Acute myocardial infarction (AMI) is a major cause of morbidity and mortality worldwide (1,2). Stress hyperglycemia is often present in patients with AMI and may increase the risk of adverse cardiovascular outcomes in this population (3,4). Admission blood glucose level (aBGL) is commonly used as a valuable and readily accessible indicator for determining stress hyperglycemia. Clarifying the role of stress hyperglycemia in myocardial abnormalities is of great significance for improving the risk assessment and clinical management of patients with AMI. However, previous studies on myocardial abnormalities in hyperglycemic patients with AMI have mainly focused on left ventricular (LV) structure and function (5-7).

The left atrium is a critical component in modulating LV filling and regulating cardiac output throughout the entire cardiac cycle (8). Atrial enlargement is an important precursor of left atrial (LA) remodeling, which is associated with atrial fibrillation development in AMI (9). Beyond LA size, LA phasic function is being increasingly recognized as an important determinant of cardiovascular events (10). As reported in previous studies (11,12), both AMI and hyperglycemia can induce complex changes in LV function, which may further lead to LA remodeling. Although some studies (13-15) have observed LA damage in AMI via echocardiology and cardiac magnetic resonance imaging (MRI), the potential additive effect of hyperglycemia on LA function among patients with AMI has not been fully explored.

Cardiac MRI can provide a reliable means of depicting cardiac structure and function due to its excellent spatial and temporal resolution (16,17). Similar to those of the left ventricle, the size and function of the left atrium can be quantified using several indices (18-20). Among them, LA strain derived from cardiac MRI feature tracking, which reflects the change in distance from the posterior LA wall to the atrioventricular junction, allows for the sensitive quantification of LA phasic function (21). Therefore, this study aimed to investigate whether hyperglycemia aggravates the impairment of LA function in patients with AMI as indicated by cardiac MRI and to characterize the atrioventricular coupling in AMI. We present this article in accordance with the STROBE reporting checklist (available at https://qims.amegroups.com/article/view/10.21037/qims-24-1757/rc).

Methods

The study was conducted in accordance with the Declaration of Helsinki (as revised in 2013) and was approved by the Biomedical Research Ethics Committee of the West China hospital of Sichuan University (approval No. 2019-756). The requirement for individual consent was waived due to the retrospective nature of the analysis.

Study population

We retrospectively screened 275 consecutive patients with AMI who underwent enhanced cardiac MRI from January 1, 2012, to July 30, 2023. The diagnosis of AMI was made based on the fourth universal definition of myocardial infarction (22). Patients were excluded if they had coexisting acquired cardiomyopathy, severe valvular disease requiring surgical intervention, congenital heart disease, poor image quality, and missing aBGL information (Figure S1). The control group comprised sex- and age-matched individuals that met the inclusion criteria, which included the absence of dyspnea, chest pain, palpitation, or any other symptoms related to cardiovascular disease, as well as the absence of any abnormalities on cardiac MRI [such as wall motion abnormality, perfusion defect, and myocardial late gadolinium enhancement (LGE)].

Finally, a total of 208 patients (168 males and 40 females; mean age 57±12 years) and 70 controls (51 males and 19 females; mean age 56±13 years) were included. Based on the presence of admission stress hyperglycemia (aBGL of ≥7.8 mmol/L) (23), patients with AMI were classified as admission normoglycemia (aNGL; n=120; 98 males and 22 females) as admission hyperglycemia (aHGL; n=88; 70 males and 18 females).

Cardiac MRI scanning protocol

Cardiac MRI scans were conducted with participants in the supine position via 3.0T whole-body scanners (Tim Trio/MAGNETOM Skyra; Siemens Healthineers, Erlangen, Germany), equipped with a dedicated two-element cardiac-phased array coil and a standard electrocardiography (ECG)-triggering device. Following each survey scan, 8–12 continuous cine images in the short-axis view and two-, three-, and four-chamber cine images in the long-axis view were acquired using a balanced steady-state free-precession sequence [repetition time (TR) =2.8 ms/3.4 ms, echo time (TE) =1.22 ms, flip angle =40°/50°, slice thickness =8 mm, field of view (FOV) =250×300 mm²/340×285 mm², matrix size =208×139/256×166 pixels]. Gadolinium-based contrast agent at a dose of 0.2 mL/kg was injected intravenously at a flow rate of 2.5–3.0 mL/s, followed by a 20-mL saline flush at a flow rate of 3.0 mL/s. After 10–15 minutes, LGE imaging was acquired using a segmented turbo FLASH phase-sensitive inversion recovery sequence (TR =750/512 ms, TE =1.18/1.24 ms, flip angle =20°/40°, slice thickness =8 mm, FOV =240×300/288×360 mm², matrix size =256×184/256×125 pixels).

Imaging analysis

Cardiac MRI image analyses were performed on dedicated software (CVI42, Circle Cardiovascular Imaging, Inc., Calgary, Canada) by two experienced radiologists blinded to the patients’ basic information. Any disagreement was through discussion.

LA volume (LAV) and function analysis

In the two- and four-chamber cine images, the LA endocardial and epicardial borders were manually delineated at maximal and minimal LAV states, with pulmonary veins and the LA appendage being excluded. Cardiac MRI feature tracking technology was used to automatically track each myocardial voxel in all frames throughout the entire cardiac cycle, with end-diastole used as the reference phase. Subsequently, three phases of LA global longitudinal strain (GLS) were automatically obtained, including LA reservoir strain (εs), conduit strain (εe), and booster strain (εa) (Figure 1). Corresponding phasic strain rates, including peak positive strain rate (SRs), peak early negative strain rate (SRe), and late peak negative strain rate (SRa), were also obtained automatically.

Figure 1 Example images of LA phasic strains in a patient with AMI and hyperglycemia. The images on the left represent pseudocolor cine images in two-chamber and four-chamber long-axis views in the states of (A) maximal and (B) minimal LA volumes, respectively. (C) The image on the right is the LA strain-time curve. LA, left atrial; εs, reservoir strain; εe, conduit strain; εa, booster strain.

LAV analysis was performed using the validated biplane area-length method (24). The maximum LAV (LAVmax), LAV prior to atrial contraction (LAVpre-a), and minimum LAV (LAVmin) were assessed at LV end-systole, LV diastole before LA contraction, and late LV diastole after LA contraction, respectively. LAV index (LAVI) was obtained by indexing LAV to the body surface area (BSA). LA ejection fraction (LAEF), including LA total ejection fraction (LATEF), LA passive ejection fraction (LAPEF), and LA active ejection fraction (LAAEF) were calculated as volumetric measures of reservoir, conduit, and booster phases, respectively. The formulae for calculation were as follows (25): LATEF = (LAVmax − LAVmin) × 100%/LAVmax; LAPEF = (LAVmax − LAVpre-a) × 100%/LAVmax; LAAEF = (LAVpre-a − LAVmin) × 100%/LAVpre-a.

LV structure and function analysis

The end-diastolic and end-systolic LV endocardial and epicardial contours were manually delineated in serial short-axis slices, and LV end diastolic volume (LVEDV), end systolic volume (LVESV), stroke volume (LVSV), ejection fraction (LVEF), and LV mass were automatically obtained. Following this, LVEDV, LVESV, LVSV, and LV mass were indexed to BSA to obtain the LVEDV index (LVEDVI), LVESV index (LVESVI), LVSV index (LVSVI), and LVM index (LVMI), respectively.

Next, in the three-dimensional feature tracking module, we manually delineated the end-diastolic endocardial and epicardial contours in long-axis two-chamber, four-chamber, and serial short-axis slices. Feature tracking was then performed using the end-diastole phase as the reference phase, and the LV global radial strain (GRS), global circumferential strain (GCS), and GLS were automatically obtained.

Intra- and interobserver reproducibility analysis

We randomly selected 30 participants (20 patients with AMI and 10 controls) to determine the reproducibility of the LA indicators. To evaluate the intraobserver variability, LA indicators were measured once more by the same radiologist after 1 month. To determine the interobserver variability, LA indicators were measured again by a second blinded investigator.

Statistical analysis

The normality of data distributions was assessed using the Kolmogorov-Smirnov test. Continuous variables are reported as the mean ± standard deviation (normally distributed) or as the median with interquartile range (IQR; nonnormally distributed), while categorical variables are reported as frequencies (%). To compare the continuous variables between three groups, one-way analysis of variance followed by the least significant difference (LSD) post hoc test or Kruskal-Wallis test was first completed, after which the Mann-Whitney test was performed as appropriate. To compare continuous variables between two groups, the Student’s t-test or Mann-Whitney test was used as appropriate. To compare categorical variables, Chi-squared tests or the Mann-Whitney test was applied. Pearson or Spearman correlation was applied for correlation analysis. Linear regression analysis was performed to determine the factors related to LA strain. Age, sex, and variables with P<0.1 in univariate analysis were included in the stepwise multivariate linear regression model. The intraclass correlation coefficient (ICC) was used to assess the variability of LA indicators. For all statistical analyses, a two-tailed P value <0.05 was considered statistically significant. All statistical analyses were conducted with SPSS 23.0 (IBM Corp., Armonk, NY, USA) and GraphPad Prism 10 (Dotmatics, Boston, MA, USA).

Results

Baseline clinical characteristics

The baseline characteristics of patients with AMI and controls are summarized in Table 1. There was no significant difference in age or sex distribution between controls and patients with AMI (both P values >0.05). Patients with AMI had a significantly higher body mass index, systolic blood pressure, and diastolic blood pressure compared with controls (all P values <0.05). Among the patients with AMI, the aHGL group, as compared with the aNGL group, had a higher prevalence of diabetes and single-vessel disease, as well as higher usage of insulin, biguanides, and sulfonylureas (all P values <0.05). Hemoglobin A1c (HbA1C) and peak troponin were significantly higher in the aHGL group than in the aNGL group (both P values <0.05). There was no significant difference in time from AMI onset to cardiovascular magnetic resonance (CMR) between the aNGL (median 4.00, IQR, 3.00–5.00) and aHGL group (median 4.00, IQR, 2.00–5.00) (P=0.118).

Comparison of cardiac MRI indicators between the patients with AMI and controls

For LA structure and function, both patients with AMI with aNGL and aHGL showed significantly increased LAVI (LAVIpre-a and LAVImin), decreased LAEF (LATEF, LAPEF and LAAEF), decreased LA strain (εs, εe and εa), and decreased LA strain rate (SRs, SRe, and SRa) as compared with controls (all P values <0.05) (Table 2). Patients with AMI were divided into a group without (n=102) and a group with (n=106) LA enlargement [LAE; defined as LAVImax >55 mL/m² (26)]. Patients with LAE showed significantly decreased LAEF and LA strains in all three phases compared with controls (all P values <0.001). For patients without LAE, LA reservoir (LATEF and εs) and conduit (LAPEF and εe) function were also significantly decreased (all P values <0.05) (Figure 2).

Figure 2 Comparison of LA function between controls, patients with AMI without LAE, and patients with AMI with LAE. LATEF, left atrial total emptying fraction; LAPEF, left atrial passive emptying fraction; LAAEF, left atrial active emptying fraction; εs, reservoir strain; εe, conduit strain; εa, booster strain; LAE, left atrial enlargement; LA, left atrial; AMI, acute myocardial infarction.

For LV structure and function, patients with AMI, regardless of glucose status, had significantly increased LVEDVI, LVESVI, and LVMI but significantly decreased LVSVI, LVEF, LV GRS, LV GCS, and LV GLS as compared to controls (all P values <0.05).

Comparison of cardiac MRI indicators between hyperglycemic and normoglycemic patients

Compared with the aNGL group, the aHGL group had significantly decreased εs [median 19.19 (IQR, 15.98–27.44) vs. 27.04 (IQR, 16.33–36.85); P=0.003] and εe [median 9.50 (IQR, 6.18–13.40) vs. 13.98 (IQR, 7.06–20.58); P=0.002]; however, aHGL had an approximately 16%, decreased εa [median 10.20 (IQR, 6.62–14.32) vs. 12.15 (6.40–16.83); P=0.097], but this difference did not reach the statistical significance. LA strain rate did not differ between the two groups (all P values >0.05). In addition, the aHGL group, as compared with the aNGL group, showed significantly decreased GRS [median 18.88 (IQR, 11.65–28.08) vs. 26.80 (IQR, 17.61–36.17); P=0.002], GCS (−10.92±4.07 vs. −12.49±4.45; P=0.005), and GLS (median −8.55±3.68 vs. −10.39±3.65; P<0.001). Infarct size was significantly increased in the aHGL group compared with the aNGL group (30.74±15.06 vs. 25.36±15.66; P=0.014).

Associations between aBGL and LA phasic strains in patients with AMI

In patients with AMI, aBGL was significantly correlated with εs (r=−0.239; P<0.001) and εe (r=−0.272; P<0.001) (Figure 3). Univariate analysis showed that aBGL was significantly associated with εs (β=−0.239; P=0.001) and εe (β=−0.272; P<0.001) (Table 3). After adjustments were made for confounding clinical factors (Model 1), the significant associations between aBGL and εs (β=−0.211; P=0.002) and εe (β=−0.215; P=0.001) remained. Results regarding the relationship between aBGL, infarct size, and LV strain are shown in Figure S2 and Table S1.

Figure 3 Correlations between aBGL and LA (A) reservoir and (B) conduit strain. εs, reservoir strain; εe, conduit strain; aBGL, admission blood glucose level; LA, left atrial.

Correlations between LV global strain and LA phasic strains in patients with AMI

As shown in Figure 4, LV global strains (GRS, GCS, and GLS) were significantly correlated with εs and εe (all P values <0.001). Univariate analysis showed that GRS, GCS, and GLS were significantly associated with εs (GRS: β=0.424, P<0.001; GCS: β=−0.436, P<0.001; GLS: β=−0.484, P<0.001) and εe (GRS: β=0.434, P<0.001; GCS: β=−0.442, P<0.001; GLS: β=−0.512, P<0.001). After cardiac MRI indicators were introduced into the multivariate regression models (Model 2), only GLS demonstrated significant associations with εs (β=−0.467; P<0.001) and εe (β=−0.455; P<0.001).

Figure 4 Interaction between LV global strain and LA strain. (A1-A3) Linear regression analysis of GRS, GCS, GLS, and εs. (B1-B3) Linear regression analysis of GRS, GCS, GLS, and εe. GRS, global radial strain; GCS, global circumferential strain; GLS, global longitudinal strain; εs, reservoir strain; εe, conduit strain.

Reproducibility

Cardiac MRI-derived LA structure and function indicators showed excellent intra- and interobserver reproducibility (all ICCs >0.9). The ICCs for LAVI, LAEF, and LA phasic strain are summarized in Table 4.

Discussion

This study adds knowledge to the existing literature on LA functional differences in patients with AMI with and without hyperglycemia and that on atrioventricular coupling in patients following AMI. Our data revealed the following: (I) compared with controls, LA function was decreased in patients with AMI, even those with normal LA volume. (II) Among patients with AMI, LA dysfunction was worse in hyperglycemic individuals, and aBGL was an independent factor correlated with LA strains. (III) LV global strain was correlated with LA phasic strain in patients with AMI, most notably LV longitudinal strain.

LA phasic dysfunction in AMI

The operation of the left atrium is marked by three phases (25). During the LA reservoir phase, the myocytes in the left atrium stretches to receive blood via the pulmonary veins, which typically represents LA compliance. In the subsequent conduit phase, blood streams divert passively into the left ventricle from the left atrium. In the final booster pump phase, the LA contracts actively to pump blood into the left ventricle, which represents the inherent contractility of the LA myocardium. In agreement with previous studies that evaluated LA structure and function using echocardiography and cardiac MRI (12-14), the cardiac MRI results in this study revealed phasic LA morphological and functional abnormalities in patients with AMI. Atrial damage in myocardial infarction has mainly been considered to be a secondary event of ventricular dysfunction since ischemic injury primarily affects the ventricles. The systemic effects during myocardial infarction, such as increased activation of the sympathetic nervous system and of inflammatory pathways, also damage the atrium. Moreover, direct hypoxic damage caused by the concomitant atrial infarctions (incidence 0.7−42%), which lead to atrial structural changes and dysfunction, cannot be ignored (27).

In addition, we found that LAEF and LA longitudinal strains of all three phases were significantly reduced, even in patients with AMI with normal LA size. This suggests that functional changes in AMI may precede morphological alterations. LA functional indicators can detect LA remodeling with sensitivity and is superior to morphological indicators. Therefore, in the management of patients with AMI, even those with normal LA size, close attention should be paid to the indicators of LA function, including LAEF and LA strains.

Hyperglycemia aggravated LA dysfunction in patients with AMI

It has been reported that 29–38% of patients with AMI also have admission stress hyperglycemia (28,29). Hyperglycemic patients with AMI have an increased mortality compared with normoglycemic ones (28). Additionally, this negative association also exists for cardiovascular complications. In our results, LA strains were significantly reduced in hyperglycemic patients with AMI as compared with those with normoglycemia, and aBGL was an independent determinant of LA strains. Stress hyperglycemia has been shown to induce LV dysfunction through multiple pathways such as increased infarct size and compromise myocardial perfusion (23,30-32), which may lead to the reduction of the atrial function given the tight relationship between LV and LA (33,34). In addition, the cardiotoxic effects of stress hyperglycemia, which includes endothelial function, oxidative stress, production of leukocyte adhesion molecules, platelet aggregation, and activation of the coagulation cascade, may directly impact the LA myocardium (27,30,32). Hyperglycemia can lead to elevated LA pressure, which may contribute to diastolic dysfunction and increased risk of atrial fibrillation in patients with AMI (35). Our results also showed that hyperglycemic patients with AMI showed significantly decreased LA strain as compared with normoglycemic patients, although LAEF was not significantly different. This may reflect the higher sensitivity of cardiac MRI feature tracking for detecting myocardial dysfunction, which helps in the early identification and early optimization of treatment. Additionally, in our study, only 42.0% of hyperglycemic patients were identified as diabetic, which aligns with previous research suggesting that hyperglycemia should be considered an additional risk factor (36).

Furthermore, when AMI was combined with hyperglycemia, LA reservoir and conduit strains decreased significantly, whereas LA booster strain decreased slightly. LA reservoir function reflects the LA filling during LV systole, and the reduction of LA reservoir strain may indicate marked impairment of atrial compensatory capacity for hyperglycemic patients with AMI (37). Previous studies have demonstrated that different degrees of LV diastolic dysfunction can influence the different phases of LA function. In patients with mild LV diastolic dysfunction, LA conduit function is impaired, and LA pump booster function is enhanced to compensate for a deceased LA emptying volume (38,39). This mechanism no longer operates when the severity of diastolic dysfunction increases (39). An echocardiography study (40) reported strong correlations between LV diastolic function and LA conduit and reservoir function, but not with LA booster function, which is consistent with our results. Therefore, our findings suggest that LA booster function may not be a good metric of LA functional capacity.

Atrioventricular coupling in patients following AMI

We further found that LA function injury is associated with LV dysfunction in patients with AMI, and there were correlations between LA and LV strains, especially GLS. Longitudinal myocardial movement is essential to the contraction of the left ventricle (33). During systole, contraction of the longitudinal myocardial fiber of the left ventricle results in the longitudinal stretching of the LA. Interestingly, when LV strains were introduced into the regression models, the correlations between aBGL and LA strains were lost. This might be because of the strong mechanical connection between the atrium and ventricle (20). Thus, clinicians should not only monitor glucose level but also cardiac function indicators in patients with AMI.

Limitations

There were certain limitations to this study which should be acknowledged. First, we employed a single-center study, and thus selection bias could not be avoided. Second, our analysis of LA deformation was limited to longitudinal strains because the reproducibility of the radial strain is poor (41). Third, the dynamic changes of glucose level were not monitored. Further studies will be conducted to investigate the impact of glycemic control and dynamic changes in blood glucose on subclinical cardiac dysfunction. Finally, several factors affect cardiac structure and function in patients with AMI, including gender (42), hypertension (43), and obesity (44). As they would require many studies to examine, we will stratify them individually in future research.

Conclusions

LA reservoir, conduit, and booster pump functions were found to be compromised in patients with AMI, even in those with normal LA size. Hyperglycemia aggravated the impairment of LA reservoir and conduit functions in patients with AMI. aBGL and GLS were independent factors associated with LA reservoir and conduit strains. Therefore, in patients with AMI with admission stress hyperglycemia, both the monitoring of glucose levels and cardiac function is necessary.

Acknowledgments

None.

Footnote

Reporting Checklist: The authors have completed the STROBE reporting checklist. Available at https://qims.amegroups.com/article/view/10.21037/qims-24-1757/rc

Funding: This work was supported by the National Natural Science Foundation of China (No. 82371925); the National Key Research and Development Program of China (Nos. 2020YFB1711500 and 2020YFB1711503); the 1·3·5 Project for Disciplines of Excellence, West China Hospital, Sichuan University (Nos. ZYYC21004 and ZYGD23019); and the Sichuan Province Science and Technology Support Program (Nos. 2022NSFSC0828 and 2024NSFSC1788).

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://qims.amegroups.com/article/view/10.21037/qims-24-1757/coif). The authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. This study was conducted in accordance with the Declaration of Helsinki (as revised in 2013) and was approved by the Biomedical Research Ethics Committee of the West China hospital of Sichuan University (approval No. 2019-756). The requirement for individual consent was waived due to the retrospective nature of the analysis.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

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